8340210073 
NATIONAL LIBRARY
NLM  0D55Tb07  b
NLM005596076 
 
 
 
 
A  TREATISE
ON
NERVOUS AND  MENTAL DISEASES,
FOR STUDENTS AND PRACTITIONERS OF MEDICINE.
                          BY


        LANDON CARTER  GRAY, A.M.,  M.D.,
                            ■flT"
PROFESSOR OF NERVOUS AND MENTAL DISEASES IN THE NEW YORK POLYCLINIC ; VISITING PHYSICIAN
  TO ST. MARY'S HOSPITAL;  NEUROLOGIST TO THE HOSPITAL FOR RUPTURED AND CRIPPLED;
    EX-PRESIDENT OF THE AMERICAN NEUROLOGICAL ASSOCIATION ; EX-PRESIDENT OF THE
      NEW YORK NEUROLOGICAL SOCIETY; EX-PRESIDENT OF THE NEUROLOGICAL
       SECTION OF THE NEW YORK ACADEMY OF MEDICINE ; EX-PRESIDENT OF
         THE SOCIETY OF MEDICAL JURISPRUDENCE; HONORARY MEMBER
           OF THE MEDICAL SOCIETY OF THE DISTRICT OF COLUMBIA |
             FELLOW OF  THE ACADEMY OF MEDICINE; MEMBER
              OF THE NEW YORK COUNTY MEDICAL SOCIETY J
                NON-RESIDENT MEMBER OF THE KINGS
                  COUNTY MEDICAL SOCIETY, ETC.
SECOND  EDITION, REVISED AND ENLARGED.
WITH 172 ILLUSTRATIONS AND 3 COLORED PLATES.
       PHILADELPHIA:
LEA  BROTHERS  & CO.
             1895. 
Gnu
m
5
 Entered according to the Act of Congress, in the year 1895, by
                LEA BROTHERS  <fe CO.,
In the Office of the Librarian of Congress.  All rights reserved.
   PHILADELPHIA :
DOR NAN, PRINTER. 
PREFACE TO  THE  SECOND  EDITION.
  The very kind reception accorded the first edition of this work  has
been a pleasant stimulus in my endeavor to make the present issue still
more  acceptable to students and practitioners.  With this purpose in
view,  I have subjected the book to much alteration.  Every portion has
been  carefully revised and five new chapters  have been  added,  viz.,
those  on  Dementia, Dementia Paranoides, Confusional  Insanity, De-
lirium, and Massage.   The Anatomical Introduction has been entirely
rewritten  in response  to many requests for a more  detailed description
of this subject, and also in view of the fact that our knowledge of cere-
bral and spinal architecture has been literally revolutionized in the last
few years.   In the chapter on Paralytic Dementia the pathological por-
tion has  been  rewritten to  conform with the newer views  that are based
partly upon the discoveries of Golgi and Cajal in cerebral histology,
and partly upon our wider knowledge of textural stains.  The chapter
dealing with Palmus  is almost new,  and details my further experience
with this disease.
   Believing most  thoroughly in medicine as a practical  science, I have
endeavored to mould this work  so  as  to equip  its readers  with the
knowledge necessary  to the  recognition  and the most  efficacious treat-
ment of  the diseases  embraced in its title.  The therapeutical sections
were  developed, with full detail, in the first  edition, and they have
been  enlarged wherever advisable in the present issue.   In every case I
have  recommended only those procedures which  have been tested by
experience. The word " treatment" has been construed in the broadest
sense to include not only medicinal and  non-medicinal agents, but  also
those hygienic and dietetic  measures which are often the physician's
best reliance.
   I have deemed myself sufficiently familiar with the uses and abuses of
Massage to devote a short chapter to the  subject; but I have not treated
of  Hydrotherapy  in  its applications  to nervous  and  mental disease
because I am not yet  convinced either that it  is practicable outside of 
iv
PREFACE.
a few large cities, or that it has more value than  mere cleanliness.  To
obtain space for these additions and alterations without expanding  the
volume  beyond the  size best adapted to the  student  and physician, I
have reluctantly omitted the bibliographical  references, solacing myself
with the thought that those possessing or having access to the first edi-
tion could readily obtain in the various annuals the literature of the two
years which have  intervened since its publication.   The  Glossary  has
been enlarged, in response  to  a  general  demand; and the Index  has
been made  more  complete.   The  series of  illustrations  has  likewise
undergone  thorough revision.  A comparison of the new edition with
the first issue  will show that many of the excellent engravings in  the
original have  been completely re-executed in order to  secure  greater
mechanical  perfection  in detail.   All the cuts  have been scrutinized,
many have been redrawn, others altered,  and  I have added considerably
to their number.   The three  colored plates which have been intro-
duced in this  edition will elucidate important facts in neural anatomy,
physiology,  and localization  with a clearness unattainable with black
alone.
                                                        L. C.  G.
  6 East  Forty-ninth Street, New York,
          September, 1895. 
PREFACE TO  THE  FIRST  EDITION.
  This book is an endeavor  to put a working knowledge of nervous
and  mental diseases into  the  hands of students and practitioners.  A
mere compilation, even of an encyclopaedia, would have been compara-
tively  an easy task, calling only for a judicious aggregation of material.
In contradistinction,  the  purpose and limits of a treatise require the
selection and clinical verification  of facts, and to this  most  important
element of my work  the  leisure of seven years has  been devoted, only
one  of which,  however, has been  required  for the actual composition.
A teacher must know what to omit,  as the force and permanence of his
teachings will depend upon his strict avoidance of non-essentials.  Super-
fluous  knowledge, like surplus food,  may clog the  activity of the mind,
and  in no department of  medical science is the temptation to expansion
and  speculation more enticing than in neurology.  Keenly appreciating
the patient toil of the scientists to whom we owe most of our knowledge,
I have held the task of the physician in yet higher esteem, as the latter
must make utilitarian application of all the facts collected by the former.
There  can be no loftier aim in medicine than the relief of human suffer-
ing,  and to this end I have endeavored to  glean from the many depart-
ments  of medical science what they could contribute.  Whether Ameri-
cans are more prone to nervous disease than other races, or whether it
is that our democratic principles set a higher value upon the individual,
his  comfort and health, than is customary elsewhere, it  is yet  certain
that Europeans, in investigating disease, regard the patient simply as its
vehicle, whilst Americans go  one  step further, and  deem  the cure all-
essential.
  Moulded by this conviction, this volume is addressed especially to the
general practitioner,  present or future, and its theme  is rigidly thera-
peutical.  Medical Nihilism is an error of youth and a confession of im-
potence, for Nature rarely afflicts  man beyond the hope of relief.  The
therapeutist has enormous resources.   Not only does the physical world
provide a great variety of medicinal  substances, and transmute its forces
to suit his will,  but likewise the psychical world is bounteous in its aid.
Far  from spurning his inheritance, the ideal physician should gather his
knowledge of disease and  its antagonists from every quarter, and  exert
every faculty for his  patient's welfare, which is his  own true success.
  Those who may use this work will  find that it  does  not assume pre-
vious knowledge of its subjects on their part.   The Anatomical Intro-
duction makes plain  all the facts of structure necessary to a comprehen-
sion  of nervous disease.   The Electrical Chapter is  entirely practical,
even in the details of selection and use of batteries.  The space assigned
to the several  diseases is  determined by the needs of the profession  at 
vi
PREFACE.
large, a consideration which has made the chapter on Neurasthenia the
largest in the book.   If apparently undue space is  devoted to Syringo-
myelia, Acromegaly, and Myxoedema, this is owing to the general inter-
est in these new types, coupled with the lack of information  apt to be
shown about them even by specialists.  Mental diseases are considered
from the standpoint  of the general physician, since the  outcome will
often depend on  his skill in early recognition and treatment.  I have
endeavored to indicate what diseases of the mind may be best treated at
home, what may need both home and asylum treatment, and the period
of committal, and what may  require seclusion from  the outset.  The
incontrovertible fact  has been generally  ignored that mental diseases,
like  hepatitis or nephritis,  are affections of a viscus, and  the result has
been a specialty within a  specialty, and  the relative  disregard  of the
usefulness of the general practitioner. A novel feature in a work of this
kind is the inclusion of the medico-legal aspects of nervous and mental
diseases.  I have presented this subject from the standpoint not of the
lawyer but of the physician;  and furthermore, have  endeavored to
qualify the reader as a medical judge of  both  sides of the questions at
issue, a  faculty of much greater value than an  ability  limited  to the
mastery of  only one side in the capacity of a medical advocate.
  In carrying out the therapeutic  aim of the book, each chapter has
been made to contain its own section on treatment.  Especial  care has
been taken to  make  the therapeutical suggestions sufficiently detailed
and  precise to cover the varying stages, symptoms, and complications of
disease, as well  as to follow the important indications afforded by differ-
ential diagnosis.   In the  chapters upon Mental Diseases  the most ap-
proved treatment is stated, and likewise the results to be expected. Only
that knowledge has  been admitted to these pages which has stood the
test of experience.
  Students will find the terminology rendered easy of acquisition by the
derivations and definitions given in the Glossary.   Throughout she
volume  simple  Anglo-Saxon  terms  and familiar synonyms have been
preferred.  The limits of the  book have  rendered necessary a certain
degree of terseness, but those who are  desirous of further  investigation
will  find a full bibliography appended  to each chapter.    I have made
liberal use of illustrations,  deeming  them essential  for explanation and
vividness.  They are largely  original, being mostly  made from speci-
mens and photographs.
  Many willing hands of kind friends have aided me in the great, often
harassing labor of this book.   To Dr.  R.  S. Newton I am indebted  for
several sections and brain specimens,  and a photograph  of a  case of
acromegaly.  Dr. W. B.  Pritchard assisted in the  preparation of a
tabulated statement of clinic cases.   Dr. R. C. F. Coombes kindly fur-
nished me with photographic portraits of typical  cases of insanity.
 6 East Forty-ninth Street, New York,
         November, 1892. 
CONTENTS.
                           PART  I.

                        INTRODUCTORY.

                           CHAPTER I.

Anatomical Introduction.  The Bloodvessels of the Cerebrum, Cere-
      bellum, Pons, and Medulla Oblongata—Cranial Topography—
      Heat-centres..........17-104

                           CHAPTER II.

Electricity.   The Faradic, or Faradaic, or Induction  Current—Static
      Electricity—Galvanic Batteries—Faradic Batteries—Stationary
      Batteries—Milliamperemeters and Rheostats—Wires and Elec-
      trode of Galvanic and Faradic  Batteries—Method of Applying
      the Batteries—The Diagnostic Uses of Electricity—Chart of the
      Motor Points of the Different Regions of the Body .    .    .  105-134

                          CHAPTER III.
Massage............135-137
                           PART  II.

                      NERVOUS DISEASES.

                           CHAPTER I.

Localization  of Lesions  in  the  Cerebrum, Cerebellum, and
      Spinal  Cord.  Localization of Cortical  Lesions—The  Motor
      Area—Cortical  Centre  of  Vision—Cortical Centre of Word-
      blindness—Centre of  Word-deafness—Centre  of  Agraphia—
      Cortical  Centre  of Aphasia—The Centres  of  Mind  Alone-
      Lesions of the Centrum Ovale—Lesions of the Internal Capsule
      —Lesions of the Corpus Striatum and Optic Thalamus—Lesions
      of the Quadrigeminal Bodies—Lesions of the Pons—Lesions of
      the  Medulla  Oblongata—Lesions of the Cerebellum  and  its
      Peduncles—Lesions of the Spinal Cord—Lesions of the Periph-
      eral Nerves—Hemianopsia.......135-153 
viii
CONTENTS.
                          CHAPTER II.
                                                              PAGES
Tests of the General Motor and Sensory Symptoms of  the
      Nervous System.   Sight—Hearing—Smell—Taste—Touch or
      Tact—Pain—Muscular  Sense—Temperature sense—Weight—
      The Tendon-reflexes—Cutaneous Reflexes—Contracture—Para-
      doxical Muscular Contraction—Muscular Inco-ordination—Mus-
      cular Strength—Cerebral Thermometry.....154-177

                         CHAPTER  III.

Diseases of the Peripheral Nerves.  Neuralgia—Neuralgia of the
      Head—Neuralgias of the Trunk and  Neck—Neuralgias of the
      Upper Extremities—Neuralgia of the Lower  Extremities—Vis-
      ceral Neuralgias—Simple  Neuritis—Multiple Neuritis—Facial
      Paralysis—Neuroma.........178-212

                         CHAPTER  IV.

Diseases of the Spinal Cord and  Medulla Oblongata.  Mye-
      litis—Myelitis of the Anterior Horns—Landry's  Paralysis—
      Spinal  Hemorrhage—Divers'  Paralysis, or  Caisson Disease—
      Progressive  Muscular Atrophy—Locomotor  Ataxia—Primary
      Lateral  Sclerosis—Amyotrophic Lateral Sclerosis—The Com-
      bined Scleroses of the Cord—Syringomyelias—Morvan's Disease
      —Tumors of the Spinal Cord—Traumata of  the Cord—Glosso-
      labio-laryngeal Paralysis—Progressive Ophthalmoplegia    . 213-298

                          CHAPTER V.

Neuro-muscular or  Muscular Diseases.  Pseudo-muscular  Hy-
      pertrophy—Thomsen's Disease......299-305

                         CHAPTER  VI.

Intracranial Hemorrhage, Embolism, and Thrombosis.    . 306-314

                         CHAPTER  VII.

Disf.ases  of  the Cerebrum.   Cerebral  Palsies of  Childhood—In-
      tracranial Growths—Hydrocephalus — Huntington's Chorea—
      Athetosis...........315-353

                         CHAPTER VIII.

Diseases  of   the Cerebro-spinal Nervous  System  and its
      Membranes. Hypersemia and Anaemia of the Brain and Cord
      —Thrombosis of the Intracranial Sinuses—Suppurative Menin-
      gitis—Cerebro-spinal Meningitis—Tubercular Meningitis—Cere-
      bral Abscess—Syphilis of the Nervous System—Disseminated
      Sclerosis—Lead-poisoning.......354-396 
CONTENTS.
IX
                        CHAPTER IX.
                                                          PAGES
The Neuroses. Epilepsy—Migraine—Chorea—Palmus (the Twitches)
     —Paramyoclonus  Multiplex—Saltatoric  Spasm—Wry-neck—
     Hysteria — Hypochondria — Neurasthenia — Occupation - neu-
     roses............. 397-472
                         CHAPTER X.
Nervous Diseases of Probably Microbic Origin. Tetanus—
     Tetany—Hydrophobia, or Rabies—Diphtheritic Paralysis   . 473-492
                        CHAPTER XI.
Certain Nervous Symptoms Common to Different Diseases.
     Vertigo—Headache—Insomnia—Coma.....493-508
                        CHAPTER  XII.
Somnambulism and Allied Disorders.  Somnambulism—Ecstasy,
     or Trance—Catalepsy—Night-terrors—Hypnotism .   .   . 509-518
                       CHAPTER XIII.
Diseases of Unknown Pathology.  Facial Hemiatrophy
     Agitans—Astasia-abasia......
                       CHAPTER XIV.
Reflex Nervous Disorders......
                        CHAPTER  XV.
Meniere's Disease........
                       CHAPTER XVI.
Friedreich's Disease.......
                       CHAPTER XVII.
Myxedema.......
                       CHAPTER XVIII
Acromegaly   .......
                       CHAPTER XIX.
Exophthalmic Goitre.....
                        CHAPTER  XX.
Diseases of  the Sympathetic Nervous System            . 563-565
—Paralysis
      .  519-530
. 531-537
538-544
. 545-549
550-554
. 555-559
. 560-562 
X
CONTENTS.
                      CHAPTER XXI.
                                                       PAGES
Alcoholism and Morphiomania.......566-572

                     CHAPTER XXII.
Railway Injuries and other Traumatic Diseases of  Medico-
     legal Interest..........573-584 r
                       PART III.
                     MENTAL DISEASES.
                        CHAPTER I.
 Classification of Insanity  ....
                        CHAPTER II.
 Delusions, Hallucinations, and Illusions
                       CHAPTER III.
 Morbid Fears and Impulses
                      . CHAPTER IV.
 Sexual Perversion.....
                        CHAPTER V.
 Simulation of Insanity.....
                       CHAPTER VI.
 The Pathology of Insanity ....
                       CHAPTER VII.
 Melancholia.......
                      CHAPTER VIII.
 Mania.......
                       CHAPTER IX.
Katatonia.......
                       CHAPTER X.
Periodical Insanity    .   .    .    .
. 586-588
. 589-592
593-597
. 598-599


. 600-607
. 608-619'
. 620-623
• 624-626
,97. 
CONTEXTS.
XI
                        CHAPTER XI.
                                                         PAGES
Furor Transitorius.........631
                        CHAPTER XII.
Epileptic Insanity..........632-637
                       CHAPTER XIII.
Delirium Grave..........638-639
                       CHAPTER XIV.
Hallucinatory Insanity    .    .       .....640-642
                        CHAPTER XV.
Dementia.   Primary Dementia—Hebephrenia—Senile Dementia-
      Dementia, or  Mental Exhaustion in the Convalescence from
      Curable Insanity—Terminal Dementia.....643-655
                        CHAPTER XVI.
Confusional Insanity.........656
                       CHAPTER XVII.
Paranoia............657-665
                       CHAPTER XVIII.
Paralytic Dementia.........666-682
                        CHAPTER XIX.
Dementia Paranoides.........683-684
                        CHAPTER XX.
 Delirium............685-688
                        CHAPTER XXI.
 Idiocy     ............ 689-690
Glossary. .
691 
 
              PART  I.

INTRODUCTORY.
                     CHAPTER  I.

                ANATOMICAL  INTRODUCTION.

  It is not  my intention  to write a text-book upon the anatomy of
the nervous  svstem.  My  purpose is only to make clear such facts
as may be necessary to  an  intelligent comprehension of the clinical
phenomena of nervous and  mental  disease;  and in carrying out
this purpose  I shall not dwell upon abstruse matters that the future
may show  to be of great  value, but  shall rather confine my atten-
tion  to the living issues of the day.
  The nerve-cell is the essential  element in nervous disease.   In it
go on all the peculiar molecular processes which endow the nervous
system with  individuality.   It is the very inner citadel of nervous
life.   To it all the other textures are subsidiary.  It is nourished by
the arterioles and lymphatics, drained by the venules, upheld by the
connective tissue.   These cells of the nervous tissue have been very
imperfectly  known until  the last few  years,  when  the wondrous
stain first suggested by  Golgi made it possible for us to see into this
hitherto hidden realm  as  no histologist had ever seen before. ^ It
was  iu 1886  that the Italian author described a method of coloring
nerve-cells and their processes  with  the bichromate  of silver,  by
placing them in a nitrate of silver  solution  after they  had been
hardened in  bichromate of potash.  In this way the cells and their
processes are outlined as distinctly as in an etching.  To obviate the
difficulty of  following these processes through the huge sections that
were made necessary by the size of the  human  brain, the genius of
Cajal hit upon the device of employing  the  brains of such small
animals as the frog, the mouse, the rat,  and the guinea-pig; and the
results thus obtained, although met at first with the usual contradic-
tion  that seems to be the fate of all original observations, were soon
confirmed at every hand.  The  result  has been that the last few
years have brought to  our knowledge more exactness in regard to
the histology of the nervous system than all the preceding countless
centuries of time.   Dictum after dictum has been ruthlessly brushed
aside, purblind theory  after purblind  theory has  shrunk  to  mere
nothingness  in the blaze of the  light of  truth that has so suddenly
                                2 
18
INTRODUCTORY.
come upon us;  and, indeed, it is almost with a blush of shame that
a neurologist, reading the latest work of Cajal, sits at the feet of this
one man, who, with bis followers, has penetrated one of the mysteries
of the ages.   It had long been known, from the time of Deiters and
Wagner, that each nerve-cell had two sets of processes—namely, one
known as the axis-cylinder process, supposed to be straight and un-
branching, and  the others known as the protoplasmic processes, which
break up into numerous branches soon after leaving the body of the cell.
The axis-cylinder process becomes  continuous with the axis-cylinder
of a nerve.   The nature of the protoplasmic processes was unknown,
some investigators maintaining that they served to connect the cells
with one another, whilst others claimed that they split into very fine
nerve-fibres,  these ultimately serving the  same purpose as the axis-
cylinder processes.   In this  condition  our knowledge  remained
stationary for several  decades, until Golgi  demonstrated that the
axis-cylinder process was not straight and  unbranching, but that it
really gave off a number of very fine collaterals, and that the proto-
plasmic expansions, instead of forming a fine network, terminated in
free extremities, after having given off numerous branches in their
course.  He  maintained that the  axis-cylinders passed  into a net-
work formed by the intermeshing  of their collaterals.   Cajal, how-
ever, has  shown that the axis-cylinder  processes all terminate in a
free end, making connection with the terminal structure by contiguity,
and not, as has been hitherto supposed, by continuity;  and that the
function of the protoplasmic processes is, in all probability, to con-
duct the nervous current into the cell.   The nervous current, there-
fore, flows out of the cell through  the axis-cylinder processes, and
into the cell  through the protoplasmic ones, being cellulifugal in the
former  and  cellulipetal in  the Jatter.   Waldeyer has suggested the
word " neuron " for the nervous unit that is composed of the nerve-
cell, the axis-cylinder and its collaterals, and the protoplasmic pro-
cess and its collaterals;  and it is probably the  patness of this term
that has caused it  to  be almost universally adopted.   The nervous
system  is  made up of such  neurons.   By means of them the  cell,
couched far  back in the screened depths of the nervous organs, is
brought into  direct  and material communication with such far-away
tissues as the skin, the muscles, the eye, the ear, the tongue, and the
other organs  to which nerves go.   If this distant tissue be intended
for the reception of impressious—as is the skin, for example—the
impression can travel  inward  to  the cell along these protoplasmic
processes.   If the tissue be a motor  one, as,  for instance, the muscle,
the cell can  make  it  contract by means of the axis-cylinder  pro-
cesses and their  collaterals.  These processes are,  as  it were, pro-
longations of the  nerve-cell into  the different motor and  sensory
tissues of  the body ; and the motor  and sensory tissues of the bodv
are in their turn, so to speak, peripheral appendages of the nerve-cell.
The cells  are mainly contained  in the gray matter,  whilst the axis-
cylinder processes or nerves run in bundles in what is known as the
white matter.  The physiological  study of  the nervous system con-
sists, therefore, in ascertaining what the functions are of the different 
ANATOMY.
19
masses of  gray matter or cells, or,  if this is  not possible,  of the
nerves or white matter.  In  other words, the cells  collected  in  the
gray matter are the ones that endow the nerves with their different
functions, and we may ascertain what these latter are either by means
of experiment upon the gray matter  or upon the nerves leading to
and  from  the  gray matter.   The complexity  of  function  of  the
nervous  system is due  to the great variety of these cells, and its
complexity of structure depends  upon  the varying topography,
according  to the needs  of the human economy, of  the masses in
which these cells and nerves  lie.  It  must  always be borne in mind,
however, that a nerve must take its origin from a cell, and  that this
cell  generally  lies  in a  mass of gray matter.   We can  therefore
understand why it  is that the  brain  and spinal cord are made up of
masses of gray matter, or cells, which are connected by means of the
nerves, or  white matter.   The chief  of these masses of gray  matter
are to be found in  the cortex of the  cerebrum  and the cerebellum,
their basal ganglia, in the horns of the spinal cord and in the nuclei
of the cord, or upper enlarged  end  of the cord,  which is known as
the  medulla oblongata  or oblong  spinal cord.   We  have painfully
gained our knowledge of the structure and functions of the nervous
system by numerous methods,  as follows:
   1.  Stilling  first  suggested the method of Continuous Sections, as,
for instance, of the spinal cord, so that the course of certain  nerves
and their relation to certain  cells could be  fairly traced.
   2. The  Coloring method, due to Gerlach,  was based upon the law
that  certain  chemical reagents and  coloring matters would affect
only certain  tissues, such as the cells and nerve-fibres, whilst the
other textures  would be either slightly affected,  or not at  all.
   3. The  Comparative Anatomy method, used with so much  success
by Meynert and his scholars, owes its value to the fact that in many
animals  the development of peripheral organs is proportional  to that
of their  central structures from which the  nerves of the former have
taken their origin.  This procedure has also the incidental value of
making  plainer the structure of the cerebrum  of higher  mammals,
by comparison with the less  complicated brains of those lower in the
series.
   4. The  Embryological or Developmental method has attained some
 brilliant results at the hands of Flechsig and  his scholars.  It
derives its value from the fact that the nerve-fibres of different por-
tions  of the  nervous system  take  on their covering of myelin at
different periods of foetal life, so that this medullary covering may
extend through a whole system of fibres, marking them  out  clearly
to the eye, whilst neighboring systems are as yet  unmedullated.
   5. Gudden employed the  Atrophic method, which is really one of
an arrest of development, proceeding upon  the assumption that cer-
tain  portions  of the  nervous system will remain in an  incomplete,
almost  fcetal  stage of development, when the central organs  from
which they receive their nerve-fibres are destroyed.  By this  method
different portions  or centres of the  brain  were  artificially injured or
destroyed in young animals, and then  the degenerative lesions were 
20
INTRODUCTORY.
traced  from the point of destruction, thus mapping out  the tract of
nerve-fibres which had begun there.   It has been found, however,
that this  method  is only of positive value, and  not  of negative—
i. e., we can only deduce  the  relationship  between two parts of the
nervous system when destruction of one leads to lesion of the other;
but we cannot, on  the  other  hand, deny such  connection  when
destruction of the one does not affect the other.
  6. Occasionally a Congenital Arrest of Development, or Malforma-
tion, has thrown great  light upon  the function of some  part of the
nervous system.
  7. The  Pathological Anatomical  method, or  that  of secondary
degeneration, first instituted by Tiirck, has been of very considerable
value,  and it rests  upon the belief that the structural integrity of a
nerve-fibre depends upon the structural  integrity of the nerve-cell
from which it takes its origin, so that lesion of the latter  induces a
degeneration of the former.
  8. The  Physiological method, or that  of Vivisection, consists in
irritation (as by electricity) of certain centres of the brain, cord, or
cerebellum, or "of destruction  of them (as by section), with a  corre-
sponding excitation or  paralysis of the nerve-fibres  proceeding  from
the irritated or destroyed parts.  This method  has given us some of
our most valuable  knowledge of the nervous system.
  9. The  Pathological Physiological method is that whereby patho-
logical lesions demonstrably destroy the function of certain parts of
the nervous system, and enable us to draw conclusions  as to the
physiology of the parts that have been injured.
  It is difficult to estimate which  one of these methods  has been of
the most value.  Suffice it to say, that from these various sources we
have gained our knowledge of the anatomy of the nervous system,
upon whose main  features I now propose to  dwell, so  far as they
are of  clinical value.
  We  will  begin  with  the  spinal cord.  In  its study I shall not
dwell upon the points  of anatomy that are familiar to every medical
student, such  as the  fact  that the  gray matter is disposed in  the
form of horns, those looking toward the belly, or ventrad, being the
anterior horns or cornu, and  those looking toward the vertebrae, or
dorsad, being the  sensory  or posterior  horns; whilst outside  these
horns  or cornu of  gray matter  are  grouped the nerve-fibres consti-
tuting  the  so-called white matter.  As a matter of fact, therefore,
the spinal cord consists in the main of a mass of nerve-fibres or white
matter, enclosing  the  gray matter, or  cornua.  Each one of these
nerves in  the white matter is the conductor of some nerve impulse
or function.   To know what this  functiou is has  been  the painful
and eager study of neurologists, according to the various methods
that have been just enumerated.
   Fig. 1 is a diagram of the spinal cord, according  to the knowledge
that we possessed  until a very recent period,  and  shows the motor
columns outlined  in white,  the  sensory being stippled, whilst  the
gray matter is seen  in the centre colored  in black.   The  motor
columns were supposed to be the lateral and the anterior pyramidal 
ANATOMY.
21
columns or pyramids,  whilst  the sensory tracts consisted  of the
columns of Goll, Burdach, Spitzka-Lissauer, direct cerebellar, and
the Govvers.   The fundamental column and the lateral column were
very imperfectly understood  at that period.   This figure should  be
studied very carefully in order to obtain a clear  comprehension of
what is to follow; in other words, the names of the columns as they
are found  in  this illustration  are those which have been sanctioned
by  usage,  and  have so far maintained themselves in  anatomical
nomenclature, and, if they are thoroughly  understood, it will be but
child's play to memorize the modifications of this diagram that the
latest  investigations  have  made  necessary.    The  student  should
therefore  observe that  the  anterior  pyramidal  column  is  small,
and is  to be  found on  either side of the anterior  median fissure;
whilst the lateral pyramidal column is at the postero-lateral portion
of the  cord.   These two columns, it  may be said at this point, are
the continuations of the motor fibres that  have come down from the
Columns of the spinal cord, according to our late knowledge.
brain the anterior  pyramidal column containing those which have
come down  from the same side of the cerebrum, whilst the lateral
pyramidal columns  hold those hailing from the opposite hemisphere.
The direct cerebellar column, it  will be noted, is contained in  the
extreme postero-lateral periphery  of the cord, external  to the lateral
pyramidal column; whilst  the  Gowers column is  on the antero-
lateral periphery of the cord,  extending from  the  direct cerebellar
column  behind  forward to the  anterior  pyramidal column.  The
column of Goll is a plume-shaped tract  on each side of the posterior
median  septum.  Outside of  it,  and between  it and  the  posterior
horn  is the  column of Burdach.   The  Spitzka-Lissauer column is
to be'seen on  each  side of  the posterior  horn.  This  is generally
known only as the Lissauer column, but as it was described simulta-
neously by Lissauer, of Berlin, and Spitzka, of New York, I have
given it  the compound name in this  and my previous edition, as it 
22
INTRODUCTORY
seems  only just to  do so.  Fig.  2 will show the modifications of
Fig. 1 that have been made by the so-called developmental studies
of Flechsig—i. e.,  by the assumption that a tract of fibres taking on
its  myelin  at a different period  from surrounding  tracts is to be
regarded  as  distinct anatomically and  functionally.   It will  be
observed  that there  are  some  important  modifications in  Fig.  2
over  what  has been represented  in  Fig. 1.   For  example, B  is
marked off from the  anterior fundamental column, and is designated
 Diagram of spinal column, junction of dorsal with the cervical region, according to the
                     Developmental Method of Flechsig.
 A. Anterior pyramidal tract; B. Fundamental tract of the anterior column ; C. Remaining
lateral column;  D. Direct cerebellar column ; E. Lateral pyramidal column; F. Lateral
limiting column; O. Anterior root-zone; H. Middle root-zone, composed of two systems of
fibres, one being those of the first system, and the other being the second system: I Median
zone of column of Goll; J. Column of Goll; K. Postero-internal  root-zone; L. Postero-
internal root-zone, or Lissauer's zone.
as the fundamental tract of the anterior column, whilst C represents
the rest of the anterior fundamental and a part of the lateral column
proper.    Then, too, F is delimited from the lateral column  proper,
under the name of the lateral  limiting column.   It is, however, in
the posterior columns between  the diverging posterior horns that the
most important modifications  are  to  be found.   For  instance, the
column of Burdach is split up  into three different tracts, namely, G,
the anterior root-zone;  H, the median root-zone, the latter contain-
ing  two systems of fibres;  and K, the postero-internal root-zone.
Nor  is the column  of Goll unchanged,  as a  portion of it  (I)  is
delimited as its median zone.
   Fig.  3 is a  diagram  of the spinal columus  as they  have  been
determined by  secondary degenerations.   At  first sight this mav
appear  very  confusing,  but it  is  exceedingly  simple  when  it  is 
ANATOMY.
23
understood that  all the  fibres  degenerating  upward  are sensory
fibres, whilst all  those degenerating downward are motor ones ; in
other  words, all  the  fibres  in  which the  degeneration  is  upward
belong to a  neuron whose cell  is below the point of degeneration,
whilst all the fibres that have degenerated downward are of a neuron

                                Fig 3
    Diagram of columns of the cord, at junction of the dorsal with the cervical region,
                according to the Degeneration Method.  (Marie.)
  A. Fibres Degenerating Upward. 1. Fibres of the sulco-marginal ascending tract; 5. Fibres
of the Gowers tract; 7. Fibres of the direct cerebellar tract; 8. Fibres of the cornu-commis-
sural tract; 9. Column of Burdach ; 10. External root zone ; 11. Zone of Lissauer; 12. Column
of Goll.
  B. Fibres Degenerating Downward.  2. Sulco-marginal descending tract;  3. Direct pyramidal
tract; 4. Intermediary tract of the antero-lateral column, some of these diverging and being
found scattered in the Gowers column, the direct cerebellar column, and especially in the
lateral pyramidal column ; 6. Lateral pyramidal column; 13. Comma-shaped tract of Schultze.

whose  cell is above  this point.   If this  be clearly comprehended,
the details of the figure become of exceeding  interest, because they
show that the columns of the cord marked out by the developmental
method do not  give  an adequate  idea of  the way in  which sensory
and motor fibres of one column may intermingle, as, for example, in
the intermediary  tract of  the antero-lateral  column (4), some of
which  go into the Gowers column, others into the direct cerebellar
column* and still others into the lateral pyramidal column ;  so that
minute examination  of  the illustration will reveal  the  curious fact
that the only pure motor columns are the anterior fundamental and
the lateral, that the single absolutely sensory column is the Lissauer,
and that the others are only mainly motor or sensory, and not exclu-
sively  so.
   What a revolution has been recently undergone in our knowledge
of the  finer anatomy of the spinal cord can be ascertained by a care- 
24
INTRODUCTORY.
ful study of Figs. 4, 5, and 6.  The first figure represents the views
held  until  the researches of Cajal and Golgi were made, whilst the
last three figures illustrate the discoveries of these authors and their
confirmers.   According  to  Fig. 4, the posterior root was composed
of fibres coming from the columns of Clark and Burdach, the lateral
column, and the  posterior  horn (a,  6, c, d, e).   The fibres of  the
column of  Clark  passed into the lateral column.   The cells of  the
anterior cornua  sent their motor fibres into the anterior root,  which
also received  the nerve-fibres from  the cornu  of the opposite side
(i,j).   The protoplasmic processes of these  same cells of the ante-
rior cornua were supposed to form a network (q) which received the
Fig. 4.
     Connections of the anterior and posterior horns of the cord, according to the view
                 formerly held.  (Compare with Fig. 6.)  (Cajal.)

  a. Posterior root-fibre originating in the cells of the column of Clark; 6. Unipolar cells of
the root-ganglion; d. Termination of a root-fibre in the network of the posterior horn;
e. Root-fibre passing longitudinally across the lateral column ; /. Fibre from the column of
Clark to the lateral column ; g. Lateral  column; h. Root-cell continued in the fibre (i);
j.  Anterior root-fibre coming from a cell (o) of the anterior horn  of the opposite side;
k.  Column of Clark ; m. Anterior fissure of the cord ; n. Column of Tiirck ; p. Anterior root-
cell whose protoplasmic branches form a network (q) where the posterior root-fibres termin-
ate ; r. Cells of the  posterior horn whose  protoplasmic  processes  form the network (q); s.
Cerebellar  column ;  t. Lateral pyramidal  column ; u, v. Posterior root-fibres terminating in
a network; x. Column of Burdach ; y. Column of Goll;  z. Posterior fissure of the cord.
fibres  from the  cells of  the  posterior  cornua (•>*), these same  cells
sending off their nerve-fibres to the  posterior roots (u, v).   Golgi,
with his wonderful stain,  showed that  these views were incorrect,
demonstrating that each axis-cylinder  process of a cell gave off col-
laterals.    He  maintained that  these  collaterals   from  the  cells
respectively of  the anterior  and posterior  horns  formed  the  net-
work of communication (Fig.  A, 5).   Cajal, however,  showed an
entirely different set  of connections,  which  have  been universally
confirmed, and his views are  illustrated iu  B of Fig. 5.   From  S
the unipolar cell  of  a  ganglion of the posterior root sends  off  a
cellulifugal  fibre to  the  spinal  cord,  through the  posterior root. 
ANATOMY.
25
When  this arrives in the cord, it bifurcates into an ascending and a
descending  branch,  both  of which  give off,  at  right-angles,  fine
horizontal  collaterals  that proceed to the motor cells of the anterior
horn, surrounding them with arborizations.   Even the trunk of the
posterior root gives off collaterals to  the cells  of the anterior horn.
Cajal has furthermore demonstrated  that the  nerve-cells are inde-
pendent  units,  that   anastomose neither with  their   protoplasmic
processes nor with their axis-cylinder ones;  that each  axis-cylinder
terminates by  varicose and  flexible arborizations  similar to those
in  the  motor  plate of  muscles; and  that, most  startling  of  all,
these arborizations are  applied  either to  the body or to the  pro-

                                 FlG. 5.
  A. Opinion of Golgi regarding the communication of the anterior and posterior roots.
m. Anterior root-fibre;  s. Posterior root-fibre, both united by networks formed in the gray
substance by the union of the terminal ramifications of the rearmost collateral of the anterior
root-fibre (m) with those of the posterior root-fibre; in these networks are the arborizations of
the fine axis-cylinder from the sensitive cells of the posterior horn.
  B. Cajal's view of the relations between the posterior and the anterior horns, s. Unipolar
cell of a spinal ganglion; m. Anterior root-fibre. The cellulifugal fibre of the spinal ganglion-
cells, passing to the posterior root of the cord, at the level of the posterior column, bifurcates
into an ascending and a descending branch, giving off at a right-angle fine horizontal col-
laterals which go to the motor cell of the anterior horn, surrounding them with their terminal
arborizations.  The trunk of the posterior root-fibre itself gives off a few collaterals in the same
direction.


toplasmic processes of cells, and  establish  connection  by contiguity,
and  not, as  has  been  tacitly  held  since  the  study  of  anatomy
began, by   continuity.   These two great  discoveries of the collat-
erals and the  connection  by  contiguity made  waste-paper of all
previous diagrams of  the cord, and brought  the oldest anatomist to
a par of knowledge with the student.   The study of spinal anatomy
now  became  a  study, not of nerves,  but of collaterals—i. e., the
branches of nerves.  These discoveries led in their train to the further
fact  that the cells of the  gray matter of the spinal cord did not
alone consist of  those  which supplied fibres to  the anterior and 
26
INTRODUCTORY.
posterior  roots, but that  there were others which had  no such con-
nection,  furnishing instead  fibres  to form  the commissures  of  the
cord  or its different columns.   Of  these we  shall have more  to  say
soon.   Fig. 6 is a diagram from Cajal, which gives the results ot his
latest studies.   It wall  repay us to study this briefly.  It will be seen
that the collaterals of the column of Goll  (a, b) go to the posterior horn,
the posterior commissure, and even as far forward as the anterior horn
(c).   The posterior root-trunk has also  its collaterals, as has already
been said.   Certain collaterals from the anterior columns take part in
Fi<;  6.
   Diagram representing a section of the cord, showing the relation between its different
               elements according to the modern discoveries.  (Cajal.)
 a. Collaterals of the column of Goll forming a larger part of the posterior commissure;
b. Collaterals of the same column going to the posterior horn ; c. Collaterals of the posterior
column reaching to the central gray substance and extending forward to the anterior horn ;
d. Posterior root-trunk and its collaterals ; e Collaterals of the anterior column ; /. Collaterals
forming the anterior commissure; g. Their course in the commissure ; h. Axis-cylinder coming
from a commissural cell, and which, after having passed through the anterior commissure, goes
to the anterior column ; i. Course of this axis-cylinder in the commissure ; j. Axis-cylinder going
directly to the anterior horn, and coming from k, a large motor cell; I. Cell of the anterior
column with a bifurcated axis-cylinder; m.  Cell with a commissural axis-cylinder; n. Cell
whoseaxis-cylinder gives off collaterals for connection ; o. Axis-cylinderof a cell of the column
of Clark; p. Axis-cylinder coming from s; q.  Transverse section of an axis-cylinder ; r. Bifur-
cation of the posterior root-fibres and ascending and descending branches ; s. Marginal cell of
the  substance of Rolando; t. Small cell of the same substance;  u. Body of the cell of the
column of Clark.

the formation of the anterior commissure (/, g).   If the course of (h)
is followed carefully, it will  be observed  that  it terminates in the
anterior column, after having crossed from the other side  of the cord
in the anterior commissure  (/) and having had its  origin  in a  so-called
commissural cell.    On  the  other  hand, (j) shows that there are cells
(k) giving off axis-cylinders directly to the anterior root.   A column-
cell  is  observed at (I), sending  its bifurcated axis-cvlinder  to the
anterior column.   A commissural cell is at (m).   At (n) is  a cell
whose axis-cylinder gives  off collaterals  for connection.   The cells 
ANATOMY.
27
of the  column of  Clark  send  their axis-cyliuders to  the lateral
columns (o).  The bifurcation of the posterior root-fibres into ascend-
ing and descending branches  is seen at  (r).  At («) is seen a mar-
ginal cell of the substance of Rolando, whose axis-cylinder is at (p).
Another small cell of the Rolaudic substance is at (t).

                                Fig. 7.
Drawing of cells from the anterior horns of the spinal cord.  Obtained by tapping
                      the fresh cord of an ox.
  As has  already been said, it used to be  thought that the cells of
the spinal  cord were only of the  one kiud  that gave origin to root-
fibres, either posterior or anterior.   The newer methods of staining,
however, have shown that there are five varieties, viz.:
  1.  Root-cells;
  2.  Commissural cells;
  3.  Column-cells; 
2 8                        INTR OD UCTOR Y.

  4.  Many-column or pluricordonal cells;
  5.  Cells with a short axis-cylinder.
  The  first four varieties all lose  their  axis-cylinders in the white
substance, so that they may be  called cells with long axis-cylinders,
whilst  the fifth kind parts with its axis-cylinder within  the gray
matter.
                                Fig. s.
 Drawing from a photo-micrograph, made by McDonald, showing the cells of the anterior
cornua as they lie imbedded in a specimen hardened in bichromate by the alum 'Weigert
method, and afterward magnified 360 diameters.

                                Fig. 9.
   .  Motor cell of the anterior horn, from the spinal cord of a newborn dog.  (Cajal )

   We  have first  to obtain an adequate  idea of the  form and
shape  of these cells  from  the bichromate of silver staining.   Our
knowledge of them  in olden times was obtained  from  tapping the 
ANATOMY.
29
fresh  spinal cord  of an ox,  when we  obtained  the shapes which
are seen in Fig. 7.   Then other  staius employed with  hardening
methods enabled  us to  see these  structures as they lay imbedded
in the spinal cord,  and we had such a view  as  is represented in
Fig.  8,  which  shows a photo-micrographic  drawing  of a  section
magnified 360 times.  How little idea we had of the vast complexity
of these minute  cellular  bodies can be gathered  from a comparison of
these  two figures with Fig. 9, which represents the motor cell of the
anterior  horn from the spinal cord of a  newborn dog.   An easy dis-
tinction  can be made between the protoplasmic and the axis-cylinder
processes.  The  former, as will be seen in Fig. 9, have many branches,
which can be divided into autero-external, posterior,  and  internal
divisions, each branching dichotomously ; and the latter are colored
in red.
                              Fig. 10.
Column-cells of the human spinal cord.  (Lexhossek.)
  The column-cells are so called because  from them  arise the axis-
cylinders which form  the different columns of the cord.  Most of
them are contained in the anterior horn, and send their axis-cylinders
into the antero-lateral column  (Fig. 6, n, and Fig. 10).  Those of
the posterior  horn have their axis-cylinder  processes directed  to the
most posterior region of  the lateral column.   Others in the substance
of Rolando and the internal portion of the posterior horn send fibres
to the posterior column.   In the column of Clark there are two  varie-
ties of  cells—the commissural cells sending fibres to  the anterior
commissure, and column-cells whose fibres goto the lateral column, 
30
INTRODUCTORY.
 probably to the direct cerebellar column.   The latter sometimes pass
 off without division, and sometimes by what is known as the T-shaped
 division, splitting the original fibre into an ascending and descending
 vertical branch.  The multiplicity of these column-cells is beautifully
 figured in 10.
   The commissural  cells  (Fig.  6, m)  are smaller,  and have fewer
 processes  than the  root-cells   They are found  in  the thickness of
 the gray substance, and usually send  their axis-cylinders through the
 white  commissure to the  antero-lateral  column of the opposite side,
 sustaining at this latter  point, however, the T-shaped division  into
 an ascending and descending fibre.
   The many-column cells are those  whose axis-cylinder splits up in
 the gray matter into  two or three fibres,  which each go to  a different
 column, so that one such division may pass into the anterior column
 of the same side, and the other division  into the same column of the
 opposite side;  or, on the other  hand, one of these branches  may
enter the  posterior  column,  and the other  the  lateral or anterior
column.
Fig. 11.
         Section of posterior rool-ganglion of a rat, eight days old.  (Cajal.)
 A. Anterior root.  B. Posterior root.  C. Body of the ganglionic cell. D.  Internal or cen-
tral branches of the dichotomous division, E, of the nervous fibre of the ganglionic cells
M.  Spinal cord.                                            so«s"umi, cens.
   Each posterior root not only contains sensory fibres, or centripetal
but  also centrifugal or motor ones.   The sensory fibres come from
the cells of  the  ganglion upon the posterior root, as will be seen bv
studying  Figs.  11  and  12.   Each  one of these ganglionic cells  i^
enveloped  in  an endothelial  capsule.   Outside of this capsule—i e
between the capsule and the  cellular protoplasm—is a very fine Deri'
cellular arborization continuous with a nervous fibre whose oriVin  \l
yet unknown, so that this ganglionic  cell receives, it would armear
not only a current  through the fibre coming from the peripherv and
transmitted to the  spinal cord, but also a nervous impulse oom  !
from some unknown quarter, possibly from a cell of the sympathetic 
ANATOMY.
31
system, as some of Cajal's researches would seem to show.  It was at
first supposed that each posterior root entering  the posterior column
passed into two divisions, one of which became vertical, passing up
to the  medulla oblongata and  the brain  in  the white substance,
whilst the other segment was lost in a nervous network formed by
the anastomoses of the protoplasmic expansions of the cells, or those
of the  collaterals and the terminal branches  of the axis-cylinders.
(See Figs. 4 and 5.)   In 1887, however, Nanseu made the surprising
discovery that in the myxina glutinosa, one of the lowest of the fishes,
of the hag or sucker order, the posterior root-fibres bifurcated in the
Fig. 12.
  Half diagrammatic longitudinal section of the posterior
column parallel to the entrance of the posterior roots.
(Cajal.)
  A. Posterior root; S. White substance ; 0.  Gray sub-
stance ; C. Cell of the posterior column with a curved
axis-cylinder ; D. Another cell of the  posterior column
with  an  axis-cylinder bifurcated  into ascending and
descending  branches;  E. Another cell with a curved
descending axis-cylinder ;  F, G. Terminal arborizations
of the axis-cylinders; B. Terminal arborizations of the
collaterals of the white substance; a'.  Collateral of the
branches of a posterior root-fibre; 6'.  Collateral of the
trunk of another posterior root-fibre.
white substance, and that the branches of these bifurcations assumed a
longitudinal direction and gave off collaterals for the gray substance.
This arrangement was soon demonstrated by Cajal in birds and verte-
brata. The centripetal fibres composing the bulk of the posterior rootare
of two varieties, one external or fine, the other internal or thick.  These
enter the posterior column obliquely, then bifurcate into an ascending
and a descending branch, both of which are longitudinal, and both
probably enter the gray substance after a course of several centimetres
in the  white  substance,  and  terminate by free  arborizations  lying
between  the  elements of the posterior horn  and  the  substance of
Rolando.   (Fig. 12.)   The external  or fine tract of the posterior 
32
INTRODUCTORY.
root has  its terminal bifurcations in  the  Spitzka-Lissauer column
and the neighboring portion of the lateral column, and its collaterals
are sparse, delicate, and  appear  to terminate alone in the posterior
horn.  The internal  tract,  or that of the thick  fibres, passes to the
column of Goll and  Burdach, and it furnishes the greatest number
of collaterals of the sensory-motor tract going forward to the cells of
the anterior horn.   From the trunk of the posterior root, as well as
from its ascending and descending fibres, a  number of fine collaterals
pass off at a right angle, penetrating the gray substance, and  there
terminating by beautiful free arborizations in contiguity with  the
bodies of the  cells  in the posterior and anterior horn.  The plan of
entrance of these posterior  root-fibres  is shown in Fig. 12, A  being
the posterior  root-fibre, a' a collateral which passes  off from  it,
b' another emanating directly from the posterior root-trunk.  S is the
white substance.  In it is seen a curved ascending axis-cylinder coming
from a cell (C) in the posterior  column, whilst from D, another cell
of the posterior column, passes off an axis-cylinder which bifurcates
into an ascending and a descending  branch.   E is still another cell
of the posterior column,  with a curved  descending axis-cylinder.
F and G are the terminal arborizations of axis-cylinders, whilst B
represents the  terminal  arborizations of the collaterals of the white
substance.   A large number of  the collaterals of the posterior roots
reunite into an antero-posterior tract  which  crosses the posterior
horn and expands, fan-like, around the motor cells of the anterior
horn.  This is the sensory-motor tract  of Cajal, or the  reflex-motor
tract of Kollicker, and, as the name indicates, it is the material  high-
way for such reflexes as  those of the tendons.
  The nervous elements are sustained by two kinds of corpuscles—
namely, the epithelial cells,  and the neurogliar, or spider, or Deiters'
cells.   The  epithelial cells cover the  cavities of the nervous centres.
They are elongated bodies, with  a nucleus, and with one or  more
ramifying and divergent processes which are lost in the neighboring
white or  gray substance.   In the embryo these epithelial cells are
very long, and are prolonged  from the central cavity to the exterior
surface beneath the pia mater, where  they form cones, and  thus con-
stitute a sort of limiting  membrane.  (See Fig. 13.)   In the brain of
certain vertebrata, as  in fishes, reptiles,  and batrachians, this disposi-
tion is maintained throughout life, and  in these organisms there is no
other connective tissue.  But in the spinal cord and the cerebrum of
birds and mammifera this tissue atrophies, for the expanding pro-
cesses do not reach to the surface of the nervous  organ, although in
the olfactory mucous  membrane and  the retina  the embryonic con-
ditions are maintained.  The neurogliar cells—sometimes called  the
spider or Deiters' cells—are  to  be found in great abundance in  the
white  substance of the  nervous ceutres, in the  framework of  the
nerves, in the ganglia of the  sympathetic,  and, in  less  quantity, in
the gray  cerebrospinal  masses.  They are small, with  very* fine
flexible or  slightly ramified processes  which  terminate free   often
by fixing themselves  upon  the surface  of the capillaries.   The con-
nective tissue of the nerve-centres is the result of a plexiform inter- 
ANATOMY.
33
crossing of the expansions of these neurogliar cells, but not of any
anastomosing,  as was formerly supposed, and the function of these
expansions appears to be to sustain and isolate the medullated fibres.
It is a matter of very great doubt, however, whether they also sustain
and  isolate the nerve-cells.   The origin of these neurogliar cells has
been the cause of  a great variety of opinions.   v\.t the present day it
is believed bymost  histologists that they are transformed epithelial
corpuscles which  have emigrated  from  their usual site  upon  the
interior  surface of the nerve-centres, and that  this  transmutation
has  been  effected  by atrophy of their central and  peripheral  pro-
cesses and by the production of secondary ones.   During this  pro-
cess of  transformation the epithelial cells would seem to be capable
of multiplying, according  to Lenhossek.   Fig. 13 shows upon the

                               Fig. 13.
Spinal cord of a human embryo prepared by Golgi's method. On the left side is the
 epithelial or ependymal structure; on the right, the neurogliar cells. (Lenhossek.)
left side the  epithelial  structure, and upon the right the neurogliar
cells.   For a  certain time the epithelial  corpuscles preserve their
peripheral  process which passes to the pia mater; but gradually this
atrophies, as well as the central process, and thus is effected a trans-
formation of the epithelial cell  into a neurogliar one.  The epithelial
cells,  however, of the anterior and posterior  fissures preserve their
form  and their primitive length.

  So  much for  the  spinal  cord  proper.   Before entering into con-
                                 3 
34
INTRODUCTORY.
sideration of the structure of its upper enlarged end, known as the
medulla  oblongata, it will  be best  to study first the  brain and cere-
bellum, and then show the connection between these three structures
  I desire to say at the outset of this portion of my  subject that al
my drawings, unless otherwise indicated, were made from actual
fresh brains, or relatively fresh ones that  had been preserved  lor  a
day  or two in  a salty  solution,  or else from  those hardened  in
alcohol, and  in some cases  photographs  or silver  plates have been
made of the brain, and the drawings from these.  In every instance,
therefore, the convolutions are exactly as they are found in  the
brain.   I am particular in calling attention to this point, because
in scarcely  one of the  text-books  is  use made of such  fresh  or
hardened brains, the representations being generally by means of
diagrams.   The result  has  been that most of the  readers of books
have become conversant with the  convolutions only through  such
	Fig. 14.	
	/F.Rolando Praecentral F. /	Parietal F.
1st Frontal F. ^	^^</w^>	
	-4 \\^VV y^ y^^i1^^	•S7 vs. Parieto-Occipital F.
/M<?
^
2nd Frontal1 F.
«N°
•rtr
v**°l
F.Sylvius

 1st Temporal'F,
       2nd Temporal F.

Convolutions of the left hemisphere.
diagrammatic representations, and I anticipate, therefore, that critics
who are not familiar with actual brains will  be surprised at the
course of some of the convolutions.  Even Meynert, Ecker, Edinger,
and Schwalbe, who are certainly indubitable authorities upon cerebral
anatomy, make use  almost entirely of diagrams.   The truth of the
matter is that the convolutions vary so much in different brains that
slight deviations  from the usual course are of no importance, and it
is very doubtful whether we know at  the  present time what really
constitutes a pathological  variation in  the direction of a fissure.
  The fissures of the brain are in the main very simple.   In Fig. 14,
which  is the lateral surface of one hemisphere, it will be seen that
there is a large fissure going upward and  backward  from the base of
the brain.  This is the fissure of Sylvius.   Coming down from above,
from the great longitudinal fissure, is another large fissure, known as
the fissure of Rolando, almost  running into  the  fissure  of  Sylvius. 
ANATOMY.
35
These two fissures can easily be found in a  brain  by the facts that
have already been stated, namely, that one runs up from the base,
that the other  runs down from the great longitudinal fissure, and
that both are large.   The fissure of Rolando is the boundary line
between the frontal lobe in front and the parietal lobe behind; whilst
the fissure of Sylvius is the boundary line between  the  frontal and
parietal lobes above and the temporal lobe below.  It will be noticed
that the convolutions behind and in front of  the fissure of Rolando
are ascending,  whilst  the other convolutions of  the  frontal  and
parietal lobe  pursue a  more or less horizontal course.   These two
convolutions, therefore, one in front of the fissure of Rolando and
the other behind it, are known as  the ascending convolutions; and
as the one  in  front  belongs to the frontal lobe, it is known as the
ascending  frontal convolution, whilst the one  behind, belonging to
the parietal lobe, is  called the ascending parietal convolution.  In
front of the  ascending frontal convolution  in Fig.  14  is seen  a
fissure  which  is  more  or less  continuous from above downward,
and which, like  the  fissure of Rolando, has an  ascending direction.
Fig. 15.
Int. Capsule\
Caudate Nucleus
    (Mead) )
Lenticular
 Nucleus
1st Frontal f.


    2nd Frontal f.
Caudate Nucleu
    (Tail)
Optic Radiation


      Pulvina
1st Temporal/.
4/ 2nd Temporal/.
Parietal/.
                        Cuneu]s  Pari^o-occipital/.
  Convolutions of the vertex, on the right; on the left, the basal ganglia, internal capsule,
                        centrum ovale, and cuneus.

This  is an accessory fissure, the prsecentral, and it is of no special
importance except that its  position must be borne in mind, so that
it  will  not be  confounded  with the  fissure of Rolando.   It will
be seen that in front of the  ascending frontal convolution there are
two  main  fissures curving  forward.  The  upper one  is known as
the first frontal fissure and the lower as the second frontal  fissure;
and  they serve to mark off  this portion of  the  frontal lobe into the
first frontal  convolution,  which  lies above  the first frontal  fissure; 
36
INTRODUCTORY.
the second frontal  convolution, between the first and second fronta
fissures; and the third frontal convolution, below the second frontal
fissure.   The  third  frontal convolution, it will be observed, has a
fork or anterior branch  of the  fissure of  Sylvius running into it
This fissure  of Sylvius contains in its depths  a series of inturned
convolutions, which are known  collectively  as  the island of Keil.
Below this fissure of Sylvius, as has already been said, is the tem-
poral lobe, and  we see in  Fig. 14 the first and second  temporal
fissures, and  the first temporal convolution lying between the fissure
of Sylvius and the  first temporal fissure, the second temporal con-
volution between the first and second temporal fissures, and the third
temporal convolution below the second temporal fissure.   Back of the
ascending parietal convolution will be noticed a  long  curving fissure
known as the parietal or inter-parietal fissure.  This serves to divide
the parietal lobe irregularly into two lobules, the upper and the lower.
These  upper convolutions of the frontal and parietal lobes will be
better seen in Fig. 15.  The convolution curving around the upper end
of the fissure of Sylvius is known as the supra-marginal convolution,
and the one around the upper end of the first temporal fissure is the
Fig. 16.
Parieto-occipita I /.
Calloso^marginal /.
Calcarine /.
                      Mammillary Body'          Optic Tract
                                   Anterior Commissure
Vertical section through the centre of the corpus callosum, showing the convolutions of
                the inturned surfaces of the hemispheres.
angular convolution, or gyrus angularis.  It will be observed that the
supra-marginal convolution and the angular convolution both really
belong to the lower parietal convolution or lobule.  The boundary line
between the parietal and occipital lobes is at the  parieto-occipital
fissure,  which is a little indentation at the point indicated in Fig. 14,
and better seen upon the inturned surface of the hemisphere (as in
Fig. 16) than upon the outward lateral surface.   The convolutions of
the occipital lobe  are illy defined upon the external  hemisphere, but
they can usually,  with some approach to  accuracy, be marked off
into the first, second, and third  occipital convolutions, as indicated
in  Figs. 14 and 15.   Upon the inturned surface of  the hemisphere,
Fig. 16, however, there is a convolution  of the  occipital lobe, known 
ANATOMY.
37
as the cuneus, from its wedge shape, and this  is the most important
portion of the occipital lobe for us to know.  The upper boundary of
the cuneus is the parieto-occipital fissure, whilst  the lower boundary
is the calcarine fissure, the name  being derived from the  adjacent
hippocampus  minor,  which is  also  called  the calcar avis or cock's
spur.  Upon  this  inturned surface of the hemisphere are a number
of other convolutions with which we must become familiar.   In front
of the cuneus is seen the prsecuneus.   In front of this again  is the
so-called paracentral  lobule,  which consists of the  surface inturned
upon this aspect of the brain of the two ascending convolutions, the
ascending parietal and the ascending frontal.  At the anterior bound-
ary  of  the paracentral lobule is seen  the calloso-marginal  fissure
curving forward, downward, and backward.   Above  this,  in front
of the paracentral  lobule, is the  inturned surface of the  first frontal
convolution, whose outer surface  upon  the  hemisphere we have seen
in Fig. 14.   Curving around the corpus callosum is the gyrus forni-
Fig. 17.
       Form of convolutions of the upper and lateral surface of the hemisphere.

catus or arched convolution, the longest of all the cerebral convolu-
tions.  It is sometimes called the limbic lobe.  Its arch around the
corpus callosum is seen in  Fig. 16, being  known in its anterior and
middle portions as the gyrus  fornicatus, but in its posterior and lower
portions  being continuous with the hippocampaP  and the uncinate2
convolutions.  The rear  portion of the  hippocampal convolution is
split by the junction of  the  parieto-occipital and  calcarine fissures,
below which junction are the lingual and the fusiform lobes, as will
be seen in Fig. 16.  The form of  a portion of these different convo-
lutions of the  upper and lateral surface of the hemispheres can be
better studied  in detail in Fig. 17.
  The base of the hemisphere is  represented in Fig. 18.   The con-
volutions of this surface  of the brain are of no practical importance

 » The hippocampal convolution, or gyrus hippocampi, is so called because it is adjacent to
the hippocampus major or the cornu ammonis, which is an eminence along the floor ot tne
adjacent horn of the lateral ventricle.
 2 The uncinate convolution, from uncinus, a hook or barb, derives its name from tne met
that it is of a hook shape, and is considered as belonging to the hippocampal convolution. 
38
INTRODUCTORY.
to us in the present state of our knowledge of localization, and they
are sufficiently indicated by the lettering of Fig. 18, so I shall not
pause to dwell upon them, the more especially as we shall have again
to consider them when speaking of the other structures at the base.
   We must now pause to state our present knowledge of the local-
ization of functions in the different convolutions of the hemispheres.
It is true that Bouillaud recognized aphasia clinically in 182o ;  that
Dax, in 1836, located  this symptom-group in the frontal lobe;  that
Broca  more precisely  located  it in the third frontal convolution  in
1863;  that Andral, in 1834, had observed paralysis of the arm and

                              Fig. 18.
                              Olfactory bulbs
           Convolutions of the base of the cerebrum and the cerebellum.

leg from cortical disease; that Panizza, in 1805, reported two autop-
sies which  showed that the function of sight was somewhere in the
parieto-occipital region of the  hemisphere.  Nevertheless, the first
proof that commended itself to the minds of medical men of there
being localized areas of function  or so-called  centres in the cortex
was afforded by the world-famous experiments of Fritsch and Hitzig
in  1870.   In  the twenty-five years which have since elapsed,  not
only has abundant  confirmation been afforded of the statements of
these two German observers, but other centres have been found in
the convolutions.  This has been  done by the several methods that
have  been mentioned  at  the  beginning of this chapter.   Let us
now see what we know about these cortical centres.  The ascend- 
ANATOMY.
39
ing frontal and the  ascending  parietal convolutions, the  rear  ends
of the frontal convolutions immediately  in front of the  ascending
frontal (Fig.  14), and that inturned surface  of the ascending parietal
and  the ascending frontal convolution which is known as the para-
central lobule (Fig. 15), contain the  motor  centres.   If the  ascend-
ing frontal and the  ascending  parietal convolutions, with the bases
of the two frontal convolutions in front of the ascending  frontal,
are divided  approximately  into four  portions, the  upper  fourth,
together with the  paracentral lobule, will contain the centre for the
leg of the opposite side  of the body,  the middle two  fourths will
contain the centre for  the arm  upon the opposite side of the body,

                                Fig. 19.
Centres of the cortex of the human brain, according to Ferrier.
  1. Centre for the movements of leg and foot in locomotion. 2, 3, 4. Centres for various com-
plex movements of arms and legs, as in climbing, swimming, etc. 5. Extension forward of
arm and hand.  6. Supination of hand and flexion of forearm.  7, 8. Elevators and depressors
of the angle of the mouth, respectively. 9, 10. Movements of lips and tongue as in articula-
tion. 11. Centre of platysma retraction of the mouth. 12. Lateral movements of the head
and eyes, with  elevation of the eyelids and dilatation of the pupils, a, b, c, d. Centres of
movement of fingers and wrist.

and the lower  fourth (together with the  portion of the third frontal
fissure  lying posterior to the ascending branch of the fissure of
Sylvius,  the so-called  operculum) will  contain the centre  for the
muscles of  the face, the tongue,  and  probably also the  larynx.
It  must  be  remembered  that this division into fourths is purely
arbitrary, and that it is utterly impossible to  say just where one centre
commences and where another terminates;  indeed,  as we shall have
occasion to  see, the centres of the cortex shade into one another to a
certain extent.  There have been considerable discussion and consequent
variance of  opinion among physiologists and pathologists as to the
subdivision  in  these fourths  of the  motor  area.    Thus   Ferrier
minutely subdivides this  motor  region,  as  is indicated  in Fig. 19, 
40
INTRODUCTORY.
basing  his localizations largely upon his experiments on  the brain
of the monkey, although he is particular to state that the centres of
the human brain, as he has indicated  them by this method of analogy,
are only approximately correct, inasmuch as the movements of the
hand and arm, for  instance, are more complex and differentiated in
man than in the monkey, whilst in the human being there is nothing
to^ correspond with the prehensile movements of the lower limbs and
tail of the monkey.   Horsley and Beevor have outlined this region
in a somewhat similar manner to  Ferrier, also by experiments upon
animals.  (Fig. 20.)  The third frontal convolution (Fig. 14) is the
centre of speech in the sense that  a lesion of it causes an inability to
articulate words properly,  although the patient may understand per-
fectly well what is said to him.  This is called motor aphasia, and
was  the symptom  to  which Bouillaud, Dax, and Broca first called
Fig
Closure o/ eyelids ,
the opposite most
         Retraction o/ 6pp
          angle o/mouth     i j i ■ RolUng Ups xElevation o/ ^Contraction o/opp. & upper
             Pouting both lips'. 'Opening mouth °PP-upper lip  hal/o/orbicularis oris
                         Raising lips
  Outer surface of the left half of the brain of an orang -outang, showing centres.  (Horsley.)
     R. Fissure of Rolando.  IP. Interparietal fissure.   PO. Occipito-parietal fissure.
                 S. Fissure of Sylvius. PC. Prsecentral fissure.

attention.   Lesion of the first  temporal convolution, and  to  some
extent of the second  temporal convolution, especially, as Mills has
recently  shown, in their  upper and posterior portions, gives rise to
the symptom which is known  as mental or word-deafness, character-
ized by the ability of the patient to hear perfectly well what is said
to him, at the same time that he  fails to understand what he thus
hears.  Singular to say, the most beautiful  exposition of this was
given by Munk through his experiments upon  the brains of dogs
He would so train a dog as to have him crouch at the word  of com-
mand or at the crack of the whip.   From this dog's brain he then
removed  the auditory centre  in the convolution analogous to the
temporal convolution of the human being, then stuffing the ear upon
the side of the uninjured nerve, so  that the dog could hear  nothing
in that way   Coming into the room suddenly behind the animal and
speaking to him or cracking his whip, the dog would  evidently  hear 
ANATOMY.
41
what was said to him, as well as the crack of the whip, because he
would prick up his ears and manifest other signs of audition, but he
would not  crouch,  as he had been  accustomed to do, showing that
although  he heard  the sounds,  he no  longer understood.   If the
cotton was  now taken from  the uninjured  ear, he again not only
heard the sound, but crouched at the word of command or the crack
of the whip—thus evidencing that, through the sound side of the brain,
he  not only heard  but  understood.  "When  there is a lesion of the
island of Reil, which, as has been said,  is a series of small  convolu-
tions buried in the fissure of Sylvius, there is caused what is known
as paraphasia, or the aphasia of conduction.  In such a case  patients
understand  perfectly well what is said to them, and articulate words
correctly, but they misplace them, saying, as did one patient of mine,
" I  see best," instead of " I  have  been;"  and making the most
curious and insensate combinations of words.   A  patient  suffering
from paraphasia  may be able  to  speak a  given word  himself, but
cannot  repeat  it  when it is  spoken  by another.   A  lesion in the
angular  gyrus  generally  causes what is  known as mental or word-
blindness; that is, an inability to recognize the meaning of a word
which is seen, although  it  may be automatically repeated.   This
word-blindness is usually associated with  true  blindness  of that
variety known as hemianopsia, which is described further on.   Word-
blindness and word-deafness are  frequently  observed together in the
same patient, due to consentaneous  implication of the temporal  and
the  angular convolutions, as might be expected from the proximity
of the posterior end  of the temporal convolutions to  the  angular
convolution.  There  is a symptom  known as agraphia, consisting
of an inability to write, although there may be  no paralysis of the
hand, no loss  of the memory of words, no word-blindness, and  no
hemianopsia.  It is by no means  certain as  to where its causative
lesion is  situated, although possibly, as has  been supposed, it may
be in the posterior portion of the second  frontal  convolution.  The
cuneus,  a  small  portion of  the adjacent  occipital lobes,  and the
lingual lobule, constitute  the  centre of  vision (Fig. 16) in the sense
that  a lesion in this  region  causes  blindness of the lateral half of
the  eye to  the  opposite  side  of the median line—i. e., if the right
occipital lobe in this region is affected, the patient fails to see anything
to the left side of the middle  line of the eye.  This defect of vision
is  that which  is  known  as hemianopsia.1   There  is a considerable
doubt at  the present day as  to exactly where the centres are of the
sensations of touch, pain, muscular sense,  and temperature.   Ferrier
and his  followers maintain  that the site  of the tactile sense is in

 i Hemiopia is derived from the Greek words rjpnavc, "half,"  and oip/c, "sight," mean-
ing, therefore, half sight.  There is another somewhat similar word,  which has led to
much confusion—hemianopsia, from rj/uovc, "half," av  (privative) and biptg, "sight,"
meaning also half sight.  It seems to be agreed at the present day that by arbitrary custom
hemiopia shall mean the condition of the retina, while hemianopsia shall be applied to the
crossing of the rays of light in the media in front of the retina. Thus a left hemiopia will
indicate that the left halves of both retinae are blind, so that the patient, not being able to see
objects to the right of either eye, shall be said to have a right hemianopsia.  This is made plain
by the diagram of Fig. 28. 
42
INTRODUCTORY.
the gyrus hippocampi (Fig. 16), and Schafer and Horsley formerly
believed  that  it was in what Broca has termed  the limbic lobe, by
which, as has already been explained, he meant the  gyrus fornicatus
as it sweeps around the corpus callosum, ending below in the hip-
pocampal and uncinate convolutions (Fig. 16).  Others have shown,
however, that lesions of the motor area may have with them some

                              Fig. 21.
  Localization of muscular sense, with motor paralysis, in a case of my own, with autopsy.

impairment of sensation.   I have myself recently reported a case in
which a round-cell sarcoma was found in the ascending parietal con-
volution  at about the junction of the upper and middle third, from
which  there had resulted a motor paralysis of the opposite arm  and
leg with a  distinct impairment of muscular sense (Fig. 21).   Hors-
ley, in a recent article, stated his  belief that there is impairment of
muscular sense in the lesions of the motor area, and reported  a case of
removal  of a  tumor from the centre for the thumb (Fig. 20), in
which, during recovery, there was considerable pain in this member.

                              Fig. 22.
   Diagram of lesion causing loss of tact and pain sense, with preservation of muscular
                           sense (autopsy).

I have recently seen a case in consultation in which there  was absolute
loss  of the sense of touch  and pain, with preservation  of  the  mus-
cular sense,  and in  which the  autopsy, made by  my friend Dr.
Frank Madden, of Plattsburg, New York, disclosed a  lesion of the
parietal lobe, as represented in Fig.  22.   In the last few years  there
has grown to be  a  belief that the parietal lobes are the terminals of 
PLATE  I.
  FIG. 1.
CHART OF  LOCALIZATION  OF CORTICAL CENTRES DETERMINED ON
              EXTERNAL  SURFACE OF CEREBRUM.
FIG. 2.
CHART OF LOCALIZATION OF CORTICAL CENTRES DETERMINED ON
                MEDIAL SURFACE OF CEREBRUM.
[To face page 42. 
 
ANATOMY.
43
sensory nerve-fibres of the general senses of pain, muscular sense,
tact, and perhapsheat; but the proof of this  has been  rather anat-
omical than physiological.  There might, indeed, be a question as to
whether it is necessary to suppose that there are  centres  of sensation
distinct from those of motion, if  we accept the views of Cajal and
Andriezen, that are soon to be explained,  of  the  mode of entrance
of the sensory nervous current to the motor cells of the cortex.
  It  will be  thus seen that our knowledge  of the  centres of the
cortex is remarkable when we consider that almost the whole work
of discovery and confirmation  has been done  since 1870.   Plate I.
represents the centres that are known as  we have been describing
them. From this it will be seen that we  know the  motor centres
for the arm and leg muscles, for the muscles of the head, face, and
larynx, for articulate speech, for word-deafness, for paraphasia or inter-
ruption of speech-conduction,  for word-blindness, for hemianopsia,
and possibly for agraphia; whilst the centres for the muscular sense,
for tact, and for  pain are possibly to be found in  the parietal lobes.
There is some dispute, however, as to the  exact localization of the
different muscular groups in the motor  region.   It is very evident
that  there is  a large portion of the cortex with whose functions we
are not acquainted.   The portion of the two frontal convolutions
somewhat in front of the ascending  frontal convolutions are  inex-
citable, and  lesions  of them  do  not give rise to motor or sensory
phenomena, but rather to purely mental phenomena, so far as we now
know.  Outside of the regions we have marked, the functions of the
cerebrum are unknown to us (Plate I.).  It is probable that every year
will add to our knowledge.   The  doctrine of cerebral localization has
been  vigorously opposed  by a  small and constantly waning school,
of  which Goltz is the most illustrious exponent.  As critics these
writers have been of great service to science,  for they have  exposed
the  absurd claims  of over-enthusiastic  localizationists, and  have
shown that, in order to destroy or even distinctly impair a centre of
the cerebral cortex, a  lesion must be destructive, and not merely
irritative;  thus,  whilst a tumor, a softening,  or a  marked com-
pression  from a  fracture may  inhibit or destroy the function of a
centre, this  may persist with a  mild degree of meningitis, especially
of  the pia  mater, or  with  slight compression.  The more localized
a lesion is, too, the more  prone it is to affect the centre.   But Goltz
and his followers have not succeeded in their attempt to demonstrate
that the doctrine of cerebral localization is  based on  faulty observa-
tion—indeed, this is the very defect of all their own reports  of cases
or experiments.  Speaking  from  my own clinical experience, I can
say deliberately that  I have never seen  a  case disproving  cerebral
localization, although  I have observed and read of many in which
an imperfect history made it impossible to reach a conclusion.

  The histology of the gray matter of the brain is quite intricate and
differs somewhat in different regions.  The late researches, to which
I have so frequently alluded, have made considerable modifications
even  in the views that were current at the time of the first edition of 
44
INTRODUCTORY.
Fig. 23.
this book, two years ago.  Let us, for example, examine the t}pjof
structure that is seen in  the  motor  area.  This  has been described
as consisting of  five layers, and even of six, but the present opinion
is that  there  are  only four, viz., the  molecular layer  that of the
small pyramidal cells, that  of the  large  pyramidal cells, and that
of the polymorphous cells.                       „  .        ,
   The  molecular  layer  (1, Fig. 23) presents a  finely granular oi
                      reticulated appearance.   It is dotted here and
                      there with some nuclei  probably belonging to
                      the neuroglia cells, especially  abundant be-
                      neath the pia mater, and it also contains a few
                      other and larger nuclei, surrounded by a tri-
                      angular or fusiform protoplasmic body that is
                      probably of nervous function.   In the  most
                      superficial  portion of this molecular   layer
                      Kollicker  and Exner discovered a group of
                      horizontal fibres.   Andriezen has recently de-
                      scribed in the outermost  region of this mole-
                      cular layer a system of neuroglia cells, giving
                      rise to  a tangential plexus of fibres radiating
                      from the bases of  these cells and also to tufts
                      of descending fibres.   This molecular  layer,
                      however, is  worthy of more extended study,
                      because of the fact that the earliest lesions of
                      general paresis  are  probably  found  in it,
                      whilst  it is probably affected in other mental
                      affections.   Fig. 24 shows some late remark-
                      able  researches regarding  it by  Cajal.  It
                      would  appear that its special cells are aston-
                      ishingly  peculiar  in the  unlikeuess  of their
                      processes to the usual  protoplasmic and axis-
                      cylinder branches of other nerve-cells.  There
                       are three varieties of these nervous structures,
                       namely, polygonal, fusiform,  and triangular
                       or star-shaped cells.   The polygonal  are of
                       medium  size (Fig. 24, D), and have four to
                       six protoplasmic processes, which are nodular,
                       fine, ramifying, and divergent,  some of them
                       descending to the layer of the small pyramidal
                       cells.  The axis-cylinder process is fine, pro-
                       ceeding from the side of the cell or of a large
 process, and it  passes obliquely or horizontally into the thickness of
 the molecular layer, ramifying greatly and breaking up into a certain
 number of wavy terminations which are very  long and  parallel to
 the surface of the cortex, but never descending to the white matter as
 do the axis-cylinders of the pyramidal cells.   The  fusiform {A, C)
 and the triangular (B)  are cells special to  this molecular layer in
 that their axis-cylinder processes cannot be  distinguished  from the
 protoplasmic ones.  Another striking peculiarity of these two cellular
 types  is that they possess  not only one, but two or  more nervous
Perpendicular section of the
 gray matter of a  cerebral
 convolution. (Cajal.)

 1. Molecular layer;  2. Layer
of the small pyramidal cells;
3. Layer of the large pyram-
idal cells;  4. Layer of  the
polymorphous cells ; 5. White
matter.  (Cajal.) 
ANATOMY.
45
processes  extending horizontally in the thickness of the molecular
layer, where they divide frequently at a right-angle, thus traversing
an enormous space.  The fusiform  cell is ovoid (A  and C), lying
along a line horizontal  with the  surface of the  cortex, and  possess-
ing two large  polar trunks which are almost  rectilinear.  These
trunks, as has already been said, give off numerous  branches  at a
right  angle, then  curve so as to approach the surface of the cortex,
and finally break up  into two, three, or more filaments which are
very long and wavy, and which ramify exclusively, almost always at
a right-angle, iu the molecular layer.  During their course, often at
the level of the bend (Fig. 24,  C), these polar trunks emit very fine
horizontal  branches which  are also very long, and which themselves
are provided with ascending collaterals.  Some  of them, as at  A,
Fig.  24,  however,  do  not change their direction,   but gradually
dwindle in size until they seem to become a simple or double nervous
filament.   The triangular or star-shaped cell (JB) is different from the
fusiform one  in that  the cell-body  possesses three or  four  polar

                              Fig. 24.
  Special cells of the molecular layer of the cerebral cortex of a dog one day old.  (Cajal. )
  A. Fusiform cells; B. Triangular, or star-shaped cell; C. Another fusiform cell; D. Poly-
gonal cell with numerous protoplasmic processes, and one axis-cylinder divided several times :
c. Axis-cylinder.

branches which take a horizontal direction through a long tract, and
gradually dwindle into a filament like that of  an axis-cylinder, and
during their course they give off, like the fusiform cell, a number of
fine collaterals which cannot be  distinguished from other  nervous
filaments of the molecular layer.   According to Cajal, these fusiform
and star-shaped cells are found in the molecular  layer in all regions
of the cortex,  most especially  in  the  deeper  or internal half of the
former; whilst the  ordinary  star shaped cell, with  only one axis-
cylinder, is generally in the external half.  To the nervous filaments
of  the molecular  layer thus made by the axis-cylinders and these
peculiar cells, there are added a number of nerve-fibres coming from
the pyramidal cells, as we shall soon have occasion to see.
  The layer of small pyramidal cells  is composed of polyhedral or
pyramidal cells (2, Fig. 23) of moderate size, their  dimension and
the length  of their trunk increasing  from above downward.   This
trunk, which is often split into two near the body of the cell, termi-
nates  in  a large  plume or  bouquet, and occupies, interlacing  with
plumes  from  neighboring cells, almost  the whole thickness of the 
46
INTRODUCTORY.
molecular layer.  The axis-cylinder is very fine, descends, and splits
up into four or five fine collaterals, each of which in its turn divides
into two.   Golgi supposed that the collaterals of these axis-cylinders
anastomosed with each other to form a continuous network in the gray
matter.  Cajal, however, has traced them in a thoroughly satisfactory
and at the same time extremely interesting manner.  Finding that they
were  extremely  long in the human being and  the  large animal, he
searched for them in the embryo and in the newly born small mam-
mals, and ascertained that they terminated with a varicose expansion
without any interlacing;  and he has even followed them in the young
foetus from their very outgrowth from the axis-cylinder up to their
final dichotomous division.  The layer of small pyramidal cells merges
insensibly with the large one of the succeeding cells.
  The large cells of the  pyramidal layer (3,  Fig. 23) have a conical
or pyramidal shape, with an inferior base from which issues the axis-
cylinder.   The  protoplasmic processes are numerous and are divisi-
ble into the ascending trunk or primordial expansion, the collaterals
of the ascending trunk, and the basilar expansions or processes of the
cellular body.   The ascending trunk is thick and points to  the sur-
face of the cortex parallel to  the trunks of other pyramidal cells.
When it has  arrived at the molecular layer it expands  into a plume
or bouquet of protoplasmic brauchlets, which terminate free among
the nervous filaments of this zone, and the commingling of all these
plumes or bouquets gives rise to a very complicated  protoplasmic
plexus, to which is due the finely  reticulated  appearance of this por-
tion of the cortex in the  ordinary carmine staining.   Golgi supposed
that these protoplasmic branchlets were in connection with the vessels
and the neurogliar cells,  but Cajal positivelystates that they distrib-
ute themselves throughout the whole thickness of the molecular layer,
and Retzius has verified  this.   The axis-cylinder of these pyramidal
cells  passes through all the lower layers of the cortex and  into the
white substance, where it bends and becomes continuous with a nerve-
tube.   During its  course it gives off six to ten  fine collaterals  at a
right-angle, which  proceed horizontally or obliquely, and split up into
two or three terminal branches.  Cajal calls these pyramidal cells the
psychical cells.  They increase in their complexity the higher the scale
of creation rises, being exceedingly simple in the frog and the lizard,
beginning to  be complicated in the rat, and reaching  their highest
evolution in man.
  The  layer  of the polymorphous  cells  contains  a few pyramidal
cells  (4, Fig. 23),  some of which are  large, and some of  medium
size, whose trunk  is  directed toward the molecular  layer.   But the
most  of the cells are ovoid, fusiform, triangular, or polygonal.  There
are certain characteristics of almost all the cells of this layer.  The
trunk is usually of less  size  and  expansion,  so that it never reaches
the molecular layer or the terminal bouquets of the  pyramidal cells.
In some of them there is no  trunk, its place being  taken by two or
more short and oblique  processes, and  there are occasionally others
with  three protoplasmic  expansions, of which two pass to  the white
substance.  The axis-cylinder furnishes two to four collaterals which 
ANATOMY.
47
ramify several times and pass by a bend or a T-shaped division into
one or two nerves of the white substance.
  Intermingled in small number with the elements of the molecular
and the small  and large pyramidal layers are two species of cells
known as the sensitive corpuscles of Golgi, and the cells of Martinotti,
with  ascending  axis-cylinder.   The former are large and polygonal
and have protoplasmic expansions all  around the body, whilst the
axis-cylinder comes off from the upper or lateral  part of the body,
marches  in various  directions, and after a short distance splits  up
into a free arborization surrounding  the  body of the  neighboring
cells.   Golgi supposed that the shortness of the axis-cylinder was an
evidence of the sensory function of the cell; but Cajal suggests that
these short axis-cylinders  are probably only meant to connect with
neighboring cells, and this seems  much more  reasonable, because we
have  no  ground for supposing  that a sensory axis-cylinder  needs to
be any shorter than a motor one, inasmuch as it carries its messages
through equal lengths of tissue.   The cells of  Martinotti,  with an
ascending axis-cylinder, are especially to be found in the  layer of the
polymorphous corpuscles,  although, as has been  said, they are found
in some  degree through all the first three layers.  They are  fusiform
or triangular, with protoplasmic expansions that are either ascending
or descending, but the axis-cylinder, which may be emitted from an
ascending protoplasmic trunk,  mounts almost like a straight line to
the molecular layer, where it divides into two or three large  branches
 ramifying horizontally and splitting up into a terminal arborization
 of great  amplitude.   With some cells it has appeared to Cajal that
 this terminal arborization  was among the  small pyramidal cells.

                               Fig. 25.
   Section magnified 3.75 diameters, showing the nerve-fibre passing into a convolution.

  Into  these layers of the brain-cells  ascend  the  medullated nerve-
fibres from the sublying nervous regions, as is  represented in Fig. 25,
which is drawn from  a microscopical section of a convolution, and
in which the nerve-fibres  are seen coming up in a sheath or bundle
and diverging gracefully to penetrate the gray matter.   The medul- 
48
INTRODUCTORY.
lated nerve-fibres constitute the white matter of the brain, and are of
four varieties :
   1. Projection-fibres;
   2. Commissural fibres;
   3. Association-fibres;
   4. Centripetal or terminal fibres.
   The projection-fibres {C, Fig. 26) come from all the regions of the
cortex  and  converge toward the corpus striatum  to pass into the
crura cerebri.  In the small mammals they emit, at the height of the
corpus callosum, a large collateral for  this  body, and then they de-
scend in small  tracts separated  by layers  of  gray substance, which
they furnish with very fine  collaterals, although there are some of
them which maintain their individuality, without giving off a single
collateral throughout the whole depth of the corpus  striatum.   Molo-
koff and other authors supposed that these  projection-fibres were the
sole continuations of the large  pyramidal cells, whilst the association
and  the commissural fibres came from  the small pyramidal cells.
Cajal, however—although he is careful to explain  that his proof is
not as yet satisfactory—maintains that they come from both the large
Fig. 26.
 Transverse section of the cerebrum, showing the probable disposition of the commissural
                      and projection-fibres. (Cajal.)
   A. Corpus callosum;  B. Anterior commissure;  C. Pyramidal pathway formed of the
                           projection-fibres.

and  the  small pyramidal cells, and even from certain of the poly-
morphous cells, and he suggests that this origin from  cells of differ-
ent dimensions explains why the axis-cylinders are of varying size.
There is every reason to believe that their lower passage is through
the pyramidal fibres of the spinal cord, although the proof of this rests
upon the well-known pathological methods, and has received as yet no
confirmation or negation from the latest histological  investigators.
   The association-fibres are divisible  into short and long ones; the
short ones,  the so-called proper arcuate  fibres,  connect  each  two
neighboring  convolutions  of the same hemisphere.   Besides  these
the  tangential fibres really belong to this system  (Fig. 29).   The 
ANATOMY.
49
long fibres of association furnish a connection between the more dis-
tant convolutions of the  hemisphere, and they consist of the superior
longitudinal fasciculus, whose fibres run in  the direction of the second
frontal convolution, and  connect the frontal convolutions with the
occipital  convolutions;  of the  sub-callosal  longitudinal  fasciculus,
running  under the corpus callosum and also connecting the frontal
lobes with the occipital;  the inferior longitudinal fasciculus, running
to the side of the posterior horn of  the lateral ventricle and connect-
ing  the occipital lobes with  the temporal;  the uncinate  fasciculus,
crossing  the entrance of the  fissure of Sylvius and connecting the
lower frontal  convolution with the tip of  the temporal  lobe; the
cingulum, passing from   the  anterior  perforated space through the
gyrus fornicatus to the tip of the cornu ammonis, its anterior portion
connecting the olfactory bulb  with the frontal lobe, and its posterior
part  connecting the hippocampal gyrus with the temporal lobe; the

                                 Fig. 27.
Tearing of the cortex and the subcortical white matter along the medial surface of the
                      cerebrum.  (From Meynert.)
  F., Tp., O. Frontal, temporal, and occipital regions.  Tr. Corpus callosum. C. C. Cingulum,
surrounding the corpus callosum and beneath the calloso-marginal fissure.  As. Association
fibres, i.e., fibres connecting adjacent convolutions. R. Cortex,  bi. Internal basal fasciculus
of Burdach. Li. Inferior longitudinal fasciculus.  OIf. Olfactory lobe.  La. Lamina perforata
anterior,  ca. Anterior commissure, unc. Hook of the hook-shaped convolution of gyrus
uncinatus. Sp. Septum pellucidum. Th. Optic thalamus,  f.d. Descending fornix,  m. Cor-
pus medullare. f.a.  Ascending fornix.  Q. Corpora quadrigemina.  A. Aqueduct of  Sylvius.
Pv. Pulvinar of the optic thalamus.  Gi. Internal geniculate body.  T. Tegmentum.  Pd. Pes
of crura cerebri.  St.i. Internal stylus of the optic thalamus. Lp. Posterior longitudinal fas-
ciculus, co. Conarium.

vertical fasciculus,  which brings the lower parietal lobe into connec-
tion with the fusiform  lobule.  (Fig. 27.)  In the cerebellum there are
also association-fibres  passing from convolution to  convolution, the
so-called garland-shaped fibres of  Stilling.   Those  of the cerebrum
probably arise from the  three layers of  cortical  cells—i. e.,  the large
and small  pyramidal  and the polymorphous cells;  but as yet  all
                                   4 
50
INTRODUCTORY.
that  has  actually been observed  has  been their  connection with  the
polymorphous  cells, and  occasionally  with a  large pyramidal ceil.
The   axis-cylinders  of these  cells  connect  with  the  association-
     Frontal section of the occipital lobe showing the association-fibres, according to
                                Sachs, of Breslau.
  v. Descending cornu or horn of lateral ventricle, f.c. Calcarine fissure, s.  Upper cleft of
calcarine fissure,  i. Lower cleft of calcarine fissure,  coll. Collateral sulcus.  s.o.I.  Parietal
fissure.  s.o.II. First occipital fissure. s.o.III. Second occipital fissure,  c.a. Calcar avis or
hippocampus minor, g.l. Lingual lobe.  g.f. Fusiform lobe, g.o.s. First occipital convolution.
g.o.m.  Second occipital convolution, y.o.i. Third occipital convolution,  c. Cuneus.
  The following are the different strands which Sachs has marked out:
  1-10. The forceps.  11-14. Internal sagittal stratum.  15.  External sagittal stratum.  16. Cal-
carine stratum.  17. Transverse stratum of cuneus.  18. Stratum proprium of cuneus. 19. Stratum
proprium of parietal fissure. 20. Stratum proprium of first occipital fissure. 21. Stratum pro-
prium of second occipital fissure.  22. Stratum proprium of the collateral sulcus.  23. Deep
stratum of convexity.

fibre usually by a simple bend, but occasionally by a T-shaped divi-
sion into equal  or unequal fibres;  so  that many  of these  association-
fibres, by means  of the direction of  the  different  connections of the 
ANATOMY.
51
two bifurcating branches, may bring a cell at one place in the cortex
into relation with a large number of others in far distant  regions.
These  association-fibres increase  proportionately to the  mass of the
gray matter, so that in man and  the large mammals they form the
principal  mass  of the white substance.   Their number and  their
extraordinary length, conjoined with their  intricate interlacing with
the projection and commissural fibres, renders it impossible to follow
any one of them anatomically, and hence it is that they have hitherto
only been studied by the so-called tearing method in  brains that
have been peculiarly  hardened.   But Cajal has made the happy dis-
covery that they can be investigated with far greater readiness in the
small brains of the rat, the bat,  the  mouse, etc., not only because of
the much more minute dimensions, but also because, singular to say,
in certain places the association, commissural, and projection-fibres are
perfectly  delimited.   Cajal  has also demonstrated that  in  many of
the association-fibres there are very often collaterals which ascend
and ramify in the different layers of the cortex, some of  them going
as far up as the molecular  layer, and  others as far down as the
white  substance.  These association-fibres terminate, like the fibres
in the spinal  cord, by means of free, wavy arborizations extending
throughout the whole cortex, even to the molecular layer.
   The commissural fibres are to  be found in the corpus callosum [A,
Fig. 26) and the anterior commissure (B).  The former consists mainly
of fibres  running from one hemisphere to another, passing  horizon-
tally across and  then  bending so as to diverge fan-like into  different
but always identical portions of  the hemispheres, with the exception
of the temporal and the basal portions of the occipital lobes and the
olfactory bulbs.  The anterior  commissure of the same side is  an
addition to the corpus callosum, and connects those identical  portions
of the  hemispheres which  the corpus callosum does not join.   In
the cerebellum there are also commissural fibres connecting  identical
portions of the two hemispheres, and again in the brain-stem between
the identical nuclei of the cranial nerves, and still again  in the spinal
cord, in which the fibres of the posterior commissure connect the cells
of the two posterior horns.   The commissural fibres (A  and B, Fig.
 26) are situated  beneath those of association  and maintain  a trans-
 verse direction in the small mammals.   They are  extremely minute,
and Cajal has determined that they have a medullary sheath.  They
arise in different regions of the cerebral cortex of one hemisphere and
terminate in the other, but in the sphenoidal lobes they are aggre-
gated into a separate tract to form the anterior commissure. Many
of them  give off very fine  collaterals at a right angle,  generally to
the number of two or three, and these  ascend to be lost in  the gray
matter above, where they terminate in a  free end.  Some  of  them
even  bifurcate, one of the divisions passing horizontally and the  other
 penetrating the  gray matter (c,  Fig. 26).  It would seem  probable
that these  commissural fibres are made up of direct axis-cylinders
and of collateral fibres of other axisrcylinders, because, on the one
hand, certain of them have been traced as collaterals of either asso-
ciation- or projection-fibres, whilst, on  the other hand, other fibres 
52
INTRODUCTORY.
have been followed from different layers of the cortex, principa ly
from the level of the small pyramidal cells, down to the corpus callo-
sum, into which they  pass with a bend.  This,  however, it should be
borne in mind, is not  yet positively determined.  The termination of
the commissural fibres is still more uncertain, although some of them
have been seen  ascending through  the gray substance and there rami-
fying, but as yet their terminal arborization has not  been actually
observed.  Sufficient, however, is  known of them to enable us to re-
gard them as nervous  connections between symmetrical regions of the
same hemisphere, as  well as probably also  between similar elements
of the different regions and layers of the cortex.

  We have learned much in the  last few years of the nervous con-
nections between  the different layers of cortical cells.   Certain thick
fibres have been observed passing obliquely or horizontally through
the gray substance and ramifying,  throughout the whole thickness of
this region, even the molecular layer, with a ramification of enormous
extent (Fig. 30, E).   These  are supposed  to come from the spinal
cord, the cerebellum,  etc.   The terminal branches of these ramifica-
tions are varicose, and especially surround  the  small pyramidal cells.
Cajal ventures the  suggestion  that  these are  probably  sensitive
nerves,  or at least axis-cylinders  coming from cells which are con-
nected with  the terminal fibres of sensitive  nerves.  He has observed
them especially in reptiles.  Be  this  as  it may, certaiu  facts are
assured  about  the connection of nerve-fibres with these cells of the
cortex.   Fig. 29 delineates a section of the cortex  stained  with
Weigert's haematoxylin  upon the left side, and according to Golgi's
method  upon the right, showing  the cells therefore on the left hand
and the fibres on the  right.  The layers of the cells  have already
been explained in  Fig. 23.  It  will  be  seen that  the uppermost
region of the cortex  contains a number of fine fibres which mostly
maintain a tangential direction.   Beneath these tangential fibres are
seen the super-radiating fibres.  At a lower level still is the layer of
Gennari, and at a still lower  level the  inter-radiating  fibres, whilst
lowermost of all are the radii themselves.  The  relation of these to the
different layers and cells is easily seen from this figure.  Cajal has
endeavored  to  show the course of the nervous currents into and out
of these cortical cells in the following manner (see Fig. 30): Starting
from  the fact  that  all the  pyramidal cells, as has  already been
described, have a protoplasmic plume or bouquet extending into
the molecular  layer,  he regards these  structures as the receptacles
of  nervous currents  from  other  cells  through  the  axis-cylinders
coming  into these protoplasmic expansions. In other  words, to use
Cajal's  terms,  the  current  is cellulifugal  in   the axis-cylinder and
cellulipetal in the cell-body or the protoplasmic processes, the latter
receiving the currents and the former transmitting them.  (See Fig. 30.)
Reasoning from  these premises, Cajal suggests that in the molecular
layer of the cortex the plume of the pyramidal  cells receives currents
(1) from the special cells of the molecular layer  through their nervous
expansions; (2) from the vertical fusiform cells of the cortex, by means 
ANATOMY.
53
of their upper  arborizations and their ascending axis-cylinders;  (3)
from the pyramidal cells of association in variously distant regions of
the cortex, through the medium of their ascending collaterals and the
terminal arborizations of their axis-cylinders;  (4) possibly also from
Fig- 29.                            Fig. 30.
the cells of the cerebellum, of the spinal cord, etc., through  the ex-
tended nervous arborizations which form, throughout the whole gray
matter, certain large fibres coming from the white substance; (5) pos-
sibly also from the cells of the opposite hemisphere through the ter-
minal brauches of the commissural fibres.   This suggestion is in the
line of  very rigid reasoning  from  the facts that have already been 
54
INTRODUCTORY.
explained, and it certainly offers a superb explanation, together with
what follows, of the widespread  commingled cerebral and physical
symptoms of general paresis, in which, as we shall  have occasion to
see, the lesions are especially in the molecular layer.  The nervous
connections between the  pyramidal and  the polymorphous cells are
extremely complicated.   They are between the cellular  body, the
trunk, and  the protoplasmic processes of these cells, upon the one
hand, and five varieties of nervous fibres upon the other, which latter
are constituted by the collaterals of the white substance,  those of the
corpus callosum, the terminal association-fibres, the terminal arbori-
zations of the so-called sensory cells of Golgi, and  the _ myriad col-
laterals coming from  the axis-cylinders  of the cells in the  three
deeper layers of the cortex.  If these conjectures of Cajal's be correct,
the pyramidal cells would receive in this  manner nervous influences
from the sensory cells of Golgi that are scattered throughout the layer
of the pyramidal cells; from the cells of the association-fibres situated
in the different lobules of the same hemisphere;  from the same cells
of the opposite hemisphere, through the medium of the commissural
fibres or the anterior commissure ; from the cells of the sensory areas
of the cerebrum, and from the cells in the layers beneath the pyramidal
cells.  The  last of these connections  appears  to  be established by
means of  the collaterals of the axis-cylinders coming from the upper
pyramidal cells, as well as by the  medium of the body, the protoplas-
mic trunk, and the basilar processes of the pyramidal cells beneath.
Each collateral is of great length, has many ramifications, and main-
tains a horizontal course,  so that it touches the  protoplasmic expan-
sions and the bodies of  many cells, enabling the small pyramidal
cells to send a nervous current to a whole series of other pyramidal
cells, both medium-sized  and small, lying at a deeper level.   Each
large pyramidal cell, in its turn, owing to its large surface of con-
tact  through its trunk, its protoplasmic collaterals, and  its descend-
ing basilar processes, can receive nervous currents from an infinity
of pyramidal  cells above it.  This is  represented in Fig. 30 {A, B,
C, D), in  which the arrows show the  direction of  the nervous cur-
rents.  Although  this matter is to some extent conjectural, yet cer-
tain  fibres have been seen terminating by arborizations in the cortical
layer of the optic lobe in birds, which is the equivalent of the molecu-
lar layer  in  the  human being; in certain mammals  fibres coming
from the olfactory lobe send collateral and terminal branches to a su-
perficial zone which is the place of union between the protoplasmic
plumes of the pyramidal  cells,  and which is therefore the exact ana-
logue of the molecular layer of the human cortex ;  whilst in reptiles
not only the olfactory fibres, but even the other axis-cylinders, prob-
ably contain sensory fibres from the cord, and ramify  in great  num-
bers in the superficial  or molecular layer of the cortex.    For these
reasons Cajal believes that a voluntary movement  begins in the pro-
toplasmic  plume or bouquet of the pyramidal cells, and that therefore
it has its origin in the midst of the molecular layer, and he would
thus explain the fact that  mechanical, chemical, and electrical stimuli
of the cerebral cortex will excite movements in determinate muscular 
                             ANATOMY.                          55

groups.   Andriezen has recently shown that the whole cortex is per-
vaded by several strata of nerve-plexuses, extending in sheet-like
fashion.   These are illustrated in  Fig. 31.  Each of  these plexuses
is for purposes of association, and contains association, commissural,
and projection-fibres, which, Andriezen maintains, connect with the
apical or basilar protoplasmic expansions of cortical nerve cells.   An-
driezen furthermore describes certain cells to which he gives the name
of " ambiguous."  These are contained in the molecular  layer, and

                                Fig. 31.
       Cortex of the human brain, showing the nerve-fibre systems and plexuses
                   (combined Weigert's and Golgi's methods).
 c. s. Clear zone (free from nerve-fibre).  M. P. Molecular plexus (Exner's) in the molecular
layer.  A. str. Ambiguous cell-stratum.   Subm. P. Submolecular plexus.  Gt. P. P. Great
pyramidal plexus.  Pol. P. Polymorphic plexus.  W. White substance. (Andriezen.)

they are fusiform, pyriform, triangular, or polygonal in shape, but
often bifurcated into  two unequal horns.  He  regards  them  as dis-
tinct in an anatomico-physiological way, and as receiving and distrib-
uting sensory excitations in the same manner as the pyramidal cells.
  This cortex  or  gray matter  of the cerebrum is the organ of the
mind, and the  so-called centres  are  simply the terminal stations of
the different peripheral nerves which are thus brought into connec- 
56
INTRODUCTORY.
tion with the mind as a whole.  The centres are therefore only com-
partments of the mind, and clinical observation constantly shows that
lesion of any one of them need not  cause mental impairment; but
that, to produce disorder of the mind, there must  be more  or less
widespread disease of the cortex involving a  number of centres.  On
the other hand, as we shall have occasion to see when studying the
insanities, mental disease may exist alone without the physical symp-
toms that demonstrate  lesion of the  individual centres.   Through
the influence largely of the  teachings of the German  school  it is
generally supposed that the  frontal lobes anterior to the motor area
must be affected  in order to have mental disease;  but this has been
again and again  disproved by clinical observation, as lesions in the
different lobes of the brain have been quite sufficient to cause marked

                              Fig. 32.
         Section of the cerebrum, showing the centrum ovale on the left side.

mental  symptoms.  We are  therefore warrauted in regarding the
cortex, as a whole, as the organ of the mind, and the so-called centres
as being  those areas of the cortex in which terminate the nerves
coming from the periphery,  or  what are known as the projection-
fibres, in contradistinction to the commissural and association-fibres
of the cerebrum,  which, as we have seen, connect the different con-
volutions.
  It will now be  our task to travel the highlv complex  route which
these  projection-fibres take  from the cortex to the peripheral struc- 
ANATOMY.
57
tures, although it  must be  borne in mind that in doing this we can
no  more  than outline the anatomical  facts which  have a  clinical
bearing.   Fig. 32 represents  upon the  left  side a transverse section
made across  the  hemisphere a short  distance below the vertex, and
shows the centrum ovale, consisting of the white matter in the centre,
fringed around with  the  convolutions.  Fig.  33 represents a still
deeper section  of the hemisphere, showing in the middle  line the
great mass of commissural or connecting fibres  running across  from
one  hemisphere to the other, the so-called corpus callosum.   When
this corpus callosum is lifted (Fig. 34) the ganglia of the base, or the
basal ganglia, are seen lying in the ventricles, the third ventricle in
the  centre and the lateral ventricles one on each side.   These basal

                              Fig. 33.
The centrum ovale and the corpus callosum.
ganglia consist of several masses of gray matter.  On each side of
the median line is seen a large pear-shaped body, the optic thalamus.
To the outside of this is a tail-shaped body, commencing anteriorly
in a large club-shaped head, and running posteriorly to  pass down-
ward  and inward and  terminating in a tail.  This, because of its
shape, is known  as  the nucleus caudatus,  or the caudate  nucleus.
When a transverse  section is  made through these basal ganglia at a
still deeper  level (Fig.  35) this  caudate nucleus will have  had  the
body  of it between  the head  and the tail cut away so that only the
head will be seen anteriorly, whilst posteriorly the tail alone will be
visible.  It is therefore evident that the caudate nucleus is arched, 
58
INTRODUCTORY.
like a tadpole, from its head to its tail, and it is this arch  that "cut
away by the section of which we are now speaking.   At tins deeper
level there comes into view another mass of gray matter, the so-called
lenticular or bean-shaped nucleus, to the outside of the caudate nucleus
(i.e., its severed head  and tail) and  the optic thalamus.   I his len-
ticular nucleus has three compartments, an outer, a middle, and an
inner one, seen in Fig. 35.  The caudate  nucleus and the lenticular
nucleus were  regarded by the older anatomists as  essentially one
structure, and were  known  by the collective name of the corpus
striatum.   Running between the head of the caudate nucleus  ante-
riorly and internally, the optic thalamus and the tail of the caudate
nucleus posteriorly and internally, and the lenticular nucleus exter-
nally, is a mass of white fibres known as the internal  capsule.  This
Fig. 34.
Lateral ventricle
interior commissure
Cau da fe-
ll Helens
Middle commissure

  3rd ventricle
 Posterior
commissure
_ Corpus
 quadrigeminum
—Descending
 cornu
          ^ / I
   'Cerebelluui"
Basal ganglia of the cerebrum.
contains the nerve-fibres coming from the convolutions and converg-
ing at this point to pass in and between the deeper masses of gray
matter.  The nerve-fibres, therefore, which have  been spread  out
over the wide surface of the overarching convolutions of the cortex,
are here narrowed into the constricted strait of the  internal capsule.
This should be carefully borne in mind, because upon this anatomical
fact depend some important points of diagnosis, as it will be evident
that a small lesion capable of injuring many fibres which are packed
together into the narrow compass of the  internal capsule would be
utterly incapable of injuring the same number of fibres if it attacked
them after they  had spread  out  over the wide area of the cortex.
At the right  side of the brain, in Fig. 35, for example, are figured the 
ANATOMY.
59
different convolutions  of the vertex of the brain.   Let the reader
contrast the size of the lesion that would be necessary to affect all the
different centres upon these convolutions with the size of the lesion
that could affect  the nerve-fibres  coming  from  these  centres  after
they have converged into the internal capsule, and he will obtain a
clear idea of what I am attempting to explain.  This internal capsule
is composed of  an  anterior  portion and a posterior portion, and the
point at which these bend into one another is known as the knee, or
genu.   The anterior portion contains the motor fibres, and the pos-
terior portion the sensory fibres; indeed, it may be borne in mind as
an invariable rule in tracing the course  of a nerve-tract in the brain
and cord, that the motor fibres  lie always anteriorly, or toward the
abdomen, or ventrad, as is technically said, whilst the sensory fibres
always lie posteriorly,  toward  the back, or dorsad.  Some of the
fibres  coming  from  the cortex pass straight through to lower levels,
whilst others terminate in these basal ganglia, and others still origi-
nate in them and pass  to  the periphery or to other masses of gray
Fig. 35.
Int. Capsule\
Caudate Nucleus
    (Head)
1st Frontal/.


    2nd Frontal/.
—F.Rolando
CaudateNuclei
    (Tail)
Optic Radiatio


      Pulvina i
1st Temporal /.
2nd Temporal/.
Parietal/.
                        Cuneus  Pari •'""ccipital/.
Convolutions of the vertex, on the right;  on the left, the basal ganglia, the internal capsule,
                     the centrum ovale, and the cuneus.
matter.  A moment's thought will convince anyone that this is only
what should  be expected, because, unless  the  basal  ganglia are to
remain isolated, they must be connected with the cortex, with the
periphery, and with other masses of gray matter.  In that portion of
the internal  capsule lying anteriorly to the knee, or genu, are to be
found  the fibres coming  from the frontal  convolutions, whilst just
about the " knee " are the fibres  supplying  the facial muscles, just
behind these the fibres supplying the tongue, just behind these again
the motor fibres going to the extremities, and still again just behind 
60
INTRODUCTORY.
 Pulvinar, optic nerve, optic chiasm, optic tract, pons, dorsal surface of medulla and upper
portion of cord, base of cerebellum, and superficial origins of the second, third, fourth, fifth,
sixth, seventh, eighth, ninth, tenth, eleventh, and twelfth cranial nerves.
which is a  narrow streak of gray matter, the claustrum.   External
to the external  capsule are those inturned convolutions lying buried
in the fissure of Sylvius, and known as the island of Reil.   The right
side of Fig. 35 will make it clear how it is that the island of Reil
comes in at this point.  From the internal capsule the fibres pass on
down  into  the  crura  cerebri, which can  be seen  at the base of the
brain  by going back to Fig. 18, where it will also be observed that
their fanciful name of the legs of the brain, given them by the early
anatomists, was not so badly chosen.  The crura  cerebri  however 
ANATOMY.
61
are more distinctly shown in Fig. 36, and this shows their relation
to the optic  chiasm and  the surrounding  uuder-lobes of the cere-
brum.  From  the crura  cerebri  the  nerve-fibres pass on through
the pons Varolii, or  the bridge of  ATarolius, which is the name
given to the mass of fibres passing over from one lobe of the cere-
bellum to the other.   Fig. 37 shows the transverse fibres cut in the
centre so that  one-half of the right side  is lifted, in order to make
clear  the course of the long or longitudinal  fibres.  In this it will
be evident how the nerve-fibres,  after having traversed the pons,
pass on  down  to  the  spinal  cord, which  is  here called the oblong
spinal cord, or  medulla oblongata.
Middle cerebellar
   peduncle
 Middle cerebellar
"""   peduncle
Specimen hardened in alcohol, showing the transverse and the longitudinal
                     fibres of the pons.
   This therefore  brings us to the connection of most of the fibres
with the spinal cord.  Before passing on, however, to a study of this
latter organ, we should have  some understanding of certain regions
lying above or dorsad of the  crura and the pons.
   Let us go back to Fig. 35.  In this, as we have already seen, the
optic  thalamus and  the two ganglia of the  corpus striatum (the len-
ticular and caudate nucleus) are demonstrated.  At the posterior and
internal  portion of the optic  thalamus is an elevation of the body
which is known as the pulvinar.   Fig. 38 shows the relation of the
optic  thalami to certain other bodies, which it is important to study
in relation to the  optic nerve.  Behind the pulvinar are seen four
elevations of nervous tissue, which are known as the corpora quad-
rigemina, there being on  each side an anterior and a posterior one.
On the inner edge of the pulvinar, just about where the posterior
quadrigeminal body joins it, is a little elevation known as the middle
geniculate body, whilst a  little further forward, just about where the
anterior  quadrigeminal body joins the pulvinar, is  seen the lateral
geniculate body. 
62
INTRODUCTORY.
  The optic fibres, which we  have seen in Fig. 34 coining  into the
posterior portion of the internal capsule, pass through the optic thal-
amus anterior to the pulvinar and into the anterior quadrigeminal
body, and  thence to the  pulvinar, from which  they  go on  down to
the optic tract.  The optic tract takes its origin in the anterior quad-
rigeminal body in a fine network coming from numerous delicate
cells in what  is known as the stratum  zonale, as well  as from the
lateral geniculate body, the pulvinar, and a deeper-lying mass of gray
matter with which we shall soon become acquainted, the subthalamic
body, and also from the gray matter at the base of the brain, near
Fig. 38.
Optic thalamus
Pulvinar-
¥lf   ^v,,ilieaI gland (stump)
    " ^ffl^    Lateral
       ^ilM ^geniculate
              body
              Corpora
            luadrigemina
aqueduct of Sylvius
4th ventricle
            Aperture into central canal
                 of spinal cord

 Specimen hardened in alcohol, showing pulvinar, pineal gland,  corpora quadrigemina,
geniculate bodies, superior cerebellar peduncle, fourth ventricle, aperture into aqueduct of
Sylvius, aperture into central canal of spinal cord, restiform bodies, and striae acousticae.
the infundibulum.   The  function of  the posterior quadrigeminal
body is unknown, although Spitzka has shown that its extraordinary
development in cetaceans and the  large bands of fibres passing from
it  to the  nucleus of the auditory nerve render  it probable  that  it
has some  relation to hearing;  and Baginski has demonstrated that
it  atrophies  after destruction  of  the auditory  nerve.   We can per-
ceive, therefore, that the course of the optic nerve is not so compli-
cated as it would seem at first sight.   From  the anterior quadri-
geminal body the optic nerve-fibres go to the cortex through the
optic  thalamus anterior to  the pulvinar, into the  posterior portion
of the  internal capsule, and thence to  the occipital lobe as  repre-
sented in Fig. 39.   From this same point of origin in the anterior
quadrigeminal body and the neighboring parts that have been men-
37839� 
ANATOMY.
63
tioned, the fibres going to the retina first pass to the lateral geniculate
body, then to the pulvinar, and  then to the optic tracts,  which
crossing  in the optic  chiasm, pass to  the retina.  Fig. 39 is a dia-
gram of  this course of the optic nerve.  It shows its cortical origin
in the occipital convolutions, thence its passage into the internal cap-
sule, through the optic thalamus into the anterior quadrigeminal body,
and  thence to the geniculate body, to the  optic tract, to the chiasm,
to the retina.   It will be observed that the optic  fibres proceed from
the left  cuneus  to the left half of each retina, which would  be  the
outer half of the left  eye and the inner half  of  the right eye.   As
the rays of light,  however, cross  in  the  optic lens when  they come
from  without to reach the retina, this blindness of the outer half of

                              Fig. 39.
                       Cuneus
Diagram of the course of tne optic fibres from the cuneus to the retina.
the left retina would incapacitate the patient from seeing objects to
the inner side of the median line, whilst the blindness of the left or
inner half of the right eye would incapacitate the patient from seeing
objects to the outer side of the median line of the right eye.  This
should  be clearly understood, for, as  has already been  stated,  the
blindness of the retina is called hemiopia, whilst the inability to see
objects with  this retina is called  hemianopsia, so that the left hemi-
opia of the case which we have been supposing would cause a right
hemianopsia.
  Fig. 40 gives us another view of these central  and basal ganglia
which we have  been describing.   It  represents a  section midway
through the corpus callosum (c c), which we have  seen  in Fig. 33
forming the floor of  the great longitudinal fissure and connecting the
two  hemispheres.  Beneath the corpus callosum is seen the  third
ventricle (3) running down into a funnel-shaped prolongation, known 
64                       INTRODUCTORY.
 Vertical section of specimen, showing corpus callosum, lateral ventricle, third ventricle,
infundibulum, aqueduct of Sylvius, fourth ventricle, upper portion of central canal of spinal
cord, corpora quadrigemina, velum medullare anterius, pons, medulla oblongata, cerebellum,
and cerebrum.
surface of the  pons (p) and medulla  oblongata.   Let  us turn  back
for a moment  to Fig. 36, so as to get the view of the under portion
of this same pons, and to Fig. 37, so as to get an idea of the course
of the  transverse and longitudinal fibres of the pons, and then in our
imagination  let us transfer the pictures of Figs. 36  and 37 to the
pons as it is  represented in Fig. 40.  Let us furthermore remember
that the ventricle is a continuation of the central canal of the spinal
cord, and that the aqueduct of Sylvius is the narrow aperture of con-
nection between the third  and fourth ventricles.  All along the upper
part of the central canal of the cord, on the floor of the fourth ven-
tricle,  along  the under surface of  the valve of Vieussens as it arches
over the fourth ventricle and the aqueduct of Sylvius, along the floor
of the  aqueduct of Sylvius, and along the floor of the third ventricle,
almost down to where it commences to narrow into the infundibulum, 
IN ATOMY.
65
is  gray matter containing nerve-cells, and in this gray matter ten
cranial nerves have their origin from the twelfth to the third inclusive,
the twelfth most posteriorly and the third  most anteriorly.   In other
words, it is evident that  the  spinal cord is thus  prolonged into the
brain, so that the medulla oblongata, as it is  called, is nothing more
than the upper enlarged end of the spinal cord, so altered in shape as

                                Fig. 41.
    Section through the valve of Vieussens and the lingula. Magnified 6.6 diameters.
  Py. Pyramid.  Po. Transverse fibres of pons.  Lm. Lemniscus. Frtg. Central field of teg-
mentum.  Flp.  Posterior longitudinal fasciculus.  Leo. Locus caeruleus.  Niv. Nucleus of
the trochlear nerve. Nvm. Nucleus of motor root of fifth nerve. Aq. Aqueduct of Sylvius.
Lng. Lingula. Brcj. Superior cerebellar peduncle. Crst. Restiform bodies.  Vm. Fibres from
motor root of fifth nerve.

to conform to the exigencies of cerebral architecture.  Let us suppose
that a number of microscopical sections are made through the regions
of the pons,  aqueduct  of Sylvius, fourth  ventricle,  and upper part of
the spinal cord,  as shown  in Fig. 40, and we will get an idea of the
topography  of  this region by the study of them.
  Fig. 41 represents  a  drawing of a  section through the  valve of
                                  5 
66
INTRODUCTORY.
    Section through the valve of Vieussens and the lingula, just behind the posterior
                 quadrigeminal bodies. Magnified 5.2 diameters.
 Py. Pyramid.  Po. Transverse fibres of pons. Frtg. Central field of tegmentum. Lm. Lem-
niscus.  Lml. Lateral lemniscus.  Lmp. Nerve-tract connecting pes of crura cerebri with
lemnisco-pedal tract. Flp. Posterior longitudinal fasciculus.  Lng. Lingula of cerebellum.
Aq. Aqueduct of Sylvius.
which have no nuclei of the  nerves of the  ocular muscles, possess
as large  a posterior fasciculus as rabbits.   The nucleus of the motor
root of the  fifth pair is seen at Nvm, and at  Vm are the nerve-fibres
passing from it.  To the outer side of these are the fibres of the sen-
sory root of the fifth pair.  At Leo is seen the so-called locus cceru-
leus or substantia ferruginea, a  collection of large,  dark, pigmented
cells—although the former term, it should be  remembered,  is some-
times applied to a dark-brown or bluish spot, four to six millimetres
in length, occasionally observed in the  floor of the  fourth ventricle.
The locus cceruleus here depicted sends off fibres  to  the  trigeminus, 
ANATOMY.
67
these passing to the median line, to the raphe, then through the pos-
terior longitudinal fasciculus, most of them reaching the motor branch
of the trigeminus.  At Niv is the nucleus of origin of the trochlear
or fourth nerve.   Lng is the lingula, the  lobe of the cerebellum lying
over  the valve of Vieussens,  which  can  also  be seen in this illustra-

                                 FlG. 43.
           Section made just behind the posterior quadrigeminal bodies.
                          Magnified 6.6 diameters.

 Py. Pyramid. Po. Transverse fibres of pons. Lm. Lemniscus.  Lml. Lateral lemniscus.
Lmp. Tract connecting lemniscus and pes, lemnisco-pedal tract.  Frtg.  Central field of teg-
mentum.  Flp. Posterior longitudinal fasciculus. Leo. Locus caeruleus.  Vd. Descending root
of fifth pair.  Aq. Aqueduct of Sylvius.  LV*. Decussation of trochlear nerve-fibres.  Brcj.
Superior cerebellar peduncle. NVm. Motor nucleus of fifth pair.


tion.   Brcj is the superior cerebellar peduncle, and Crst is the resti-
form body, forming the inferior cerebellar peduncle.
  Fig.  42 is a microscopical section made higher up, so that it comes
just behind the  posterior quadrigeminal  bodies,  as  represented in
Fig. 38.   In it the motor fibres running to the periphery are seen in
the pyramids, Py, and  passing between these from side  to side are 
68
INTRODUCTORY.
the transverse  fibres of the pons, Po.   Dorsad of these is the lem-
niscus,  Lm, and the  lateral lemniscus, Lml, whilst  at  Frtg  is  the
central  field of  the tegmentum.  The superior cerebellar peduncle is
seen laterally to the  tegmental field  at  Brcj.   Just  above the  teg-
mental  field is seen the  section transversely of the posterior  longi-
tudinal fasciculus, Flp.   The aqueduct of Sylvius  is very clearly
shown at Aq, and above it  is the lower portion of the lingula.
Sqs
Fig. 44.
Jzuu^^rcj
Nlml
      Section through the posterior portion of the anterior quadrigeminal bodies.
                          Magnified 6.6 diameters.
^ ZSTTid\?°- Transverse fibres of Pons.  Lm. Lemniscus. Lml. Lateral lemniscus
Nlml. Nucleus of lateral lemniscus. Lmp. Tract from lemniscus to pes, lemnisco-peXuract
^Central field of tegmentum. Flp. Posterior longitudinal faseicuL  ZLocusciruk»
JP. Descending root of trochlear nerve.  Yd. Descending root of fifth pair  ^SupTrior
Sies   ?     "  ^ AqU6dUCt °f  SylVlUS-  *"■ SU1CUS  ^neathPthe quSrigeminal


   In Fig. 43 is represented a section also made at the posterior portion
of the quadrigeminal bodies, and in it are again shown the relations of
the various parts which we have been  considering : the pyramids at
Py,  the transverse fibres of the pons at Po, the sensory fibres 0fth
lemniscus and  the lateral lemniscus at Lm and Lml, the central field 
ANATOMY.                           69
of the tegmentum, Frtg,  the posterior longitudinal fasciculus at Flp,
and the superior  cerebellar peduncle at Brcj.   Certain other struct-
ures,  however, here come into view.   1 "d is the  descending root of
the trigeminus; Lmp the tract  connecting  the sensory fibres of  the
lemniscus with  the motor structures of the crura—what I term  the
lemnisco-pedal tract—and at IV1 are seen the fibres of the trochlear
nerve crossing in the roof of the  fourth ventricle.
  Fig. 44 represents a section made through  the posterior  portion

                                Fig. 45.
  Pp. Pesor foot of the crura cerebri. Sns. Substantia nigra. Csth. Subthalamic body or body
of Luys.  Nig. Red nucleus.  Al. Ansa lenticularis. F. Forel's tegmental decussation. M.
Meynert's ventral decussation. N3. Nucleus of oculo-motor nerve. Flp. Posterior longitudinal
fasciculus.  Aq. Aqueduct of Sylvius.  Rsp. Subpineal recess.  Cop. Posterior commissure.
Vd. Descending root of fifth.  QA. Anterior quadrigeminal body. Lm. Lateral lemniscus.

of the anterior quadrigeminal  bodies.   The same structures can be
studied in this as in Fig. 43, which we have just  considered, except
that the descending fibres of the trochlear nerve are distinctly repre-
sented at the side of  the aqueduct at IV1, whilst at Sqs,  above the
aqueduct of Sylvius, is seen the sulcus between the anterior quadri-
geminal bodies, the so-called sulcus corporum quadrigeminorum sagit-
talis, and at Nlml is the nucleus of the lateral lemniscus. 
70
INTRODUCTORY.
  Fig. 45 is  a section  through  the region of the pineal  gland, as
represented in  Fig. 38, exclusive  of the  pulvinar.   Here we see
that the  motor  and  the sensory fibres are  widely separated,  the
motor  fibres  lying  in the so-called foot or pes of the crura cerebri
at Pp, and  the sensory  above or dorsad in  the lemniscus at Lm  the
posterior  longitudinal fasciculus at  Flp, and at Al a set of fibres,
probably  sensory, that pass around the lenticular  nucleus  into  the
internal  capsule, and  which are therefore  known  as the  ansa len-
ticularis.   At N* is  seen a portion of the nucleus of the  hird  or
motor  oculi nerve.    At M is seen the tegmental  decussation  de-
scribed  by  Meynert,  and called after him, whilst at  F is another
tegmental decussation described  by Forel, to which his name  has
Anterior perforated
     space
      Fig. 46.
Gray matter at base of frontal lobes
   I
   \   Posterior longitudinal fasciculus

   1   \
        1  Ascending radicle of fornix
Island of
  Reil
    Optic tract-
Caudate nucleus_
       (tail)
Hippocampus'-^-------
                 3d ventricle
                                     ( Valve of V lcussens
                           Aqueduct of Sylvius
Transverse section of lowermost portion oi cerebrum and basal ganglia, showing the main
        structures at this level. (Dalton's Topographical Anatomy of the Brain.)

been  given.   At  Cop  is  seen  the posterior commissure;  beneath
it, at Rsp, the subpineal  space,  and  above  at  the side,  QA, the
anterior quadrigeminal  body.   The descending root of the fifth pair
is still  seen at this level, as represented at Vd.   But this figure
beautifully represents three masses of gray matter which are coming
to be of considerable  importance in our modern  anatomical  knowl-
edge.  The red nucleus is  represented at  Ntg as  a round body sur-
rounded by fibres, whilst the substantia nigra, a collection of darkly
pigmented cells, is seen at Sns, just above the  pes of the crura cerebri,
and at Csth is the subthalamic body, or body of Luys.
   If we now go  back, and from the superior aspect view this region
99999915 
ANATOMY.
71
in which we have been making sections, we shall have such a picture
as is presented in Fig. 38.  Above we see the optic thalamus on each
side, between  them the stump of the pineal gland, just back of them
the corpora quadrigemina, and still further down the fourth ventricle,
a side view of which we have had in Fig. 40.  At the upper end of the
fourth ventricle is seen a narrow aperture passing into the aqueduct of
Sylvius, and at the lower end of the fourth ventricle is another narrow
passage into the central canal of the spinal cord.  Turning back to
Fig. 40 it will be readily perceived that the roof of the fourth ventricle
is formed posteriorly  by a portion of the cerebellum, and in front of
this by the valve of Vieussens and the corpora quadrigemina, whilst
the floor of the fourth ventricle consists simply, as has already been
said, of the gray matter of the spinal cord which has  come to the
surface, instead of being buried in the centre, in the shape of horns,
or cornua.   In other words, the fourth ventricle is nothing  more
than a continuation of the central canal of the spinal cord.
   In Fig. 46 is seen a horizontal  section through the lowermost part
of the upper portion of this region.   It illustrates  how  the  motor
fibres  come down in the crura cerebri, how the sensory fibres descend
in the region  of the tegmentum, and  the relative  position of the red
nucleus and the substantia nigra.   Contrast this with Fig. 45.

                                Fig. 47.
Horizontal section through the cerebellum. The section cut across anteriorly under the
             corpora quadrigemina.  (From Stilling's Atlas.)
 R, P. The superior cerebellar peduncles; between them the lingula.  In front of this is seen
the nucleus tegmenti (m) of the vermis, the nucleus globosus (Ng), the embolus (Emb), and the
corpus dentatum of the cerebellum (Cdc), which are in the hemispheres on each side; at Com
is the decussation of the anterior commissure, and at Sem is the semicircular fibres.

   Novv that we have seen the principal parts of the  hemispheres, the
basal ganglia, the pons aud medulla, and have studied the details of
these different figures, we are in a position intelligently to trace the
course of the nerve-fibres through them to the periphery.
   The  cerebellum is an important organ which I  have not  as yet 
72
INTRODUCTORY.
studied, because I have thought  it best to leave it until we  had
reached the  present point and  could understand  the fibres coming
into it from  the  structures of the  pons and the subthalamic  region.
The cerebellum has been one  of the mysteries of the nervous system,
although Stilling, in  his wonderful Atlas, embodied  thirty years of
research concerning it.   Its outward  shape  is  familiar  to  every
physician, and we have seen it  partially represented in  Figs.  36
and 37.  A horizontal section through it is shown in Fig. 47, which
is taken from Stilling's Atlas.  In  the centre are seen the  white sub-
stance of the vermis and the nucleus of the tegmentum, and anterior
to these the  decussation of the  anterior commissure.   On each side
are the hemispheres, and in  their white matter are  seen  the nucleus
globosus, the embolus, and the nucleus dentatus.  Between the supe-
rior peduncles, R R is the lingula, upon the valve of Vieussens.  The
Fig. 48.
        The three peduncles ot the cerebellum. (From Hirschfeld and Sappey.)
  1. Rhomboidal fossa of the fourth ventricle.  2. Stria acousticae.  3. Inferior peduncles,
 or restiform bodies.  4. Columns of Goll.  5. Superior cerebellar peduncles.  6. Lemniscus.
 7. Middle peduncles.  8. Corpora quadrigemina.

 cerebellum is connected with the cerebro-spinal  nervous  system by
 three peduncles:
   1.  The inferior peduncle, or restiform body, 3, Fig. 48.
   2.  The middle peduncle, or peduncle of the pons, 7 Fig 48
   3\ Tht s"Perior Peduncle, or the peduncle of  the corpora quadri-
 gemina, 5, Fig. 48.                                        ^
   The  inferior peduncle  or  restiform body is  composed of fibres
 from the direct cerebellar  column  of the cord which begin in the
 ^Vlw  *  " -a.nd t!rminate  in the vermis superior of the same
 side; of fibres arising from the nucleus of the column of  Burdach,
 or the nucleus cuneatus (Plate II., nucl. cun.), and these also pass to
 the vermis superior; of fibres from the nucleus of the column of Goll
 of the same and opposite sides (Plate II., nucl. grac), also goin* to
the superior vermis;  of fibres arising in  the cells of PurkinjeYn°the 
ANATOMY.
73
cerebellar cortex and  running  to  the  lower olivary bodies of the
opposite side; of fibres arising in the cells of the Deiters' nucleus and
running to the nucleus tegmenti of the opposite cerebellar hemisphere,
connecting the vestibular nerves and the cerebellum, and  probably
passing  into  the  superior  peduncles  and  thence  to  the  cerebral
cortex.
   The  middle peduncle  is composed  of fibres originating in the
cerebellar cortex and  running to  the  cells of the pons of  the  same
and the opposite side, and  thence onward to the cerebrum with the
fibres of the antero-lateral column ;  whilst others cross in the raphe
and go  to those cells of the pons in which terminate the  fibres coming
down from the cerebral cortex of the frontal and occi pi to-temporal
lobes, thus establishing a connection between the cerebellum and the
cerebrum.
   The  superior peduncle obtains  its fibres mostly from the nucleus
dentatus and  the cortex of the cerebellum, thence passing to the red
nucleus of the opposite side; and  from this red nucleus other fibres
go to the optic thalamus, and  from this to the cerebral cortex, prob-
ably to the central convolutions, thus  establishing a second connec-
tion between the cerebrum and the cerebellum.
   The cerebellum is an organ of co-ordination.   It receives different
sensations  from the periphery and transmits them to the cerebrum,
to whose cortex they bring images  of space and position.  From the
-cerebral cortex go other nerve-currents to the cerebellum,  probably
exercising a certain control or inhibition over co-ordination.  These
sensory impressions from  the periphery are  through  the direct  cere-
bellar column, which  is thought to  convey  the visceral sensations;
the  fibres arising  from the nuclei of the columns of Goll and  Bur-
dach  possibly conveying  the  muscular sense; the so-called sensory
cerebellar tract, running  from  the vestibular nerve to the nucleus
tegmenti and  bringing the cerebellum into connection with the circu-
lar canals of the labyrinth, which plays so  important  a part in the
maintenance of equilibrium.  The tracts conveying all  these sensory
impressions from  the  cerebellum  to the cerebral cortex lie in the
superior peduncle,  whilst those through which the  cerebral cortex
exercises its  inhibitions over the cerebellum are to be found in the
middle  peduncle.  There is  some doubt as to the course of the motor
tracts direct from the cerebellum to the periphery, but  it is  probable
that they are to be found in an indirect  and a direct route, the former
lying in the fibres  running from the cerebellum to  the motor  zone
of the cerebral cortex, although  there is a variance of  opinion  as to
whether these are in the superior or middle peduncle; and the latter
in the fibres passing from the cerebellum through the inferior peduncle
or restiform  body to the spinal cord, where  they may  surround the
cells in  the anterior horns.   Kolliker supposes that these  impulses
go through the fibres running from the cerebral  cortex to the lower
olivary  bodies of the opposite  side, and thence  through the lateral
columns of the cord to the anterior horns.
   Our kuowledge of the histology of the cerebellum has been much
advanced by the studies of Cajal, Golgi, and those whom they  have 
74
INTRODUCTORY.
incited.   They have shown that the cortex of this organ is composed
of three layers :
   1.  The superficial or molecular layer ;
   2. The granular layer, which is gray, yellowish, or reddish in color;
   3.  The zone of white substance.
   The  molecular layer contains  two varieties  of  cells,  those  of
Purkinje  and  the small  star-shaped  cells.   The former  are seen
in Fig. 49, a.  From the  upper part of  the cellular body proceed

                                Fig. 49.
  Semi-diagrammatic transverse section of a cerebellar convolution of a mammal.  (Cajal.)
  A. Molecular layer. B. Granular layer.  C.  Zone of the white substance, a. Cell of Pur-
kinje.  b. Small star-shaped cell of the molecular layer, d. Terminal descending arborizations
surrounding the cells of Purkinje.  e. Superficial star-shaped cells.  /. Large star-shaped cells
of the granular layer,  g. Granules with their ascending axis-cylinders bifurcated at i.
h. Mossy fibres, j.  Neuroglia cell with plume,  m.  Neuroglia cell of the granular layer.
n. Climbing fibres,  o. Ascending collaterals of the axis-cylinders of the Purkinje cells.

one  or  several nervous  trunks which, penetrating  the molecular
layer, expand  into a  flat and  luxuriant arborization  that  is pro-
longed to the  surface of  the cerebellum.   All the  branches of this
arborization terminate free, and have in their  course a  great num-
ber of collateral spines  inserted perpendicularly.   These  arboriza-
tions are  flat,  and  extend laterally, so that a longitudinal section
along their axes shows them perfectlv.   The axis-cvlinder of these 
ANATOMY.
75
cells of Purkinje takes on  a covering of  myelin immediately after
leaving the cell, and descends to the white substance, emitting, how-
ever,  at the  level of two or three constrictions of the  medullary
layer, certain ascending collaterals which ramify in  the inferior por-
tion of the molecular layer and probably  serve as means  of connec-
tion between the different cells of Purkinje.  A beautiful specimen
of one  of these cells  is shown in Fig. 50.   The  star-shaped  cells
(b, Fig. 49)  are small, and flattened transversely.   Cajal claims  to
have  discovered that they possess a very long  axis-cylinder of an
arched shape, which proceeds transversely, and that their  descending
collaterals, as well as the  terminal  arborizations of their  axis-cylin-

                              FlG. 50.
       Purkinje cell of the cerebellar cortex of a young cat.  (Van Gehtjcten.)

ders, surround the cells of Purkinje, so that  these latter bodies are,
as it were, enclosed  in a basket formed by the terminal ramifications,
which  are  excessively thick  and  wavy,   (d, Fig.  49.)   To  these
structures Kolliker has given the name of the " end-baskets."   The
entirety of these fibres thus surrounding the cells of Purkinje is con-
densed at the  inferior portion of the cellular  body and envelops the
axis-cylinder of the cell of Purkinje  just at  the  point where the
myelin is still lacking.
  The granular layer is composed of very small bodies scantily sup-
plied with protoplasm, and forming a very complicated mass beneath 
76
INTRODUCTORY.
the molecular layer.   According to Cajal, their  protoplasmic  pro-
cesses are short, two or three in number, and terminate in a finger-
shaped arborization which  appears to surround or touch the body of
the neighboring granules.   Their axis-cylinder  is  very fine, and
ascends to the molecular layer, dividiug in the form of a T at differ-
ent levels of this zone, to become a longitudinal fibre which proceeds
parallel to the cortex and therefore perpendicular to the arborization
of the Purkinje cells.   The parallel fibre does  not give off any col-
lateral in its  course, but is prolonged to the limit  of the lower layer
of the cerebellum, where it terminates, almost at the white substance,
by free and  wavy thickening.  Cajal  has followed these  parallel
fibres throughout the small brains of the inferior vertebrates, reptiles,
batrachiaus, and the foetus of small mammals, and he believes that they
connect the granules and the cells of Purkinje.  It  would thus appear
that each granule may send a nervous current to all the cells of Pur-
kinje  situated in its radius and in the whole length of the cerebellar
layer, or inversely, in the event that the nervous current should pro-
ceed in two directions, each cell of Purkinje can  transmit its action
to all the granules of the subjacent layer.  The large  star-shaped
cells are found in the  granular layer (Fig. 49,/).   They are few in
number,  and their  protoplasmic processes diverge in all directions,
whilst their axis-cylinders split up into a great number of branches,
which are lost among the granules.  It  is probable that these axis-
cylinders terminate free.
   The white  substance of the cerebellum is composed of three varie-
ties of nerve-fibres : 1, descending axis-cylinders  coming from  the
cells of Purkinje;  2,  thick  nerve-fibres ascending  and ramifying
among the granules, the so-called mossy fibres; 3,  thick fibres which
ascend and ramify in the  molecular  layer, the  so-called  climbing
fibres.  The  mossy fibres (h, Fig. 49) derive their name from  the
fact that they emit from place to place certain nodular  thickenings
resembling the moss of trees.   At first they were  considered as arti-
ficial productions, or artefacts, but their existence has been determined
in all the vertebrata.   They are found  only in the granular layer,
and terminate by free nodosities or by means of ascending moss-like
expansions.  Cajal thinks that they are possibly the continuations of
the fibres from the direct  cerebellar layer of the  spinal cord.   The
climbing fibres (n, Fig. 49) are  thick and medullated, either do not
ramify at all,  or but very little, and pass through  the granular layer
into the molecular, where they climb the ascending trunk of the cell of
Purkinje and  terminate in a wavy or plexiform arborization applied
to the large primary and secondary branches of these Purkinje bodies.
As yet, however, it is not known from what nerve-cells  these climb-
ing fibres arise.
   According to Cajal,  the protoplasmic arborizations and the bodies
of all these cells transmit the nervous currents as well as their axis-
cylinders, and this  he believes because axis cylinders have been seen
to ramify and terminate free upon these protoplasmic processes.   He
also maintains that a nerve-cell may have independent connections
with other nerve-elements, inasmuch as in the cells of Purkinje each 
ANATOMY.
77
portion of the body and of the protoplasmic arborizations is enveloped
by  an entirely  different kind of nerve-fibre.  Thus, the  body is
brought into relation, by means of the terminal baskets, with the
star-shaped  cells of the molecular layer; whilst the trunk of the
main  ascending branches have a connection, through the climbing
fibres, with  the  elements of the spinal cord or the brain; and, still
further, the terminal protoplasmic branches are  brought into con-
tact with the axis-cylinders of the granules,  or the so-called parallel
fibres.   In most of these cases the connections are bj' contiguity and
not by continuity, although it cannot as yet be absolutely stated that
this is a universal  law.

  We  are now in a position to try  to  unravel the course of the
fibres from the spinal cord upward to the brain and the cerebellum.
  The first  peripheral station is  formed by the cells of the ganglion
upon the  posterior root (a,  a, Plate II.  See also Fig. 5, B).  The
cells of these ganglia emit a nerve-process which splits into two, one
going to the periphery (E,  Fig.  11), the other passing to the spinal
cord and forming, with other similar fibres, the posterior root (D,
Fig. 11). These fibres of the posterior root pass into the spinal cord,
and each one splits into an ascending and a descending one (Fig. 12).
They proceed longitudinally in the posterior columns.  All the de-
scending ones are short (Plate II., V, 2', 3', blue), pass longitudinally
a short distance downward, then bend at a right-angle and penetrate
the gray matter, where they end in free nodules.  The ascending fibres
are divisible into short and long ones.  The short ones (Plate II., 2, 3,
blue) run for a short  distance longitudinally upward,  and then bend
at a right-angle and pass into the gray substance of the cord,  there
to terminate  in  the usual free manner.   The  long ascending fibres
(Plate  II., 4, blue) pass longitudinally  upward  through  the  whole
spinal  cord, and, as with the others, bend at a right-angle  and termi-
nate with the usual free nodules  in the gray substance of the medulla
oblongata, in the  region of the  nucleus of the column  of Goll and
the nucleus of the column of Burdach, called respectively the nucleus
gracilis and  the nucleus cuneatus.   All ascending and descending
fibres give off collaterals in  their  course (Plate II., col).   These pass
horizontally and penetrate the gray matter.  It is thus evident that
the terminals of all  the descending and  ascending  fibres,  together
with their collaterals, pass  into the gray matter of the cord; and as
the terminations of the  long fibres  may be  regarded as  their final
collaterals, it may be said that all the fibres coming into the cord
penetrate the gray matter.
  As these posterior root-fibres pass into the spinal cord they diverge
and split into  two  portions—namely, a lateral and a medial.  The
lateral (Plate II., 2, blue) pass up longitudinally, and the most lateral
of them  constitute the Spitzka-Lissauer column, the ascending fibres
being  short.   The medial  portion (Plate II., 3, 4, blue)  is much
larger  than  the  lateral, and consists of fibres which bend inward to
constitute different portions of the column of Burdach, and here they
first split up into ascending and  descending fibres, the course of the 
78
INTRODUCTORY.
latter being unknown, whilst the former are divisible into short and
long fibres.   The short fibres (Plate II., 3, blue) bend  into the gray
matter after a longer or  shorter course, whilst the long ones (Plate
II., 4, blue)  run toward the  cerebrum through the whole  course of
the spinal cord and terminate in  the medulla oblongata.   These
longer of the ascending  fibres are pushed more and  more in their
course toward the middle line of the cord by the constant entrance
of new fibres from the posterior roots (Plate II.) ;  so that  the long
ascending fibres  of the sacral nerves are pressed inward by the fibres
entering  the  lumbar cord, these  again by the dorsal, these by the
cervical,  and thus it comes to pass  that in the cervical cord the sen-
sory ascending  fibres  of the  sacral nerves are  most medial, whilst
those of  the cervical nerves are most lateral.  The columns of Bur-
dach  contain mainly the short ascending fibres, although  in them
there are many long ascending fibres, which, however, are found near-
est  the median  line, and they evidently pass over into the columns
of Goll, through which they take their way to the medulla oblongata
(Plate II., 4, blue).  The columns of Goll consist almost exclusively
of long ascending fibres, and they terminate in the nucleus of the
column of Goll and the nucleus of the column of Burdach (Plate II.,
nucl.  grac. and nucl. cun.),  so that  the cells of these nuclei are
analogues of  the  column-cells of the cord.   From  these nuclei
the sensory fibres proceed as follows: The axis-cylinder processes
of their  cells  pass  into  the lemniscus (Plate II.), cross toward the
median  line,  decussate with  analogous fibres of the other  side (so-
called decussation of the lemniscus) and thus form the medial or upper
lemniscus.  Most of the sensory cranial nerves of the opposite side
pass into this medial lemniscus and proceed with it  to the cerebral
cortex (Plate II.),  the fibres of the medial lemniscus through the
medulla  oblongata, the pons, and the crus.   In the latter they lie in
the  tegmentum.   They then  pass  into the internal capsule in its
posterior  portion (Plate II., caps,  int.), behind the motor fibres, and
thence into the  white matter constituting the corona radiata, and
so on into the cortex, probably the ascending parietal convolution,
the  parietal lobe,  and perchance also into the parietal, occipital,
and temporal convolutions.   All of these fibres give off collaterals
in their course from  the  medulla  oblongata to the cortex.  Many of
these do  not  reach  the cortex, but end in different masses of gray
matter on the way, such as the auterior quadrigeminal body, the optic
thalamus, the lenticular nucleus, etc.
  Besides this best  known of the sensory paths,  there  are others
through the anterior and lateral columns.    Some of the nerve-fibres
which have been described send collaterals to the column-cells of the
spinal cord, and  many of the short ascending and all of the  descend-
ing fibres terminate  in  close contiguity  to these same cells.   The
axis-cylinder  processes of these column-cells become mainly the long
fibres of  the anterior and lateral columns.  These in their turn give
off collaterals to the gray matter of the cord, and  finally bend at a
right-angle to terminate, as do their collaterals, in  the gray spinal
substance.  These longitudinal fibres compose the fundamental ante- 
PLATE II.
Sup. Cerebclla
  Peduncle""
Middle Cerebella
  Peduncle
DIAGRAM SHOWING COURSE OF  SENSORY FIBRES FROM PERIPHERY

         TO CORD, CEREBRUM AND  CEREBELLUM.-(Flatau)
[To face page 78. 
 
ANATOMY.
79
rior column, the fundamental lateral column, the Gowers, and the
direct cerebellar column.
  The anterior fundamental  column is found throughout the spinal
cord, and  in the region of the pyramidal decussation it is pressed
inward, but passes up from there as the so-called posterior longitudinal
fasciculus.   (See Figs. 41, 42, 43,  44, 45, Flp,  and also Fig. 46.)
The fibres of this fasciculus gradually end in the groups of cells of
the medulla oblongata, pons, and subthalamic region, in the so-called
gray reticular substance, finally terminating in the neighborhood of
the nucleus of the third nerve and the anterior quadrigeminal body.
In  their  course they give off  collaterals  to the motor nuclei of the
eye-muscles and to the hypoglossal nerve, so that they are the prin-
cipal  means  of communication  for  the reflexes  from  the sensory
spinal nerves to the muscles of the eye and the tongue.
  The lateral fundamental column is also fouud throughout the whole
cord, and its fibres terminate in the  cell-groups of the gray substance,
especially in the nucleus reticularis tegmenti.  It is  probable that
they end near the  superior central  nucleus immediately behind the
posterior quadrigeminal  bodies.  In  their course they give off col-
laterals to the  motor nuclei of the fifth, seventh, ninth, tenth, and
eleventh  cranial nerves.
   The column of  Gowers first becomes  visible in the  lumbar  cord,
and the fibres are lost above in the neighborhood of the small olivary
body.
   It  will  thus be seen  that the anterior and  lateral fundamental
column and the Gowers column have been followed  into the cellular
groups well up near the subthalamic region.  These different cellular
masses have been designated by Kolliker by  the name  of the nucleus
magnocellularis diffusus,  and it is possible that fibres proceed thence
to the medial lemniscus and through this to the cerebral cortex.  If
this be true, the physiological importance of the lateral and anterior
fundamental columns  and the  Gowers  column would be thus ex-
plained :  The nervous current coming from the periphery first passes,
by means of the sensory fibres, to the column-cells  in the gray matter
of the cord. Thence go axis-cylinder processes which are either short,
as  in the anterior and lateral fundamental  column ;  or long, as in
the Gowers column, the direct cerebellar column, and individual fibres
of the anterior and lateral fundamental column; or  crossed, as in
the anterior fundamental column and partially in the  lateral funda-
mental column and the Gowers  column ; or  uncrossed,  as partially
in the lateral fundamental column, the Gowers, and the direct cere-
bellar column.  The longer of these fibres carry the sensory impulses
from the column-cells to the cortex; first passing into the nucleus
magnocellularis diffusus, which has been described above, and from
there to  the cortex through the medial  lemniscus.  These long col-
umns decussate in the  spinal cord in the anterior commissure.   The
short fibres proceed for only a short distance upward, give off collat-
erals, and  end  in  the  gray matter  of the cord and the brain-stem.
It is therefore possible that there is a direct  and an  indirect sensory
path.  The direct one consists of the peripheral  fibre, the ganglion 
80
INTRODUCTORY.
 on the posterior root,  the  posterior root-fibre,  the  long ascending
 fibre in the posterior column, and the termination in the cells of the
 columns of Burdach and Goll (nucleus gracilis and nucleus cuneatus);
 thence, through the axis-cylinder processes of these cells, to the lem-
 niscus, the medial lemniscus, the posterior part of the internal cap-
 sule, and the cortex.   It has been supposed that this sensory path
 carries sensations of touch and muscular sense from the periphery to
 the cortex.  The indirect sensory route lies in the anterior and lateral
 fundamental and the Gowers column, and  consists of the peripheral
 nerve-fibres, the ganglion upon  the  posterior  root, the fibres in the
 posterior column, the  short ascending fibres, the collaterals of all
 the  ascending and  descending fibres, and the terminals near  the
 column-cell;  thence through the  anterior commissure, the  lateral
 and anterior fundamental and the Gowers  column, to the cells of the
 nucleus  magnocellularis diffusus; thence again through the  medial
 lemniscus to the cortex.  This indirect sensory path (Plate II., 11,
 12, blue), possibly conducts the sensations  of temperature and pain.
 It is also possible that the short longitudinal fibres form a part of this
 path, through the intercallation of  the column-cells of the cord.   It
 is thus evident that the direct and the indirect sensory paths undergo
 a  decussation, the first in the brain-stem, the second in the spinal
 cord.  The direct cerebellar column, however, does  not decussate,
 and probably has no other function than to conduct  impressions of
 coordination.   The decussation of the indirect sensory path through
 the anterior commissure of the spinal cord has, however, been doubted
 by many authorities, and the question  has not yet  been positively
 decided.
   We  have  seen that  the ganglion  upon the posterior root of the
 spinal  cord contains cells which give origin to the sensory nerve-
 fibres  proceeding inward.   The  fibres of the sensory cranial nerves
 take their origin  in  the same  manner from cells outside the brain.
 From  them the fibres  of the sensory cranial nerves  proceed to the
 cerebrum, where they—like the posterior root-fibres — divide into
 ascending and descending fibres, which have collaterals and terminals,
 the latter surrounding  the sensory nuclei with their free ends.   Thus
 the cells of these sensory nuclei are analogous to the column-cells of
 the gray matter of the spinal cord and those in the nuclei of the
 columns of Burdach and Goll.   The axis-cylinders of these cells are
 either long or short  The long ones decussate in the  raphe and pass
 to the  cortex.  The short ones terminate in different cells of the gray
cerebral substance and  probably conduct the reflexes.
   The course of the motor fibres from the cortex to the  periphery is
much  simpler  than the sensory highways which have  just been
described.  The motor impulses proceed  from the pyramidal cells
of the  motor  area  of  the cortex to  the  pyramidal  fibres, passing
through  the  corona radiata  to the motor nuclei of the cranial and
spinal  nerves, the former lying  in the brain-stem, the  latter in the
anterior horns of the spinal cord.  The axis-cylinder processes from the
cells of these motor nuclei  constitute the fibres of  the peripheral
motor  nerves, and end  free in the  muscles.   The beginning of the 
ANATOMY.
81
C 1.
Dl.

motor path is in the large pyramidal cells            FlG-5L
of the motor area of the cortex, which is
composed of the ascendiug parietal  and
ascending frontal convolutions, the bases
of the three frontal convolutions and the
paracentral  lobule  (Plate  III., 1, 1,  1,
etc.).   Hence the  nerve-fibres  proceed
through the white matter of the centrum
ovale, or the so-called corona radiata, into
the internal  capsule (Plate III., 2, 2,  2,
etc., caps. int.).    From  this point the
motor fibres pass into the crura cerebri,
lying most veutrad in what is known  as
the pes.  Then they go into the pons and
the medulla oblongata, where they are
visible as two compact bundles, so-called
pyramids (Plate III., Py.), and these pyra-
mids can be followed to the lower end  of
the medulla oblongata.1 At this point, in
the region of the first and second cervi-
cal nerves, there is a  decussation  which
extends over a distance of about six mil-
limetres, and the pyramidal  fibres split
into two portions, one decussating and the
other not.   The decussating portion goes
down the spinal cord in the lateral pyram-
idal column; the  non-decussating part
passes down on the same  side in the an-
terior pyramidal column  or  column  of
Tiirck.   The fibres of the  lateral pyram-
idal column give off collaterals (Plate III.,
3,4, 5, col., red), which proceed, at a right-
angle from the main fibre, into the gray
substance of the same side,  where their
terminal ends surround the  cells of the
anterior horn ; and the main fibres them-
selves finally terminate in  a similar man-
ner.  For these reasons the  number  of
the lateral  pyramidal  fibres  diminishes
gradually downward  until  the column
terminates in the lumbar enlargement  at
the region of  the third and fourth  sacral
nerves.  The fibres of the anterior pyram-
idal column also give off collaterals (Plate
III., 6, 7, 8,  CO^., green) at right-angles,   The mutual relations of the verte-
and these pass through the anterior com- bral bodies and sPines t0 the st«-
        ,  L ,        °   ,,   /> . ■        ..  ments in the cord and to the exit of
missure to the motor cells of the opposite the nerves.  (goweks.)
■10
•1L
-IS
 1 The student should follow the different columns of the medulla oblongata and the cord
(Figs. 1, 2, 3, 41, 42, 13, 44, 45, and 46); and he had best do this in a second reading.
6 
82
INTRODUCTORY.
side, and the main fibres terminate in the same manner.   This antero-
pyramidal column ends about the lower third of the dorsal cord.  It
will be thus seen that these pyramidal fibres have two decussations, one
in the region of the first and second cervical nerves, and the other at dif-
ferent levels of the cord through the anterior commissure.  The axis-
cylinder processes of the cells of the anterior horns pass into the anterior
root-fibres of the same side and terminate free in muscles  or glands.
The motor cranial nerves all pass into this  pyramidal tract at the knee
of the internal capsule (Plate III., x, t, tr, ab, f g, h, v), and they all de-
cussate before reaching it.  The course, however, of these cranial motor
nerves from their respective nuclei to this point in  the internal cap-
sule has led to considerable differences  of  opinion among anatomists.
It is an undoubted fact that many of  the muscles  supplied by these
motor cranial nerves functionate bilaterally, as the muscles of masti-
cation, of the eye, of mimic movements, and of the pupil, and for this
reason it has been supposed that each motor cranial nerve receives fibres
not only from its own nucleus, but also from that of the opposite side.
But this belief has not yet met with complete anatomical confirmation.
   In Fig. 51 is  shown  the relation of the various segments of  the
spinal cord to the bodies and spinous processes of the vertebrae.  This
is  of importance from a surgical point of view,  since  the segments
do not correspond  to the vertebrae after which they are named.  The
following table  is given  by Starr, and  has been  modified  by him
recently, as the result of the analysis of a large number of cases, to
show the localization of function in the different segments:
Segment.	Muscles.	Reflex.	Sensation.
II. and III. 0. IV. c. V. c. VI. c.	Sterno-mastoid. Trapezius. Scaleni and neck. Diaphragm. Diaphragm. Deltoid. Biceps. Coraco-brachialis. Supinator longus. Rhomboid. Supra- and infra-spinatus. Deltoid. Biceps. Coraco-brachialis Brachialis anticus. Supinator longus. Supinator brevis Rhomboid. Teres minor. Pectoralis (clavicular part). Serratus magnus. Brachialis anticus. Serratus magnus. Triceps. Extensors of wrist and fingers. Pronators.	Hypochondrium (?). Sudden inspiration pro-duced by sudden pres-sure beneath the lower border of ribs. Pupil. 4th to 7th cervical. Dilatation of the pupil produced by irritation of neck. Scapular. 5th cervical to first dorsal. Irritation of skin over the scapula produces con-traction of the scapular muscles. Supinator longus. Tapping its tendon in wrist produces flexion of forearm. Triceps. 5th to 6th.cervical. Tapping elbow-tendon pro-duces extension of forearm. Posterior wrist. 6th to 8th cervical. Tapping tendons causes extension of hand.	Back of head to vertex. Neck. Neck. Upper shoulder. Outer arm. Back of shoulder and arm. Outer side of arm and forearm, front, and back. Outer side of fore-arm, front, and back. Outer half of hand.
 
ANATOMY.
83
SEGMENT.		Muscles.
VII.	c.	Triceps (long head). Extensors of wrist and fingers. Pronators of wrist. Flexors of wrist. Subscapular. Pectoralis (costal part). Latissimus dorsi. Teres major.
VIII	c.	Flexors of wrist and fingers. Intrinsic muscles of hand.
I.	D.	Extensors of thumb. Intrinsic hand-muscles. Thenar and hypothenar eminences.
II.	to	Muscles of back and abdo-
XII.	D.	men. Erectores spinse.
 I. to
Il.s.
Ilio-psoas.
Sartorius.
Muscles of abdomen.
Ilio-psoas.  Sartorius.
Flexors of knee (Remak).
Quadriceps femoris.

Quadriceps femoris.
Flexors of knee.
Inner rotators of thigh.
Abductors of thigh.

Abductors of thigh.
Adductors of thigh.
Tibialis anticus.
Outward rotators of thigh.
Flexors of ankle.
Extensors of toes.
Flexors of ankle.
Long flexors of toes.
Peronei.
Intrinsic muscles of foot.
Perineal  muscles.
Anterior wrist.
7th to 8th cervical.
Tapping anterior tendons
 causes flexion of wrist.
Palmar 7th cervical to 1st
 dorsal.
Stroking  palm causes
 closure of fingers.
Epigastric, 4th to 7th dor-
 sal.
Tickling mammary region
 causes retraction  of  the
 epigastrium.
Abdominal.  7th to 11th
 dorsal.
Stroking side of  abdomen
 causes retraction of belly.

Cremasteric.  1st to 3d lum-
 bar.
Stroking inner thigh causes
 retraction of scrotum.
Patella tendon.
Striking tendon causes ex-
 tension of leg.
Gluteal.
4th to 5th lumbar.
Stroking  buttock  causes
 dimpling in fold of but-
 tock.
Plantar.
Tickling sole of foot causes
 flexion of  toes  and re-
 traction of leg.
Foot-reflex.  Achilles' ten-
 don.
Overextension of  foot
 causes rapid flexion ;
 ankle-clonus.
Bladder and rectal centres.
    SEN8ATI0N.


Inner side and back
 of arm and fore-
 arm.
Radial half of  the
 hand.
Forearm and hand,
 inner half.

Forearm,  inner
 half.
Ulnar distribution
 to hand.

Skin  of chest and
 abdomen, in hori-
 zontal bands run-
 ning around and
 downward cor-
 responding to
 spinal nerve.
Upper gluteal
 region.

Skin  over groin
 and front  of
 scrotum.
Over  back  above
 buttocks.

Front of thigh.
Front and  outer
 side of thigh.
Outer side of leg.
Inner side of thigh
 and leg to ankle.
Inner side of foot.

Back of thigh, back
 of leg, and outer
 part  of foot and
Back of thigh,
 foot, outer side.
Buttocks.
Skin over sacrum,
 anus,  perineum,
 genitals, and
 lower  part  of
 buttocks. 
84
INTRODUCTORY.
  Before entering into the details of the origin of the different cranial
nerves, Fig. 52  should be carefully studied.  It is  an  excellent dia-
gram from Edinger, showing the relative position of^e nuclei, and
it can be greatly elucidated by Figs. 36, 40, 41, 42, 43, 44  and 45.
  The cranial  nerves may be divided  into the motor and sensory.
To  the  former belong the oculo-motor, the trochlear, the abducens,
the facial, the ninth, and  the hypoglossal, as well as the motor por-
tions of the three mixed nerves, the trigeminal, the glossopharyngeal
and the vagus.   As with  the motor spinal nerves, the tracts of each
cranial one can be divided  into a central and a peripheral portion.  The
central tracts begin in the large pyramidal cells of the motor area of
Fig. 52.
     Relative location of the nuclei of the different cranial nerves. (Edinger.)

the cortex, pass through  the knee or genu of the internal capsule,
thence downward to  decussate  and go to their motor  nuclei, which
are all in  the brain-stem.    (Plate III., iv., v., vi., vn., vm., ix.,
x., xi., xn.)   There is much divergence of opinion as to  the exact
peripheral tract of these cranial nerves. If one were to rely upon the
physiological fact that the muscles  supplied by the motor cranial
nerves  functionate bilaterally, as do the muscles  of mastication,
the eye, mimic movements, the  pupil, etc., it might be supposed
that each  motor cranial nerve received fibres not only from its own
nucleus, but also from the opposite one, or that the  motor nuclei of
the two sides were connected with each other. Anatomical investiga-
tions have not  as yet, however, as has already been stated,  confirmed
either of  these suppositions thoroughly.
   The Oculo-motor Nerve, or the Third Pair, has its central tract from
the cortex, from a point as yet not exactly determined  in the human
brain, thence to the internal capsule, and thence by decussating fibres
to  the cells of  its motor  nucleus.  (Plate III., in.)   Its peripheral
tract is from the nucleus just beneath the anterior quadrigeminal
bodies, downward, probably to split into two  portions, one passing
to  the eye-muscles on the same side, and the other to those on the
opposite,  although the decussation has as yet only been demonstrated 
PLATE III.
h»j-
-Oil.
DIAGRAM SHOWING COURSE OF MOTOR  FIBRES FROM THE CEREBRUM
              AND CORD TO THE PERIPHERY.-(Flatau.)
[To face page 84. 
 
ANATOMY.
85
for a portion of its fibres.  Although  the axis-cyliuders of the cells
of the nucleus pass  over into the peripheral  nerve-fibres, the col-
laterals are  supposed to be surrounded by the central motor tract
of the nerve, by the sensory fibres from the spinal cord through the
posterior longitudinal fasciculus, and by the fibres of the optic nerve.
The  fibres from the spinal cord are presumably the medium of the
reflex acts of the eye-muscles.
  The Trochlear,  or Fourth  Nerve, has its  central tract  from an
unknown point in the cerebral  cortex to its  nucleus.  (Plate III.,
IV. t.)  The peripheral tract is from the nucleus just beneath the pos-
terior quadrigeminal bodies to a decussation  shown in Plate  III.
It is  uncertain as to whether fibres come  from  the other nucleus.
Through its collaterals the cells of the nucleus of this nerve re-connect
with its fibres going to the cortex, with fibres coming from the spinal
cord,  and with others from the optic.
   The Abducens  Nerve, the Sixth, has its   central  tract from an
unknown point of the cortex to its nucleus.  (Plate III., a, b.) This
lies in the anterior portion of  the floor of the  fourth ventricle (Plate
III.,  vi.), and its cells are connected with the cortical fibres, with
sensory spinal fibres, and with fibres from the optic.
   The  Facial Nerve, the Seventh, has its central tract from the
lower third  of the ascending parietal and ascending frontal convolu-
tions to its nucleus (Plate III., vn.,/), which  lies lateral and ventrad
from  the abducens nucleus at  the lower end of the pons.   (See Fig.
52.)  It is well known that in cerebral hemorrhage producing what
is known as hemiplegia only  the lower branch of the facial is  im-
plicated, whilst that to the orbicularis  oculi  and frontal muscle are
unaffected.  The  probable explanation of this lies in  the fact that
the motor nucleus  for the upper branch is in the posterior portion of
the oculo-motor nucleus of the same side, the axis-cylinders of whose
cells pass into the  fibres of the facial  upon  the same side, whilst the
central tract connecting it with the cortex probably runs in the upper
branch of the facial, which is not affected in most cases of  cerebral
hemorrhage.  The cells of the motor nucleus  are connected with the
cortical fibres, with  sensory spinal fibres, and with fibres  from the
trigeminal and cochlear nerves.
   The Accessory Nerve of Willis, or  the Eleventh, has its  central
tract  from an unknown point in  the cerebral cortex  to its nucleus
(Plate III., XI.) in the lowermost portion of  the medulla oblongata.
The posterior portion of  the motor nucleus  of  the pneumogastric
constitutes the motor nucleus  of  the cerebral portion of the eleventh
nerve, whilst the  anterior horn cells  from the  region of  the fifth
cervical nerve and somewhat upward constitute the motor nucleus of
the spinal portion.   The axis-cylinders of the  motor nucleus pass into
the fibres of the nerve on the same side.  The roots of the eleventh
nerve passing from the medulla oblongata are  closely connected with
those of the pneumogastric.   The roots of  the spinal portion of the
eleventh pass from the side of the spinal cord, from the fifth cervical
nerve upward.  The cells  of  the  motor nucleus are connected with
the cortical  fibres and  with sensory spinal fibres. 
86
INTRODUCTORY.
  The Hypoglossal Nerve has its central tract from the lower third
of the ascending parietal  and ascending  frontal convolutions to its
nucleus.  (Plate III., xn., h.) This is about 18 mm. long, and stretches
along the median sulcus on the  floor of the fourth ventricle to the
region of the strim acusticoz.  The nuclei  on the two  sides are con-
nected by commissural fibres.  It is  probable that the fibres coming
from  one nucleus are joined by those from the other.   The cells of
this  nucleus are connected with  cortical fibres, with sensory spinal
fibres, and with fibres from the  sensory portion of the ninth and tenth
nerves.
  The Motor Portion  of the Trigeminus, or Fifth Nerve, has its
central tract probably from the lower third of the ascending parietal
and ascending frontal convolutions to its nucleus (Plate III., v., tr.),
on the upper portion of the floor of the fourth ventricle, as well as
to certain motor cells which lie scattered in the lateral portion of the
central gray matter up  to  the region of the anterior quadrigeminal
bodies, and  also in the so-called locus coeruleus. (Fig. 52.)  The nerve-
processes of the cells of the motor nucleus pass into the fibres of the
motor trigeminal root, as well  as into the descending root.  These
axis-cylinders are probably joined by others from the opposite nucleus.
The  nucleus is connected  with  cortical fibres, with sensory spinal
fibres (the latter being the  means of conduction of reflex movements,
as in  trismus, peripheral  irritation, etc.),  and with  fibres of the
sensory portion of the trigeminus.
  The Motor Portion of the Glosso-pharyngeal Nerve, or the Ninth,
has its central tract from an unknown point in the cerebral cortex to
its nucleus  (Plate III., ix., g), which is known as  the nucleus  am-
biguus, lying fused with the motor nucleus of the pneumogastric on
the floor of the fourth ventricle.  (Fig. 52.)  From the  nucleus fibres
pass  to the peripheral nerve of the same side.  The  motor portion of
the vagus or pneumogastric nerve, or the tenth, has the same tracts
as the ninth.  The cells of the motor nuclei of the ninth and tenth
nerves are  connected with cortical fibres, with  sensory spinal fibres,
and with fibres of the sensory  portion of the trigeminus.
  The tracts of the sensory cranial nerves are analogous to those of
the spinal sensory nerves or the posterior roots.   Just as these latter
have their origin in the cells of the ganglia upon the posterior root,
so do the sensory cranial nerves begin in cells lying outside the cra-
nium, and from these the  fibres pass into the cerebrum, where they
divide, like the posterior root-fibres of the spinal cord, into  descend-
ing and  ascending fibres,  which again split up into collaterals and
end-fibres, the  latter surrounding with  their terminals the  cells of
the so-called sensory nuclei.   The cells of these sensory nuclei are
analogous to the column-cells of  the  spinal cord and to those of the
nuclei of the column of Burdach and the column of Goll.  The axis-
cylinders of these cells are  either long or short.   The long  ones de-
cussate in the raphe of the medulla oblongata aud carry their nerve-
impulses uninterruptedly to the cortex, probably to the ascending
parietal convolutions and the parietal lobe, thus constituting the cen-
tral sensory tract.   The short ones terminate in different  cells of the 
ANATOMY.
87
gray cerebral substance, and serve mainly to conduct the reflex move-
ments.
  The sensory portion of the trigeminal or  fifth  nerve is from the
cells of the Gasserian ganglion  through the sensory root to the  sen-
sory nucleus  of the fifth pair (Plate II., v.) at the upper end of the
floor  of the  fourth  ventricle.   Thence long  fibres  (Plate II., 16)
decussate in the raphe  to pass into the medial lemniscus and go with
this  to  the cerebral cortex.  The short ascending fibres go to the
motor nuclei  of the  trigeminal, the  facial, and the hypoglossal, and
probably also to the motor portion of the ninth and tenth nerves, and
serve mainly as media for the reflex movements.  The sensory root-
fibres and the fifth nerve  split up into ascending and descending
branches upon their entrance into the brain and stem.  The descend-
ing branches form the tract known  as the ascending  trigeminal  root
(which is really the  descending), whose terminals surround the cells
of the sensory nucleus of the fifth  and those  of the posterior spinal
cornua as low down as the region of the first  cervical nerve.
  The sensory portion of the glosso-pharyngeal and vagus nerve, or
the ninth and tenth, arises as follows :  The fibres of the ninth come
from the jugular and petrosal ganglia, whilst those of the tenth have
their origin in the jugular and  cervical  ganglia.  This tract, by its
terminals, surrounds the cells of the sensory nucleus  (Plate II.,  ix.,
x.) lying to  the side  of the hypoglossal nucleus.  From this long
fibres (Plate  II., 13, 14) ascend to  decussate  in the raphe and pass
into the medial  lemniscus, and thence to the cerebral cortex.   Short
nerve-fibres and collaterals go to the  nucleus of the hypoglossal nerve,
and probably are the media of the reflex movements.   The descend-
ing fibres of  the ninth and tenth  nerves form the so-called solitary
fasciculus, or the respiratory tract of Krause, and descend to surround
by their terminals the cells of the sensory nucleus, as well as the cells
in the posterior horns of the spinal cord as far down as the  eighth
cervical nerve.
  The optic  nerve is quite  complicated in its tract.  In the  middle
layers of the retina there are certain bipolar cells that are analogous
to the cells in the posterior ganglia of the spinal cord; whilst in the
deeper retinal strata are large ganglion-cells akin to the column-cells
of the cord.   From the bipolar cells axis-cylinders pass to surround
the large ganglion-cells, and  from  the latter  arise the fibres of the
optic  nerve.   These decussate partially, as has been  described, Fig.
39, in the chiasm, in such a way that  fibres from the lateral or tem-
poral half of the retina run in the lateral half of the  chiasm,  thence
into the optic tract to the posterior portion of the internal capsule, and
thence to the cortex of the cuneus, the occipital convolutions, and the
lingual lobule of the same side.  The fibres from the nasal or medial
half of the retina—constituting  the smaller portion of the tract—de-
cussate in the chiasm, pass into the optic tract, thence into the posterior
portion  of the  internal capsule to the  cerebral cortex just described,
but of the opposite hemisphere.   These two central tracts are repre-
sented by the long ascending axis-cylinders of the large ganglion-cells
of the retina.  The shorter fibres end in the so-called primary optic 
 88                      INTRODUCTORY.

 centres—i. e., mainly in the lateral geniculate body, the anterior quad-
 rigeminal body, the pulvinar, the medial geniculate body, and prob-
 ably in the lenticular nucleus (Fig. 39), probably serving the purpose
 of the reflex movements.   From these primary optic centres fibres
 pass to the cerebral cortex.   The cells of the anterior quadrigeminal
 body, which are surrounded by the terminals of the short optic nerve-
 fibres, give off axis-cylinders that pass to the nuclei of the eye-nerves
 (the third, fourth, and sixth), which is a pathological and physiological
 fact of great importance.
   The olfactory nerve  takes its origin from certain  bipolar  cells of
 the nasal mucous membranes analogous to the cells of the spinal
 ganglia, as well as from the axis-cylinders of these bipolar-cells in the
 olfactory bulb, and which in their turn are akin to the  column-cells
 of the cord.  From these cells arise the fibres of the olfactory tract, a
 part decussating in the anterior cerebral commissure and  passing to
 the gyrus hippocampi, the gyrus  uncinatus, and  the  cornu ammonis
 of the opposite side; but the greater portion of the fibres do not de-
 cussate, going  to the  corresponding  portions of the cerebral  cortex.
 It is supposed that short fibres arise from  these long ones to go to
 the  cells in the olfactory tract, and these  make possible  the reflex
 movements.
   The auditory, acoustic, or eighth nerve  is extremely complicated.
 Near  its entrance into the  brain-stem this  nerve  divides into two
 roots  surrounding the restiform  body, namely, the  lateral or outer
 root, the  so-called  cochlear nerve, and the  medial or inner root, the
 so-called vestibular nerve.   The  former is most  important to hear-
 ing, as the latter has nothing to do with audition, probably aiding in
 the  perception of equilibrium.  The fibres of  the  vestibular nerve
 arise in the ganglion of Scarpa, thence go through the medial root to
 surround the cells of  the sensory nucleus (Plate II., vm., 15), from
 which they proceed to decussate in the raphe,  pass into the medial
 lemniscus and thence to the cortex.   Another  portion is very prob-
 ably connected with the cerebellum.   The cochlear nerve arises in
 the ganglion of Corti.   Its fibres pass through the lateral root to  sur-
 round the cells  of the sensory nucleus, the  so-called accessory and
 acoustic nuclei.   The  nerve-processes from the  latter form the fibres
 of the  acoustic  striae,  whilst  those of  the  former make up the so-
 called trapezoid  body.  The acoustic  striae pass dorsad, then bend
 downward toward the centre, to split into two portions.   One goes to
 the  upper olivary body of the same side, and  thence to the  lateral
 lemniscus.  The  other decussates in the raphe and goes to the olivary
 body of the opposite side, thence wending its way to the lateral lem-
 niscus.   There thus arises  a partial crossing  of the fibres of the
 acoustic striae, as in a chiasm.  The trapezoid  body is  composed of
 nerve-processes  from the cells of the accessory nucleus.   Its fibres
 pass to the medial line and divide into two portions.   One immedi-
 ately goes into the lateral lemniscus of the  same side.   The other
 passes to the raphe, and in its course its fibres are connected with the
 upper  olivary body and the trapezoid nucleus of the same side, and
ends in these nuclei, from which others pass to decussate in the raphe, 
ANATOMY.
89
 and thence  pass to the lateral lemniscus.   It will thus be seen that
 the lateral lemniscus is really the central auditory tract of the coch-
 lear nerve,  and is to be distinguished from  the  medial lemniscus,
 which constitutes a central pathway for the sensory spinal nerves of
 the fifth, ninth,  tenth, and  vestibular nerves.   When this  lateral
 lemniscus has reached the upper portion of the pons it divides into
 two portions, namely, the inner and the  outer tract.   The fibres of
 the inner tract end in the anterior and posterior quadrigeminal bodies
 of the same  and the opposite side.  They represent the  short ascend-
 ing fibres that serve mainly for reflex movements.   The fibres termi-
 nating in the anterior quadrigeminal body are of especial importance,
 as they surround the large cells  that are connected with the nuclei of
 the nerves of the eye-muscles, namely, the third,  fourth, and sixth.
 These same  cells are also  surrounded by fibres from the optic nerve,
 so that they are centres for the optic and  auditory nerves, and make
 possible  the movements of the  eye that result from optic and audi-
 tory sensations.  The trapezoid body sends off collaterals in its course
 to the nucleus of the facial nerve, which  serve the purpose of reflex
 movements, such as those of mimicry and  the  pointing  of the ears
 in animals from auditory impressions.  The collaterals to  the central
 gray matter carry auditory impressions to the respiratory  and vascu-
 lar centres.   The fibres of the outer bundle of the lateral lemniscus,
 joined by nerves from the posterior quadrigeminal bodies, pass into
 the posterior portion of the internal capsule, and thence to the cortex
 of the posterior portions  of  the two temporal convolutions.  They
 belong to the long ascending fibres, and  constitute the  outer central
 auditory tract.  It is possible, however, that shorter fibres may also
 connect different levels of nerve-ganglia with  this portion of  the
 cortex.

 THE BLOODVESSELS OF THE  CEREBRUM, CEREBELLUM, PONS,
                 AND MEDULLA OBLONGATA.

  Heubner and Duret have made most important researches into the
 vascular supply of the cerebrum, and have shown  that there are two
 great sets of arterioles—one for  the brain cortex,  and  the other for
 the brain stem, as the intra-cranial organs below the cortex and the
 centrum  ovale are called, i. e, the basal ganglia and the sub-lying pons
 and medulla oblongata.   The arteries of the brain stem arise at right-
 angles from the larger branches of the circle of Willis, and, entering the
 cerebral substance, branch in this without communication with each
 other.  According to Heubner, they possess the peculiarity of taking
 their origin  from the first portion of the large cerebral arteries as they
 pass over the white substance.   These cerebral arterioles are  beauti-
 fully shown  in Fig. 53.   From  the short angle which  is  formed by
 the  first  portions  of the  Sylvian artery and the anterior  cerebral
 artery, or the artery of the corpus callosum, arise only the vessels for
 the anterior half of the brain stem.  From the anterior communicating
branch of the anterior cerebral artery branches are given off to  the
head of the nucleus caudatus; from the point of the angle, the vessels 
90
INTRODUCTORY.
for the anterior limb of the internal capsule and the inner and middle
segments of the  lenticular nucleus;  whilst  from the lateral portion
of the Sylvian artery are supplied the outer segment of the lenticular
nucleus, the middle portion of the caudate nucleus, and  the external
capsule.  The ganglia of the tegmental or dorsal portion of the crus
are supplied  from the  commencing portions of the large arteries
Fig. 53.
      3 1   2
     Branches of middle cerebral, anterior cerebral, and posterior cerebral.  (Duret.)
 1. Carotid artery.  2. Sylvian, or middle  cerebral artery. 3. Anterior cerebral artery. 4.
Posterior cerebral artery.  5. Arteries of the corpus striatum. 6. Anterior choro'ideal artery.
7. Posterior communicating artery,  8. Postero-lateral choro'ideal artery. 9.  Postero-median
choro'ideal artery.  10. Termination of callosal arteries. 11. Middle quadrigeminal arteries.
12. Postero-internal optic artery.

forming the circle of Willis.  The choro'ideal artery and the posterior
communicating  supply the anterior, and the posterior cerebral  the
posterior ganglia.   It must be borne in  mind  that although there
is  communications  between these larger  arteries at the  base, there
is none between the branches after they have plunged  into the cere-
bral substance, and that these latter, therefore, are terminal  arteries.
The optic chiasm, the cranial nerves, the  pons, the medulla  oblon-
gata, are thus  supplied directly from the  arteries of the circle of
Willis without any intervention  of  the arteries coming  from the  pia
mater.   Duret has shown, furthermore, that many of these branches
of the arteries of the anterior cerebral  artery are inconstant.   They 
ANATOMY.
91
supply only the head of the caudate nucleus, and they produce very
circumscribed lesions, which  are the  more dangerous because they
may easily break into the ventricle.   He  has  also  shown that from
the Sylvian artery there  pass  off the internal striated vessels going
to the first and  second segments  of the lenticular  nucleus and the
internal capsule,  and  the external  striated  arteries,  which  are so
called because they first supply the  outer  portion of the third seg-
ment and  the lenticular nucleus, and then pass into the gray  matter
of the same and ascend.   These  latter branches are subdivided into

                                 Fig. 54.
                           Cf D"GQ'QVC
               Arteries of the pons and the choroid plexus.  (Duret.)
  0. Part of optic thalamus not covered by choroid plexus.  0'. Choroid plexus beneath the
optic thalamus. C. Posterior portion of choroid, thrown back from its normal position above
the crura cerebri and the quadrigeminal bodies.  D. Choroid plexus.  D'. Its anterior portion.
D". Where it curves to reach the lateral ventricles.  G. Internal  geniculate body. G/. Ex-
ternal geniculate body. Q. Anterior quadrigeminal body. Q'. Posterior quadrigeminal body.
P. Section of crura cerebri just above the pons.  Pi. Pineal gland.  1. Carotid artery.  2. Syl-
vian, or middle cerebral artery.  3. Anterior cerebral artery.  4. Posterior cerebral artery.  5.
Point of origin, from  the carotid, of the anterior choro'ideal artery. 5'. Its course in the
choroid plexus. 6. Postero-lateral choro'ideal artery. 6'. Its branch to the choroid plexus.  6",
Its branch to the velum interpositum.  7. Postero-external optic arteries, traversing the crura,
near the  geniculate bodies, to enter the optic thalamus.  8. Middle quadrigeminal artery,
branching into the anterior and posterior quadrigeminal vessels.  9. Postero-median choro'i-
deal artery.  10. Termination of callosal artery in the pineal gland.  V. Veins of Galen.


the lenticulo-striated vessels  anteriorly, and  the  lenticulo-optic ves-
sels posteriorly.   The lenticulo-striated arteries are large, ascend into
the third segment of the lenticular  nucleus to the upper part of the
internal capsule, and pass over to  the  caudate nucleus, terminating
far forward in this.   They are the  most  usual site  of hemorrhages.
The lenticulo-optic arteries pass through the posterior portion of the
internal capsule, and into the anterior and outer portion  of the optic
thalamus.   Duret has  furthermore demonstrated that the posterior
cerebral artery not  only supplies the optic  thalamus, but also the
corpora quadrigemina and the tegmental  region of the crus.  One of
these branches to the optic thalamus, the postero-internal optic artery, 
92
INTRODUCTORY.
supplying the inner surface, is prone to minute hemorrhages  which
are very dangerous because of their tendency to break into the ven-
tricle;  whilst another branch, the  posterior external  optic artery,
passes over the cms before reaching the hinder portion  of the optic
thalamus, and hemorrhages of it may therefore involve both the optic
thalamus and the crus.
   The arteries of the cortex  are subdivided into secondary and ter-
tiary branches within  the pia, and  from  the plexus so  constructed
arise nutritive vessels  which pass perpendicularly into  the cerebral
substance.   (Fig. 56.)  There  is  a  difference  of  opinion  between
Heubner and Duret as to whether the areas to which these arterioles

                                 Fig. 55.
Transverse section of the cerebral hemispheres, about 1 cm. behind the optic commissure.
  Ch. Chiasma.  B. Section of the optic tract.  L. Lenticular nucleus. 1. Internal capsule.
C. Caudate nucleus.  E. External capsule.  T. Claustrum.  R. Island of Reil. V, V. Section
of the lateral ventricle.  P, P. Anterior pillars of the fornix.  0. Gray substance of the third
ventricle.
  Vascular Areas: I. Anterior cerebral  artery.  II. Middle cerebral artery. III. Posterior
cerebral artery.—1. Internal carotid  artery.  2. Sylvian artery. 3. Anterior cerebral artery.
4, 4. External arteries of the corpus striatum (lenticulo-striate artery).  5, 5.  Internal arteries
of the corpus striatum  (lenticular arteries). 6. Arteries of the chiasma.  7. Arteries of the
commissure and anterior pillars of the fornix. 8. Arteries of the convolutions of the insula
and claustrum.  The opto-striate artery is not represented in the figure.  (Duret.)

are  distributed  communicate  with each  other, Heubner contending
that they are connected by small vessels of the calibre of a millimetre,
whilst Duret maintains that each area is isolated.   From the pia mater
two sets of arteries  pass  into the  cerebral substance: long or medul-
lary vessels,  and  short  or cortical ones.   The long  or medullary
vessels, twelve or  fifteen  in  number  in the section  of a convolution,
pass vertically three to four centimetres deep, nearly to the end of the
vessels coming up from  the base, but without communicating with
them ;  and it is in these  badly nourished neutral territories  between
the two sets of arteries that certain senile softenings are especially to
b% found.  The short  or cortical vesels  supply only the cortex and 
ANATOMY.
93
the neighboring white matter.   From them  is formed the fine  net-
work in the cortex in the different layers of the nerve-cells.   Through

                                  Fig. 56.
                         A
 Distribution of arteries to gray and white matter. 1,1. Medullary branches passing directly
through the gray matter to the white matter, and then terminating in branches that do not
anastomose with their neighbors  (" terminal arteries").  1. Medullary arteries in the sulcus
between two convolutions. 2, 2. Cortical arteries.  (Duret.)


                                  Fig. 57.
An artery of the cortex.  Magnified 360 diameters.
obstruction  of one of these arteries there will be formed a superficial
softening of the cortex and the  neighboring white matter, forming a 
94
INTRODUCTORY.
triangle whose basis will lie toward the surface.   This is the so-called
yellow softening [plaque jaune).   In Fig. 57  is  represented an artery
of the cortex, with its peri-vascular space.

                                      Fig. 58.
Outer surface of the left hemisphere.  (After Duret.)
                                Distribution of Vessels.
  The region bounded by the line (_______) represents the territory over which branches of the
anterior cerebral artery are distributed.
  The anterior regions bounded by the line(______________) represent the territories over which
branches of the middle cerebral artery are distributed.
     I. Is the region of the external and inferior frontal artery.
    II. Is the region of the anterior parietal artery.
   III. Is the region of the posterior parietal artery.
   IV. Is the region of the parieto-sphenoidal artery.
  The posterior and inferior region bounded by the line (.-----------------) represents the
territory over which branches of the posterior cerebral artery are distributed.

                              Fissures and Convolutions.

  F. Frontal lobe.  P.  Parietal  lobe.  O. Occipital lobe.  T.  Temporo-sphenoidal lobe. S.
Fissure of Sylvius ; S', horizontal;  S", ascending ramus of the same.  c. Sulcus centralis or fis-
sure of Rolando.  A Anterior central or ascending frontal convolution.  B. Posterior central
or ascending parietal convolution.  F1, superior; F2, middle ; and  F3, inferior frontal  convo-
lutions,   fi, superior, and f2, inferior frontal sulcus,  f3. Sulcus prsecentralis.  P1. Superior
parietal or postero-parietal lobule.   P2. Inferior parietal lobule, viz.: P2. Gyrus supra-margi-
nalis.   P2'. Gyrus angularis.  ip Parietal fissure,  cm. Termination of the calloso-marginal
fissure.  O1, first; O2, second ; O3,  third occipital convolutions,  po. Parieto-occipital fissure.
o1. Sulcus occipitalis transversus.   o2. Sulcus occipitalis longitudinalis inferior.  T1. first; t2,
second; T3, third temporo-sphenoidal convolutions,  t1, first; t2, second temporo-sphenoidal
fissures.


   According to  Duret, the  larger arteries of  the cerebrum are only
connected  by the fine  branches of longer  or shorter vessels  and  he 
ANATOMY.
95
thinks  that  this is  the  reason  that  the  areas  of  the  central  dis-
tribution  of these arteries  are much  more prone to soften, whilst in
the  peripheral areas a distribution  may, when  the supply of blood
from  the true nutrient  artery is  cut  off, be supplied by a collateral
vessel.
                                    Fig. 59.
Vascular areas of the upper surface of the cerebrum.  (After Duret.)
  F. Frontal lobe.  P. Parietal lobe.  O. Occipital lobe.  s. End of the horizontal ramus of the
fissure of Sylvius,  c. Fissure of Rolando.  A. Ascending frontal convolution.  B. Ascending
parietal convolutions.  F1,F2,iF3. Superior, middle, and inferior frontal convolutions,  f1, f2.
Superior and inferior frontal sulci, f3. Sulcus prsecentralis.  P1. Superior temporal lobule.  P2.
Gyrus supra-marginalis.  P2'. Gyrus angularis.  ip. Parietal fissure, cm. Calloso-marginal
fissure,  po, po. Parieto-occipital fissures, t1. Superior temporal fissure.  O1.  First occipital
convolution,  o. Transverse occipital sulcus.
  Arteries: The line (..................) marks the limits of the distribution of the anterior cerebral ■
the line (______________) on the left side of the figure limits the distribution of the Sylvian
artery.  I. External and inferior frontal artery.  II. Anterior parietal artery.  III. Posterior
parietal artery.  IV. Parieto-sphenoidal artery.  The line (----------) on the right side of the
figure limits the distribution of the posterior cerebral.


  The Sylvian  artery gives off  four or five main branches,  which
pass over the  island of  Peil  to reach  the surface of the  cerebrum.
The first one supplies  the  first frontal convolution,  especially in its
rear portion,  and   hence  arise  the  isolated  softenings  of  Broca's 
96
INTRODUCTORY.
centre, which  cause  aphasia alone.   The fourth branch supplies the
lower parietal  lobe and the upper portion of the first temporal con-
volution, whilst  the fifth branch supplies the remaining portions of
the  first  and  second temporal convolutions.  The anterior cerebral
artery is divided into three branches, the first supplying the two con-
volutions on the under surface of the  frontal lobe,  the second going
Fig. 60.
   „_____A  c B
Inner surface of the right hemisphere.  (After Duret.)
                             Distribution of Vessels.
  The regions bounded by the line (.....) represent the territories over which the branches of
the anterior cerebral artery are distributed.
     I. Is the territory of the interior and anterior frontal artery.
    II. Is the territory of the internal and middle frontal artery.
   III. Is the territory of the internal and posterior frontal artery.
  The regions bounded by the line (---------) represent the territories over which the branches
of the posterior cerebral artery are distributed.
    II. Is the territory of the posterior temporal artery.
   III. Is the territory of the occipital artery.
                            Fissures and Convolutions.
  CC. Corpus callosum, longitudinally divided.  Gf. Gyrus fornicatus. H. Gyrus hippocampi.
ft. Sulcus hippocampi. U. Uncinate gyrus,  cm. Sulcus calloso-marginalis. F1. Median aspect
of the first frontal convolution,  c. Fissure of Rolando.  A.  Ascending frontal; B, ascending
parietal convolution.  Pw. Precuneus. Oz. Cuneus.  Po. Parieto-occipital fissure, o. Sulcus
occipitalis transversus.  oc. Calcarine fissure,   od. Superior; oc"., inferior ramus of the same.
D. Gyrus descendens.  T4. Gyrus occipito-temporalis lateralis (lobulis fusiformis).  T3. Gyrus
occipito-temporalis medialis (lobulus  lingualis).


to the gyrus  fornicatus,  the corpus callosum, the second and third
frontal  convolutions,  and  the  upper  end of the  ascending frontal
convolution, whilst the  third  branch  supplies the precuneus.   The
posterior  cerebral artery splits  into  three branches.   The first sup-
plies only the hook-shaped  end of the gyrus hippocampi,  the second 
ANATOMY.
97
supplies  the  fusiform lobule and  the neighboring  portion  of the
second temporal convolution, whilst the third branch nourishes the
lingual lobe, the cuneus, and the occipital lobe.
  Duret has shown that the pons and  medulla are supplied by three
different systems—the median, the radicular, and the indifferent ves-
sels.  The median arteries have a calibre of one-fourth  to one-sixth
of a millimetre, and arise  from the basilar and the anterior spinal.
They ascend perpendicularly in the raphe nearly to the gray matter,
and supply  the nuclei  and the ependyma  of the fourth ventricle,
breaking  up  into fine  networks for the different nuclei.  They are
terminal arteries.   The anterior  spinal  artery  is sometimes pres-
ent on only one side, sometimes double, sometimes arising from each
vertebral, but  these branches generally unite in one stem.   When
there is only one, it generally arises from the left vertebral;  if there
are two, they  are generally strongly anastomosed.   The left verte-
bral is usually larger than the right.   The radicular arteries  arise
from one of the larger  branches that have been spoken of, and pass
into the vessels that terminate on  the nerve-roots in arterioles which
have a diameter of one-third  to one-fourth  millimetre.   These con-
sist of ascending and descending  branches, the latter passing to the
nucleus, breaking up into a capillary network.  It is therefore evident
that each nucleus has  two sources of arterial supply: one from the
median and the other  from the radicular arteries, the former being
by  far the most important.   The indifferent arteries of the pons and
medulla  are supplied from the other larger vessels of  the circle of
Willis.   The  inferior cerebellar artery passes to the lateral portions
of the medulla oblongata and the  lower inferior cerebellar peduncle,
and gives rise on each side to a posterior spinal artery which nour-
ishes the posterior columns and finally divides into three branches :
one for the vermis, anastomosing with its fellow  of the opposite side
and two  lateral branches;  one  supplying the inner surface of the
cerebellar hemisphere;  the  other  the  under surface of the same.
These three arteries have enormous anastomoses on the surface of
the cerebellum and also  communicate with  the posterior cerebral
artery.
                    CRANIAL TOPOGRAPHY.

  Of late years, since the localization of cortical  centres  has come so
largely into play in neurological diagnosis, much attention has  been
paid to the relative position of the  different fissures and convolutions
of the brain and cerebellum and to the cranial sutures and  bones.  The
subject was first studied in 1857 by Gratiolet, in 1861 and again in
1877 by Broca, and  since then by Bischoff, Heftier, Turner, Fere,
Fouillehouze,  Ecker, Lucas-Championniere, Pozzi, Horsley, Thane,
Hare, and Dana.
  Broca  has  given certain names to the different points  of union of
the  sutures, and these are marked out on the accompanying diagram,
and with them the surgeon and neurologist should be familiar.  The
principal  ones are  the  nasion, the  inion, the glabella, the lambda,
the  stephanion, the pterion, and the asterion.  The nasion is at the
                               7 
98
INTRODUCTORY.
junction of  the  nasal and the frontal  boues; the inion is  identical
with  the  occipital  protuberance; the glabella is a protuberance just
above the nasion;  and the asterion can be felt just behind the upper
part of the  mastoid process of the temporal  bone; whilst the others
are marked so  plainly upon  the diagram that they need no further
description.
                              Fig. 61.
Diagram illustrating prominences of the skull.
   The shape and various dimensions of the skull vary with age, sex,
race, individuals, pathological  conditions, and artificial deformities;
but there  is no great  difference  in the skulls of the European and
the American  races.  The principal types of skull are the dolicho-
cephalic, the brachycephalic, and the mesocephalic.   The first is that
in which the antero-posterior diameter is to the transverse as 100 is
to 75 or less;  the brachycephalic is that in which the antero-pos-
terior diameter is to the  transverse as  100 is  to  80 or more • the
mesocephalic is that  in which the antero-posterior diameter is to the
transverse as 100 is to 70 or to 80.  The physiological limits in varia-
tion  in  the ratio of the antero-posterior to  the^transverse diameter
are from 100 to 70, or 100 to 90.  No great variations are  found
between  the skulls  of  the  two sexes, although  in female skulls the
bony ridges and protuberances are less marked,  the inion less prom-
inent, and  the volume less, whilst the posterior half of the naso-
occipital arc is  greater.   Nor has the shape of the skull been shown
as yet to be of  any particular importance among the different races,
although it may be  stated roughly that  the English and  Iri^h and 
ANATOMY.
99
Scandinavians are dolichocephalic,  whilst  the negroes,  Arabs, and
Chinese are less  long-headed in the ratio in which they are named ;
that  the Germans, Russians, and Turks  are  brachycephalic; and
Photograph from Fraser, showing the cerebrum and the cerebellum in the cavity of the
     skull covered by the membranes ; also the upper portion of the spinal cord.
that the American  Iudians,  Dutchmen, and Parisians are meso-
cephalic.  The Italian school have attempted  to demonstrate  the
existence of a pathological or criminal skull, but they have not been
successful.
  Of much more practical value than all these variations of the skull
are  the relations of the  different convolutions to the sutures.   It
must be borne in  mind, however, that it is  no longer necessary to
define very minutely the  relation  of  a suture  to the  skull-bone, be- 
100
INTRODUCTORY.
cause antiseptic surgery has rendered trephining nearly as harmless
an operation as circumcision, and in most all cases the  skull  should
be so liberally removed as to lay bare the whole cerebral lobe, or at
least  several convolutions.   The approximate relation, therefore, of

                               Fig. 63.
Photograph from Fraser, showing the cerebrum, the cerebellum, and the upper portion
            of the spinal cord, the membranes having been removed.
the different cerebral fissures to the different sutures of the skull is
all  that  it is necessary for the neurologist and the surgeon to know.
Figs. 62 and 63, taken from Fraser's beautiful atlas, will give a true
idea of the relative position of the main fissures and convolutions to 
ANATOMY.
101
the skull, as the intra-cranial contents  usually lie within the intra-
cranial cavity.   The fissures and convolutions can be  readily identi-
fied by comparison with Fig. 14.  Various instruments have  been
devised for marking off the skull,  so-called cyrtometers,  but an
ordinary tape-line is as good as anything else.  The rules following
will be quite sufficient.
   I. The longitudinal fissure corresponds  with  the median line of
the vertex from  the glabella, or junction  of the nasal  and frontal
bones, to the inion, or occipital protuberance.
   II. To find the fissure  of Rolando:  Measure the  distance from
the glabella to the inion, or occipital protuberance.   Find 55.7 per
cent, of this distance, and this  will indicate the upper  end of the
fissure of Rolando, which is generally from 15.7  to 26.8 centimetres
from the glabella.   To find the course of this fissure, mark off from
the upper end a line that shall form an angle of 67 degrees anteriorly
with the longitudinal fissure.   This  will  give the direction of the
upper  two-thirds of the fissure of Rolando, or about 1\ inches, or
5.6 centimetres.   The lower third of this  fissure, about 2.1 centi-
metres in length, is somewhat more vertical, the  total length of the
whole fissure being 8.5 centimetres.  To find the lower  end of the
fissure of Rolando, mark off a line from the stephanion to the asterion,
and another from the bregma to the external auditory meatus, and
the point of intersection of these two lines will be  just over the lower
end of the  fissure, about one centimetre above the fissure of Sylvius.
The upper end of  this  fissure of Rolando varies somewhat in its
position  in  adults  of different  races  and  sexes,  but the  average
variation is only  about twenty millimetres, and  the  lower end  has
about the  same variation.   In  idiots,  whose cerebral growth  has
been impeded, the upper end is  nearer the bregma, being only 30 to
32 centimetres behind it; but the lower end is not usually changed.
In children the upper end of the fissure in  the first months of life is
from  30 to 35 centimetres  behind the  bregma, in the  second and
third years of life about  42 centimetres behind the bregma, and after
this it rapidly approaches with every year to the distance of the adult
brain.
   III. The fissure of Sylvius:  To find this draw a vertical line
from the stephanion  to the middle of the zygoma.   Then draw a
horizontal line from the  external angular process to the highest point
of the squamous suture.  Prolong this latter line, gradually curving
upward until it reaches the parietal eminence.  The junction of the
two lines will indicate the beginning of the fissure of Sylvius.   The
vertical line indicates approximately the position of the  anterior or
vertical branch of the fissure, whilst the posterior  part of the hori-
zontal line indicates the position of the posterior branch of the fissure.
The third froutal fissure lies just anteriorly  to the vertical branch of
the fissure,  i. e., just anteriorly to the  junction of the two lines that
we have indicated.  The tip of the temporal lobe is just back of the
posterior edge of the orbital process of the malar  bone.   In children
up to the third or fourth year the fissure of Sylvius is  more oblique, 
102
INTRODUCTORY.
and lies  somewhat  more above the squamous suture than  the  lines
which I  have indicated.
   IV. The parieto-occipital fissure:  Measure the distance from the
nasion, or junction of the nasal  and frontal bones, to the  inion or
occipital  protuberance, and take 22.8 per cent, of this, and this will
indicate  the position of the lambda.  Its average distance from the
occipital  protuberance in adults is  7.42 centimetres.   It must  be
remembered, however, that this  parieto-occipital fissure is subject to
great variation.  Thus Heftier found it just above the lambda, Ecker
several millimetres anterior, whilst Fouillehouze located it from 5 to
21 millimetres anterior;  Fere, found it uuder the lambda in 39 out
of 62 cases, and a few millimetres above it in 24 cases; and Turner,
Broca, Reid, Horsley, and Hare are  not agreed.   In children, too,
this parieto-occipital fissure  is from 5 to 31 millimetres  in front of
the lambda.    In all cases,  therefore,  the occipital lobe should  be
generously uncovered.
   V. The parietal fissure : The finding of this fissure  is a somewhat
complicated matter, if its exact  site is to be  determined  from the
skull.  The fissures of Rolando and Sylvius and the parieto-occipital
fissure should be marked out in the manner that has been described.
The anterior end of  the parietal fissure can then be found about one
inch above and  behind the angle formed by  the fissures of Rolando
and Sylvius, whilst the posterior part lies about one-half inch outside
the parieto-occipital fissure.   As this parietal fissure, however, is ex-
tremely variable, the best  way to localize it is to uncover the parietal
lobe, through  the centre of which it runs.
   VI. The preceutral fissure and the first and second frontal fissures:
These fissures can best be found by first ascertaining the  position  of
the fissures of Sylvius and Rolando.   The  precentral fissure at its
lower end is about 1 centimetre above the Sylvian fissure, whilst its
upper end is about 2.5 millimetres anterior to the fissure of Rolando.
The first frontal fissure  begins at about 2.5  centimetres in front  of
the fissure of  Rolando, running forward parallel to the longitudinal
fissures.  The secoud frontal fissure passes forward from the precen-
tral fissure  at a point a  little above the stephanion, and  continues
its course under the froutal part of the temporal ridge.
   VII. The temporal lobe and the first  and second temporal fissures:
The upper  boundary of the temporal is the fissure of Sylvius and
the lower boundary is a line drawn from a point slightly above the
zygoma and the external meatus to the asterion, and continued along
the occipital curve to the inion.   The anterior border of the temporal
lobe is about beneath the posterior edge of the orbital process of the
malar  bone.   Bergmaun states that a trephine placed  one-half inch
above the external auditory meatus would enter the lower part of the
lobe, whilst the middle part is in the vertical line from the posterior
border of the  mastoid  process.   To find the first temporal fissure a
line should be drawn about 2.5 centimetres below and  parallel  to
the Sylvian fissure, whilst the secoud temporal fissure is about 2  cen-
timetres  below the first  These are Reid's rules, and  I believe they
are reliable. 
ANATOMY.
103
  VIII. The occipital lobe and anterior occipital fissure can be found
by curving a line from the lambda to a point about two-thirds of the
distance between the inion and the asterion, and regarding this as the
anterior border of the occipital lobe, whilst the superior occipital
curved line may represent the lower border.
  IX. The central  ganglia of the corpus striatum and optic thala-
mus :  Draw a line from the upper end of the fissure of Rolando to
the asterion.  This  may be taken to  be the posterior boundary of
the optic thalamus.  Draw a second line parallel to the first, slightly
in front of the  beginning of the fissure of Sylvius.   This may be
taken to be the boundary anteriorly of the corpus  striatum.  The
upper surface of the ganglia will  be about 45 millimetres below the
surface of the scalp at the bregma.

                        HEAT-CENTRES.

  Very little indeed is known about the heat-centres.  Twenty-five
years ago  Tscheschichin found that a heat-centre existed  somewhere
above the pons Varolii in the brain.  H. C. Wood had arrived at the
same conclusion. Richet, in 1884, found that there was a  heat-centre
somewhere in the anterior part of the brain.   In April, 1884, Isaac
Ott located this heat-centre in the anterior and inner portion of the
corpora striata of rabbits.   In December of the same year Aronsohn
and Sachs found that a puncture of the brain caused an  increase of
the temperature of the body.  In July,  1885, Ott published a further
communication upon the subject, stating that he had localized a heat-
centre  at the anterior and  inner portion of the optic  thalami.   In
October of the same year Sachs and Aronsohn again returned to the
matter, localizing this  heat-centre that they had previously described
in the nodus cursorious of the optic thalami of the rabbit.  Schreiber,
Budge, Lussana, and  Christiani had shown that various  sections at
the base of the  brain and at the vertex were capable  of causing rises
of temperature; but it would seem as if the precise  observations of
Aronsohn, Sachs, and Ott had localized the heat-centre of which the
other observers  had  merely seen the effects.   Schreiber, for instance,
found a marked increase in temperature after section of the medulla
oblongata  at  its junction with the pons, whilst Budge had located
vasomotor fibres in  the crura  cerebri.   Schiff, Brown-Sequard, Eb-
stein, and  others  also showed that hemorrhages had been found in
the pleura, luugs, stomach, intestines, and kidneys, after injuries of
the corpora striata,  the pons, the optic thalamus, the crura cerebri,
and the medulla oblongata.  Lussana located vasomotor fibres in the
optic thalami, and Christiani ascertained that removal of the hemi-
spheres caused fever.   Aronsohn and  Sachs have, however, shown
that the vasomotor fibres are not the cause of the increased tempera-
ture, that removal of the  hemispheres alone will not cause fever, and
that there  is no increased production of heat in the  muscles nor any
marked vasomotor changes.  At the present time, therefore, the only
heat-centre that has been localized is that at the anterior and inner
portion of the optic  thalami in rabbits, and probably in  an analogous 
104
INTRODUCTORY.
location in the human being.  It has long been known clinically that
some lesions of the spinal cord are capable of causing considerable
increase  of temperature, but exactly how this  is produced  is not
known.  Eulenberg and Landois have also shown that excitation of
one cerebral lobe can  produce a notable elevation of temperature in
the opposite limb, although they do not speak of the general tempera-
ture.   Richet has performed a number of experiments upon rabbits
and dogs, showing that the excitation of different convolutions is
capable of causing a general thermic rise.  Thus injury to the ante-
rior lobes caused an elevation of temperature of 3.6° C. in forty-five
minutes, whilst cauterization produced the same phenomenon.  The
method of production of this  increase of temperature is largely a
matter of speculation. 
CHAPTER  II.
                         ELECTRICITY.

  It is not my purpose to do more than deal with the applications
of electricity in nervous  and mental disease.  I  am  not writing a
text-book on electricity, aud I shall therefore not deal with theoretical
considerations, except so far as may occasionally be necessary in order
to banish the confusion existing in the average medical mind about
electrical terms  and  still more about electric  phenomena.   If by
some magic power I could at this very moment unroof the office of
every physician  in  the United  States, I hesitate to mention what I
think would be the proportion of  worthless  batteries, or worthlessly
used batteries, or  worthless  rheostats, or  worthless   milliampere-
meters, or electrodes entirely unfitted for the purpose to which they
are  daily  being put.   I believe, therefore, from experience as a
teacher and consultant, that a  brief space  can  be advantageously
devoted  to the instruments with which electricity is used and  the
methods of handling them.
  Electricity, as we use it in medicine, is of three kinds :
  The Galvanic, which is  sometimes called the voltaic or the con-
tinued current.
  The Faradic, which is sometimes called the faradaic, or the inter-
rupted.
  The Static, which is made by friction, generally in  the Holtz or
similar machines.
Fig. 64.
            A cell.  z. Positive plate,  s. Negative plate,  a. The fluid.

  Galvanic electricity is a force produced by  the  immersion of two
dissimilar  metals  in a fluid  capable of inducing chemical action.
The two metals, or plates, immersed in a  fluid, and the jar which
holds  them, are called collectively a cell (Fig. 64).  A collection of
cells constitutes a battery.  One of these metals, or  plates,  is called 
106
INTRODUCTORY.
the positive, and the other  the negative.   The current flowing from
the positive  plate  is called  the positive current and that from the
negative plate is termed the negative current.   The two plates differ
in their chemical and physiological properties.   We may assume for
practical  purposes that the metal which is the most actively attacked
by the liquid is the positive  metal.  All metals, therefore, can be
ranged in a  comparative series from the  most positive to the most
negative, each one being  positive or negative to other members of
the series.    Within the  cell  the current flows  from the  positive
plate  Z, to  the negative plate  S, Fig. 64.   If to each one of these
plates is attached a wire, and the wires are  joined, the current flows
through them and back again into the cell, but in the opposite direc-
tion to the current in the  cell.   These wires are called the poles.  If
between the  two poles a human body is so interposed that  the  cur-
rent  must  flow  through  it,  the  direction  of the  current  will be
unchanged.    The  distinction   that  is here  described  between  the
plates in the cell  and the  wires outside the cell should be fixed
clearly in the mind  of the reader, as it is a matter about which there
is much confusion.  The  positive  pole is known as  the anode, and
the negative  pole as the cathode.
   Cells vary in construction according to the uses to  which they are
to be put.  If a wire is simply to be brought to a white heat, as in
the electric cautery, the  cell  should be constructed in  an entirely
different  manner from what  is  required when  the  wire is simply
intended to  pass a current  of electricity through the human body.
When a  galvano-caustic  is needed,  the  largest  possible amount of
electricity should come from  the cell,  as,  the flow of the  current
being through  a metallic wire which conducts electricity well, the
resistance opposed  to  the current will  be very slight, and therefore
the power  that the current  has of overcoming the resistance, or the
electro-motive force,1 as  it  is  technically called, need only be very
slight.   If, on  the  other  hand, a moderate quantity  of electricity is
to  pass  out of  the  cell and push its way through the human body
with  its enormous resistance, the quantity of the current is unimpor-
tant in comparison with its  capacity for overcoming resistance, and
the electro-motive force must accordingly be great.   In other words,
the quantity  of the current and its  capacity for overcoming resist-
ance, or its electro-motive force, are two entirely different things, and
for this reason the battery which is used for electric cauterization can-
not be used for electrification of the human body.  It is of importance

  1 The electro-motive force is the result of the difference of electric potential of two bodies, or
two different parts of the same body, and it is proportional to this difference.  It is often com-
pared—and justly—to the difference in pressure of the water in a water-pipe at two different
levels.  Practical electricians, however, have come to use the term as synonymous with its
power of overcoming resistance; and although this idea is not strictly accurate, I have found
that it conveys a  more definite idea to the average  mind, because the whole doctrine of poten-
tials is confusing from its very arbitrariness. The zero potential, for example, is assumed to
be the potential  of a spot infinitely distant from all electrified bodies, and the earth is dog-
matically asserted to be this zero potential. Anything positively electrified is asserted to be at
a higher potential than the earth, whilst anything negatively electrified is at a lower potential
than the earth.  If the difference of potentials between two bodies connected with each other
is maintained by the friction of a Holtz machine, or the chemical action of a galvanic battery,
an electric current results, and the difference between the potentials of these two bodies
determines the electro-motive force.  But the difference between  these two potentials, pro-
ducing the electro-motive force, is to all intents and purposes the capacity of overcoming
resistance. 
ELECTRICITY.
107
 for the physician to know what cell is best adapted to the exigencies
 of practice, what cell is most easily carried about, lasts the longest,
 gives the most constant current from day to day, and is the cheapest.
 All  these details will  be  considered later.   For example, the teleg-
 rapher makes use of  a Daniell's cell  that  is large and cumbrous,
 and that has to be replenished every day or two; and as his instru-
 ment is never moved, and as it is very easy for him to replenish one
 or two cells, which  are all that  he needs, the Daniell's cell answers
 his purpose very well.  But it would be entirely too large and require
 entirely too much attention  for the physician, more  especially as a
 number of them would be needed by the latter to furnish the requisite
 current.  Then, again, the stationary cell, which the  physician uses
 only in his office, may be much larger and more cumbrous than those
 which he has to carry around with  him in his carriage to the bed-
 sides of his patients.
   Owing to its low resistance, its flexibility, and its cheapness, copper
 is the metal generally used in the wires or poles.  If brought directly
 in contact with the naked human body, these wires  would  be found
 to be painful, since  they concentrate  the current upon too small an
 area of skin.  To prevent this pain and to diffuse  the current over
 a wider  surface  of tissue the  poles have attached to them  a  dif-
 fuser or electrode, a  device varying iu size,  shape,  and  material,
 according to its purpose.  If, for example, the current is to be con-
 centrated upon a small nerve,  a small piece of copper is preferred.
 If the current  is to be diffused over a large area, the electrode may
 be such as  shown in Fig. 67.   Electrodes  are  usually constructed of
 copper, covered with sponge or absorbent cotton in order still further
 to diminish the painfulness of  the  naked copper when placed upon
 the textures of the body.  In some cases they are made of clay.
   It is necessary to have some accurate means of measuring the cur-
 rent,  and for this purpose an instrument known as the milliampere-
 meter has  been  devised.   The ampere is  the unit that has  been
 adopted of late years for the quantity of electricity, and the milliam-
 pere,  or thousandth part of the ampere, is the unit of quantity which
 is best adapted to the uses of the medical electrician, since we scarcely
 ever use the full ampere, but rather  proportion our doses of electricity
 in quantities that range  from  one  to ten or twenty milliamperes in
 medico-electric therapeutics, and from three hundred to five hundred
 milliamperes in  electrolysis.    The  different kinds  of milliampere-
 meters will  be considered in their proper place.  Until recently the
 importance of accurate  dosage of electricity has not been appreciated.
 To follow the old custom of measuring the current by the sensations
 of the patient is no more rational or scientific than to direct a patient
 to take as  much  quinine as  he thought would produce cinchouism.
 Another equally faulty method  has  been to  use a given number of
 cells  for a case, but this is grossly  inaccurate, since  the resistance of
 the  humau  body varies  enormously under  varying  circumstances,
and the current developed from the cells is likewise subject to much
 fluctuation.
  It is also  necessary to have a regulator of the current, so that we 
108
INTRODUCTORY.
can admit  as  much electricity as we want.  Such an instrument is
called a rheostat.   The old fashion  was to  turn  on a sufficient num-
ber of cells, and then, if that did  not give enough current, to turn
on another cell, and so on until the requisite amount of current was
admitted.  The difficulty with this  method should be very apparent.
Suppose that we  turn on five cells, and then we  find that we  have
two  milliamperes of electricity measured off;  but we want three
milliamperes.   We therefore turn  on another cell, but we find that
this gives us four milliamperes.  Now, what are we going to do?  If
we turn back to three cells, we will only have two milliamperes; if
we turn on four cells, we have four milliamperes.   If we have some-
thing in the circuit that will  accurately regulate the admission of the
current, so  that we can turn on just three  milliamperes, it is very

                              Fig. 65.
Battery table showing arrangement of galvanic and faradic apparatus, rheostat, and
                       milliamperemeter.
apparent that we are very much more precise.   Besides this, it may
be very unpleasant to turn on each  additional cell, for in doing so
we  give  the  patient a shock.   If we were passing electricity only
through the human trunk, the shock caused by adding a whole cell
would be very slight, and the patient would not complain much; but
if we were passing electricity through the human brain, a single addi-
tional cell would give a  shock  so unpleasant as to cause vertigo, a
flash of light, and often considerable distress.   It is therefore further
apparent that a  regulator  that will  turn on or turn off the  current
very gently,  without shock, is eminently desirable, and such a regu-
lator is the so-called rheostat.  The different varieties of rheostats will
also be considered hereafter. 
ELECTRICITY.
109
  Let us now suppose that we have a patient to whom we want to
give  galvanic electricity, and that we desire to make use of the cell
with its wires or poles attached, these wires being armed with the
proper electrodes, and that we also wish to make use of a rheostat or
regulator of the current, and of a measurer of the current, or milli-
amperemeter.  Fig.  65 shows  how this is done.  To the battery
are attached the two poles or wires, 1 and 2. Disregarding wire 1 for
a moment, wre turn our attention to the other pole or wire (2) going to
the rheostat, thus conducting the current into and through it.  On the
other side of the rheostat the current is carried off through another wire,
3. This runs to the milliamperemeter, conducting the current into and
through it.   From the other side of the milliamperemeter the  cur-
rent is taken by wire 4.  The wires 2, 3, and 4, with the intervening
rheostat and milliamperemeter, therefore constitute one  pole of the
battery just as the wire 2 does before it has been connected with the
rheostat and the milliamperemeter.   If we put an electrode on wire
4, and another electrode on the other wire, 1, which constitutes the
other pole of the battery, and if between these two electrodes we put the
human body, the current flows through the body and  around again
into  the cell of the  battery.   The current-collector shown in Fig. 65
has  the wires  attached to it, and  has a simple  switch which can be
turned to either binding-post, and thus enables us to direct the  posi-
tive  or the negative current into either one  of the wires 6 and 7.


THE FARADIC, OR FARADAIC, OR INDUCTION CURRENT.

   The faradic current differs considerably from the so-called galvanic
current.  The  latter, as we have  seen, is a  current that flows out of
a battery through the human body  back again into  the battery, not
being interrupted in its course in any way.  In the galvanic battery
we usually make use of several  cells, varying in number from  five
up to fifty, or even a larger number if electrolysis  is to be effected.
Galvanic electricity, therefore, may be defined, for  our present pur-
poses, as a continuously flowing current of  large quantity, with  suffi-
cient electro-motive force  to enable it to overcome the resistance of the
human body; and its therapeutic  effects depend mainly upon the
quantity of  the  current which  is endowed with sufficient power of
overcoming  resistance, or electro-motive force, to enable it to pene-
trate the body.   Faradic  electricity, on the other hand, is the current
which flows from one or two cells, but which, by means of various
mechanical devices, is interrupted constantly, and made to have  more
electro-motive force  or much more power  of overcoming resistance
than galvanism.  The general principle underlying  this phenomenon
we will  now endeavor to demonstrate.  Suppose that  there is a cell
to the plates of which are attached the usual poles or wires.  Let us
join  these poles or wires so that  the current will run around  them
back into the cell.   Let us  now place near  these wires another  wire,
and  in the latter we intercalate a milliamperemeter, so that we can
detect any current of electricity that shall  pass through this  wire. 
110
INTRODUCTORY.
At the  moment when the current passes through the wires attached
to the cell we shall see that the needle of the milliamperemeter inter-
calated  in the wire fluctuates, indicating that a current of electricity
is passing through this wire.   Yet the wires do not touch, and it is
evident that while  the current in the milliampere wire is due to the
passage of the current in the battery wires, it is not due to the  con-
tact of  the two wires.   It  must  therefore be by induction without
contact.  A current is induced in one wire by the passage of a cur-
rent through  a neighboring wire.  The battery wire is called  the
primary wire, and the milliampere wire is called the secondary wire.
In this  secondary wire the milliamperemeter is intercalated.   It is a
curious  fact  that the current in the secondary wire  is not observed
while the current is quietly passing through  the primary wire, but
only at  the moment when the  current  is suddenly turned on in the
primary wire, or suddenly  turned off in the same.   Let us suppose,
therefore, that in the battery wire we  have a  mechanical contrivance

                              Fig. 66.
       Diagram illustrating the primary and secondary wire of a faradic battery.
                        (From De Watteville.)

for turning on and turning off a current, for making or breaking the
current, as it is  technically called, or  interrupting it.  It is evident
that such an  interruption will be a great convenience in producing a
current in the secondary wire.  This  principle of induction and in-
terruption constitutes the  keynote of  the faradic  battery, and hence
we can understaud why it is called  the interrupted  current, in con-
tradistinction to the steadily flowing current of the galvanic battery.
In every faradic battery, therefore, there is a device for interruption,
and also a primary wire which carries the current and which induces
the secondary current in the secondary wire.  This  primary wire is
usually in the shape of a long coil wound around a bobbin, and over
it or in it is another long coil holding the secoudary wire, also wound
around a bobbin.   Fig.  66,  taken from  De Watteville, illustrates
this.  This shows  the  primary wire, A B, one  end of which is con-
nected to the battery, e, and  the  other end  is  connected to the
hammer, h.  Inside the coil of the primary wire  is a bundle of iron
rods, o, and c d is the  secondary coil, which is entirely independent
of the rest of the apparatus.  The current from the primary wire 
ELECTRICITY.
Ill
can be  collected from the two poles, P and p', and the current from
the secondary wire can be collected from  the two poles, s and s', so
that either the  primary or the secoudary coil  can be used.   When
the current  flows in  the primary  coil, A b, the iron, o, becomes a
magnet by the passage of the electricity through it and the hammer,
H, is immediately attracted by this magnetic  action, and is  drawn
away from the screw,  sc.  Then the current ceases flowing.   When
the current  ceases to flow, however, the iron ceases to be a magnet,
and ceases to attract the hammer magnetically, and this hammer flies
back, by means of the elastic spring, to the screw, sc.   Then again
the current from the primary wire  flows  around, and the same pro-
cess is repeated.  The distance of the hammer, h, from the screw, sc,
will determine the rapidity of the interruptions, and  therefore every
apparatus has a means of regulating the swing of the hammer, so
that the interruption may be quick  or may be slow.
   It is thus apparent, as we have said, that the faradic or induction
current is a current  of small quantity, which, by means of interrup-
tions, is made to produce another current by induction.  The primary
wire, therefore, of a faradic battery would conduct exactly the same
electricity as the wires of a galvanic  battery if it were not  for the
interruption ; but the secondary  wire of  a faradic battery not  only
differs  from the galvanic current by means of the interruption, but
also because of the fact that it is an  induced  current and  does not
flow  directly from  the cell.  It  is, therefore, evident, as we have
said, that the faradic battery is an  interrupted current, and also an
induced current, and the result of this interruption and induction is
that its electro-motive force, or capacity  for overcoming resistance,
is increased.  The galvanic current, on the other hand, is a continu-
ously flowing current.  As experience has  shown that one or two cells
are usually quite sufficient to give  the requisite  current to a faradic
battery, whilst it has also been demonstrated that from  twenty to three
hundred cells are necessary to give the requisite current for  a gal-
vanic apparatus, there  is the further distinction that faradic electricity
is a small amount of electricity made more penetrating, or endowed
with a  higher electro-motive force,  by the mechanical devices which
have been described; whilst the galvanic current is a current of large
quantity with just sufficient electro-motive force, or power of over-
coming resistance, to enable it to penetrate the human body.
   The  wires, or poles, and the electrodes are the same for the faradic
battery as they are for the galvanic battery.  The measuring-appa-
ratus and the regulating-apparatus of a faradic battery are, however,
very different from  those of a galvanic battery.   Galvanism, as we
have seen, can be measured by a milliamperemeter and  regulated by
a rheostat.  In the faradic battery, however, there is no precise means
of measuring the current.  The galvanometers that are necessary to
this form of current are very expensive, and only indicate the quan-
tity of  the current,  but  they do not indicate the suddenness  of the
interruption,  upon which, as we have seen, depends the flow  of the
current  in  the primary aud the secondary wires.   In  measuring
faradism, therefore,  there is usually a scale along  which the outer 
112
INTRODUCTORY.
 bobbin containing one of the wires is pushed, and this enables us to
 say that to-day at a certain point we  have produced such an effect,
 and that to-morrow we shall probably produce the same effect when
 the bobbin is  pushed to the  same point.   This measurement is, as
 must be apparent, dependent  upon the assumption that the cell and
 the resistance  of the body shall not vary daily, and we  know as a
 matter of fact that cells and the resistance of the human body do not
 remain the same from day to day.  Practically, therefore, we can only
 speak of a faradic current as  moderate, strong, or  painful, determin-
 ing this by the sensations  of the patient and by the amount of mus-
 cular contraction that is obtained by applying the current to a muscle
 or  to the nerve attached to a muscle.


                   STATIC ELECTRICITY.

   Static electricity is manufactured for medical purposes by means of
 the Holtz machine, which, as I scarcely need  to say, consists of two
 upright jars—so-called Leyden jars—and a revolving wheel fixed in
 front of a  stationary plate of glass.   This revolving wheel is made
 to revolve  by means of a handle affixed to the same wheel, to  which
 is attached a rubber cord  encircling a revolving axle, on which the
 wheel is fixed. As this wheel revolves it brushes against several
 small wire brushes, and the electricity is generated by means of this
 friction and flows off on to the metal combs, which conduct it to the
 Leyden jars.   From these it flows on to the handles  above  the
 Leyden jars,  and to these handles is affixed a metal chain armed
 with  the different electrodes, consisting of glass  rods tipped with
 metal cones; so that the electricity passes off in the form  of electric
 air, or electricity diffused through  the  atmosphere,  or in the form of
 sparks.  When it is desired to obtain the electric air, the handles are
 separated widely so that a spark  cannot pass across from the bulbs
 on  the handles.  If the sparks are to be carried directly into the
 body of the patient, the bulbs on the handles are approximated, and
 the length of the spark passing into the human body will be approxi-
 mately proportionate to the length of the spark between the bulbs.


                  GALVANIC  BATTERIES.

  In  selecting a battery a physician  should always be assured that
the cells composing the battery will afford a constant current—in
other words, a current which will not vary greatly from day to day,
and which  shall not need frequent refilling of the cell.  It is not too
much nowadays to require of a cell that it shall run at least eighteen
months to  two years without replenishing; and I have frequently
had cells that have so run from  three to five years, although I have
never had  one  that lasted over two years if it was in constant daily
use.  If it is intended to use the battery stationary in  the  house,
office,  or hospital, the size and weight of the cell will  be a matter
of little consequence, and  attention  should only be paid to the con- 
ELECTRICITY.                      \\^
stancy.  If, on the other hand, it  is desired to use the battery  as
a portable one, so that it  can be carried  around to the  houses  of
patients, the size of the cell becomes of very great importance.   The
physician  must, therefore, make his selection among the cells that I
am now about to speak of with regard to these requisites
   The different cells which are now used in  this country in making
galvanic  batteries  are: the Grenet, the Leclanche, the chloride  of
silver, the Stammers, the Axo-Leclanche, the Law, and the Edison-
Lalande.
   The Grenet cell  is a fairly good one  as long as it lasts, but  unfor-
tunately it needs  to be replenished every few weeks, and this is a
matter of some little inconvenience.  Moreover, as it is an open cell
and  contains fluid, it  is liable to  spill, and although the battery-
makers maintain that this can be prevented by what is called a hy-
drostat, or a board covered with padded rubber, which  is slid in over
the top of the cells and pressed down by a rod from the  lid  of the
battery, yet it will be found  that  leakage will occur as the rubber
grows old and shrinks, whilst the rubber is apt to adhere if  left  in
place over the cells for any length of time.
   The Leclanch§ is made as a liquid, and  also as a dry cell.  The
 liquid cell gives a fairly constant current  as long as it lasts, and it
 will ruu from six mouths to a year, when it will usually have to
 be refilled.  This refilling process is simple, consisting only of pour-
 ing in some sal ammoniac in solution, but, nevertheless, it consumes
 some little time.   The size of the liquid cell  militates against  its
 being used as a portable battery, in view of the equally, if not more,
 efficient portable cells  that are now to be had.  The dry Leclanche
 cell is certainly an excellent one ; and it is claimed that, with proper
 care, it will  run  for about eighteen months.   I have run one for
 thirteen months.   The small weight of the  cell certainly renders it
 invaluable for portable batteries.
   The chloride of silver is an admirable cell for galvanic  purposes,
 if properly constructed.  The one used in this country is the Barrett
 chloride of silver cell, and  was first made for me some thirteen years
 ago by Mr. John A.  Barrett.  These earlier ones were extremely
 durable, for a battery  in my possession lasted practically unimpaired
 for three years, although  in  daily use, and  was finally broken by a
 fall; and I know of one now in this city (New York) that has lasted
 for five years, although I  am  not  aware how much use  it has had.
 Since this  time, however,  it  has sometimes  been very poorly, and
 sometimes very well made.   In  every case  in which it is used it is
 only proper that some guaranty from the makers should be had of its
 durability.   It is the most portable of all the cells, each one weighing
 only six ounces.
   The Stammers cell  has  the  advantage of being a very cheap one,
 as it costs  only twenty cents.  The  maker claims that  it will run
 eighteen months.   I  have never used it, and cannot, therefore, say
 anything of my own personal experience.
   The Law cell is very constant and requires scarcely  any attention.
 I have had a battery made of it in daily use in  our large clinics at
s 
114
INTRODUCTORY.
the New  York Polyclinic  for  two years.  Its size,  however, will
prevent its use in portable batteries, although I should  prefer it, for
my own part, to any other cell for a stationary battery.
  The Edison-Lalande  is  a new cell, and, as  the  name indicates,
is a modification of the Lalande cell  by Thomas A. Edison.  It is
claimed that  it is  practically indestructible—that  is,  it will run as
long as it is  not  absolutely worn out, and this is about a year.  I
have  had  no experience with  it, but  I should certainly think it
worthy of a  trial  in stationary batteries, although  its  size will not
allow it to compete with the smaller cells for portable  batteries.
  The liquid Leclanche cell is used in this country in both stationary
and portable  batteries, although  its  weight makes  it  unfit for  the
latter.   The  dry Leclanche  cell is used in some portable batteries,
An accessory battery is  also made, containing any  number  of cells
that may be  required, and that can be attached to the main battery
at any time when  more  current  is required, as for purposes of elec-
trolysis.   These are extremely useful.
  Each one of these batteries has its  own devices for collecting the
current at certain binding-posts, to which wires or rheophores can be
attached.   Great attention should be paid to these binding-posts.
It is customary to make them in  such a manner that the wire con-
ducting the current to the  patient's  body passes either into a split
post which holds it  by its elasticity, or else passes  into a hole and
has a screw to screw down upon it.   The split binding-post should
be entirely discarded, for it loses its elasticity with use, and the wire
is apt to slip and give unpleasant shocks to the patient.  The other
binding-posts, perforated  with a  hole through which the  wire  is
passed, and  with  a screw which screws  down upon the  wire, is
always the best, aud it should  be  carefully ascertained that the
screw works upon a strong  thread and holds well, as many batteries
are defective  in  this  detail.  Kidder makes  a spring binding-post
which is said  to be excellent.  In some of these batteries there is a
current-selector, whose purpose it is to take into the circuit as many
cells as may be desired.   This ought to be entirely discarded, as the
current-regulator,  or rheostat,  is  a  far better  instrument.   When
this rheostat  is used, all  the current from all the cells can be col-
lected directly from the  binding-posts,  and the amount of current
that is admitted into the patient  is thus regulated  by means of the
rheostat, and  this can be done gradually and without shock, whilst
the current-selector invariably causes a slight  shock as the  handle
passes from  cell  to cell.   An attempt has been made to obviate this
latter defect of the current-selector by having the handle make con-
nection with  one cell  before it leaves the other;  but  this does not
answer, as can readily be demonstrated when the current is passing
through the human  brain, for however carefully and gently  this col-
lection may be made, the patient will see sparks or  have  a  slight
sensation  of dizziness. 
ELECTRICITY.
115
                   FARADIC  BATTERIES.

   There is no great difference in the efficiency of the different faradic
batteries upon the American  market, with the  possible exception of
the chloride of silver cell, which has not worked well in my hands in
the faradic apparatus, being quickly exhausted.   The only criticisms
that I have to make of most of the faradic batteries are that gener-
ally the secondary coil is too short to give sufficient intensity of cur-
rent when  it is  intended  to affect  such deep-lying structures as the
abdominal  organs, and that  the long interrupting apparatus is apt to
be  defective.  As we seldom need very intense currents, however,
and as the long  interruption  is a therapeutic measure of infrequent
application, these two defects are not usually of much importance.
In a stationary apparatus,  however,  I should  always  make use of
the Dubois Reymond coil, which has a long interrupter of excellent
workmanship, and in which the secondary coil is adequate for all
purposes.  This is represented in Fig. 65.


                 STATIONARY  BATTERIES.

   In having a stationary  battery constructed I  think that the physi-
cian will usually do best with  the Law, the wet Leclanche, or the
Edison-Lalande cell, and of these I should give the preference to the
Law.  The cells of the stationary  battery may either be in a closet
in the physician's office,  in the kitchen, the  cellar, or a so-called
cabinet.   In  all cases, however, the connecting wires  leading from
the battery to the rheostat and milliamperemeter should be easily ac-
cessible, so that any defect in the conduction may be readily remedied
by the physician himself.   The connection between the cells of the
battery  itself will usually  require the  attention of  an  electrical
mechanic if conduction  becomes impaired.   In my own office I have
not  made  use of a cabinet because of this desire to have  the con-
nections, so far as feasible, immediately under my own eye.   I there-
fore place the rheostat, milliamperemeter, binding-posts, and  Dubois-
Reymond coil upon an ordinary fiat table, which can  be  purchased
at any furniture store.  (Fig. 65.)  This  table can be covered, if
desired,  with a glass cover to protect it from the dust and from med-
dliug.
  In some batteries there  is  a device for sending the galvanic and
faradic current through the same wires.   This is  apt  to get out of
order, however, and is  of no  practical value whatever, as  it is no
therapeutic gain, but rather  a disadvantage, to give the galvanic and
faradic currents simultaneously.  I had one in my office for a number
of years, but finally abandoned it.
  It is an easy matter for the  physician  to find  out where the fault
lies if the current does not  pass well.   Fig. 65  shows how this can
be done.  It is evident that  the defect  must lie either in the  battery
supplying the electricity, or  else in some of the conducting apparatus
between  the battery and the  patient.  Let us, therefore,  go over each 
116
INTRODUCTORY.
segment outside the battery.  First one electrode should be removed,
and  the tip of the wire from which it has been  removed applied to
the other electrode.  If the current now passes, it is evident that the
fault has been in the electrode that has been removed.  If the current
still does not pass, remove the next electrode and touch the tips of
the two wires together, and, if the current passes, the fault must have
been in this electrode just removed ; or if it does  not pass, then re-
move wire 7 and put a reliable one in its place;  and in this  manner
wire 6 should be tested, then wire 5, then the  rheostat, and, finally,
in succession, wire  4, the milliamperemeter, and wires 3,  2, and 1.
The defect will be found to be in one of the segments removed, or it
must be in the binding-posts, or the wires  leading  from the binding-
posts to the cells of the battery, or the cells themselves.
  It should be borne in mind  that the more  delicate of these cells
that have  been described, such as the chloride of silver cell and the
Leclanche, are destroyed by what is called " short-circuiting."   If the
current be  passed around from the cells through the  different wires
of Fig. 65, and back again to the  cells without  the  interposition of
some body between  the  two wires  whose resistance is equal to that
within the body of the cell, this will  be what is technically known
as the  " short circuit," and it will paralyze the delicate cells.  For this
reason the  tips of the wires or the electrodes should never be allowed
to come into contact when the current is turned on, unless  there is a
rheostat in the circuit; and a still  better method  is  always to keep
the pole-changers on the galvanic apparatus away  from the binding-
posts leading to the  battery.   In the faradic batteries this  short cir-
cuiting need not be taken into account.


        MILLIAMPEREMETERS AND  RHEOSTATS.

  Until within a very short  time a good milliamperemeter was not
obtainable  in this country, and I believe that the first reliable one was
made for me some twelve years ago.  In purchasing one there are cer-
tain  requisites to which the physician  should carefully look.  In the
first place, the scale should be graduated according to the needs of the
particular person using it.  If electrolysis alone is to be employed, the
scale should run up to four or five hundred milliamperes and over, and
it is of small importance whether a fraction of a  milliampere can be
measured  off.   If galvanism of the spinal cord  and the brain alone
is to be done, the scale  that mounts  to thirty milliamperes will be
quite sufficient; but it should  be distinct enough to  indicate a half
or a quarter of a milliampere.   If both spinal and cerebral galvani-
zation  and electrolysis are to be done, there should be a combination of
these two  scales, so that it will be  possible,  on  the one hand, to
measure off a fraction of a milliampere, and. on the other, to obtain
four or five hundred   In the second  place  the  needle should move
with very  little oscillation, so that, after marking off  the requisite
amount of electricity, it shall either not swing at all or come to a stand
in a  second or  two.   In this particular most of the instruments are 
ELECTRICITY.
117
exceedingly  defective.   In  the  third  place, the  milliamperemeter
should always have an upright  scale, numbered with sufficient dis-
tinctness to be easily read at a  distance of several feet, or otherwise
it will  be  exceedingly awkward  to employ it.   Most milliampere-
meters in  this country are  not  graded by one  general  standard, so
that when  one milliamperemeter  measures one milliampere, another
may measure two or three;  indeed, in a trial about two year ago in
the office  of Dr. A. H. Goelet, of this  city, there wrere found to be
startling variations between the different instruments, although since
this time the instrument-makers claim that the instruments are almost
alike.   Still another requisite of a milliamperemeter is that  it should
be portable.  As best  combining these requisites I  unhesitatingly
recommend the Vetter milliamperemeter.   The one which is pictured
in Fig. 65 was  made by Hirschmann, of Berlin, and it is a very
accurate instrument which  has  stood years of wear; but  it is  too
cumbrous  to  be  portable, and  the needle  swings  exceedingly.
Edelmann, an instrument-maker of Germany, also makes  an excel-
lent instrument which can be purchased in this country.
   The rheostats in use at  the present day for physicians are either
the water or the carbon ones.  The objection to the former is that
chemical changes take place in the water, so that after an instrument
has been in use for awhile unpleasant shocks are apt to be given,
and some  accidents have occurred  in this way.   The  new Bailey
rheostat is the best of all the water-rheostats, and it is  claimed that
all previous  defects have been  overcome  in it.  The best  rheostat
made  in this country, however,  is the carbon  instrument  made by
Vetter, which is shown in Fig. 65.  I have an instrument by which
I can  turn on |- of a milliampere with  perfect ease and without the
slightest shock.  Vetter and Stammers also have rheostats, or  con-
verters, which can be affixed to the ordinary Edison light in such a
manner as to control the current and adapt  it to  purposes  of spinal
and cerebral galvanization.  I have given up the use of the Edison
current, however, for cerebral galvanization, as exceedingly unpleasant
though slight shocks are frequent, probably due to variations in the
current; moreover, the quality of the current is apt to  be unpleasant.
But I find it unobjectionable when employed about the trunk or the
limbs, except when the nerves are sensitive, as in  some cases of neu-
ralgia and neuritis.   For running  the  galvanic apparatus,  however,
these converters  are exceedingly convenient, as, indeed, they are for
galvanic purposes.  For purposes of electrolysis, however, and for
electric lighting, the Edison and alternating currents can  be made
approximately safe by a proper rheostat.


    WIRES AND ELECTRODE  OF GALVANIC AND
                   FARADIC  BATTERIES.

   The wires, or  rheophores—the latter term being very  seldom used
by American  electricians—should always be made of tinsel cord
woven of  a  large  number of  well-made tinsel threads, as  this has 
118
INTRODUCTORY.
 been proven to be the best conducting material for medical batteries.
 This tinsel thread is always  covered with silk as an insulator of the
 current, and it does  so insulate as long as the silk is not wet.  As we
 shall have occasion  to see, however, water must be freely used in the
 administration of electricity for  medical purposes,  whereby the  silk
 thread is  very apt to become soaked and thus allow the electricity to
 pass to the body of  the patient when the thread accidentally comes in
 contact with the skin, so that slight, unexpected, and annoying shocks
 will be given in this way and unnecessarily  frighten timid patients
 and children.  To obviate this the wires should be run through little
 rubber tubings (which can be obtained of all the instrument-makers),
 and thus  be  completely insulated.   These wires  should always be of
 a generous length, so as to enable  them to reach  out a good distance
 from the  patient and facilitate applications, more especially when  the
 patient lies upon a couch or lounge.  I have mine  always made at
 least two  and three-quarters yards  in length, as  almost all the com-
 panies supply wires of very defective length.  At  one time I made
 use of copper wires, but I found that they were not only brittle and
 awkward to  handle, but experiment has  since demonstrated that they
 are  really not so good  conductors as tinsel wires  woven of many
 threads of perfect tinsel.
  The size of the electrode is a matter of very considerable moment.
 The object always is to  get  a certain amount of electricity into  the
 body of the  patient  and to impinge it upon the organ  that it is  de-
 sired to affect.   There are certain peculiarities of the distribution ot
 the electric current  that should  be borne in mind  in  attempting to
 effect this purpose.   If two electrodes, each being two inches in
 diameter,  are placed, for example, upon the spinal  cord, and  a current
 passed, a certain amount of the current will pass in an approximately
 straight line directly  from  electrode  to electrode,  whilst a certain
 other portion of the current will be diffused  in  curvilinear lines to
 each side of this straight line.   If the same amount of current is
 passed from two electrodes  placed exactly in the  same places, but
 these electrodes are made four inches  in diameter instead of two,
 more of the current  will be diffused in curvilinear lines and less will
 pass directly in the straight line.   If, therefore, we wish to  reach  the
 spinal cord lying deep beneath the muscles of the  back, the vertebrae,
the  loose areolar tissue of the spinal canal, and the membranes of the
 cord, we  must do it by the diffuse current  as  represented in these
 curvilinear lines; and therefore the greater the size of the electrodes
 and the consequent greater diffusion of our current, the more it will
 affect the  spinal  cord.   For this  reason the small  electrodes which
 are  usually sold with  batteries are absolutely worthless for purposes
 of  spinal applications, and  in  their  place should  be used as large
 electrodes as  practicable, so that in  the adult the electrode of Fig. 67
should be employed, and in  the child  the  electrode of Fig.  68 or
69.   If, on  the other hand, it is desired  to have the  current impinge
upon a nerve-trunk, it must not  be too diffused.  It will, therefore,
be best to make use  of a large electrode (Figs. 67 to 71) for the one
pole which is not to  be placed upon the nerve, and one of the smaller 
ELECTRICITY
119
electrodes, such as the electrode of Figs. 72 to 76, for the other pole
which is to be  put directly upon the nerve.   There is a limit, how-
Fig. 67.
18 x 6 centimetres.
Fig. 68.
Fig. 69.
18 x 15 centimetres.
Fig. 70.
10 x 5 centimetres.

     Fig. 71.
so
      5x4 centimetres.

Fig. 72.    Fn;. 73.     Fig. 74.
Fig. 75.
7.3 x 7.3 centimetres.

      Fig 76.
    3 cm. square. 5 cm. square. 13 cm. square. 15 cm. square.     20 cm. square.

ever to the diminution in size of the latter, because if it is too small
it will  cause  pain,  and  practically the  smaller electrode  should be
99999999999 
120
INTRODUCTORY.
made use of for this purpose, and not the smallest one, Fig. 72.   The
large electrode that has been  mentioned  admits the  current  more
diffusely, whilst the  smaller  one causes it to  impinge, in entering
the body, upon the particular nerve that it is desired to affect.  If both
the electrodes are as small as the electrode  of Fig. 72, it will be found
that the administration of the current will  be more painful.   The
electrodes must, therefore, be made of different sizes and also of dif-
erent shapes, according to the purposes for which  we desire to use
Fig. 78.            Fig. 79.
  a                 h
Fig. 80.
Roller electrode.
them.   Erb has  suggested that it would be well to have  electrodes
of definite sizes, so that electricians  throughout the world could com-
pare results with  more approach to precision, and  he has therefore
figured the different sizes and given them numbers.  These are repre-
sented in Figs. 67  to  76.   They  are  made of malleable  copper,
which should be of sufficient  thickness to bend without breaking 
ELECTRICITY.
121
and to preserve  its shape after being bent.   Most of them are very
defective in  this respect.  They should  be covered with  absorbent
cotton, taking  care  to  pad this carefully around the edges and  the
angles, so that  the electricity may not cause smarting at these points,
which it is very apt to do when the electrode is bent around the neck
or a limb.  The cotton can  be  held in place  by  muslin or linen
stitched on, which  can be removed in a moment and is a great  ad-
vantage in point of cleanliness.   Most manufacturers cover their
electrodes  with a fine sponge, glued on.   This is a filthy contrivance,
and ought to be  entirely discarded, in view of the fact that we have
so cleanly, so easily affixed, and so cheap a cover as the absorbent cot-
ton.   For applying electricity to the pelvic organs of the male, I have
had made  an electrode which is six  inches wide and thirteen inches
long.   It consists of a malleable copper plate, below which is attached
a plate of rubber projecting well beyond the edges of the copper and
serving as a protection against the water which must drain off.  Be-
tween the  plate and the rubber is placed a thick mass of absorbent
cotton, held  in place by muslin  or  linen stitched  on as has been
described.   This electrode is placed upon a stool, the  patient sits down
upon  it in such a manner that the perineum  comes in contact with
the cotton, which should be  thick and abundant, and thus the elec-
tricity is conducted  well  up into  the perineum.  Dr. A. H. Goelet,
of New York, has  devised  a  clay  electrode, which is valuable  in
uterine and vaginal applications.
   The ordinary  uterine, rectal, urethral, nasal, and  aural  electrodes
are too well known  to need reproduction here.
   Wetting the skin with water is the simplest method of diminish-
ing the resistance  offered by the skin, and this water should be as
warm as  can  be borne conveniently according  to  the season of  the
year.   Water does not reduce  the cutaneous resistance quite as much
as acidulated solutions, yet there is  no practical difference.  Every
physician  using a battery much in his  office  should therefore have
upon his table a large jar to hold this water, which should be changed
for each patient, and in it  should be a  large sponge with which to
wet the skin; or a wash-basin  with running  hot and cold water
should  be at hand.  The cotton  or sponge coverings of the elec-
trodes must also be wet, as  they are  very poor  conductors when
dry.   Great attention  should  be  paid to  this  wetting of the skin
and electrodes, and  I insist upon this, as I  have  again and again
heard complaints about the  feeble currents of batteries,  and have
found the real reason to be that neither the skin of the patients  nor
the electrodes were thoroughly wet.
  The resistance of the human skin varies very considerably in dif-
ferent places and somewhat under different circumstances.   The most
conclusive researches on  this subject  have been  undertaken  by
Jolly, of  Strassburg.   He  has  shown that,  contrary to what is
generally  supposed, the  inner surface  of  the hands  and the soles
of the feet  offer but  a  relatively  slight resistance;  yet on  this
inner surface of the hands, which were examined in ten  males,  the 
122
INTRODUCTORY.
resistance  varied between 22,000 and  55,000  Siemens units/ and
in ten females  between  16,000 and  50,000 Siemens units,  whilst in
the feet the variations were in males between 15,000 and 32,000,
and in females between  20,000 and 55,000  Siemens units.  In the
face, upon the skin of the cheeks, the average resistance was 43,300
Siemens units in males, and in females 78,000, whilst  the temporal
region of the face was on the average 92,500 in males, and in females
109,000.   For all other  areas of the skin the average resistance was
over 100,000 Siemens units, generally between 200,000 and 300,000
Siemens units.   These facts concerning the resistance of the human
skin have  been marvellously little known, and it is an actual matter
of evidence that when killing by electricity was first recommended in
New York a few years ago, the commission reported a method based
upon the assumption  that the  average resistance of the  human skin
was only 2400 ohms !  These cutaneous resistances vary  enormously.
The following average resistance of the different regions is given by
Jolly,  in Siemens units :
    Soles of the feet.............23,000
    Palms of the hands............41,300
    Cheeks......       ........42,500
    Temporal region.............92,500
    Neck ................21,900
    Dorsal surface of the feet...........236,000
    Thigh...............275,000
    Back................289,000
    Dorsal surface of the hands...........304,000
    Leg................324,000
    Arm................355,000
    Forearm...............364,000

   The resistance of the  skin is  enormously reduced  by the passage
of a galvanic current.  Thus, in one case of Jolly's where the resist-
ance in the  forearm was 113,700 Siemens units before the passage
of the current, it was reduced  in  five seconds by the  passage of a
current from twelve Stohrers cells to  52,000 Siemens units.  But this
resistance  to  the passage of the current  varies in different cutaneous
areas,  so that, for example, the resistance of the  skin  of the inner
surface of  the hands and the soles of the feet will  not  be very much
reduced  by  the passage  of the current.   As I  have  already said,
moistening the skin will also reduce the resistance, and the warmer
the water the more the  resistance will  be  reduced.  Saponification
of the water will answer still better,  and also acidulation of it, and
many  of the text-books  recommend this latter method ;  but anyone
who has had any practical experience in giving electricity will know
that this  consumes much time and  tarnishes the metallic fittings of
the electrodes.   The resistance  of the  skin  will also  vary in dif-
erent persons with different states of the weather  and with different
diseases.
   It  is a  very convenient matter to  have what is called  an inter-

  1 The Paris or legal ohm is the  usual American and British unit for measuring resistance,
and is arbitrarily understood among electricians to be a  standard coil of  copper wire one
square millimetre in diameter and about 48.5 millimetres in length, attached to a freshly
charged Daniell cell, or a column of mercury one square millimetre in area 106 centimetres
in height, at  a temperature of 0° C.  The Siemens unit would be represented by the same
column of mercury with a height of 1 metre ; so that one ohm is equal to 1 0600 Siemens units.
It has recently been proposed to have still another unit of resistance, to be called the Kolvin,
after Colvin, the electrician, but this has not yet come into use 
ELECTRICITY.
123
rupting electrode ; that is, one in which the current can be turned off
or on with a mere  pressure  of the finger.   If, for example, we are
giving electricity to  a patient, and it is necessary to turn  off the cur-
rent, or to turn it on, or to break and make the circuit, as it is tech-
nically called, this cau be done by taking the electrode away from
the skin, and thus breaking  the current, and putting it  back on the
skin, and thus making  it.   But the disadvantage  of this method  is
that a fine nerve, which it may be very difficult to locate, such as the
popliteal in fat people, may slip from under the finger.  Some device,
therefore, that will break  the current without taking away the elec-
trode from the skin, is advisable, and this is simply done in the so-
called  interrupting  electrode.  The best one  of these is that figured
in Fig. 79, which I  have had made for  myself, and  in which the
circuit is made by pressing down the little trigger, and thus allowing
the current to pass, whilst taking the finger away from the trigger
breaks the current   The trigger in this electrode works as easily  as
the hair-spring of a  revolver, and the mere tap of the finger is  suffi-
cient.  Fig. 78 represents the interrupting electrode of a make that is
very objectionable, in my opinion.  In this the current is broken by
pressing down upon the handle, and then, when the finger is taken
off, the circuit is made, so that the current is turned on unless  there
is pressure made upon the trigger; but in delicate manipulations it
may be very tiresome to  keep the  fiuger pressed upon  the trigger
when it is not desired to make a circuit.
   About these electrodes  certain matters of practical detail should be
thoroughly understood.  The binding-screws should be first carefully
looked to.  A split holder, into which the end of the wire is to  go, is
very untrustworthy,  because, as has been  said  already, its elasticity
diminishes very quickly, and it does not hold the wire reliably.   A
hole, through which the wire can be pushed  so that a screw can be
screwed down upon  it and hold it in place, is always the best method,
and the screw should be a strong, well-made one.  In those electrodes
which have handles, the handles should  be of a generous  length, and
should not be less than  eight inches in length.  They should be  suffi-
ciently thick to be grasped by the hand and held without undue  effort
in flexing the fingers, and they should be hollowed out somewhat on
the shank for this purpose and allowed to bulge well at the upper end.
The handles of almost all the electrodes that are sold with the batteries
are radically defective in  these two  details of the binding-screw and
the length and thickness of the handle.


       METHOD  OF APPLYING  THE  BATTERIES.

  Let us suppose that, having provided a galvanic and faradic bat-
tery, it is desired to  know how to make application  to  the human
body, and for this purpose let us take the galvanic battery and speak
of some of the ordinary applications.   Our apparatus is  arranged  as
in Fig. 81, so that  the rheostat  and the milliamperemeter are  in
the circuit.   AVe now attach the electrodes  that are needed to the 
124
INTRODUCTORY.
Battery table showing arrangement of galvanic and faradic apparatus, rheostat, and
                         milliamperemeter.
carefully  over the brow,  gently shaping it.   These  two  electrodes
are now committed to the care  of some person who has a steady
hand, and who  is carefully instructed to place  the hand upon the
neck-electrode firmly and yet  gently, and to  hold  the forehead-
electrode  gently  and  firmly in  place  by means  of the  handle.
This  attendant must  not touch  the copper of  the two  electrodes,
or else the circuit will be diverted through  his or her  body, and
a  shock will be  given to the  patient.   When the  electrodes are
in place,  the  current-collectors are  turned on to the binding-posts 
ELECTRICITY.
125
so  as  to  permit the passage of a current.  Now the screw of the
rheostat is  gently screwed down until it is felt that some resistance
is being encountered to its revolutions, and then the screwing should
be done very carefully, whilst the eye is kept upon the milliampere-
meter to see by the fluctuation of the needle  whether the current has
begun to  pass.  It should be remembered that very slight pressure
upon the milliamperemeter  may cause  a  difference of one or  two
milliamperes, and if this is made suddenly the patient will perceive
a flash of light or  experience a slight vertigo.   A current of one or
two milliamperes is now turned on; never  more than this at first,
although  in the course  of time  it may  be increased to three or four.
The  current is then  allowed to pass  quietly for three minutes at
first, and afterward, as  the  patient  becomes  accustomed  to  it, for a
greater length of time.   During the passage of the current the per-
son holding the electrodes should not allow the hand to move at all,
because a very slight  movement will cause  an unpleasant shock or
a  sensation of  vertigo.   In this  cerebral  galvanization  patients
often have  a copperish taste in the mouth, but this is a matter of no
consequence.  When the current has been running for three minutes,
the screw of the rheostat should be very delicately and very gently
unscrewed, allowing  the current  to diminish,  as indicated  by the
milliamperemeter, by  a  fraction of a milliampere at a time, until the
current has been entirely turned off, and then, and not till then, the
electrodes should be taken away.  This description should  be read
and  re-read until  the details have become  familiar, because  it is a
lack of attention to these little matters that  makes the difference be-
tween success and failure in cerebral galvanization, and I have heard
many men  speak of their failures in this  respect when courtesy has
prevented me from  saying that they did not  know how to apply the
electricity.   When  the  spinal cord  is  to be taken into  the circuit,
the electrodes of Figs. 67 to 70 should be  used, but  it will not be
necessary to exercise as  much precaution  in turning the current on
and  off as should  be observed when  the brain  is  taken into the
circuit.   When it is desired to concentrate the galvanic current upon
a  peripheral nerve, the right ulnar we will say, one electrode of
Figs. 67 to  70 should  be  placed   upon the right shoulder,  and a
smaller electrode,  Fig.  73  or 74,  should  be put over the  ulnar
nerve, as it  is indicated in the charts at the end of this  chapter.
The current should then be turned on as before, although it will not
be necessary to be so  extremely  cautious about it  as when the brain
is in the circuit, unless  the  nerve is very tender.   In applying the
faradic current the procedure is very simple.  All that is necessary
is to attach the necessary electrodes to the wires and turn  on as much
current as may be desired.


      THE  DIAGNOSTIC USES  OF  ELECTRICITY.

  The diagnostic use  of electricity depends upon the altered reaction
of nerve and muscle to the galvanic and faradic currents.  In order to 
126
INTRODUCTORY.
understand this it is necessary to comprehend  the normal reaction of
these structures to these currents.   If a muscle is to be set into con-
traction in the human body, it must be done through the nerve leading
to it, because it is practically impossible to limit electricity to a muscle
without  at the same time  implicating the nervous filaments in the
muscle, and the practical uses of the current in the human body are
therefore quite different from experiments upon frogs wherein muscles
are bared with merciless impunity.  The reaction of nerve and muscle,
for this  reason,  simplifies  itself  into a reaction of the  muscle to
stimulation through the nerve.  If a nerve  of the human body is
tested with the two currents, the faradic and the galvanic, in order to
produce a muscular contraction by application of the  current to the
nerve, it will  be found that the response of the muscle varies very
greatly according to the current  used.   If the  ulnar nerve,  for
example, is tested by the faradic current, the resultant  muscular con-
traction will be in proportion to the strength of the current, and this
muscular contraction will be be practically about the same in strength,
whether  the  negative  pole  is  placed upon the nerve or whether the
positive  pole  is so placed; in other words, excitation  of a nerve by
the faradic current causes muscular contraction in proportion to the
strength  of the current, and this  muscular contraction is practically
the sme with the negative and the positive pole.   With the galvanic
current, however, the reaction of the nerve and muscle is more com-
plicated.    If the current is turned on from the  galvanic battery in
the manner that has been indicated, one electrode of Figs. 67 to 70
being placed  upon the shoulder or upon the sternum,  and  the inter-
rupting  electrode, Fig. 79, being put  upon the  ulnar nerve, it will
be seen that there is a very  great difference accordingly as this elec-
trode is  made  the negative or the  positive pole.  It  will be found
that the  first contraction of the muscle will  come from the applica-
tion of the negative  pole to the nerve;  in  other words,  a current
being gradually turned on,  and the nerve  being first tested with the
positive and then with  the  negative pole,  it will  be found that  the
first contraction is produced with the use of the negative pole to the
nerve.  Nor is this all.   Curiously enough, it  will  be discovered
that this contraction with the negative pole will not come whilst the
current is passing through the uerve, nor will it come  when the cir-
cuit is broken, but only when the circuit is made, or closed.  Let us
understand this  more  clearly, for  my  experience in innumerable
lectures has taught me that  this is a matter about which men are apt
to become confused.   The  one electrode,  as we have said, is  placed
upon the sternum; another electrode, the interrupting  one, is  placed
upon the ulnar nerve.   The latter electrode can be made the positive
pole or the negative pole by changing the pole-changer of the battery.
Besides, this interrupting electrode can make  the  current  by having
the trigger-handle pressed  down  to come in  contact  with the little
button, or it  can break   the current  by withdrawing the  finger
from the trigger and letting the latter press back.   The current  now
being gradually turned on, and the interrupting electrode being made
first the  positive and  then the negative pole, it will  be found  that 
ELECTRICITY.
127
a muscular  contraction  comes  with  the  use of the  negative  pole
for  some time  before it will come with the positive pole, that this
muscular contraction with the use of the negative pole is only at the
time that the trigger of the interrupting-handle is pressed down and
the  current is made, and that there is no muscular contraction whilst
the  trigger is kept in place so that the current passes, or when the
trigger is  allowed to fly back and the current is broken.   In-other
words, the first muscular contraction results with the negative  pole
at the closing of the current.  This should be read aud re-read until
it is thoroughly understood, aud  then only should  the reader go on
with what I  am  now about to say.  The current is then gradually
increased,  when  it will  be found  that the  muscular contraction
becomes more marked with the  negative pole  at the closing;  and
after a while, as the current is  still gradually increased, it will be
found  that a  muscular contraction can  also be produced with the
positive pole.   This contraction  with the positive pole is generally
first with the opening of the current, and then, with  a  little stronger
current, at the closing of  the  current.   It will thus be seen that
with the galvanic current, as the  current is gradually made stronger,
the first muscular contraction is with the negative pole at the closing,
and then, when a little more is  turned on,  with the positive pole,
generally first at the closing, and  then at the opening.  If we now go
on  increasing the current still more, it will be  found  that the mus-
cular contraction obtained in these three different ways  becomes more
pronounced.  If, however, we keep on increasing the  current until
it becomes so strong  that  it is  uncomfortable to  the patient, we
may become impressed with the fact that we have as yet obtained no
muscular contraction with the negative pole at the opening of the
current; and we  can only  obtain a contraction with  this negative
opening when the  current  has  become unpleasantly strong, some-
times not until  it  is  almost unbearably strong, even in  healthy
persons.   This, therefore, is the reaction of the  healthy nerve to the
galvanic current.   First we have the  contraction  produced only by
the negative  pole  at  the  closing of the current; second, as the cur-
rent is made stronger, there  is superadded  a muscular contraction
upon the application of the positive  pole, aud at  the opening aud the
closing ;l and third, we only obtain the  muscular contraction  with
the negative  pole at  the  opening  when the  current has become
unpleasantly  or unbearably strong.   There is therefore a perceptible
interval between  the strength of  the current needed to produce the
first contraction with the negative closing, and that required for the
contraction with  the positive opening and  closing, and there is  a
very marked  increase  in  strength of  current needed  to produce  a
contraction with   the  negative   opening.    Suppose now  that we
endeavor to simplify this reaction  of the nerve and   muscle by  a
formula.   As I  have already said, the positive  pole is  known as
the  anode, which is usually indicated by  the letter  A., and the

  1 It is a matter of no importance whether this muscular contraction with the positive pole
comes first with the opening or first with the closing, as this varies in healthy individuals. 
128
INTRODUCTORY.
negative pole is  known as the cathode, designated  by the letter C.
The letter O. will stand for opening, and the letter C. will stand for
closing.   We can thus represent the foregoing galvanic reaction of
nerve and muscle by this formula :

                    Negative closing = C. C.
                    Positive opening = A. O.
                    Positive closing = A. C.
                    Negative opening = C. O.

  In some  text-books the  final c. is added to all these to designate
closing, but this is unnecessary and apt to confuse.
  This formula I call the progression of the poles.   It is the answer
in galvanic language of the healthy muscle when asked a question
by the healthy nerve.   It is very obvious  that  any  interruption in
this formula would denote disease, so that if we got  C. O. with the
same strength of  current  that  gives  us  C. C, this would be so con-
trary to what should be observed in the  healthy nerve aud muscle
that it would  be  conclusive evidence of some pathological process in
one or both of them.  And, for the same reason, if the ulnar nerve
on the right  side responded to a gentle faradic current, and on the
left side did not  respond  to  the  strongest faradic current, it would
mean that there  was some lesion in the nerve and muscle in the left
side.   If we examine a nerve  that has  gradually become impaired,
as after  section of the sciatic of the frog, or in a traumatic neuritis
in the human being,  or in the degeneration of certain  peripheral
trunks resulting   from  a myelitis of the  anterior horns  in a child,
we will find that there  are marked and characteristic alterations in
the response of both the nerve and muscle to the  galvanic and faradic
current.   For these alterations Erb has suggested  the  significant
name of reaction  of degeneration (Entartungsreaction). Let us study
the peroneal nerve after a sudden onset of paralysis in a little child,
in whom a diagnosis has been made of myelitis of the anterior horns.
In  the first week or  ten days there will  be  diminishing response
to galvanism  and faradism, so that  it will  take increasingly larger
currents to cause  a muscular contraction through galvanization and
faradization of the affected  peroneal nerve than it does in its fellow
of the unimpaired side.  In the first few days, when the galvanic
and  faradic currents are applied to the nerve itself,  the  decreasing
muscular contraction day by day shows that  the  nerve-excitability
to galvanism  and faradism  is diminishing, and this may go on to
total  loss of  response to both  currents in a severe case  toward the
end of the second week.   If the current during  this time is applied
directly to the muscle, it will be found that the muscular  response to
faradism is rapidly diminishing and may be entirely lost toward the
end or beginning  of the second week, as has been said ; but the mus-
cular response to galvanism is not.nearly so much diminished as is
the  response to faradism, and, indeed, toward the end of  the second
week the muscular response to galvanism begins actually  to increase.
This increase of muscular response to galvanism, which is known as 
ELECTRICITY.
129
the quantitative reaction of degeneration, rapidly augments, so that
at the end of the second week it may be extremely marked.  Simul-
taneously with this increase of muscular  response to galvanism goes
an alteration of the normal polar reaction, or what I have called the
progression of the  poles, so  that A. C. may equal C. C, and after a
while C. 0. may equal A. O., or C. O. may even come with  a less
current than A. O.   Simultaneously with this quantitative reaction
of degeneration and this alteration of the  polar progression  there is a
change, in response to galvanism, of the character of the muscular con-
tractions, which are quick and shock-like in the  normal muscle, but
which, at the stage we  are  describing, become sluggish and worm-
like.  It is therefore evident  that the  reaction  of degeneration is
characterized by a diminution  or loss of the faradic and galvanic
excitability of the nerve and the faradic excitability of the muscle;
whilst the  galvanic  excitability of the muscle remains—indeed, is
often  increased—the normal progression  of  the poles is altered, and
the muscular contraction is  sluggish aud worm-like.  In some cases
all these different phenomena  of the  reaction of degeneration may
be obtained, whilst in others some of them may be lacking.
   In  the cases in which there has been a permanent injury inflicted
upon  the nerve and the muscle, this reaction of degeneration becomes
permanent and will be found year after year.   In cases which recover,
however, the different degenerative phenomena may  gradually disappear
until  the nerve reacts in a normal or almost normal way to the two
poles.  As a matter of prognosis, therefore, the extent and duration
of the reaction of degeneration become of great  importance.   If a
nerve has been injured, and shows only a slight  loss of response of
nerve and muscle to the galvanic current at the end of  two or three
weeks, and there is no increased response to galvanism, no alteration
in the progression of the poles,  and but slight alteration in  the char-
acter  of the  muscular movements in  response to the currents, the
prognosis  will  be  a very favorable one;  whereas the opposite of
these  phenomena would  be  of very unfavorable  augury.  Between
these  two extremes there are all grades.  Even  in some cases, as I
have  repeatedly seen, there may be an  excellent return  of  motor
power in a nerve and in a muscle which  do not yet respond in a
perfectly normal way to galvanism and faradism.
   In  all cases where reaction of degeneration is found, either complete
or partial, it indicates disease in the nerve  and in  the  muscle such
as is described  in neuritis, although the neuro-muscular alteration
may be of central  origin.  It must  be remembered, however,  that
there  are certain diseases of the muscles, as in pseudo-hypertrophic
muscular  paralysis,  in  which  there  is  scarcely any  alteration to
galvanism and faradism.
9 
130
INTRODUCTORY.
CHART OF  THE   MOTOR  POINTS  OF  THE  DIFFERENT
                       REGIONS OF  THE BODY.

                                       Fig. 82.
  A diagram of the motor points of the face, showing the position of the electrodes during
electrization  of special muscles and nerves.  The anode is supposed to be placed in the
mastoid  fossa,  and the  cathode in the part indicated  upon  the diagram.  (From Von
ZlEMSSEN.)

  1. Occipito-frontalis (ant. belly).  2. Corrugator supercilii. 3. Occipitc-frontalis (post. beUy).
4. Orbicularis palpebrarum.  5. Retrahens et attollens aurem.  6. Pyramidalis nasi. 7. Facial
nerve.  8. Lev. lab. sup. et alae nasi.  9. Deep posterior auricular branch  of  facial nerve.
10.  Lev. lab. sup. propr.  11. Stylo-hyoid.  12. Dilator naris ant.  13. Digastric.  14. Dilator
naris  post.  15. Buccal branches of facial nerve.  16.  Zygomat. minor.  17. Subcutaneous
branch of inferior maxillary nerve.  18.  Zygomat. major.  19. Splenitis capitis. 20.  Orbicu-
laris oris. 21. External branch of spinal accessory nerve.  22. Branch of levator menti and
dep. ang. oris.   23. Sterno-mastoid.   24. Levator menti.   25. Sterno-mastoid.  26. Dep. lab.
infer.  27. Levator anguli scapulae.  28. Dep. ang.  oris  29. Phrenic nerve.  30. Subcutaneous
nerves of neck.  31. Posterior thoracic nerve to rhomboid muscles.  32. Sternc-hyoid.  33. Cir-
cumflex  nerve.  34. Omo-hyoid. 35.  Posterior thoracic nerve to serratus magnus.  36. Sterno-
thyroid.  37. Branch of brachial plexus.  38. Branch for platysma. 40. Sternc-hyoid. 42. Omo-
hyoid.  44, 46. Nerves to pectoral muscles. 
Fig. 83.
Serratusimagnus.

Latissimus dorsi.
Rectus abdominis.
Intercostal nerves.
Intercostal nerves.
Diagram of the motor points of the trunk.  (From Von Ziemssen.)

                            Fig.  84.
       Diagram of the motor points of the arm, under side.  (From Von Ziemssen.)
 1. Musculo-cutaneous nerve.  2. Musculo-cutaneous nerve.  3. Biceps.  4. Internal nerve of
triceps.  6. Median nerve,  8. Brachialis anticus.   10. Ulnar nerve.  12. Branch of median
nerve to the pronator teres.
                                       Fig. 85.
                                        3   2          1
               Motor points of the arm, outer side.  (From Von Ziemssen.)
 1. External  head of triceps.  2.  Musculo-spiral nerve.  3. Brachialis anticus.  4. Supinator
longus.  5. Extensor carpi radialis longior.  6.  Extensor carpi radialis brevior. 
132
INTRODUCTORY.
Motor points of forearm, inner surface.         Motor points of forearm, outer surface.
                             (From Von Ziemssen.)
  Fig. 86.—1. Flexor carpi radialis.  2. Branch of the median nerve for the pronator teres. 3.
Flexor profundus digitorum.  4. Palmaris longus.  5. Flexor  sublimis digitorum.  6. Flexor
carpi ulnaris.  7. Flexor longus pollicis.  8.  Flexor sublimis digitorum (middle and ring
fingers).  9.  Median nerve.  10. Ulnar nerve.  11. Abductor pollicis.  12. Flexor sublimis digi-
torum (index and little finger).  13. Opponens pollicis.  14. Deep branch  of ulnar nerve.  15.
Flexor brevis pollicis.  16. Palmaris brevis.  17. Adductor pollicis.  18. Adductor  minimi
digiti.  19. Lumbricalis (first).  20. Flexor brevis minimi digiti.  22. Opponens minimi digiti.
24. Lumbricales (second, third, and fourth).

  Fig. 87.—Extensor  carpi ulnaris.  2. Supinator longus.  3. Extensor minimi digiti.  4. Ex-
tensor carpi radialis longior.  5. Extensor indicis.  6. Extensor carpi radialis brevior.  7. Ex-
tensor secundi internodii pollicis.  8. Extensor communis digitorum.  9. Abductor minimi
digiti.  10. Extensor indicis. 11. Dorsal interosseus (fourth).  12. Extensor  indicis and extensor
ossis metacarpi pollicis.  14. Extensor ossis metacarpi pollicis.  16. Extensor primi internodii
pollicis.  18. Flexor longus pollicis.  20. Dorsal interossei. 
ELECTRICITY.
133
Fig. 88.                                         Fig. 89.
Motor points of thigh, anterior surface.                  Posterior surface.
                              (From Von Ziemssen.)
 Fig. 88.—1. Tensor vaginee femoris (branch of superior gluteal nerve).  2. Anterior crural
nerve.  3.  Tensor vaginae femoris (branch of crural  nerve).  4. Obturator  nerve.  5. Rectus
femoris. 6. Sartorius.  7.  Vastus externus.  8. Adductor longus.  9. Vastus  externus.  10.
Branch of crural nerve to quadriceps extensor cruris.  12. Crureus.  14. Branch of crural nerve
to vastus externus.

 Fig. 89.—1. Adductor magnus.  2. Inferior  gluteal nerve for gluteus maximus.  3. Semi-
tendinosus. 4. Great sciatic nerve.  5. Semi-membranosus. 6. Long head of biceps. 7. Gas-
trocnemius (internal head).  8. Short head of biceps.  10. Posterior tibial nerve. 12.  Peroneal
nerve.  14. Gastrocnemius (external head).  16.  Soleus. 
134
INTRODUCTORY.
           Motor points of the leg, outer side.                        Inner side.
                                 (From Von Ziemssen.)

  Fig.  90.—1.  Peroneal  nerve.  2. Peroneus  longus.  3. Gastrocnemius (external head). 4.
TibiaUs anticus.  5. Soleus.  6.  Extensor longus pollicis.  7. Extensor communis digitorum
longus. 8. Branch of peroneal nerve for extensor brevis digitorum.  9. Peroneal brevis.  10.
Dorsal interossei.  11. Soleus.  13. Flexor longus pollicis.  15. Extensor brevis digitorum.  IV.
Abductor minimi digiti.
  Fig. 91.—1. Gastrocnemius  (internal head).   2.  Soleus.  3. Flexor communis digitorum
longus.  4. Posterior tibial nerve.  5. Abductor pollicis. 
CHAPTER  III.
                          MASSAGE.

  The  manipulations  employed  in  massage are four  in  number,
namely:
  1. Stroking;
  2. Rubbing;
  3. Squeezing;
  4. Striking.
  The stroking should be in the direction of the venous current—i. e.,
toward the heart.   It is done by varying degrees of pressure with the
flat of the hand, its ulnar or radial edge, with the ball of the thumb,
with the base of the hand, and with the thumb and forefinger, either
one hand  being used, or  both, as when one completely  encircles an
extremity.
  Rubbing is with the dorsal side of the thumb or with the last
phalanx of the middle  three fingers.  The finger-tips should move
in small circles over  a small area, but the direction is not important.
  Squeezing is performed  by grasping the tissues between the thumb
on one side and the other fingers on the other, bringing the fingers of
the two  hands closely together, and making a series of pinchings or
kneadings.  The  tissues may be lifted somewhat out of their ordi-
nary position ; or  the one hand should be placed  on the outer side of
a limb and the other on the inner, and all the tissues raised together
and wound around  the bones, as it were.  This squeezing calls for
a good deal of muscular strength and practice.
  Striking is  by  blows given by the flat of the hand  at  its ulnar
edge, by the tips of one or more fingers, by the dorsal surface of the
fingers spread  apart,  or by the side of the fist.
  This simple division  of  the manipulations employed in massage is
quite sufficient for all practical purposes.   The  technique, however,
has been refined to a  marvellous degree, and some of the refinements
are no doubt useful in  massage of certain delicate organs, but what
has been described above is quite sufficient for all general purposes.
  Of these different methods, stroking, rubbiug, and squeezing are
the ones which are most useful, and should be generally employed in
cases of nervous and mental  disease.   Striking is seldom necessary.
When the massage is general  it should be begun at one  foot.  This
should be  grasped with both  hands and  treated with squeezing and
rubbing, at the same time that the thumbs are pressed into the de-
pressions between the bones.   The leg should then be stroked and
rubbed with  a long, rubbing motion, and the  different groups of
muscles should be squeezed or kneaded, aud then the leg should be 
136
INTRODUCTORY.
given a  final stroking all over.  The thigh should  be treated in a
similar manner, aud then the lower extremity.  The massage should
next  be  applied  to the back  in  the  same manner, and  the chest
after  that.  In treating the abdomen  the  procedure should be as
follows:  The patient  should raise  his head slightly, bend his legs,
breathe  freely, and  relax  the abdominal  muscles—which  latter,
by the way, will often  need  some little  practice.   The masseur
should then place the tips of the middle  three fingers, held closely
together, upon  the abdominal wall, and rub in small circular move-
ments.  The stomach  can be reached by making these manipulations
in the gastric and left  hypochondriac regions;  the  large  intestine by
beginning at the caecum, following the ascending and descending por-
tions of  the colon and the  sigmoid flexure down  to the symphysis
pubis; and the small intestine by similar movements  in the um-
bilical and lumbar regions.  The upper extremities should then be
gone  over in the same manner as that in which the lower has been
treated.
   Simple as these manipulations  seem, it yet requires considerable
practice  to do  them  properly.    In all cases the  limb should be
put in such a position as to relax the muscles, which can be done
by anybody endowed with  ordinary intelligence.   Certain physical
qualifications  are necessary in the person giving  massage.   He
or  she   must,  for example,  have a  certain  amount of physical
strength  so that  they can make the squeezings with sufficient force,
in order, on the one hand, to manipulate the squeezed tissue properly,
and, on the other, to do it with a steady, strong muscular movement
that will  not be painful.  The movements of the masseur or masseuse
should under no circumstances be painful.   Then, too, a dry and
firm hand is an absolute requisite for a masseur or a masseuse.  Some
authors  advise the use of  some oleaginous substance wherewith to
anoint the skin, but this is never necessary unless it is desired to make
use of this unguent for purposes of nutrition.  Firm hands, steady
movements, and  practice make a  fat  of any kind upon the skin
totally unnecessary, and it  is only uncleanly.  There  is no doubt
whatever but what the general  circulation  and the temperature of
tissues can be greatly increased by massage, and also that the strength
of the muscles can be increased to a degree only short of that of actual
volitional exercise.  In cases of individuals who for various causes
are unable to use their muscles, or in others who are necessarily con-
fined to their room or to bed, massage is an invaluable therapeutic
agent.   The  great difficulty about it is that there are very few per-
sons expert iu  the  giving of it.  For  several years I almost  aban-
doned its use for this  reason, and it has only been since I have kept
in my employ a masseur and a masseuse that I  have been able to
rely upon  it.   In some few instances  I  have known of physicians
instructing some nurse so as to obtain very creditable results.
   In no  instance  should massage be begun at bedtime, because there
are many people for whom the first manipulation means an absolutely
sleepless  night.   In most cases, however, they soon become accus-
tomed to it at any hour. The first manipulation should never extend 
MASSAGE.
137
beyond a half-hour, and then as the patient becomes  accustomed to
it, and he has  a beneficial  result, the  time should  be  lengthened
to forty-five minutes, and finally to  an hour.  The  patient should
always lie in bed for an hour after the massage, and even longer
where there is much weakness.
  The directions for the use  of massage in individual diseases will
be given in the different chapters. 
 
             PART   II.

NERVOUS  DISEASES.
                    CHAPTER  I.

LOCALIZATION OF LESIONS IN THE CEREBRUM, CEREBELLUM,
                     AND SPINAL CORD.

  The diagnoses of the different lesions of the brain and spinal cord
are treated of in their proper chapters in this book, but I propose to
outline briefly the localization of them in this chapter, so as to  ob-
viate the necessity for repetition.

           LOCALIZATION OF CORTICAL  LESIONS.

  As we have seen,  the centres which have so far been localized in
the cortex are the  motor areas, the centres  for vision, word-deafness,
word-blindness, motor aphasia, and aphasia of interrupted conduction,
and possibly also the centres for agraphia and the  muscular sense,
pain, and touch.
                     THE MOTOR AREA.

  The  lesious of the motor area usually produce mouoplegic paral-
ysis ; i. e., they affect one limb  or a group of muscles.   It  is very
important, from a diagnostic point of view, that this fact  should be
remembered.   The reason for  it is very apparent.  The centre  for
the leg is contained, as has been said, in the upper fourth of the motor
area, that for the arm in the  middle two fourths, and that for the mus-
cles of the head and face in  the lower fourth, whilst the centre of  the
motor mechanism  of speech  is to be found in the third frontal convo-
lution.   These different centres  are therefore spread over a consider-
able area  of the cortex, and in order  that they should  all be  im-
plicated by one cortical lesion,  this would  have to extend over  the
ascending parietal  and frontal convolutions and over the third frontal.
As the nerve-fibres, however, pass from these various centres toward
the  base of the brain, they must  be converged into the  narrowed
strait of  the  internal capsule,  as is seen  in  Fig. 81,  and,  packed
together in this narrow inlet, they can be caught  by a very small
lesion,  such  as may be due to a pin-head  hemorrhage  from  the
bursting of a capillary bloodvessel.  Besides producing monoplegic 
140
NERVOUS DISEASES.
paralysis, the lesions  of the motor  area have a tendency to cause
convulsion, which is either localized  throughout the entire limb that
has been or is to be paralyzed, or else the convulsion starts in this,
and, after being confined to it for a distinct though short period,
extends to the other members of the same side, or may even become
generalized.  It has  been asserted  that when a convulsion due to
cortical disease begins in one limb, this is always  evidence that the
lesion is in the cortical centre of this limb, although  the convulsion
may extend to the other extremity  or  to other muscles.  This so-
called  primary convulsion  has  been called by Seguin the signal-
symptom.   But  it is not  always  proof  that the  centre  of  the
convulsed limb  is alone affected, for in some cases in which several
centres are  affected  by  a lesion the convulsion will commence in
one of them and then extend to the  others.   Nevertheless, when
the convulsion has been  for weeks or months confined to one limb,
and is  evidently due to cortical  disease, it  is almost invariably the
case  that the  centre of the limb  primarily couvulsed was the first
one attacked by the lesion.  It was for  some time supposed that loss
of consciousness, with a more or less localized convulsion, preceded
or followed by  monoplegic  paralysis,  was diagnostic of  a cortical
lesion as distinct from  a subcortical lesion; but this has been proven
by further cases of my own not to  be  a reliable  criterion, as some
cases of cortical lesion may be attended by no loss of consciousness,
whilst  some cases of subcortical lesion are.  The diagnosis, there-
fore, of a cortical lesion of the motor area is to be made mainly by
means  of the presence of a monoplegic paralysis, with or without
monoplegic convulsion, and exclusion of subcortical areas.

                CORTICAL  CENTRE OF VISION.

  As we have already seen (Fig. 39  and Plate I.), the cortical centre
of vision is in the cuneus and the adjacent occipital convolutions; and
the defect of sight produced by the lesion in  this centre is that which
is known as hemianopsia.   We shall have occasion to examine sub-
cortical lesions also capable of producing hemianopsia.

           CORTICAL CENTRE OF  WORD-BLINDNESS.

  This, as we have seen (Plate I.),  is supposed to be located in the
angular gyrus, although there is still some doubt about the matter.

                 CENTRE OF WORD-DEAFNESS.
  Recent cases by Mills have demonstrated  that this peculiar lesion
is located more particularly in the rear ends of the first and second
temporal convolutions, so that we can  readily understand why it is
that  word-deafness is  so often associated with word-blindness.

                   CENTRE OF  AGRAPHIA.

  As has already been stated, agraphia is an inability to write, al-
though there may be no paralysis of the  hand, no loss of the memory 
        LOCALIZATION OF BRAIN AND CORD LESIONS.     141

of words, no word-blindness, and no hemianopsia.   Its centre is not
positively known, but is supposed  to be in the posterior portion of
the second frontal convolution.

              CORTICAL  CENTRE OF APHASIA.

   When the third frontal convolution is affected, the patient suffers
from what used to be known as ataxic aphasia, but what has recently
been termed motor  aphasia—i. e.,  the patient understands perfectlt
well  the meaning of words and can recollect them well enough, buy
he cannot pronounce  them properly.  When the  island of Reil is
affected  there is  what is  known  as aphasia of conduction—i. e., the
patient utters words entirely unlike those which he  had intended  to
speak, and, being thus  unable to  express  himself with the words
which he had desired to use, seemingly gives vent to gibberish.
   A sharp distinction must be made between four varieties of defect
of expression—namely, motor or ataxic  aphasia, aphasia of conduc-
tion, word-deafness, and agraphia.   The patient who  has  motor  or
ataxic aphasia  can remember words perfectly well, as is evident by
his being able to write them, being able to  express his appreciation
of their meaning in writing, and by being able to make some defective
attempt at the pronunciation of them. The patient who has aphasia
of conduction  can also  appreciate the  meaning of words perfectly
well, as  is shown by his being  told  to do a certain thing and his per-
formance of the  act in a perfectly intelligent manner; and  he can
also write  the words which are given to him, but he cannot make
even a defective attempt at the pronunciation  of  them, but simply
utters some word that has no relevancy.  The patient who has word-
deafness can pronounce a word perfectly well, and  repeat it when it
is pronounced  by another, so that  he has evidently no defect in the
mechanism of speech; and he can also  write the word which  he is
told to write, showing that there  is no fault in the mechanism neces-
sary to writing; but lie does not understand the  meaning of the word
which he repeats.  You can say  to him, for example, " This is your
watch,"  and he will repeat the word "watch," and will also write it;
but if asked the meaning of it, not only  will his facial expression
evidence that he  does not know what it means, but he will confess, if
he is intelligent, that he does not know the meaning of u watch."  If,
however, he is  shown the watch, and often when he has written the
word " watch," his face will brighten up with a look of intelligence,
and he will tell you that he knows  what you mean; in other words,
through the sense of sight he has gained  a comprehension of the
meauing of the word by seeing the article.   He can also gain  an idea
of the meaning  of the word by other  senses than sight, as by the
sense of touch  in feeling the watch, or the sense of  smell in smelling
a flower, or the sense of taste in tasting an object, or by the muscular
sense, when he is asked  the meaning of the word " forefinger," and
you move his forefinger,  or by the sense of  pain when you ask  him
the meaning of  the  word  " pin,"  aud  then prick him with  one.
Finally, when  a patient  has agraphia  he is  not able  to  write, 
142
NERVOUS DISEASES.
although he may be  able to understand the meaning of words per-
fectlv well, may be able to pronounce them properly,  may have a
perfect memory of them, and may have no word-blindness, hemian-
opsia, or paralysis of the hand.

               THE CENTRES  OF MIND ALONE.

  It was formerly held that the  frontal lobes anteriorly to the motor
area were the only centres of mind—i. e., that only a iesion of them
could produce mental  symptoms purely,  without  any  such as are
due  to  implication of the  centres of the  limbs, sight, hearing, and
aphasia. Even  at  the  present  day is an  idea of this  kind dimly
floating  in  the  neurological  mind;  but as  cases multiply, this
doctrine is gradually being disproved, and it is being shown more
and  more clearly that the metaphysical entity which we call mind
is dependent upon the structural integrity of the cortex as a whole,
so that a lesion anywhere in the cortex, if  sufficiently destructive,
may produce mental symptoms,  and the more widespread  such it is,
the greater will be the mental impairment, although a small area of
disease may seem to a superficial observer to leave the mind unim-
paired, when careful examination of the patient will show that this
is only seemingly so.  Nevertheless, it remains true that involvement
of the frontal lobe anterior to the motor area and the third  frontal
convolution produces only mental symptoms, and not physical ones.
Some cases, notably the celebrated  crowbar one, have been vaunted
in contradiction of this; but  an analysis of the history has shown
that there were mental  changes  sufficient to prevent the individual
from following his occupation,  whilst subsequent cases have abun-
dantly proved the statements just made.

              LESIONS OF THE CENTRUM  OVALE.

  The centrum ovale, it should be remembered, is nothing more than
the nerve-strands coming down from the cortex to pass to the sub-
lying ganglia, and  lesions of it  therefore do not differ from lesions
of the  cortex except in the fact that the deeper  the level of the
lesion, the more  convergence  and interlacing will there  be of dif-
ferent nerve-fibres  coming from different  cortical centres.   (See
Fig. 92.)  Thus, a  lesion  just  below the centre  for the  leg and
sufficiently localized to affect only the nerve-strands coming from
it, would cause exactly the same symptoms  as a  lesion of the leg-
centre itself—viz., paralysis or  convulsion, or both, of the leg.  If
the  lesion  were still deeper seated, so as to implicate  the nerve-
strands coming  from the leg  and the arm-centres  and  converging
so as to reach  the internal capsule, the symptoms produced would
be that  of simultaneous affection of the  arm- and the  leg-centres,
namely, paralysis or convulsion, or both, of the arm and leg.  The
deeper  down we go into  the  centrum  ovale, therefore,  the more
complex will  be the symptoms.  It  is often extremely difficult to
make a diagnosis between a cortical and a subcortical lesion, and we 
LOCALIZATION OF BRAIN AND CORD LESIONS.     143
Fig. 92.
Lea,
Cortical centres and subcortical nerve-
    strands leading up to them.
are generally obliged to seek aid from clinical facts as well as ana
tomical ones.  Thus, if there is a monoplegic paralysis and convul
sion at the  start, and this  paralysis
and  convulsion  remain monoplegic
through  months, there is  a greater
probability of the lesion being cortical
than of its being subcortical, for the
reason that   there  would   be  more
space in  the cortex for the lesion to
develop and  affect only one limb than
there would  be in the centrum  ovale.
Again, if the diagnosis of a  tumor
can be made, and the  symptom is a
paralysis  or convulsion which  has
remained monoplegic for months, the
probability  is greatest  of  the  lesion
in the cortex, because a tumor  in the
centrum ovale would be likely to im-
plicate nerve-fibres from other centres
more quickly in its growth.  Again,
if the lesion  has been a trauma  of the
skull, the probability is greatest of the
trauma  having  impinged   upon the
cortex rather than upon the subcortical regions.   Again, if a diagnosis
has been  made of a meningitis, it is certain that the cortex would be
affected by the meningitis long before the subcortical tissue was impli-
cated.  Again, if a diagnosis can be made of an arterial lesion, as in a
condition of general endarteritis with attendant atheroma or embolism,
the probabilities are far greater of the centrum ovale being  impli-
cated, because the vessels from  the pia mater inosculate freely in the
cortex, whilst the subcortical matter  is fed with relative sparseness
by loug, straight arterial branches dipping down into it.  (Fig. 93.)
When, however, the paralysis is not monoplegic, as when both limbs
on the same  side are affected, or when there is an affection of several
limbs, or  of the muscles of the  head and  trunk  with coincident
aphasia,  it may be a  very difficult matter  to  make the  diagnosis
beween a cortical aud  subcortical  lesion, and  in most cases  it is
almost impossible.   To sum up, therefore:
   1. A cortical lesion is most probable when one centre alone is af-
fected, and remains  affected.  Thus, if there should be paralysis of
one arm,  with  or without  convulsion limited  to that one arm or
starting in it, the probability would be exceedingly great that there
was a lesion  in the middle twTo fourths of the motor area.  So, also,
when there are paralysis and convulsion of one leg, or of the muscles
of the head and face, or aphasia alone, or  word-deafness alone, or
agraphia alone,  or hemianopsia  alone, it would be extremely probable
that the lesion was cortical  in  the respective centre.  If, moreover,
there should be a paralysis  of a few muscles  in  one limb, as  of the
thumb, and  this paralysis should remain for  some time before other 
144
NER VO US DISEASES.
symptoms supervened, the probability would pass into certainty of
there being a cortical lesion.
  2.  A cortical lesion would be rather more probable than a subcor-
tical one when there were persistent attacks of loss of consciousness
with the localized symptoms, although, as I have said, the weight to
be attached to this loss of consciousness is rather problematical.

                               Fig. 93.
Distribution of arteries to gray and white matter.  (Dueet.)
 1,1. Medullary branches passing directly through the gray matter to the white matter, and
then terminating in branches that do not anastomose with their neighbors (" terminal arte-
ries"). 1. Medullary arteries in the sulcus between two convolutions. 2, 2. Cortical arteries.

  3.  A cortical lesion is most  probable when one centre is affected
first, and then, a distinct  interval  of time having  elapsed, another
centre is affected, and still  more if there is a progression of symp-
toms to a third centre, and  so on.   But this must be nevertheless
taken into consideration: If centres are closely approximated, as are
those of the arm and leg,  the head and neck, and  those of motor
aphasia  and aphasia of conduction, the  subcortical  nerve-strands
from these centres  are  also close together, so that a growing lesion
could readily  extend subcortically  as well as cortically.   But  it
centres as far apart as those for the leg and hemianopsia should be
affected in  progression, it  would then be most  probable that the
lesion in both cases was  in the cortex,  and  multiple,  because  it
would be impossible to conceive of  a subcortical  lesion that should
extend from beneath the upper third of the motor area away back
to just beneath the occipital lobe without causing enormous  general
symptoms, not only of implication of the whole cerebrum from such 
        LOCALIZATION OF BRAIN AND CORD LESIONS.     14,5

a large lesion, but also from  impairment  of various  nerve-centres
between the two main ones which we have named.
  4. Meningitis and  traumata are more likely to affect the cortex
than the centrum ovale.
  5. Tumors are  somewhat  less likely to affect the centrum ovale
than the cortex, although subcortical tumors are found  often enough
to prevent this fact from being conclusive.
  6. Cortical tumors and meningitis, so far  as we now know, are
alone capable of causing a distinct rise  of  cerebral temperature, as
indicated by my cerebral thermometry.  This fact, it should be borne
in mind, has  only the positive value of making  a distinct rise  of
cerebral temperature  probably indicative of a tumor or meningitis,
but, conversely, the absence of rise of cerebral temperature is of  no
value for or against.
  This difficulty of diagnosis  between a cortical and a subcortical
lesion is of very great importance to the  surgeon.   In  any case
in which it cannot  be made many  a sore  disappointment will  be
avoided by carefully  explaining to  the  patient and the friends the
uncertainty of the localization of the lesion.   To this difficulty should
be added the further one of finding the exact site of a lesion  in the
centrum ovale, even when it has been localized there.  This, however,
will be dwelt upon  fully in the chapter upon intra-cranial growths
(Chap. VII.).

            LESIONS OF THE INTERNAL CAPSULE.

  Lesions of the internal capsule are almost invariably due to arterial
trouble, either of the nature of endarteritis,  embolism, or thrombosis.
In Fig. 55 it has  been shown how the terminal arterioles coming  off
from the Sylvian  artery supply the  internal capsule.   At page 59,
the location of the different nerve-strands in the internal capsule has
been described.   Just behind the knee or genu (Fig. 35) lie the fibres
from the motor area, the so-called pyramidal tract.  Immediately in
front of them run the nerve-strands  from the facial and hypoglossus
centres, which probably are situated, as we have seen in Plate I., in
the lower portion  of the ascending frontal convolution. Behind the
pyramidal tract in the posterior third of this portion of the internal
capsule run the sensory fibres, which  are  on their way to the teg-
mentum.   Back  of the  sensory  fibres  are the  optic-nerve  fibres
coming in from the occipital lobe.  Somewhere in this region are also
fibres from the temporal lobes to the  auditory nuclei, and others from
the olfactory lobes.  Besides these main motor and sensory fibres there
are other  short ones whose  existence we know of anatomically, the
lesions of  which  produce symptoms  that are not known  to  us.
Anteriorly to the  knee or genu, there are fibres from the frontal lobe
to the pons, and  from the cortex to the optic thalamus ;  whilst in
the posterior or sensory portion of the internal capsule, behind the
genu, are fibres to the optic thalamus that are probably sensory, and
from the temporo-occipital cortex to the pons.   Lesions, therefore, of
the internal capsule  produce either  motor  or sensory  symptoms, or
                               10 
146
NERVOUS DISEASES.
commingled motor and sensory symptoms.   In the majority of cases,
however, the symptoms are motor and but  slightly sensory, aud the
portion of the internal capsule affected is that supplied by the lenticulo-
striated artery.  (Fig. 55.)  The form of  paralysis is  hemiplegic;
i.e., paralysis of motion or sensation, or both, most frequently motor
alone, of the upper and lower extremity and of the lower part of the
face, the eyelids and eye-muscles being unaffected.   (See p. 85.)  The
diagnosis of a lesion of the internal capsule is readily made.  As has
been said, the paralysis is generally motor only, though sometimes both
motor and sensory; the onset is relatively acute, being either sudden
or extending over a few hours or a day;  aud in the vast majority of
cases the lesion is one due to some arterial trouble,  such as an endar-
teritis, embolism, or thrombosis.  The lesion, therefore, occurs mainly
in certain classes of individuals:  first, those who have the chronic end-
arteritis of middle age, associated with general  atheroma, hypertro-
phied heart, aud chronic degenerative kidney lesion ; second, those who
have an intracranial syphilis producing syphilitic endarteritis; third,
children who have hemiplegia,  either without mental defect or with
very slight mental impairment; fourth, in rare cases those who have
a premature endarteritis from alcoholism ; fifth, those who  have the
endarteritis that is associated with nephritis.  Tumors of the internal
capsule hardly ever occur, and  traumata  impinging only upon  this
narrow strait of the internal capsule are  equally rare, except where
there is existing arterial disease  that renders the arterioles excessively
fragile.

LESIONS  OF THE CORPUS STRIATUM AND OPTIC THALAMUS.

   These cannot  be diaguosed.   It is possible, however, that the re-
cent localization by Ott of a heat-centre (see  p. 103) in the optic thala-
mus will be the means of our  making a diagnosis, although as yet
this has not been done, and this centre has only been localized in the
dog and the rabbit.

          LESIONS OF THE QUADRIGEMINAL BODIES.

   As  has  been seen in Figs. 36, 38, 40, 45, and 48, the quadrigemi-
nal bodies are in close relation  to the  optic-nerve  fibres, to the teg-
mentum, to the superior and middle cerebellar peduncles, to the pineal
gland, to the pulvinar of the optic thalamus,  and also to the nuclei
and nerve-fibres of the ocular nerves.  It  can well  be  seen, there-
fore, how much doubt there is as to whether the symptoms are due
to lesions alone of the quadrigeminal bodies  or to associated  lesion of
the surrounding structures.  Such  cases,  however, as have so far
been published, some twenty-five in number, would  seem to show that
the symptoms are : first, au unsteady, reeling gait appearing early in
the course of the symptoms; second, ophthalmoplegia of the muscles
of both eyes, but  not quite  symmetrically, nor implicating all the
muscles in equal degree.   Nothnagel believes that the reeling gait is
due to the  quadrigeminal lesion  alone, as  several cases have  been 
        LOCALIZATION OF BRAIN AND CORD LESIONS.      147

reported in which the cerebellar peduncles were  not affected.   Thus
Feilchenfeld, Pontoppidan, and Fischer have reported three cases of
tumor of the pineal gland alone, with pressure upon  the quadrigem-
inal  bodies, whilst  Massot has  reported a case of  a tumor of the
pineal gland in which the quadrigeminal bodies were  not compressed
and there was no reeling gait.   The reeling gait  is like that of cere-
bellar lesion, and consists  of a stumbling  or titubatiou similar to
that of a drunken man, aud it is entirely dissimilar to the ataxia of
locomotor ataxia, in which the patient walks erectly,  but brings his
heels down with a stamp or a  tendency to  a stamp, and the upper
extremities  are  not affected at all.  The ocular muscles which are
most prone to be affected are those supplied by the third pair, although,
as has been already stated, other ocular  muscles  may be  affected so
as to give rise to an ophthalmoplegia.  The lesion of the ocular muscles
is due to compression or extension  of the quadrigeminal lesion to the
nuclei and nerve-fibres of the ocular  nerves.  As has been said, this
ophthalmoplegia is not apt to be complete or bilateral.   Thus, when
the third nerve is affected, it is generally the superior and inferior
recti which are paretic or paralyzed,  or  the lateral  movement of the
eye may be abolished, or ptosis may be the  most marked symptom ;
and  although ophthalmoplegia occasionally occurs, it is seldom as
complete as when the nuclei themselves are affected (see Progressive
Ophthalmoplegia).   Nystagmus alone, or in conjunction with paral-
ysis of ocular muscles, may occur.  It has also been claimed that the
trochlear or abducens nerve alone can be affected, and it was  at  one
time thought that this was a diagnostic symptom, but it has not been
proveu.   Nothnagel has recently expressed the belief that lesions of
the quadrigeminal bodies  may  leave the vision entirely unimpaired,
but in making this statement he does not seem to have taken account
of any other impairment of sight than  amblyopia or amaurosis, the
cases which he cites do not seem  to have  been  definitely examined
for hemianopsia, and in other cases he admits that choked disk and
optic neuritis were present in such degree as to make  it impossible to
examine thoroughly the visual acuity ; moreover, the recent experi-
ments and  cases of von Monokow have proven  that the anterior
quadrigeminal bodies, together with the lateral geniculate body, are
connected with the  optic nerve-fibres.   Diagnosis of  a  lesion  of the
quadrigeminal bodies may therefore be made by means of the reeling
gait,  associated  with  ophthalmoplegia or isolated paralysis  of the
trochlear or  abducens nerve,  or with  nystagmus, and  also  by the
absence of other motor, sensory, or vasomotor symptoms.   I think
it  is  probable  that the future will  show that hemianopsia is asso-
ciated with these symptoms, especially when the anterior quadrigem-
inal bodies are implicated; and it  must not  be  forgotten that  the
posterior quadrigeminal  and  middle geniculate bodies  have been
shown by von Monokow and Spitzka to be connected with hearing;
deafness has been a sign of lesion in this region in a number of cases
analyzed by Weinland.  Flechsig, Bechterew, Roller,  Monokow, and
others have claimed, indeed, that a portion of the  lateral lemniscus
running  to  the  posterior quadrigeminal bodies contains fibres from 
148
NERVOUS DISEASES.
the cochlear nerve; but Weinland fouud the lateral lemniscus totally
destroyed on  the side opposite the deafness and the diseased quad-
rigeminal body.
                    LESIONS OF THE  PONS.

   Homen, Meyer, and Spitzka have carefully studied cases of lesion
of the pons.   Of these three, the most minutely and therefore thor-
oughly described is Spitzka's.  In these three cases the age was forty-
eight, forty-eight, and fifty-eight, respectively, aud the lesion was an
arterio-sclerosis causing either hemorrhages or softening.   It must be
remembered that, as has been shown in Figs. 36, 37, 38, and 48, the
pons  is a very complicated  structure, containing motor and  sensory
fibres passing  from the cortex down to the spinal cord, as well as
nerve-fibres and nerve-nuclei of the different cranial nerves, the cere-
bellar peduncles, and transverse fibres connecting the two lobes of the
cerebellum.   The exact lesions, therefore, will  vary to  some extent
according to the level of the pons that  is  affected, but these three
cases of Homen, Meyer, and Spitzka, together with the  knowledge
gained from other sources, have enabled  us to  speak with some cer-
tainty of the main diagnostic symptoms.   In the former there were:
1, paralysis of the tongue, which deviated  to the side of the lesion;
2, hemiansesthesia of the opposite side; 3, constant dizziness; 4, ataxia
of the limbs of the opposite side; 5, exaggerated knee-jerk of the oppo-
site side; 6, diminution of cutaneous  reflex of the opposite side; 7,
subjective sense of muscular cramping of the extremities of the opposite
side.  The hemiansesthesia consisted of impairment of touch, tempera-
ture, sense of weight, and muscular sense—the latter to a slight degree.
The ataxia was greater on closing the eyes,  but  was not increased by
placing the feet close together.   In Meyer's case there was a loss of
faradic excitability of nerve  and muscle in  the  face, and  of galvanic
excitability of the nerve in  the same region.  Meyer's case had also
contracture, muscular atrophy, and trophic disturbances of the arm
opposite to the lesion.   In Spitzka's case the pupil became somewhat
contracted nearly three years after the first symptoms appeared, whilst
in Meyer's case the pupil was unaffected; and this is a contradiction
of the prevailing view that a lesion of the pons must be necessarily
accompanied by a contracted  pupil, although cases do occur in which
there  may be  myosis, at the same time that other cases have been
observed in which they have been found dilated.  The reaction of
the pupils to light is an equally unreliable symptom  for  purposes of
diagnosis.  The lesion  in Homen's,  Meyer's,  and  Spitzka's cases
implicated the lemniscus, and  in Spitzka's case it was about at  the
level  that is figured in  Figs. 42 and 43, about  at Lm and extending
downward.
   Lesions of  the pons may be diagnosed  by  the  following symp-
toms :  1, paralysis of sensation  or  motion, or  both, of the  side of
the body opposite to the  lesion ; 2, paralysis of the trigeminal, ab-
ducens, facial, or hypoglossal  nerves, and possibly also of the auditory,
all upon the same side of the  body as the lesion;  3, vertigo; 4, exag-
gerated knee-jerk on the side of the body opposite to the  lesion; 
        LOCALIZATION OF BRAIN AND CORD LESIONS.     149

5 subjective sense of cramping of the extremities of the side of the
body opposite  to the lesion;  6, absence of mental disturbances;
7, possibly conjugate deviation of the eyeballs and head toward the
side of the lesion; 8, difficulty of deglutition and articulation ;  and,
9, ataxia of the opposite limbs.   As we have already seen, the pupil-
lary contraction is an unreliable sign, although it is probably of value
in  the diagnosis  of a sudden hemorrhage into the pons, when it has
been frequently observed as a temporary symptom.  If disease should
be situated high in the pons, however, near where the crus passes into
it,  there  would be a unilateral paralysis—i. e., the cranial nerves and
the limbs would be affected upon  the same side, opposite to the lesion.
This can be readily understood  when we remember that the nerve-
fibres from the different cranial nerves  have here reached  the side
upon which they are going up to the cortex, just as they have in the
internal  capsule.   (Figs. 36 and  46.)

          LESIONS  OF THE  MEDULLA OBLONGATA.

   Lesions of the  medulla oblongata assume either the form of pro-
gressive ophthalmoplegia  or labio-glosso-laryngeal  paralysis, which
are treated of in separate chapters.   Lesions of the individual nerve-
nuclei are difficult to diagnosticate, unless symptoms of impairment
of a cranial nerve are observed in the course, of one of these symptom-
groups, or of a progressive muscular atrophy.

    LESIONS  OF THE  CEREBELLUM AND ITS PEDUNCLES.

   The diagnosis  of cerebellar lesions is a very difficult matter.  It
was formerly supposed that a swaying, staggering gait was  pathogno-
monic, but since it  has been shown to be present  in  the two care-
fully observed cases  of pons lesion recorded  by Spitzka and Meyer,
this view is no longer tenable.   When, however, to the staggering,
swaying  gait  there  is  added a  marked  tendency to staggering per-
sistently in one particular direction, this would be indicative of lesion
of the cerebellar peduncles, and therefore the probability of a coinci-
dent cerebellar lesion would  become stronger.   These movements in
one particular direction may consist in  staggering  to one  side,  or
backward, or forward, or in a semi-rotary movement around a circle.
A peculiar condition of the eyes was observed in one case of Monat's:
they were motionless, and one looked  downward and outward, the
other upward  and inward.  In three cases of my own I have also
observed a symptom to which I have seen no allusion, namely, a pecu-
liarly tight drawing  of the scalp over the skull during the paroxysms
of headache and dizziness.   Many cases of disease of the cerebellum
and its  peduncles have been latent so far as regards symptoms.  It
is, therefore, a matter  of  considerable  doubt as  to  whether we can
positively make a diagnosis between lesion of the cerebellum and  its
peduncles and that of the pons  ; although the probability would be
strongly in favor of a disease of the cerebellum or its peduncles when
there existed  a  swaying,  staggering gait, especially when this was 
150
NERVOUS DISEASES.
accompanied with forced movements in certain directions, and when
there was no motor or sensory paralysis of the extremities and no
implication  of cranial nerves.

               LESIONS OF THE SPINAL CORD.

   The symptoms of lesions  at the different levels of the  cord can
be ascertained by means of the table upon page 82.  The localiza-
tion of symptoms  in  the various portions of the gray and white
matter can only be  made to a limited extent.   Thus, motor paralysis
with  muscular atrophy and  entire  absence of  sensory symptoms
would indicate that the anterior cornua of the cord are implicated,
as in poliomyelitis anterior and some forms of progressive muscular
atrophy;  and a  lesion may  be localized  in  the  lateral pyramidal
column when there are exaggerated tendon-reflexes, contracture, and
hasty micturition, as in secondary descending degeneration of this
tract from some  higher level in the cord, pons, or cerebrum.  But a
disease of the  posterior cornua cannot be diagnosed, nor of such
white strands of  the cord as the columns of Goll, Burdach, Spitzka-
Lissauer,  direct cerebellar and Gowers'  columns, aud the anterior
fundamental column.   It has  been supposed that  the posterior
columns  of Burdach and Goll contained  the  tactile  and muscular
sense nerve-fibres,  and  the  lateral and anterior  fundamental and
the Gowers' column the temperature and pain nerve-fibres, but many
clinical  observations have failed  to  prove this view,  as well  as the
belief that lesions of the direct cerebellar columns are always the
cause of ataxia in spinal lesions.

           LESIONS OF THE PERIPHERAL NERVES.

  Lesions of the  peripheral  nerves can be diagnosed by the symp-
toms that will be  detailed in the chapter upon Neuritis.

                        HEMIANOPSIA.

  At the  outset of  this subject it should be clearly understood that
there  is  a technical difference in the meaning of the  two words
hemianopsia and  hemiopia,  although their etymological derivation
is  almost  the  same {vide page 41).  Hemiopia is  the blindness of
bilateral  halves of the retina.  As is well  known, the rays of light
coming  from the outside cross  in the optic  lens, and  therefore a
person who  has a left-sided hemiopia will fail to see  objects to the
right  side of the  median line, and this external blindness is called
hemianopsia—i. e., a left hemiopia will cause a right hemianopsia.
  As has been shown  in the diagram, Fig. 39, page  63, the course
of the optic  nerve  is a very complicated  one.   The  cuneus of the
occipital  lobe, the adjacent occipital convolutions, and probably also
the gyrus angularis and the lingual lobule (Fig. 16) are the cortical
centre of sight, and a lesion of the region thus constituted produces
a hemiopia of corresponding  halves of the retina, or hemianopsia of 
        LOCALIZATION OF BRAIN AND CORD LESIONS.     151

the opposite side.   From the cortical centre of sight the optic fibres
pass through the centrum ovale  to  the  posterior portion of the in-
ternal capsule, as shown in Fig. 15. From the internal capsule they
then pass through the posterior portion of the optic thalamus, the
pulvinar, into  the anterior  quadrigeminal body, and  thence to  the
lateral  geniculate body (Figs. 38 and 39), receiving fibres from ad-
jacent structures.   From the anterior  quadrigeminal  body and  the
lateral geniculate body the fibres then pass back and across the optic
thalamus to the base of the brain into the  optic tract (Fig. 39), and
through the optic tract to the optic chiasm and thence to  the  eye.
Most of the fibres, as has already been said, pass from the  cortical
centre of sight through these intermediate structures (optic thalamus,
anterior quadrigeminal  body, and  lateral  geniculate body) to  sym-
metrical halves of  the retina upon  the same  side as the cortex from
which they have taken their origin.  Besides these, however, certain
fibres pass to the outer portion of the retina upon the same side as
the cortex,  and other fibres pass in front of the chiasm to  connect
the two  retinae.  The chief stations, therefore, at  which  the  optic
fibres are apt to be implicated are :  the cortical centre of sight,  viz.,
the cuneus, the adjacent  occipital  convolutions, probably  also the
lingual lobule or the angular gyrus; the centrum ovale, the internal
capsule, the region of the corpora quadrigemina, the optic tract, the
chiasm, the optic nerve in front of  the chiasm, the retina.
  A lesion of the cuneus or the other convolution just named  is a
cortical lesion, aud will have the general symptoms of cortical lesions,
besides the localizing ones.   The latter can be diagnosed by the fact
that the blindness is bilateral, affecting the eye  on the same side as
the cortical lesion, the dividing-line of the  blindness  being nearly
vertical.  This variety is called  homonymous hemiopia, or hemian-
opsia.   The dividing-line is generally precisely on the vertical me-
ridian, and straight;  but this  is  not  always  so, for it  may be
sinuous or oblique or forming an  angle, and it is  not always the
same in  each  eye.   Hun  has also shown that the blindness  may
be in the upper quadrant of each retina on the  same  side, although
Von Monokow believes that several cases warrant him in affirming
that these quadrant defects are generally, if not always, due to im-
plication of the anterior quadrigeminal  or lateral geniculate bodies.
This cortical lesion causing  hemiopia  may be  the  only localizing
symptom present,  but there sometimes  coexists  word-blindness, due
to coincident lesion of the angular gyrus, and mental blindness, due
to lesion of the posterior portion of the  first and  second temporal
convolutions (page 41);  but there will usually be no other symptoms
of cortical  implication.
  When hemianopsia is due to  a  lesion  of  the centrum ovale, the
diagnosis may  be very difficult, inasmuch as the  same symptoms will
be present as when the cortex alone is affected.   The reason  for this
will be evident when we consider that the  same symptoms are  pre-
sented in case of a cortical centre or centres being implicated, as when
the nerve-strands  running from these cortical  centres through the
centrum ovale are involved ;  in other words, it is as difficult to  make 
152
NERVOUS DISEASES.
a diagnosis of a subcortical lesion in this portion of the brain as it
is in others.
  A lesion of the posterior  portion  of the  internal  capsule can be
diagnosed with more ease, because at this point with the hemianopsia
there will be  general  sensory symptoms which  are  known by the
name of "hemiangesthesia," namely, impairment of touch, pain, mus-
cular sense, taste, and sometimes temperature-sense, upon one side of
the body.   But this hemiansesthesia will  be upon the opposite side
to the hemiopia and upon the same side as  the hemianopsia, and in
some of these cases of  lesion of the internal capsule the motor fibres
lying in the anterior part of this latter structure will also be affected,
so that hemiplegia will be present.
  When there is a  lesion in the region of the corpora quadrigemina,
conjointly with the  hemianopsia will be general symptoms of implica-
tion of this region  (page 146 ), namely, a staggering gait and some
implication  of the  ocular  muscles.   It is claimed that Wernicke's
pupillary reflex is of aid in this diagnosis; i. e., in lesions behind the
pulvinar,  anterior  quadrigemina, and  lateral geniculate  body the
pupils will respond to light thrown upon the blind side of the eye,
although they act sluggishly; whilst  this reaction of the pupil will
be absent when the lesion  is at these ganglia or  in front of them.
This symptom of  differential diagnosis has  been verified by Wer-
nicke, Seguin, and  Brieger.  Haab has recently called attention to
another pupillary reflex which he designates as the pupillary cortical
reflex.   This  is tested in the following manner: A  light is placed
about forty-five degrees  sidewise from the  patient,  the  examina-
tion being made in  a dark room  and  care being taken not to throw
too much light upon  the  pupil.  The patient is then made to fix
one  eye  of the examiner and  to maintain  the  fixation steadily.
After he has  done  this a  short while he is  asked  if  he can  see the
laterally  placed flame  of the light, and  at the  moment when the
patient turns  his attention to  this flame, whilst  he  keeps  his eye
fixed upon  the examiner's eye,  a  contraction of the pupil can be
distinctly seen in the normal eye.   It  must be remembered, however,
that this examination must not  be prolonged, because it is difficult
for  a person to keep his attention fixed upon the lateral flame; but
this length of time  can sometimes be increased by having the patient
regard some peculiarity of the examiner's eye, and, whilst he is regard-
ing this intently, suddenly turn  his attention to the light, when the
examiner must watch the pupil.   This examination may also be made
by placing the flame above or  below or at different places.   Haab
regards this, with seeming reason, as  a cortical reflex of the pupil,
and  believes that it may be of value in making the diagnosis between
a cortical lesion and a lesion of the lower structures  through which
the optic fibres pass.  He does  not, however, cite any pathological
cases; nor, according to a letter recently received from him,  does he
know of any clinical material in support of his views.
  When the lesion is at the base of the brain (Figs.  18 and 36) the
optic symptoms will be usually accompanied by those due to lesion of
the structures at the base, such as the third nerve especially, or of the 
        LOCALIZATION OF BRAIN AND CORD LESIONS.     153

sense of smell from implication of the olfactory, and, when the lesion
extends backward, of the pons and the different cranial nerves which
take their origin at the sides of the posterior part of this  structure.
In such cases the  hemianopsia is usually bitemporal, as by a lesion
at the middle of the chiasm involving  the crossing-fibres from both
tracts.  In  some very rare cases  the hemianopsia is binasal, and is
due to a lesion on both sides  of the chiasm or on the outer side  of
each optic nerve.  If there is a lesion of the optic nerve in front of
the chiasm, or on  the lower or upper part of the chiasm, or of both
optic nerves, there will be  a  blindness  of half  of the field in only
one eye.  These lesions at the base of the brain usually include not
only loss of sight, but also  of color- and form-sense, whilst the pres-
ervation of light-sense, with a loss of either color-sense or form-sense,
is frequently found with lesion of  the cortex or  of the region of the
corpora quadrigemina. 
CHAPTER   II.
TESTS OF THE GENERAL MOTOR  AND  SENSORY SYMPTOMS
                   OF THE NERVOUS SYSTEM.

   The different senses which are  to  be  tested are:  sight, hearing,
smell, taste, touch, pain, muscular sense, temperature, weight.

                              SIGHT.

   The eye should be tested as to vision, color-sense, condition of the
retina, and pupillary reaction.
   In a text-book of this kind it  would be impossible, of course, to
go into all  the  methods of examination of vision which would  be
appropriate in a text-book upon the eye, and I need  only call atten-
tion very briefly to those matters which are of more especial impor-
tance in connection with neurology, such as the condition of the pupil,
the external ocular  muscles,  the  eyelids, the determination of gross
defects of sight, and the state of the retina.
   The pupil should be examined to ascertain its size when in repose,
the size relatively of the two pupils, the reaction to light, and the re-
action to accommodation.
   The following table, and most  of the text explanatory of  it, are
taken  from  Soelberg-Wells, edited by Bull, and  will be of use  in
enabling the reader to  remember  more  easily the manner in  which
the different movements of the eye are  produced:

           Movement                   Is produced by the action of the
      Upward.                 Superior rectus and inferior oblique-
      Downward.              Inferior rectus and superior oblique.
      Inward.                 Internal rectus.
      Outward.                External rectus.
      Upward and inward.       Sup. rectus, inf. rectus, and inf. oblique.
      Upward and outward.      Sup. rectus, exter. rectus, and inf. oblique.
      Downward and inward.     Inf. rectus, inter, rectus,  and sup. oblique.
      Downward and outward.    Inf. rectus,  exter. rectus, and sup. oblique.

   In other words,  the effect of the recti  muscles is to draw the eye
into the orbit; that of the oblique muscles is to draw it out.  Paral-
ysis of the external rectus is easily determined.   It  is supplied by
the sixth nerve.  The third nerve supplies the superior, inferior, and
internal rectus, the inferior oblique, the levator palpebral superioris,
the  constrictor of the pupil, and  the ciliary  muscle.   This third
nerve  divides  in the  orbit into  an upper and a  lower branch, the
former supplying the  superior rectus and  the levator  palpebral supe-
rioris, the latter  the internal  rectus, the inferior rectus, the inferior
oblique, the sphincter pupillse, and ciliary muscle, and this latter also 
         TESTS OF MOTOR AND SENSORY SYMPTOMS.      155

sends a small branch  to the superior oblique and  external  rectus.
Paralysis of the third nerve may affect all the muscles completely or
partially, or some  may be completely paralyzed, whilst the rest are
only partially affected,  or there may be au isolated paralysis  of one
muscle.   In complete  paralysis of the  third nerve the upper eyelid
droops, and when it is lifted, and an object is  moved before it  in
various directions,  the  eye  fails to follow it in the upward, inward,
and downward direction; but it can still move outward by means of
the external rectus, and somewhat downward and outward by  means
of the superior oblique, although generally secondary contraction of
the external rectus soon supervenes, and a marked divergent  squint
ensues with crossed diplopia. The pupil will be somewhat dilated and
immovable.   This branch of the sphincter pupillse may, however, be
paralyzed in advance of the paralysis of the whole nerve,  and  this I
have frequently observed in cases of intracranial lesions.  Finally,
the eye will lose its power of accommodation.   If the healthy eye is
closed and the patient be directed to walk up to an object,  he becomes
vertiginous and rolls  slightly,  from the mental illusion as  to the
position of the  object.   There  is also generally some protrusion of
the eyeball on  account of  the  paralysis of the  three recti  muscles.
Marked ptosis is also generally present, and by  relaxing the orbicu-
laris and contracting the frontalis, the upper eyelid can still be slightly
lifted.  In paralysis of the internal rectus, we will say of the left eye,
both eyes can follow an object  nearly to the middle line, but beyond
this the  left  eye will  lag behind, giving rise to a divergent  squint.
In complete paralysis of the left  internal  rectus a  rotatory, zigzag
movement inward  is observed when the left eye is moved inward, and
this is due to the action of the  superior and inferior rectus.   When
the superior rectus, say of the left eye, is paralyzed, the movements of
the eye above the horizontal line will cause the left eye to lag behind,
and this deviatiou  will increase  proportionately  to the height  of the
body which is being moved, and there will also be a divergent squint
due to the unantagonized action outward of the inferior oblique.   If
the right eye is covered, and  the patient  looks with the left eye at
an object held slightly in the upper half of the  visual field, the left
eye will  move upward and inward, according to  the amount of paral-
ysis, showing that  it  had before deviated downward aud outward,
and the covered eye will simultaneously make a  considerably greater
associated movement  upward  and  inward.  The patient will carry
his  head thrown back, so as to make as much use as possible  of the
lower half of the  visual field, and in endeavoring  to hit an object
will  strike too  high.   In paralysis of the inferior rectus the  symp-
toms are just the opposite of those of paralysis  of the superior  rectus.
Paralysis of the inferior oblique is very rare, and the symptoms are
the  opposite of those that obtain in paralysis of the superior oblique.
Paralysis of the superior oblique requires some care  to detect, and is
often overlooked.   Let us suppose that the left superior oblique has
been paralyzed.  The patient would see objects  in the lower half of
the  field  double and  irregular in outline, but above the horizontal
median line there  would be no diplopia.   If a body is  held in the 
156
NER VO US DISEASES.
horizontal  median  line, or a  little below it, there would be a slight
deviation of the left eye upwardly  and inwardly,  becoming more
marked the more the object is moved into the lower half of the field,
especially to the right.   The left eye also moves distinctly downward
and outward when the right eye is closed, but it must be remembered
that  this can  only be perceived with a little care.  In some cases a
still  more  careful test should be made in paralysis of the superior
oblique in order to determine the differences in the double images, but
this is a matter for which reference must be made to the special text-
books.   A secoudary contraction of the inferior oblique often super-
venes after paralysis of the  superior oblique has existed  for some
time.
  Nystagmus is a spasmodic affection of the muscles of the eye, and
consists  in  an oscillation of  the eyeballs,  generally horizontal but
occasionally rotatory, and in some rare instances vertical.  Spasm of
the orbicularis palpebrarum, or blepharospasm, varies from a moderate
temporary twitching to a firm pressure of the eyelids together, so that
it may be impossible for the  patient or the physician to open them
even to a slight degree, and if this attempt is  forcibly made, it may
be very painful and  cause convulsion.
  Conjugate deviations of the eyes consist of simultaneous movement
of both eyes to one side.
  Strabismus  is  that condition of the eye in which the patient is
unable  to bring  both  visual  lines to bear simultaneously upon one
point.   The inward  strabismus is called  convergent strabismus; the
outward, divergent; the upward, sursumvergens; the downward,
deorsumvergens.   Convergent and divergent strabismus are usually
due to errors of refraction, the former to hypermetropia, the latter to
myopia, and therefore they are of little interest to neurologists.
  That condition of asthenopia of the  ocular  muscles which is also
known  as insufficiency  of the  recti muscles has played a great role
during  the  last few years in this country as the supposed cause of
almost every affection of the  nervous system  from neuralgia up to
general paresis, and  it therefore deserves  some  little attention.  It
is a  very common  affection,  and  distresses the patient by  causing
the eyes to feel  warm, uncomfortable, and strained in working or
reading, so that  the  print becomes obscure, the letters run together,
and  there  is often  some pain through  the temple,  or  forehead, or
vertex, or au aggravation of existing neuralgic trouble of the trigemi-
nus, and most especially of a tendency to migraine (vide Chapter IX.,
" Migraine").  In this condition vision and accommodation are good,
and there is a  normal appearance of the eyes.  Direct the patient to
look steadily with both eyes at an object; gradually bring this nearer
to the eye, and when the object comes within about six inches of the
patient, one eye becomes unsteady and wavering in its fixation, and
then deviates in  the direction of the weaker muscle, either gradually
and  slowly, or  suddenly  and  spasmodically.    When one eye  is
covered with  the hand  the  same  deviation occurs.  If a prism is
held with its  base  upward  or downward  so as to produce diplopia,
this deviation, when dependent on a weak externus or internus, will 
TESTS OF MOTOR AND SENSORY SYMPTOMS.       157
also be shown.   It must be remembered, however, that the external
rectus is  able  to overcome a prism ten, fourteen, or eighteen degrees
for  distance.   In some  cases of  very latent insufficiency  the eyes
should be tested in a room which  is moderately darkened ; a lighted
candle- should be placed about twenty feet from the  patient; this
the  patient fixes, then a red glass is put over one eye,  then over the
other  eye a prism of five degrees, base upward.  Two flames will
then be  seen.  If the  red glass  is placed  over the  right eye and
stands directly over the white of the eye, there may be an equilibrium
of ocular movement; but  if the  red light go to the left, there will
be insufficient adduction, and if it  go to the right, insufficient abduc-
tion.  If the lights, however, stand vertically, the candle should be
moved several  feet to  the right or to the left, or the patient should
be made to turn his head far to  the right and then to the left, still
regarding the  flame;  and  in these lateral positions  lack of perpen-
dicularity will detect  the faulty muscle.   If the abductive power is
more  than eight  degrees,  insufficient adduction may  be  suspected,
and this should  be tested for by prisms with the base  outward,
increasing the strength of these prisms until the patient is  no longer
able to fuse the images.   But as these tests should not be undertaken
without  proper correction of any error of refraction,  the thorough
method cannot be described in a book of this  kind,  and reference
must be had to treatises upon the  eye.
Fig. 94.
Fig. 95.
Atrophy of the disk from spinal disease.
       (From Nettleship.)
Atrophy of the optic disk after papillitis.
       (From Nettleship.)
  An ophthalmoscopic examination of the eye is of great importance
in many cases of nervous diseases, whether of  the  cord, brain, or
peripheral nerves.  This is a matter which belongs  to the specialty
of eye diseases more particularly, and for an  explanation of the
method of using the ophthalmoscope reference must be had to treatises
upon the eye.  Every neurologist should be fairly expert iu the use of
this instrument, sufficiently so,  at  least, to be able to distinguish the
types of retinal lesion, such as ordinary retinitis, albuminuric retinitis,
choked disk, and  atrophy of the optic nerve.  Although there is not
sufficient space at my disposal to go into the minutiae of these types,
I have yet thought  it would be of great practical value to insert the 
158
NERVOUS DISEASES.
accompanying illustrations.  Fig. 94 represents an atrophy of the disk
from spinal disease.  Fig. 95 illustrates an atrophy of the disk after
papillitis, the upper and lower margins being still hazy, the veins still
Albuminuric retinitis due to fatty degeneration.  (From Ayee.)

                    Fig. 97.
Apoplectic retinitis of renal disease. (From Ayre.1 
         TESTS OF MOTOR AND SENSORY SYMPTOMS.      159

tortuous, but the arteries nearly normal, aud there is disturbance of
choroidal pigment at the inner and outer border; although the disk is
not represented quite white enough. Fig. 96 portrays an albuminuric
retinitis due to a fatty degeneration of the fibrous tissue of the retina,
especially localized in  the  radiating fibres of the retina around  the
origin of the yellow spot, whilst in Fig. 97 is seen an apoplectic form
of neuro-retinitis sometimes seen with renal  disease.
   Testing for hemianopsia is readily done, but the distinction between
hemiopia and  hemianopsia should not  be  forgotten.  A rough test
is for the  physician  to hold  up his forefinger before one  eye of
the patient, the other eye being closed by the patient's fingers gently
pressed  upon  the  lids.    A white object,  such  as a handkerchief
or a piece of  chalk,  is  now  brought  from  the  side  toward  the
examiner's finger, and the patient is  asked  if he can see this object
whilst he is looking straight at the  finger.  If he can, this  lateral
field of vision  is good.   In this manner the  upper, lower, lateral,
and median fields of vision can be tested.   For cases that are to be
recorded, so-called  perimeters are useful iu  exactly marking  off the
defects of the field of  vision, and charts for  recording these measure-
ments are sold at all the instrument-stores.


                           HEARING.

   The hearing should be  tested in order to determine the capacity
 for hearing, as well as for that symptom which is known  as  mental
 deafness or inability to understand the  meaning of what is heard.
   The tests for  simple  hearing are ordinary conversation, the tick
 of a watch, and the  tuning-fork.  Really  the best  test is  that  by
 means of conversation ; but as this is apt to consume too much time
 in the hurry of office-work, the next best  means would be by some
 such test-sentences as  those suggested by Buck, two of which are  :

                Pour oil on the waters of Lake Erie ;
                All hail!  thou  hero of fourteen wars.

   Each of these sentences contains  eight  long vowel sounds and is
 equally free from  non-resonant consonant or  short  vowel sounds.
 The next best test is  by means of a watch, although  experience has
 taught me again and again that this must be corrected by the test of
 sentences.  The watch should  be placed at a distance where its ticking
 cannot  be heard by  the  patient, and then gradually approached to
 where  the ticks can be so heard, and the latter may be regarded as  the
 farthest point  of distinct hearing.   The objection to first placing  the
 watch  close to the  ear and then removing it to a distance is that when
a sound is once perceived, it is easy for the patient to imagine that he
 hears it beyond where he really does perceive its sound.  The ear that
 is not undergoing  examination  should  be  closed, of course.  There
 is no hard-and-fast rule as to exactly the distance  at which a watch
can  be heard  by a normal ear, because watches vary greatly in  the
loudness of their sound, most of them being heard best immediately 
160
NERVOUS DISEASES.
after being wound, and also when held so that the physician's hand
covers the back, or when held by the  patient.  But four feet from
the ear may be taken as the proximate normal distance, although, as
I  must  reiterate, there  are many exceptions to this rule.   Some
measuring-instrument, as a  tape-or a  yard-measure, should be em-
ployed in order to determine the distance from the ear to the watch.
   The  tuning-fork is generally  employed  in  order to determine
whether there is disease of  the middle  or internal ear, and also  for
testing hearing, but it has not been popular with aural surgeons.  If
we close our ears and speak, the sound seems  to be confined  to the
cranial cavity, so to say, and its reflection is to a certain extent pre-
vented by the occlusion of the external auditory canal.   If the audi-
tory nerve be normal, and if there be cerumen in one auditory canal,
or a thickening of the  mucous  membrane of the tympanic cavity,
there will be a condition similar to closure of  the external meatus of
a  healthy ear by the finger, and the  vibration  of the tuning-fork
placed upon the bones of the head will be  heard most distinctly by
the affected ear, although a conclusion cannot  be reached in this way
if both ears are equally implicated.  If there  is disease of the audi-
tory nerve, either from a direct lesion  of it,  or  from disease which
has extended from the middle ear to the internal ear, no such marked
difference will  be noticed when  the  external  meatus is closed.   If
there is no serious lesion of the auditory nerve, although the tick of
the watch may not be heard, the vibrations of the tuning-fork placed
upon the teeth, forehead, or mastoid process  will be distinctly per-
ceived.   If there is serious lesion of the auditory  nerve, causing
absolute deafness, these vibrations will not be perceptible in the head.
Some persons who are not trained to observation will maintain that
they hear the tuning-fork better  from the better ear, because they
believe that they ought to do so, but it  is much more reliable to take
the statement of a patient as to whether the tuning-fork is heard more
distinctly and longer when  its vibrations are conducted through the
ear or through the bones of the head  than it is to rely upon his state-
ment as to which side he hears it better on.  The large tuning-forks
of the note C should always be employed.  If hearing is impaired,
and  the conduction of the vibrations  of the tuning-fork is  better
through air than through bone, there is disease of the auditory nerve,
and this may be either primary, or secondary  to disease of the mid-
dle ear.    If the conduction  of the  vibration of the tuning-fork
through bone is increased, and lasts longer than aerial conduction,
there is disease  of the middle or external ear.  In order to test the
conduction of the ear and the bone-conduction relatively, the tuning-
fork should be  struck on the knee of the examiner, and then held in
front of the meatus to test the vibrations through the air, then again
set in vibration and its handle  placed  on  the mastoid process near
the centre to  test the bone-conduction.   The explanation of the fact
that the tuning-fork is  heard best through the bone when there is
disease of the middle ear is because the  increase of diseased tissue
increases  the capacity of resonance of the parts, and when there is
disease  of the  auditory nerve the vibrations  pass through the ex- 
         TESTS OF MOTOR AND SENSORY SYMPTOMS.       161

ternal auditory canal, the tympanic cavity, and the fenestra ovalis,
which constitute the best channels of conduction.
  In dealing with the symptoms of Meniere's disease (vide Chap.
XV.,  "'Meniere's Disease") the  neurologist has  often  to make a
diagnosis between disease of the middle  ear and  disease of the laby-
rinth.  This can be done mainly by attention to the following facts :
  Air-conduction  is best through  a normal ear, so that such conduc-
tion is heard  three or four times  better than  bone-conduction.   In
disease of the middle ear, however, bone-conduction  is greater  than
normal, and air-conduction is  less, so that the relations of air-con-
duction to bone-conduction are precisely the opposite to what is the
case with the normal ear.   When there  is disease of  the internal ear
the bone-conduction is weakened, and the air-conduction is also weak-
ened, but it frequently happens  that the  relation between  the bone-
conduction and  the air-conduction is greatly in favor of the latter;
i.  e., air-conduction is better than bone-conduction,  although  both
are weakened.   In mixed cases in which  disease of  the  middle ear
and disease of the labyrinth are combined  there are:  l,the  disturbed
relation between air-  and  bone-conduction which is usually found
in middle-ear disease; and 2, the bone-conduction  is weaker  than
normal.
   Pomeroy subtly calls  attention to the fact that  when the normal
ear is stopped with the finger, and the bone-conduction is therefore at
its maximum for  such a normal  ear, an incautious examiner might
compare  it with the bone-conduction of an ear suspected of dimin-
ished  bone-conduction, but which had not been closed by the finger.
Pomeroy also states that while the rule  is that a normal ear stopped
with the  finger will have its bone-conduction at a maximum, yet iu
some diseases of the middle ear,  with the  meatus stopped,  the bone-
conduction is somewhat better than normal, although these are some-
what exceptional cases.
   The symptom  of word-deafness is that in which, as  has  been
explained, the  patient hears distinctly what is said, but fails to
understand the  meaning of it, and it is due to a lesion of the pos-
terior portions of the  first and second temporal convolutions, or to
the conducting-strands leading from them down to the periphery.

                            SMELL.

   In testing smell, distinction should be made between the impres-
sion made upon the fibres of the trigeminus that supply the nostrils
aud that made upon the  olfactory fibres.   The former can be tested
by pungent odors, such  as ammonia, alcohol, etc., whilst the latter
should only be  tried  by the pure odors, of which the best  are the
odor of violet, oil of cloves, and musk.   One nostril should  be gently
closed by the physician's hand by pressure inward until the septum
is  gently felt, and then the other should be tested by means of the
odorous substance, the nature of which  should not be made  known
beforehand to the patient.  The difficulty in this test is, that the
olfactory nerves iu the human being soon weary, so that a test cannot
                                   11 
162
NERVOUS DISEASES.
 be repeated  more than a few times.  A careful examination of the
 anterior and posterior  nares  should  always be made in order to see
 that any loss of smell is not due to some lesion of the mucous mem-
 brane or the bones.

                              TASTE.

   In  testing the sense of taste it should be remembered that the
 gustatory filaments of the tongue come from two different nerves, the
 anterior half being supplied by the lingual  nerve issuing from the
 chorda tympani, whilst the posterior half is supplied by the  glosso-
 pharyngeal nerve.  The test should be made  by  means of a bitter,
 such as quinine; by a sweet,  such  as sugar;  by a  sour, such as vine-
 gar; and by a salt such as  common salt, and it is  best to test  succes-
 sively with sugar, then salt, then vinegar, and last of all the quinine,
 as the bitterness of the quinine will blunt the subsequent gustatory
 impressions if  it be used first.  The patient  should be  made to  pro-
 trude  the  tongue, when first  one posterior half and  then  the other
 should be  tested, and after this the anterior half, the patient having
 been instructed beforehand  not to draw in the tongue and allow  it to
 come in  contact with the roof of the mouth,  but to indicate whether
 he tastes the substance by shaking  the head for a negative and point-
 ing the finger for an affirmative.   In this way the sense of taste can
 usually be localized in an intelligent person.   The electrical exami-
 nation of the sense of taste is of very little value, because the sharp
 and acrid taste of the electric current is not so fine a  test as the dif-
 ferent  substances that have been mentioned.

   There has been great discussion  among physiologists as to whether
 the senses of touch, pain,  temperature, muscular sense, and weight
 are really distinct, or whether  they  are not variations of feeling in the
 same nerves.   However this  may  be, it is certain  that  clinically we
 constantly find one or more of these senses disturbed when others are
 intact, and it has even been claimed in late years that the loss  of the
 temperature-sense especially is a diagnostic mark of syringo-myelitis.
 I have no hesitation, therefore, in discussing them  separately from
 the clinical point of view.

                        TOUCH, OR TACT.

  The best method of testing  the sense of touch or tact is to see if the
patient can distinguish  between different  substances lightly brought
in contact with the skin, such as a  piece of cotton or a silk handker-
chief and the touch of the physician's finger.   In order  to do this in
the fingers, for example, the  patient's eyes should be closed and some-
thing held in front of them, when the finger-tips should be lightly
touched,  first with the  cotton or handkerchief, then with the  physi-
cian's  own finger-tips, and  the patient should tell which  is which.
This test, simple as it  may seem,  yet requires a certain amount of
care.   If a test is first  made  with  the cotton, for instance, and then 
TESTS OF MOTOR AND SENSORY SYMPTOMS.      163
with the finger, and this rotation is regularly kept up, first cotton and
then finger, the  patient may become  accustomed to it and  anticipate
rather than feel.  The best way is first to take the patient's  hand, and
then, not touching it at all with the  cotton or the  handkerchief, ask
him what he feels.   If he says  that he feels either the handkerchief
or the cotton, he should be at once  informed that he has not  been
touched at  all, so that in this way he will be  made  more  alert, and
the examination should not actually be made until the patient is really
seen to be informing the physician of what he  feels rather  than of
what he imagines.   The cotton  or the finger should then be brought
very lightly in contact with the finger so as to test the degree  of sen-
sation, whether there is impairment of it or whether there is increase
of it.  The examiner should be familiar with the degree  of sensitive-
ness of different parts of the skin, and this can only be  acquired  by
a certain experience. Slight differences cannot be  determined except
after repeated examinations, because the sensitiveness of  touch varies
very greatly from one  individual  to another, and also  in the  same
person according to varying corporeal conditions.   But  no test of
the sensation of touch can be properly made if the skin is cold, and
in all examinations of the feet or hands they should be carefully felt,
and if cold, they should  be gently warmed before the test is made.
It is a familiar fact  that typesetters will make many mistakes in set-
ting type if the temperature of the room goes below a certain point,
and this is also true of typewriting.   The  instrument known as the
sethesiometer, invented by Sieveking, is, as the following figure shows,

                              Fig.
            +Tm+mr+1|......ilinilimli.............I mil 3^'- j^ffi ||lllll||||l|l||| ll
                          yEsthesiometer.

a movable slide upon a horizontal bar measured off into inches, or
metres and millimetres.   By means of this the distance to which the
two points need to be separated in order to be felt as two points can
be determined, and this distance has been found to vary in the differ-
ent areas of the skin, as is shown  in the following table of Weber:
  Tip of the tongue,  1 millimetre.
  Finger-tips,  2 millimetres.
  Lips, 3 millimetres.
  Dorsal surface  of the first  and second phalanges and the median
surface of the fingers, 6 millimetres.
  Tip of the nose, 7 millimetres.
  Thenar and hypothenar areas, 8 millimetres.
  Chin,  9 millimetres.
  Tip of the great toe, the cheeks, the eyelids, 12 millimetres.
  The glabella, 13 millimetres.
  Heel, 22 millimetres.
  Back of hands, 30 millimetres. 
164
NERVOUS DISEASES.
  The neck, 35 millimetres.
  Forearm, leg, and back of the feet, 40 millimetres.
  Back of the trunk, 60 to 80 millimetres.
  The upper arm and thigh, 80 millimetres.
  The difficulty about the sesthesiometer is practically that unintelli-
gent people, such as the mass of those who come to our  clinics aud
hospitals, are very apt to become confused, as a little experience will
demonstrate, and the differences are very great from one examination
to another.  This is not surprising when we reflect that  this instru-
ment appeals to a peculiar form of tactile sensation which is unfam-
iliar to the  ordinary human being; and for this  reason, at the first
examination I prefer the test for the tactile sense spoken of above,
employing the sesthesiometer only in order to determine with approxi-
mate accuracy the variations which may occur in the course of treat-
ment.   This table  of Weber's, however, must be taken with due
allowance, as  these distances  vary very greatly from individual to
individual and  in a given  individual on different days, because of
the  varying bodily conditions and because of the unfamiliarity of the
instrument. Variations, therefore, should not be  regarded as abnor-
mal unless they are decided ; thus, if the instrument had to be sepa-
rated four millimetres in order to be felt  at the finger-tips, this would
be  abnormal,  or if on the  thigh  they were felt  at forty instead of
eighty, this would be abnormal, but  a variation  of one-half or one
millimetre in the finger-tips or of one to  two millimetres in the thigh
should not be  hastily interpreted.  In testing for medico-legal pur-
poses,  or where there is  any  suspicion of malingering, it may be
necessary to resort to indirect tests of the tactile sense.  Thus, if a
person claims  that he has  lost the sense of touch and cannot feel the
difference between  silk or cotton  and the finger, or  that he cannot
feel the  points  of the sesthesiometer widely separated beyond what
should be the  normal point, the subject  may be quietly changed and
an  opportunity sought for  during the examination to touch lightly
with the finger the part that is claimed to  be anaesthetic, when the
patient's attention is attracted to something else ; and then some evi-
dence of the touch  having been felt may be obtained.  In this way
I have often detected malingering; in one case  lightly touching the
patient's neck  when her back was toward me, whereupon she turned
her head sharply around, and in another case by lightly tapping the
man's  hand with mine as his head was directed away from me, when
the  immediate quick turn of the head and the inquiring look made
it evident that the touch had been accurately felt.  A quick-minded
and alert examiner can almost invariably throw a malingerer off his
guard  by this  method.

                              PAIN.

  The best test of the sense of pain  is by the hidden needle, or
aigue  cache. ^ This is a needle within a  hollow  cylinder, and to the
upper  end of it is attached a spring, which in its turn  is attached to a
spiral thread running up and down through a slot by the working of 
         TESTS OF MOTOR AND SENSORY SYMPTOMS.       165

a little circular cap.   The extent to which the needle can be made to
protrude can be determined beforehand.  This  instrument is placed
upon the patient's skin, very few people knowing what it is, and the
needle is  pressed quickly down and  inserted into the skin, so  that
it is a beautiful test—as perfect as can be devised—of the pure sense
of pain, without any anticipation upon  the  patient's part.  Unfor-
tunately, however, it will sometimes  happen iu this day of damage
suits against  corporations that individuals  are acquainted with the
instrument, and it requires very little fortitude  to stand the prick of
this pin without any manifestation of pain, which is not surprising
wheu we reflect how readily patients become accustomed to  the inser-
tion of hypodermic needles for inches  under the skin, whilst most
schoolboys  are familiar with the schoolboy trick of  doubling up the
leg under the thigh,  then drawing  the skin  over  the  knee tense,
and suddenly jabbing in  a pin  without expressing any  feeling of
pain.   In any  doubtful case  it is well, therefore, to make use of
some other test than the hidden  needle,  and  this can always be
done by means of an  electric  battery.   The battery should be well
tested beforehand, in order to ascertain that a powerful current can
be turned ou at will.   Small electrodes of copper (Figs.  72 to 76)
should be used, and should be  separated only a few inches.  A gentle
current should  be first used, and if the patient claims that any  pain
is felt, a feint should be made for a minute or two of testing  with
this gentle  current, and  then,  after the examiner has apparently sat-
isfied  himself that no pain is felt and the  patient is thrown off his
guard,  a  powerful current should be  suddenly turned on.  This,
however,  will not be conclusive, because the patient  may really  have
an impairment of the sense of pain and yet not  an absolute loss of it,
so that a lighter current might  really not be  felt, whilst the  most
powerful  current would be.   However, this primary procedure has
the advantage in many cases  of causing the patient to break down
at once and admit  that  he has been shamming.  If he does not do
this, the  examination should be  resumed, aud starting  with the
 moderate current, it should be  gradually increased until it is deter-
 mined relatively what current  is really felt.  By the time this second
examination is in process a shamming patient has usually  become so
demoralized that any further shamming will be easily recognized,
whilst  a  partial ansesthesia iu a truthful person will  be determined
 with equal readiness.  Marked degrees of ansesthesia, however, can
often be determined by the needle, because it often happens that such
anaesthesia  is accompanied by an ischsemia of the  anaesthetic  part,
which is demonstrated by the sluggish flow of blood  following a deep
needle-prick,  and this blood  is usually venous in character.   More-
over, the  needle-prick can be made to serve  a good purpose by being
 used upon the anaesthetic part when the patient's attention is attracted
to other matters.
                      MUSCULAR SENSE.

   The muscular sense should  be tested  by bending a joint or a limb
with the patient's eyes blindfolded, and then  having the patient tell 
166
NERVOUS DISEASES.
what  movement is made.  In the slighter degrees of impairment of
the muscular sense the small joints can be moved without the patient
knowing it, whilst the larger joints cannot, and it is a high degree
of ansesthesia that permits of the larger joints or a whole limb being
moved without  the patient being  aware of it.   If anyone has a
doubt of the difference  between the muscular and  tactile sense, they
have only to have an  experience, as I  have daily in my clinics and
lectures, of absolute impairment of  tactile sense and preservation of
muscular sense, and vice versa.
Fig. 99
                     TEMPERATURE-SENSE.

  The simplest test of the temperature-sense for clinical  purposes is
to take three tumblers or test-tubes of water, one cold, one luke-
             warm, and  one hot, and have the patient tell which is
             which with  blindfolded eyes.  Care should be taken,
             however, that the eyes are blindfolded before the water
             is brought into the patient's  presence, otherwise quick-
             minded individuals will see the slight steam from the
             water or notice the greater transparency of perfectly
             cold water.   A more  accurate  test can  be  made by a
             series of test-tubes  with water at different degrees of
             temperature as tested by an ordinary axillary thermom-
             eter.   In the  Salpetriere,  in  Paris, the  instrument
             shown in Fig. 99  is  used.   It is difficult  to  test the
             temperature-sense in malingerers, but I have sometimes
             succeeded  in exposing  individuals who  claimed that
             they could not feel differences of temperature  by sud-
             denly spilling some  hot water upon the hand when
             their  attention was directed to other subjects.

                                  WEIGHT.
Blocq's thermo-
Eesthesiometer.
  The sense of weight has not been shown to be clinic-
ally of much importance, and we know very little about
the significance of variations in it.   It can be tested by
superposition of varying weights.  The hand should be
well  supported by being  laid gently upon a table, and
the weights should be superimposed at regular intervals
as measured by the second-hand of a watch.
                   THE  TENDON-REFLEXES.

  The  tendon-reflex consists of  the muscular  jerk which results
from  mechanical irritation of the tendon  of the muscle, and it is
something  entirely  distinct from the muscle-reflex, which  is due, as
the name indicates,  to mechanical irritation  of the muscle itself.  All
muscles have their tendon-reflexes, of course, so that in order to speak
of them fully we should  catalogue every muscle in the body.   As a
matter of fact, however, there are only a few muscles which are of 
         TESTS OF MOTOR AND SENSORY SYMPTOMS.       167

sufficient  size and  anatomically so situated as to enable us to play
upon  their tendons  and obtain a jerk of the  muscle in  health,
although  in  many diseased  muscles  we can  obtain  reflexes  which
are impossible in the normal condition.   The tendon-reflexes which
are of clinical importance are the patellar tendon-reflex or knee jerk,
the triceps tendon-reflex or elbow-jerk, the jaw-jerk or tendon-reflex
of the masseter muscles, and the tendon-reflex of the  leg-muscles, or
the  so-called ankle-clonus.   The most  important of  these  is  the
patellar tendon-reflex—the knee-jerk, or the tendon-reflex par excel-
lence.  This  can be evoked  in  several ways.  The  patient can be
made to cross one knee over the other, and whilst it is thus  hanging
percussion can  be made upou the tendon of the quadriceps extensor,
as it is stretched  over the flat surface of the tibia.  The best  means
of percussion, I think, is that which I am accustomed to use in my
clinics.  The middle finger of the right hand is extended, the  index-
finger placed back of it so as to support the distal phalanx, and the
thumb is put in front of it in  a corresponding situation.   By  this
means a strong and delicate percussion-hammer of Nature's making
is ready at hand, with which one can tap strongly  or tap lightly,
so as to bring out a feeble tendon-reflex or show the great irritability
of a very much exaggerated one. A percussion-hammer may also be
made use of, or the tendon may  be tapped with the side of the hand,
but none  of these methods  is equal to  that just described in pre-
cision and facility  of range from  a  light to a heavy blow.   This
knee-jerk when  feeble can often be made more forcible by what is
called the method of  u reinforcement."   Jendrassik does this  by
having the patient lock the fingers  of  each hand  and pull them
forcibly apart; and Mitchell and Lewis have shown that the same
effect  can be obtained  not  only by  powerful muscular  acts,  but
even by winking, speaking, coughing, laughing,  pulling  the hair,
touching  the skin with iron or something hot, pinching, or electrical
excitation upou any part of the  body.  The jerk forward of the  foot
should be carefully observed for two kinds of phenomena :  first, the
amount of muscular  movement; and, second, the spastic element
evident in  the  muscles.  Thus,  a simple increased jerk  may be
obtained, or a spastic jerk, or a combination of the  two.  Clinical
observers have not, in my opinion, by any means laid  the stress upon
these two kinds of phenomena  that they deserve.  It may often be
extremely difficult  to determine what is a normal knee-jerk forward
of the foot, because  the range of the  normal is so great;  but a
spastic element, a quick jerky twitch  forward, is always abnormal,
even when the  muscular range of the  movement is  small.   The
tendon-reflex varies  very  greatly in health.  Thus, among  200
healthy  medical students whom  I examined, in 5 I found  the
tendon-reflex absent, in 180 of  an approximately normal range, and
in 15 apparently exaggerated, but  in  none of these did I find  any
spasmodic element.
  The jaw-jerk  is tested in the following manner:  The patient is
made to open the jaw, and then  the masseter muscles are tapped with 
168
NERVOUS DISEASES.
a percussion-hammer or the  finger held in the way just described.
This tendon-reflex is seen only in disease.
   The  foot- or ankle-clonus  (also formerly called spinal epilepsy by
Brown-Sequard) is evoked in one of two ways: 1, the patient is
made to extend his leg and  thigh, when the physician  should grasp
the back part of the calf with the  left hand and the anterior portion
of the sole of the foot with the right hand.   The patient should then
be  instructed to remove his  voluntary control  from the muscles of
the foot, and whether this has been done should  be determined by
gently flexing  the  foot upon  the leg, as the same difficulty is often
met with in uneducated  people  in this  regard that will be spoken
of in describing the test  for slight contracture.   When it is cer-
tain that the patient has " let go "  of his foot,  the  latter should  be
quickly and forcibly  flexed  upon  the  leg,  when any  exaggerated
tendon-reflex will be made evident to the examiner's hand by a series
of throb-like extensions of the foot, which will pass into a continuous
coarse tremor  if  flexion  of  the foot  is  firmly maintained;  2, the
patient should be seated upon a stool and then instructed suddenly
to tap the toes of one foot firmly upon  the floor, keeping  the heel
well elevated, when an exaggerated tendon-reflex  may  be shown by
a series of rhythmical contractions  of the  muscles of the legs, con-
stituting a coarse tremor also   In  some  cases  the ankle-clonus can
be evoked  by only one of these methods, but in others both  methods
will  produce it, and I have  frequently been able to call it  forth by
one method one day and  then failed to obtain it the next day in the
same patient except by the other method, and perhaps upon a further
day failed  to evoke it in this  individual by either method.
   It  is  still a matter of doubt as to whether the knee-jerk is a direct
muscular process or a spinal  reflex  act.   It has been observed that
the duration of the reaction-period is shorter  than that of spinal
reflexes.  Nevertheless, section of either the sensory or  motor spinal
nerve-roots abolishes the knee-jerk, so that it is apparently dependent
in some way upon  the spinal  cord.   This I have verified in  my own
experiments, and  I have also found that such a slight inhibition as
lifting the crural  nerve  lightly upon a  string abolishes the knee-
jerk of a rabbit, and that this knee-jerk immediately reappears when
the  string is withdrawn.  Another theory  has been that  nervous
excitations  continuously  transmitted  from the spinal  cord to  the
muscles  maintain the so-called muscular tonus, but Lombard could
find  no proof that muscular tonus was continuous, or  that the irri-
tability of a muscle to a  mechanical stimulus was dependent on its
tension.  H. C. Wood, refining the matter still further, has suggested
that  the irritability of the nerve in the  sarcolemma of the muscle
might be dependent on the  spinal cord, and that the knee-jerk was
dependent  upon  the irritability of these nerves, so that it might not
be a  reflex act,  and yet not be dependent upon muscular tonus.
But,  as Bowditch  pointed  out, the irritability  of the  nerve is  not
lessened  for  some  time after  section, although  the  knee-jerk is lost
immediately.  As to how the " reinforcement" method  increases the
knee-jerk we are equally in the dark.   There are two theories upon 
TESTS OF MOTOR AND SENSORY SYMPTOMS.
169
the subject : one is that the inhibitory action of the cerebrum is cut
off from the parts below through the nervous  energy being diverted
to other  paths by the voluntary act of reinforcement of such mus-
cular efforts as coughing, singing, etc.; and the other theory is that
an excess of energy is expended in these acts of reinforcement which
exalts  the  excitability of other  centres.  Neither  theory, however,
has  been proved or  disproved.    The  knee-jerk varies in  healthy
individuals  to a considerable extent under the influence of  fatigue,
sleep, changes in the weather, emotions, different sensory impressions,
or mental effort, and,  as we shall  have occasion to see in the various
chapters of this book, alters  greatly from time to time in  cases of
disease.
   Gowers believes  that the  essential condition to  all these tendon-
reflexes is that of passive tension of the  muscle, not necessarily of
the tendon, and he,  therefore, suggests for them the  name of myotatic
contractions (from totikoc, extended).

                   CUTANEOUS REFLEXES.

   The chief cutaneous reflexes are  the  cremaster, the plantar, the
mammary,  and the abdominal.
   The cremaster reflex can be tested by having the  patient stand up,
so that the  testicles and the penis hang, and then scratching gently
with the nail or with a blunt instrument along the  inner side of the
thigh, when the testicle will be seen to be drawn up.  This reflex can
generally be evoked within an area  covering  the  inner side of the
thigh, about to the middle line in front and about to the edge of the
curve of the  thigh  inwardly; but when it is exaggerated  it can  be
elicited by excitation of farther-lying portions of the thigh, even the
back of it, or by irritation  of the abdominal cutaneous surface.   It
has not yet been proven to  be a sign  of much diagnostic importance,
but I have  seen it notably exaggerated in many cases of reflex spastic
symptoms, pain  from  stricture, disease  of the  seminal vesicles, and
occasionally from disease of the prostate gland.
   The plantar reflex is the reflex contraction provoked by tickling the
sole of the foot, the muscles of the leg, or even of the thigh.   In some
cases mere  tickling will not call forth this reflex, but it will  have to
be elicited by pricking with a  needle, or by the faradic brush,  or by a
sponge dipped in hot water, or even by putting the limb into hot water.
  The mammary reflex is obtained by tickling  the  breast, when the
nipples are erected by the contraction of the muscular fibres.
  The abdominal  reflex is  the contraction of the muscles of the
abdominal wall when the skin over the  abdomen is irritated by the
finger-nail, or by a  blunt object, or with  something  cold  or some-
thing hot.   The upper part of this reflex is known as the  epigastric
reflex.
                        CONTRACTURE.

  Contracture is a  condition of the  muscles which differs radically
from contraction.   In  the  latter the  muscle is locked, as by fixation 
170
NERVOUS DISEASES.
of a joint or by callus.   In the former the muscle is contracted, but
the contracture is not fixed, and can be overcome  by gently pressing
upon the muscle, the  contracting muscle giving  to the examiner's
hand the sensation  as  of wax gradually yielding.   This  condition
generally, almost invariably, affects the flexor muscles, and varies in
degree from the slight contraction that can only be evoked by careful
examination  to the pronounced degree in which  the muscles are
drawn into positions of great deformity, as  in Figs. 100 and 101.
When the condition is very marked there  is no difficulty whatever
in detecting it, but slight degrees of it  require some care to elicit,
and I have  for  years  been in the habit of employing the following
methods in my clinics : We will suppose that the muscles which we
are examining are those of the lower extremity.   The patient is
instructed  to extend the leg and then to give it up passively to the
examiner.   Many uneducated people find it very hard to remove ab-
Fig. 100.                            Fig. 101.
  Contracture of the hand in a case of hemi-    Contracture of the hand in a case of hemi-
 plegia from hemorrhage into the internal   plegia from hemorrhage into the internal
 capsule.  Dorsal view.                   capsule.  Palmar view.

solutely their voluntary control of a set of muscles, and therefore the
leg  must be bent at the knee several times in order to determine that
the patient  has allowed it to extend and flex with perfect flaccidity.
When  this  has been satisfactorily determined, the leg is gently ex-
tended upon the thigh, one of the examiner's hands  grasps it above
the ankle, whilst the other hand of the examiner is placed upon the
thigh, and then a sudden movement of flexion of the leg  should be
made.   If there is any slight  contracture of the muscles,  the exam-
iner's hand will become aware of a sudden  movement of resistance in
the leg, like a muscular " click," aud the hand  is thrown  back to a
varying degree, usually sufficient, even in the  slightest  cases, to  be
perceptible  to  the  eyes of the  class.  A very little  experience will
enable a person to make a quick distinction between this involuntary
muscular resistance or click of the leg whose muscles are contractured
and the resistance which may  be  made voluntarily by the patient,
and I never  have any difficulty in teaching my class  to make this 
         TESTS OF MOTOR AND SENSORY SYMPTOMS.      171

distinction in one lecture.  I believe that  this method of mine is of
very great value in determining slight degrees of contracture, and
in several cases I  have been  able by it  to  solve the  question  as
to whether there was any malingering.   When the  contracture is
marked, this seusation of muscular resistance or click is very distinct,
and the examiner's hand  will be  thrown back several  inches as he
attempts to  flex the leg.   The  great mistake made by  most of my
students is that the movement of flexion  is not quick enough, as a
slow movement of  flexion  will  not evoke  this muscular click.  The
phenomenon is evidently dependent upon  the  increased  muscular or
tendinous  excitability—I  am  not certain which it  is,  although I
believe that it is the latter, as iu all of these cases the tendon-reflexes
are exaggerated, while the  muscular excitability is not always above
normal.  Indeed, it may be laid down as a rule that tendon-reflexes,
muscular contracture,  and  hasty micturition are symptoms that  go
together; and  in some cases of  paraplegia, especially when  due to
spinal syphilis, these three  symptoms become annoying to the highest
degree, so  that the  urine  must be passed at very frequent  intervals
during day and night, the legs are painfully flexed upon the abdo-
men by the contracture, and, as I have seen in several instances, the
tendon-reflexes are so  enormously exaggerated that the  least move-
ment with the bedclothes,  or a loud sound, or a tap upon the limb,
will cause the legs to be drawn  up with a series of twitches and jerks,
whilst, if  the patient  is placed  in a chair, the  legs will be seen in
constant but irregular motion, sometimes in  movements of  flexion
upon the abdomen, first upon one side and then upon the other, then
in rigid, bar-like extensions of the legs upon the thigh, or in  flexion
of the legs upon the thigh, until life is made more than miserable.

         PARADOXICAL MUSCULAR CONTRACTION.

   This phenomenon was first described by Westpbal as  a slow tonic
contraction in a muscle which has been suddenly relaxed.   It is best
seen in the tibialis auticus, and can  be evoked by  grasping the foot
and passively flexing it on the  leg.  It has also been observed in the
extensors of the toes, occasionally in the flexors of the knees, rarely
in the arm-muscles.  It is not  accompanied by muscular rigidity or
by exaggerated reflex of the muscle itself, although there has some-
times been diminution  of the latter.  It is as yet a clinical curiosity,
and its cause is unknown.

               MUSCULAR INCO-ORDINATION.

  Ataxia is that condition  of muscular inco-ordination in which pre-
cise combined movements of the  muscles cannot be performed  with
the normal exactness, although  there is no  loss of muscular  strength.
Muscular inco-ordination,  or ataxia, can be detected in several ways.
The best test of the  lower extremities is to have the patient walk along
a straight line, such as a crack  iu  the  floor, the edge of a rug,  or a
straight line  running through the carpet, and  do this with  the eyes 
172
NERVOUS DISEASES.
closed, so as  to  be entirely dependent  upon  the  sensations coming
through  the  sensory  nerves  of the lower  extremities.   A normal
person can walk this  straight line with  steadiness and ease, whereas
a person who has ataxia will stagger slightly, occasionally throw one
leg out to maintain  the equilibrium, or in the greater degrees be
totally unable to hold himself erect.  Ataxia of the upper extremities
can be tested by having the patient shut the eyes and then swing one
arm up from the side of the body with  a long swinging movement,
so as to touch the tip of the nose with the tip  of the forefinger, when
inability to co-ordinate the  muscular movements will be seen by a
failure to bring the finger to the nose, the finger either hitting the side
of the nose, or wavering as the nose is  approached,  or, in the severe
cases, hitting only the side of  the head, or the ear, or  failing alto-
gether to perform any purposive movement toward the nose.  This
ataxia of the muscles of the  extremities is called  motor ataxia.
The ataxia which a person has  in the trunk in the sitting position is
called static ataxia, and it  can be seen by the swaying and  inability
to maintain steadily upright  the trunk of the person who is seated.
Some authors speak of the  so-called Romberg symptom as an  evidence
of ataxia.  When this  is present, the patient,  standing with the eyes
closed and the  feet closely approximated,  sways  to one side or the
other, or backward and forward.  I do not regard this, however, as
a sign of muscular inco-ordination or pure  ataxia, but rather a dis-
turbance  of  equilibrium due to so many  different diseases of the
central and peripheral  nervous system   that  its  diagnostic value is
very small.   Other authors,  again, speak of  the standing upon one
foot with the other raised as  a good  test of ataxia, but there are
many perfectly healthy people who cannot  do this well, and it is a
very unreliable  aud clumsy  test.
   In  these tests which I have spoken of for ataxia, great care  must
be exercised to have the patient's eyes  closed, and not to have him
touch with the hand any neighboring object or any person, because,
as I shall show when treating  of  locomotor  ataxia, a patient who
may have so  pronounced an inco-ordination  of muscles  as to  be in
danger of breaking his neck in attempting  to walk with  the eyes
closed  may yet  so walk with security and  relative ease when  he is
simply allowed barely to touch  his  own finger to the finger of an-
other person, as by this  method  he obtains, through the sense of touch
and the muscular sense of  his  uuaffected or  slightly affected upper
extremities, a guide to his movements which is lacking in his affected
lower extremities.
   The causes of muscular inco-ordination  are varied.  It has been
observed in lesions of the  peripheral nerves,  in locomotor ataxia, in
lesions of the pons—especially of  the  lemniscus—in  disease of the
cerebellum and  its peduncles, in affections of the  cerebrum and also
of the auditory  nerve.   It is  probable, therefore, that ataxia may
be produced by any defect  in any of the nerves conducting  the vari-
ous kinds of sensation.  We know, as  has  already been said,  that  a
defect in the  conduction of the  waves of sound will produce it, as in
lesions of the auditory nerve.   We know  that it is often seen in 
         TESTS OF MOTOR AND SENSORY SYMPTOMS.      173

those cases of peripheral neuritis in  which there is only impairment
of the sense of touch and pain.   We know that it can be produced
by lesions of the lemniscus, which is a sensory tract.  We know that
it can be produced in such a spinal disease as locomotor ataxis.  We
do not know, however, exactly which one of the four senses of tact,
muscular sense, pain,  and temperature,  must be impaired  in  order
to produce  it, although it is  very probable  that it is  never due to
lesion of the temperature- or pain-sense.   I am inclined  to  think
that it is often due either to lesion of both the muscular sense and
the sense of touch, or of the  sense of touch alone.  That it is not
dependent upon loss of the muscular sense alone, I  have demon-
strated several  times to my classes by exhibiting ataxic  patients in
whom the muscular sense  was either normal or so  slightly impaired
as not to be able to account for the very pronounced ataxia, as well
as other patients whose muscular sense was greatly affected and who
yet had no ataxia.


                    MUSCULAR STRENGTH.

   Muscular strength  is to be tested, of course, by determining the
muscular power  of the different muscles.  Fig. 102  represents  an
instrument for testing the strength of the muscles of the hands.  By

                             Fig 102.
taking it into the palm and squeezing it, the strength in kilogrammes
is indicated upon the lower scale, that for pressure; whilst locking a
finger in each oval end and pulling will  indicate the strength upon
the scale for traction. The defect in this instrument is that the spring
is variable in its elasticity and soon becomes weak,  so that the meas-
urements are not  absolute.  It  is preferably used, therefore, to test
the  strength from time to time in a given case.   The best means of
testing the strength of the hand-grasp is, I think,  the one which I
have devised:  I  give the patient my hand in  such a  way  that he
cannot grasp it above the knuckles, so that he cannot hurt me unless
he possess  unusual strength, because my fingers roll over one  another
and prevent him  from obtaining a firm hold.  One soon becomes an 
174                   NER VO US D IS EASES.
expert in hand-grasps if this method is used, for all civilized man-
kind is already familiar with the varying degrees of hand-pressures
and their shades of meaning.   Just as the gynecologist has an edu-
cated finger, so should the neurologist have an educated hand.  I can
readily detect  slight variations of strength by my method.
  There is no convenient instrument for testing and recording the
muscular  strength of the foot and  leg; but, after all, in every case
of muscular impairment, anatomical knowledge, beyond the possi-
bility of any instrument, is needed to detect the individual muscles at
fault.  In most cases, too, the gait is of great value in diagnosis, for
the drop of the toe in extensor paralysis, the flop of the foot in flexor
impairment, the wrist-drop in lead-paralysis, and other characteristic
deformities tell as much as an instrument or a careful examination
of the muscles involved.

                  CEREBRAL THERMOMETRY.

  In 1878 I presented to the American Neurological Association the
results of an  investigation of cerebral temperatures of 102 indi-
viduals.   The places at which I placed the thermometers I denomi-
nated stations, and they were situated as follows : One on each side

          Fig. 103.                                Fig. 104.
     Cerehral thermometer.              Cerebral thermometer with cover and pad.

somewhat back of and  above the commencement of the external
angular process of the frontal bone, the frontal station; one on each
side just above the ear, the parietal station; and one on each side of
the occiput, the occipital station.   About over the fissure of Rolando
—i. e., about six and seven-eighths inches back from the furrow formed
by the junction of the nasal bones with the nasal process of the
frontal—was the vertical station, two  on each side.  I had  made a
series of surface-thermometers, great care being taken to see that they
registered perfectly and that the flat bulbs were not sufficiently plia- 
         TESTS OF MOTOR AND SENSORY SYMPTOMS.       175

ble to have the registering scale of mercury altered more than one-
half a degree by strong pressure.  These thermometers were held in
place by a strip of soft morocco running around the head and upward
over the line of the great longitudinal fissure to the occiput, and per-
forated so as to permit the insertion of the thermometer at the requi-
site stations.   In addition to this, each  thermometer had around the
bulb, sliding over the  upright scale, a round padded cushion of silk,
and over the upright scale was slipped  a glove of silk, these precau-
tions being  taken to prevent the environing temperature from affect-
ing the mercury.  (Figs. 103  and 104.)  The conclusions which I
arrived at were these :
  1.  The average temperature of the left frontal station was 94° 36',
the right being 93° 71'.
  2.  The average  temperature  of  the  left parietal  station  was
94° 44', the right being 93° 59'.
  3.  The average temperature  of the  left occipital  station  was
92° 66', the right being 91° 94'.
  4. The average  temperature of  the left  side of  the head  was
93° 83', the right being 92° 92'.
  5. The average  temperature of the  whole head, exclusive of the
vertex,  was 93°  51'.
  6. The average temperature of the motor region of the vertex was
91° 67'.
  7. The average  temperature of the whole head, inclusive of the
vertex, was 92°  66'.
   8. If there  be an alteration of temperature at any of the lateral
stations, this fact will justify a suspicion of abnormal change at that
point.
   9. If there  be an alteration of temperature at any of the lateral
stations of more  than two degrees above or below the average of such
station, this fact will  constitute strong evidence of the existence at
this station of abnormal change.
   10. In proportion as the alteration of temperature at any individual
station  is increased or decreased  beyond the  figures just mentioned,
in exact proportion will the strength of the  evidence  be increased,
until, the maximum or minimum having been passed, the evidence
will  become almost conclusive.
  11. If it should so happen that  such elevation of  temperature
above the average should be at any lateral stations on the right, caus-
ing a rise at this point beyond the average temperature at the corre-
sponding station on the left, this  would  strengthen the suspicion or
the evidence.
  12. These remarks apply with equal force to the average for the
whole of either side, as well as to the average for the whole head.
  13. It is necessary to the validity of  these  conclusions that the
contemporaneous bodily temperature should be normal, or that there
should be a marked disproportion between it and  the  cerebral tem-
peratures.  •
  I then put on record the first case of diagnosis of an intracranial
lesion by cerebral thermometry—a glioma of the brain, in which the 
176
NERVOUS DISEASES.
clinical symptoms pointed to an implication of the base, but which I
located at the lateral aspect of the cerebrum, aud iu which the autopsy
confirmed my diagnosis.  In this the  tumor was found between the
horizontal branch of the fissure of  Sylvius  and  the first temporal
fissure, while the whole of the right occipital lobe was converted into
a colloid, extremely vascular  mass,  giving way under examination,
this  also  extending anteriorly to the  tumor as far as the fissure of
Sylvius.   The temperatures at the different stations were as follows:

     Frontal, left              :........?i°75'-
     Frontal, right.............98® 33'.
     Parietal, left.............9o°-
     Parietal, right.........     ...  99° 75'.
     Occipital..............96° 75'.
     Occipital, right,............100° 6Q>.

The average of the  left side  was  96°  16', and of the  right was
99° 52', and of the whole head 97° 84'.  Since then Mills has reported
two  cases, one a case of frontal tumor, another a gumma  involving
the basal termination of the corpus callosum, its peduncles, the lamina
cinerea, and the anterior perforated spaces, and Eskridge  a case of
tumor of the cerebellum with monocular hemianopsia.  Mary Putnam
Jacobi has also  reported a case of tubercular meningitis.   In all of
these my statements were fully confirmed.   Maragliano  aud Sep-
pilli, of Reggio-Emilia, Italy, have made a series of investigations
upon the cerebral  temperature of the insane and the sane.  They
ascertained that it was exceptional to find the average temperature of
the head higher than normal in simple  melancholia and dementia;
that the  highest temperature is found in furious mania, then in de-
creasing  ratio in melancholia  agitata, paralytic dementia,  agitated
dementia, imbecility and idiocy, simple mania,  simple melancholia,
simple dementia;  that in all  mental diseases the occipital  lobes are
of lower  temperature than the others;  the  temperature of the frontal
lobes, which equals that of the parietal in  agitated dementia, idiocy,
and imbecility, is higher in mania, in simple melancholia and simple
dementia, whereas  in paralytic dementia  and agitated  melancholia
the temperature of the parietal lobes is higher than that of the frontal.
In all  the principal groups of mental disease the averages of the two
side of the head are  almost equal, with the exception of congenital
forms, in which the right shows a higher figure than the left.   The
general temperature of the body of the insane taken in the axilla and
rectum is higher in melancholia agitata and furious mania, and gen-
erally  goes on  decreasing in regular order in paralytic  dementia,
agitated  dementia, simple mania, idiocy and  imbecility, tranquil de-
mentia, simple melancholia. These Italian authors found the cerebral
temperature of the sane to  be higher than I did, their figures for the
individual lobes being on the average l$fa° greater than mine, whilst
they found the whole head 1-jftfr0 warmer.  They explained this dis-
parity  by  the fact that they  did their work  in  June, July, and
August, whilst mine was done in the winter and early  spring, so
that when they  made some observations  in  December  their figures
were very nearly those that I had given,  and they thus themselves
admit  that the disparity is explained by  the difference of the tern- 
         TESTS OF MOTOR AND SENSORY SYMPTOMS.       177

perature of the surrounding  atmosphere.  Maragliano ascertained
that thermometers placed on the skull were accurate indices of the
temperature of the contents of the  skull.  He  filled  a skull with
water  at different temperatures, leaving the integument and hair in
place,  and  found that  the  thermometers placed externally followed
faithfully the  oscillations of the temperature of the water within as
denoted  by thermometers placed therein.  Amidon has made some
interesting observations confirming my results.   During the seventeen
years that have since elapsed I have  made a number of observations,
and have had  no reason to  modify my original  conclusions.   I have
not, however,  found that cerebral thermometry is  always of value,
inasmuch as there  are many organic diseases of  the  cerebrum in
which the  alteration  in  surface-temperature is not  sufficient to lead
to a positive  diagnosis.  In  all cases,  however, in which  I  found
a variation to the  degree  which  I  have indicated I always found
organic disease;  so that in doubtful cases of intracranial neoplasm
cerebral  thermometry  may be of great  value when there is a local
rise of temperature implicating one  or more  stations on one side of
the head.  Absence of rise, however, is of no diagnostic importance
one way or the other.
12 
CHAPTER  III.
           DISEASES OF THE PERIPHERAL NERVES.

                           NEURALGIA.

   Definition.   Neuralgia is a  functional  affection of the sensory
 fibres of the peripheral nerves, and manifests itself by pain.
   Clinical, History.   The pain of neuralgia varies extremely iu
 degree from a mild ache to a severe  pain, and also in quality, run-
 ning through all the gamut of sensations of which the sensory nerves
 are capable, so that it  may be boring, dragging, burning, stabbing,
 shock-like, creeping, etc.   The pain  of neuralgia  has  certain char-
 acteristics that distinguish it from pain  in  a nerve due to organic
 cerebral,  spinal, peripheral, or visceral disease, and these peculiarities
 are the tendency to shift from one nerve or set of nerves to another,
 and the presence of certain tender points (points douloureux).  The
 tendency to shift manifests itself in the most remarkable  manner at
 times, whilst the  tender points are almost invariably found  at the
 levels where the  nerves pass from  a deeper to a superficial  level,
 Every nerve in the body may be  the seat  of neuralgia, so that a cata-
 logue of  all the different forms would be an anatomical list, but for
 practical  purposes neuralgias may be divided into those of the head,
 trunk, and neck, the upper extremities,  the lower extremities, and
 the visceral neuralgias.

                   NEURALGIA  OF THE HEAD.

   The neuralgias of the head are migraine and trigeminal neuralgia.
 Migraine will be considered in a special  chapter, because it is more
 of a neurosis than  a neuralgia.  The trigeminal neuralgias are the
 ordinary  neuralgia of the trigeminal nerve and tic douloureux.  The
 ordinary  trigeminal  neuralgia may mauifest  itself in either  of the
 three branches of the fifth  pair, or in  all the three branches simulta-
 neously.   The painful points in the ophthalmic division are (1) the
 supraorbital, at or a little  above  the  supraorbital  foramen; (2) the
 palpebral, in the upper eyelid; (3) the  nasal, at the junction of the
 nasal bone with  the cartilage; (4) the  ocular, vaguely in the  globe
 of the eye ; (5) the trochlear, at the inner side of the orbit.  In the
 second division of the fifth, the supramaxillary branch, the painful
 points are the cheek, eyelid,  the  side of the  nose,  the  upper lip)
 zygoma, upper temporal  region, the upper row of the teeth, and iu
the nasal  cavities and gums; whilst  in the infraorbital  branch of
the secoud division  the painful points  are (1) the infraorbital; (2) 
DISEASES OF THE PERIPHERAL NERVES
179
 malar; (3) superior labial; (4) the palatine.  When the third divi-
 sion or inframaxillary division of the fifth is  affected, the painful
 points are (1) the temporal;  (2) the inferior dental, and, rarely, the
 inferior labial and to one  side of the tongue, the so-called lingual
 point.
   In all  these simple  forms of neuralgia, while the pain may vary
 in degree, as I  have said, from a mild  ache, coming on at certain
 irregular times, to a  severe and shock-like pain, yet it should be
 sharply distinguished from that variety to which has been given the
 name of tic douloureux, in which the pains come on in paroxysms of
 great severity, so that the patient  holds the face and  sits  in  mute
 agony, and which, being very intractable and apt to continue through
 years, is entirely  different in course and prognosis  from the simpler
 forms.

          NEURALGIAS OF  THE  TRUNK AND NECK.
   The neuralgias of the trunk and neck are—
       Cervico-occipital;
       Phrenic;
       Cervico-brachial;
       Dorso-intercostal;
       Lumbar.
   Cervico-occipital neuralgia is in  the regions of distribution of the
 four upper cervical  nerves, and is therefore felt iu the occipital aud
 posterior parietal regions to the vertex as far forward as the parotid,
 and  down the neck to the clavicular and upper thoracic regions, or
 it may be limited to  the area of the great  occipital  nerve, the small
 occipital nerve,  the inferior  subcutaneous  nerve,  and  the supra-
 clavicular nerves.
   In phrenic neuralgia  the pain is at the lower and forward region
 of the thorax, at  the points of' insertion of the diaphragm, and at the
 mid-portion of the neck, where the phrenic nerve branches off  from
 the cervical plexus, as well as in the chest and in the shoulder.
   Dorso-intercostal neuralgia is in the area of the sensory branches
 of the dorsal nerves, mostly in the anterior divisions, and the tender
 points are found  laterally in front and behind.
   Lumbar neuralgia has  its site  in  the  first four lumbar nerves
 which supply the loins, the inguinal  regions, the hypogastrium, the
 mons veneris, part of the scrotum  and the labia majora, the antero-
 lateral  and median regions of the  thigh, the anterior portion of the
 knee-joint, the median surface of the leg, and the inner border of the
 foot  to  the great toe.   It is rare to find simultaneous implication of
 all of this region, aud it has therefore been divided  into two groups,
 lumbo-abdominal neuralgia, or lumbago, and femoral neuralgia, the
 former beiug by far the most frequent.  There  is a form of neuralgia
 due to urethral stricture, or disease of the prostate or seminal  vesicles,
 which is very apt to be confounded with lumbago, aud  yet  which I
 have never seen described.   It follows the  pelvic lesions mentioned,
 often in neurotic or impressionable individuals, aud is very intract-
able and difficult  to treat,  as I shall state further on. 
180
NERVOUS DISEASES.
         NEURALGIAS OF THE  UPPER EXTREMITIES.

   The  neuralgias of the  upper  extremity belong  to the cervico-
brachial group and  nerves in the branches of the brachial plexus or
the posterior branches of the four lower cervical nerves, so that the
pain is  in the upper arm or forearm, often extending  into the hands
and fingers, and the painful points are (1) the axillary point corre-
sponding to the brachial plexus; (2) a scapular point; (3) a shoulder-
point at the emergence of the cutaneous branches of the circumflex
through the deltoid; (4) the median  cephalic point, at the bend of
the elbow  answering to the musculo-spiral nerve; (5) an external
humeral point three inches above the elbow at the emergence of the
cutaneous division of the musculo-spiral; (6) the superior ulnar-point
upon the ulnar nerve between the olecranon and the epitrochlea; (7)
the inferior ulnar point, upon the ulnar just in front of the annular
ligament of the  wrist; (8) a radial point,  where the  radial nerve
issues at the lower and outer part of the forearm.
   But neuritis of these nerves is much more common than neuralgia.

         NEURALGIA OF  THE  LOWER EXTREMITIES.

   Neuralgia of the lower extremities consists chiefly of sciatica or
pain in the sciatic nerve, and the painful point, as Gibney has shown,
is usually best found in the following manner: Placing the thumb
upon the great trochanter of the femur, and the second finger upon
the tuber ischii, press down midway between the two with the index-
finger, when the sensation of the patient  will be a guide to having
reached the sciatic nerve.

                    VISCERAL NEURALGIAS.

   Visceral neuralgia is mainly of the kind known as colic, or accom-
panying organic affections of the intestines, the liver, or the female
pelvic organs.
   In all the different forms of neuralgia the  various functions of the
different nerves,  motor, sensory, and sympathetic, may be affected,
Thus, in trigeminal neuralgia  there may occur spasm of the facial
muscles, pallor or redness and  even swelling of  the  face, increased
lachrymation, salivation,  herpes,  changes  in  the hair,  periosteal
alterations,  even erysipelas and neuro-paralytic ophthalmia,  whilst
hypersesthesia and ansesthesia may sometimes be temporarily present;
and in all the neuralgias analogous symptoms to these are common,
   Pathology.  A great  deal of energy has  been  spent  in discus-
sion as  to whether neuralgia is  due to changes in the  central cells
of the sensory nerves, in the nerve-fibres  themselves, or in the end-
organs,  and also  as  to whether  these changes are secoudary to vaso-
motor disturbances; but it is useless  to go  into these differences of
opinion, because they are entirely speculative, with scarcely a respect-
able fact to prop any one  of them up.  The truth of the matter is,
that we do not know the molecular changes which  constitute neural- 
DISEASES OF THE PERIPHERAL NERVES
181
gia, and we never shall  know until we  have instruments  delicate
enough to enable us to  dip down  into a living cell of cord or skin
and  have a microscopic  view  of molecular life,  or until we have
gained such knowledge of all the cells of peripheral nervous struc-
tures  that we can appreciate a  slight  departure  from the  normal.
The congestions and the shifting and  turnings of  the nerve which
were described by the  earlier authors were really cases of neuritis,
and  not  neuralgia.   But although we  do not know the  molecular
changes which are at  play in  a  pain-suffering nerve, we do  know
many of the factors which can  set up that pain.
  Causation.  The causes of neuralgia may be :
       Heredity;
       Gout;
       Neurasthenia;
       Anaemia;
       Malaria;
       Eye-strain ;
       Dental disease;
       Disease of antrum;
       Genital irritation  ;
       Neural tumors;
       Trauma;
       Influenza;
       Changes of temperature;
       Toxic influences;
       Kidney disease;
       Syphilis;
       Hysteria.
   Heredity is often a  cause  of neuralgia, and, indeed, most of the
cases of generalized or  recurrent neuralgia will be found to be hered-
itary, although it must  be confessed that this hereditary causation
may well be  overestimated.    I  do not believe, for  instance, that a
person has ever lived who  has  not had neuralgia at some time, and
yet it would not be fair  to say that this  individual could transmit
neuralgia hereditarily, as could a person who was constantly subject
to the malady.   This  wide distinction  between the  constantly neu-
ralgic individual and the occasionally neuralgic one is generally lost
sight of by patients in giving a history of their heredity.   But aside
from a  purely neuralgic heredity,  neuralgic patients will very fre-
quently have a neurotic heredity, such as epilepsy, migraine, neuras-
thenia, iusanity, etc.
   Gout  is a frequent  cause of  neuralgia.   But  the gout which is
described  by English  authors  is seldom  met with  in this country,
even  among  people living luxuriously and daintily, and it  is more
apt to be relatively slight joint-aches and disturbance of the chylo-
po'ietic system than the full-fledged attacks of the disorder which the
text-books describe.  In  many  neuralgic individuals, however, whose
parents  have not been gouty,  there has been a tradition of gout in
the family
  The neurasthenic is  subject  to aches aud pains that are generally 
182
NERVOUS DISEASES.
vaguely neuralgic, but  at  times he has  outspoken attacks of neu-
ralgia.
   Syphilis  is not so frequently the cause of neuralgia as the abun-
dant literature upon the subject would seem to prove, but, of course,
it undoubtedly occurs.   The intracranial exacerbations of this dis-
ease upon which  so much  diagnostic stress is laid are, however, su
common in many forms of neuralgia as to have but little weight in
my estimation.
   Anasmia  should always  be sought for in any  case of neuralgia
where the cause is not  certain, and reliance should not be placed
upon the color of the lips,  the face, and the conjunctiva, but exami-
nation should always be made of the heart and  the great vessels for
the characteristic blowing-sounds, and in  doubtful cases an examina-
tion of the  blood should be made.
   Malarial  neuralgia  occurs in two forms : in the  first place, with a
regular  periodicity, aud, in the second place, as a sequel of malaria;
and a sharp distinction should be  made between these two forms for
purposes of treatment.   The periodicity of  malarial neuralgia  will
sometimes have to be carefully looked for.  Thus,  I have known an
obstinately  recurring neuralgia to resolve itself  under patient exami-
nation  into an attack every second day at 9 o'clock in the morning,
to which was added on  every fourth day au  attack at  2 o'clock in
the afternoon, aud  it was  not until the antiperiodic medicine  was
carefully administered at the time immediately preceding these peri-
odical occurrences that  relief was  obtained.  Nor  is  it  always the
case that a rise in temperature will accompany the periodical returns,
so that absolute reliance cannot  be  placed upon this means of diag-
nosis.   It is  frequently  said that the brow-ache is characteristic of
malaria, but this statement should be viewed with some caution.  It
is undoubtedly true that brow-ache is observed in malaria, but this
should  not  blind us to the  fact that neuralgia of other nerves of the
body may also occur in  the same disease, especially of the different
branches of the fifth pair and the sciatic, so that too much dependence
should not be placed upon the anatomical localization of the neuralgia
as a diagnostic factor.
   In any case of obstinate  neuralgia about  the trigeminal nerve a
careful  examination  should  be  made  for errors of refraction  and
muscular insufficiencies  of  the eye-muscles;  but if I may judge by
my own experience, these are rare causes.  In any case,  however, it
is well to remove any possible reflex irritation from the eye.
   Dental disease  is a frequent  cause of neuralgia of the different
branches of the trigeminus, and iu any case  of pain commencing in
the jaw and radiating through  the  cheek a careful examination of
the teeth should  be  made   by a competent dentist.   Any doubtful
filling should  be  removed  and  repacked.  Any persistently pain-
ful teeth or  any from which the  pain starts should be drilled into,
even if outwardly and above they seem perfectly sound, for I have
in several  instances known  a  tooth which  had been  pronounced
healthy yet to have imbedded in  its fangs  a mass of pus and gas that
was  incredible in  its fetidness when provided with an outlet,  and 
DISEASES OF THE PERIPHERAL NERVES.
183
these cases had  had recurring neuralgias for several years.   On the
other  hand, the mere  presence of pain generally through the teeth,
even though  the teeth may have commenced to decay, is no reason
whatever why they should  be removed in the wholesale manner that
is so often done.  Nor will such  removal usually give even tempo-
rary relief.
  Disease of the antrum  occasionally causes neuralgia of the tri-
geminus, and it should, therefore, not be overlooked in any case of
persistent pain in the fifth pair.
  The subject of genital  irritation has  been much exploited in the
last few years as the cause of all sorts of nervous  disorders, among
others of neuralgia,  but  in my experience it  is one  of  the minor
causes.   Of  course,  any well-marked vaginal, uterine, or ovarian
disease may give rise to neuralgia, but the case then  is  not one of
neuralgia, but of the malady which sets up the pain, whilst slight
disorders of the genital organs seldom cause neuralgia unless joined
with causes of general debility.
  When neuromata cause neuralgia, the pain is generally limited to
the nerve-trunk or branch  upon which the tumors sit.  In all cases
of neuralgia, however, it is wise to  make  careful search  for a pos-
sible tumor, which can usually be found with ease about the scalp,
neck,  rectum, female pelvis and trunk, aud upper and lower  extremi-
ties.
  Trauma  setting up neuralgia usually does it by implicating a nerve
in a cicatrix, or by fracturing a bone aud  imprisoning the  nerve in
it or in the callus which  is occasioned.   I  have never seen trauma
induce neuralgia by itself without  some local  lesiou  of this kind,
although neuralgia is a constant accompaniment of traumatic neuras-
thenia.
  The late epidemic  of influenza which has swept around the world
has been a cause of  neuralgia,  mainly in this country of the dorso-
intercostal form, and I think that this form should be considered as
one of the  diagnostic points of  influenza.
  Changes of temperature from heat to cold,  sometimes from cold
to heat, and barometric disturbances, are frequent causes of neuralgia,
as are the changes of temperature and environment constituting the
main  factors  iu the process of acclimation, which, in a  minor degree,
is seen by  us New  Yorkers every  summer on the arrival of our
city-dwellers at the mountain and seashore, and again in the autumn
upon  the return of these  individuals to the city.   Some persons are
most  affected by the approach of a storm, others by the passage of it,
whilst some  of the  most painful  forms of neuralgia—those of the
character which the French call foudroyant—are seen  after a storm,
during the  presence of what is called the anti-cyclone,  which is a
period of  blue  skies,  bright sunshine, high barometer,  and slight
atmospheric motion.   It  is well  to  study in any intractable case the
behavior of the patieut to these barometric disturbances,  so as  to be
on the watch for severe  attacks and  know about when to anticipate
them.
  Various toxic influences may cause neuralgia, such as arsenic, lead, 
184
NERVOUS DISEASES.
 ordinary illuminating-gas, some sewer-gases, alcoholism, and diabetes,
 In any obstinate case careful examination should be made of the urine,
 both quantitatively and qualitatively, and  microscopically, if neces-
 sary, for I have had a number of cases of ueuralgia come to me in
 individuals suffering from  fatal  nephritis, which had not been diag-
 nosed.   Usually,  however, the  pallor,_ the oedema of the eyelids and
 lower extremities will cause a  suspicion of the real trouble, but in
 the  cases of which I have  spoken there were none of these outward
 signs, and the high  arterial tension, to which attention should always
 be paid, was one of the first  symptoms to arouse my suspicion.
   Hysteria is a frequent cause of neuralgia, so that it should not be
 forgotten that genuine pain may exist  in an hysteric.
   Diagnosis.  The study of the  causes which I have just dwelt
 upon will make  apparent many points of  diagnosis, which I  need
 only allude to again ; thus, it should always be  borne in mind that
 a so-called  neuralgia  may  really be anaemia,  neurasthenia, malaria,
 eye-strain,  dental disease, disease of the antrum, genital irritation, or
 neuromata.   In other words, neuralgia is  but a symptom, and in all
 cases we should ask what  it is  a symptom of.   The different causes
 which I have enumerated should be carefully thought of, and the
 diagnosis made thus  by a discovery of some one cause or by exclu-
 sion of many.  The diseases which are most apt to be  mistaken for
 neuralgia, however, are—
      Brain-tumor;
      Intracranial syphilis;
      Spinal tumors;
      Pott's disease;
      Spinal caries;
      Neuritis;
     Topoalgia.
   A brain-tumor may cause either a general headache or pain limited
 to one distribution  of a nerve,  aud be so slight as to picture well a
 neuralgia.   Thus, in one patient who died in the course of six weeks
 with a tumor of the centrum ovale as big as a medium-sized potato,
 the symptoms at the onset  were entirely those of a slight neuralgic
 pain  over the forehead -, whilst in another case of cerebral tumor, the
 patient dying in six  months with a melano-sarcoma as big as a hen's
 egg imbedded  in the temporo-sphenoidal lobe, the only symptom for
 the first  four weeks  had been that of neuralgia limited to the supra-
 orbital branch of  the fifth pair on the same side as the tumor; and
 in still another case, of a patient with a tumor of the cerebellum, the
 first symptom  had been recurring attacks of obstinate  neuralgia of
 the vertex.   The diagnosis, however, can usually be made by a care-
 ful study of the case.   A  neuralgia should always excite suspicion
 when  it appears  gradually or  suddenly in a patient who has  not
 been  subject to it, with some slight motor  or sensory  symptoms of
 other nerves;  with  some mental alteration  perhaps;  with attacks
 of nausea or vomiting ;  or subsequently to the appearance of tumors
 in other  parts of the body.  If an optic neuritis occurs, or any slight
changes in the optic disk, the diagnosis is still more easily made; but 
DISEASES OF THE PERIPHERAL NERVES.
185
unfortunately in many cases of tumor optic  neuritis  is either a late
symptom or does not appear at  all.  The development of a case of
brain tumor, with its pronouuced motor and sensory paralysis and
mental symptoms, will  inevitably make clear a diagnosis that may
have been obscure at the start.
   Intracranial  syphilis in  many of its forms is very  frequently
mistaken  for simple neuralgia, but the  diagnosis can be  made  in
many instances  by the three  symptoms  which I  have discovered,
and of which I speak  at length in the chapter upon that subject,
namely, the quasi-periodical headache,  either nocturnal  or at  some
stated time  of  the day, aud the obstinate insomnia; the headache
and  the insomnia disappearing upon the supervention of any con-
vulsive or paralytic symptoms.  But  it is in the early period of  the
headache, when it is only  accompanied by obstinate  insomnia, and
before the superventiou of convulsions or paralysis, that the  diag-
nosis must  be  made.  Great  suspicion, therefore,  should attach  to
any violent headache accompanied by obstinate insomnia, and careful
search should be made for large glands of the head, neck, and groins,
and the patient should be  carefully interrogated as to any syphilitic
infection ; but even  if no  suspicious glauds or history of infection
are found, the patient should be put upon proper syphilitic treatment.
In any case of obstinate headache not yielding to ordinary analgesics,
whether a specific history of syphilis is given or not, syphilis should
be regarded as one of the possibilities.
   The pain of spinal tumors or caries is a fixed, severe, and persistent
pain, limited to the distribution of one or two nerves, and is accom-
panied by local tenderness of the  vertebra and by vertebral immo-
bility, to which in time  may be superadded symptoms of ansesthesia
and paralysis.
   The differentiation of Pott's disease from neuralgia is a matter of
no difficulty when the former malady is well developed, and even in
its early stages careful examination will detect some vertebral immo-
bility, deviation, or tenderness, or some impairment of motion  or
sensation beyond the possibility of a  neuralgia, or some muscular
atrophy, or some marked alteration in the reflexes.
   The diagnosis between neuritis and neuralgia is usually an easy
one,  but it  may  sometimes become a matter which requires careful
consideration.   In neuralgia the  pain  is  apt to leap from one nerve
to another, or even from one side of the body to the other.   It is
seldom accompanied by  ansesthesia, aud never by muscular atrophy,
motor paralysis, glossy  skin, or  reaction  of degeneration, whilst all
of these latter symptoms are usually present in neuritis.
   Topoalgia is the name given by Blocq and Ouanoff to  pain in dif-
ferent regions that are not anatomically or physiologically delimited.
It may occur by itself, but  is generally accompanied by neurasthenia,
hysteria, or hypochondria.
   Prognosis.   The prognosis will depend upon the kind of neu-
ralgia aud upon the cause; but as a general thing the prognosis is
excellent, excepting where the cause is not removable either by medi-
cation or the surgeon's knife.  Neuralgia of the trigeminus is of good 
186
NERVOUS DISEASES.
prognosis, except when it occurs in the form of tic  douloureux or
accompanying great facial spasm.  Other neuralgias of the head have
also an excellent prognosis.   The prognosis of the neuralgias of the
upper extremities  is almost  invariably excellent, too,  as  is the case
also  with neuralgias of the trunk, excepting in that curious form
which seems to bear some relation to antecedent urethral, prostatic,
or seminal lesions  of the  male, which may  be  mistaken for ordinary
lumbar neuralgia,  and of which I  have  never seen  a  case cured.
The neuralgias  of  the  lower  extremity  are _ usually of doubtful
prognosis,  especially of the  sciatic  nerve; mainly, I  think, because
of the fact that  it  is so  extremely difficult to put the limb at rest,
for when this is done  they improve as quickly as do neuralgias in
other parts of the body.  Visceral  neuralgias are, as a rule, of good
prognosis if they are not connected with  some  irremediable  visceral
lesion.
   Treatment.   Before entering upon the treatment of a case it
may be  well to realize  that for therapeutic  purposes all forms of
neuralgia  may  be divided  into  two great classes ;  namely, those
depending  upon  general causes weakening  the whole organism,
and  those dependent  upon  local irritations; whilst  occasionally a
neuralgia  may  be produced by  both  causes, the general condition
acting as a predisposing,  whilst the local irritant acts as the exciting
cause.   I think that a great many difficulties may be cleared away
when these statements are  thoroughly understood.   In  every case,
therefore, our first duty  should  be  to search for the local irritant-
such as a neuroma, a cicatrix, a fracture, a callus, a tumor, a  marked
error of  refraction, or great  muscular  insufficiency  of  the ocular
muscles—and remove it if that be possible, and then, if the neuralgia
persists,  take measures to bring  the vitality of the whole organism
up to the plane of health.   To effect this latter purpose is  often a
work of art.  If ausemia is present, it should be removed. Anaemia
sufficient to cause  persistent neuralgia must usually be treated with
vigor, and  the  best plan, in my opinion,  is the following :  Cut off
the expenditure of energy  in the  patient by one-half, either by
keeping  him in  bed  until  noonday  and  having  him  go to  bed
early in  the evening, or  by forbidding all  exercise  whatsoever,
ordering the use of a carriage in going around ; or by making him
rest  three  or four hours  every afteruoon.  The  morning rest is
usually the best, however, inasmuch as ausemic patients are generally
at their worst in the morning.   Use large doses of iron, either the
dialyzed iron, «r>j after meals in a cup of water ;  Dree's albuminate oi
iron, 5j also after meals in a cup of  wTater ; or the peptonate of iron
in the form of compressed tablets, gr.  ij-iij after meals, three times
daily ; or the subcarbonate of iron, gr. xx-5j, when a tasteless pow-
der is  desired for  children, to put  in the  food perhaps,  or  when a
cheap  preparation is  needed.   Lately I  have  been using ferratin,
gr. iv-viij  three times daily, in capsule, because it  not only has no
constipating effect, but seems to be slightly laxative at times.  Tonic
doses of quinine should  be given with  the iron, or  five grains of
sulphate of quinine every  night at  bedtime.   Administer large 
DISEASES OF THE PERIPHERAL NERVES.
187
quantities of red meat, having it  prepared hot at the three meals
of the day, and  in addition use a strong  beef-tea, making a pound
of meat  into a pint  of  beef-tea, dividing it  into  three  portions
daily;  if needed, also  use  use  bullock's blood,  obtained fresh from
the abattoir every moruing, and  frozen  hard into cakes and thus
eaten,  which, gruesome as it may  sound, is  by  no  means un-
pleasant  to  many people.   Administer small  doses  of bichloride
of mercury,  -fa to -fa  of  a grain three  times  a day.   If  there
should be malaria, this must  be  carefully removed.   If the neu-
ralgia  come  in the  malarial  paroxysms, the  treatment  is  quite
different  from  what  it is  when  the  neuralgia  succeeds this.  The
malarial  paroxysms  must  be  broken up  by large doses of quinine
(ten, twenty, or thirty grains, according to  how the patient is known
to bear the drug or the  severity of the malaria), administered a
couple of hours before the attack is expected ; or if the attack occurs
very early in the morning before waking, the quinine should  be given
at bedtime, and  the dose should always be sufficient to produce dis-
tinct cinchonism.  When the  paroxysms  have disappeared, the qui-
nine may be gradually reduced, and when  the dose has become very
small it  may be left  off entirely,  and arsenic given  for a week or
two—best Fowler's solution of arsenic, three drops three times a day,
in a wineglass of water, or arsenious acid, y-^g-  grain three times a
day.  Some individuals, however, can take neither quinine nor arsenic,
although in my own experience those who cannot take  quinine in
truly malarial paroxysms are very few in  number.   In such a case
cinchona bark may sometimes be  borne, preferably in  the  form of
the elegant elixirs which are prepared by  the leading  pharmacists of
our large cities, the dose varying  from §ss to oiv, according to the
amount of cinchona used ; or the tinct. cinch, comp. (U. S. and B. P.),
is a cheap and  effective preparation for the lower classes, but it  is
very disagreeable to  people of delicate palates.   Its dose is  5j  three
times daily.   If cinchona  will not answer, the  iodide of potash in
continuous doses of ten to fifteen grains three times a day, or the tinc-
ture of iodine fifteen  to twenty drops at a  dose, three times a day, in
a tumbler of water, or lemon-juice, 3j-5iij in a glass of water, steadily
used two or three times a day, may one of them answer the purpose
of overcoming the periodicity ;  or arsenic may do in conjunction with
cinchonidia or chinoidin, and I have found the following prescription
of considerable value:

       R.—Chinoidin.......3}}.
           Hydrastis.......^['   .
           Ferri sulph.  exsic......3j-—M.
  Ft. in pil. no. xxx.  S.—One three times daily one hour after meals.

  If arsenic  cannot be taken after the quinine in  antiperiodic doses
has been  stopped, resort may be had to the foregoing prescription, or
the patient may be put upon dilute nitro-muriatic acid, 20 drops three
times a day, after meals, in a wineglass of water; or an alkali may
be used, even so mild a one as Vichy or Giesshuebler; or a change
of climate may be tried.  In the neuralgia  which may have succeeded 
188
NERVOUS DISEASES.
malaria, quinine may be of great value, or it may be perfectly useless,
and a test must be made to determine this point.   In many of these
cases the pain is kept up by anaemia, which can be readily removed
by one of the preparations of iron just mentioned.   If this should
prove useless, the acids or the alkalies will be all the treatment that is
needed, although a  change of climate is usually beneficial, provided
that the climate selected is  one  that usually agrees with the patient.
The  treatment of gout or lithsemia (which is the American gout)
should be  in accordance  with the  rules laid  down in speaking of
lithsemic neurasthenia  (Chap. IX., "Neurasthenia"),  and to the
same chapter the reader must turn for directions as to the treatment
of the neuralgia of neurasthenics.   I have  much  more faith  in
the general treatment of neuralgia than I have in the local treatment
of it;  in other  words,  I believe that neuralgia is almost invariably
the cry of a debilitated  organism—not of impoverished blood, as was
said many years ago at  one stage of our knowledge—oftener than it
is the cry of an independently damaged  nerve.   In every instance,
therefore, the general treatment should be given the preference.  If,
however, it be impossible to carry this out, or if the pain  is persistent
in spite of the general treatment, then local measures for the relief of
pain should be used—very cautiously, however, and not with the free
hand  with which they must be employed in neuritis, as I shall  have
occasion to point out.   The best analgesics, in my estimation, are:
opium and morphine, codeia, phenacetine, antipyrin, aconitia, aconite,
aquapuncture and acupuncture, veratrum  viride, counter-irritation
by blisters and rubefacients, hot applications, and electricity.  Of all
these, by all  means the  best is opium in the form of its distinguished
extractive, morphine, and the best of all the morphines, in my opinion,
is the sulphate, although it may be that some people in whom the
sulphate cannot be employed will bear the muriate well, but it is very
seldom that the sulphate cannot be borne if  care is taken, as it always
should be, that  the  opium  is obtained from some  perfectly reliable
manufactory in  packages marked with the guaranteed aualysis.  The
opium and morphine that are usually found at the druggists are very
unreliable drugs, and not only do I take particular care that all used
by my patients should  be obtained  as  I have directed, but also that
the solution of it shall be made fresh every few days, put into bottles
with glass or cork stoppers, or the tablet triturates shall be put into
a bottle with a screw top, and that over them, as they lie iu the bottle,
shall be placed a thick pledget of cotton.   The hypodermic adminis-
tration of morphine is by far the best means of relieving acute  pain.
Unfortunately, however, it is a very dangerous drug to use with neu-
ralgics, and I make it a rule never to employ it except in such  acute
pain that the paroxysms cannot otherwise  be  controlled, aud then I
never let the  patient use the hypodermic himself.  In some cases mor-
phine will have its effect enhauced by the addition to each dose of jfo
grain of atropine, as will be pointed  out shortly, whilst in other cases
the effect is diminished  by this combination. Codeia is, next to mor-
phine, the most valuable  extract of opium for its effect upon the
visceral neuralgias.  Phenacetine has not been a reliable drug in ray 
DISEASES OF THE PERIPHERAL NERVES.
189
hands except in dorso-intercostal neuralgia, especially when caused by
influenza.   Antipyrin is undoubtedly a most effective analgesic, but it
is also a depressant that is dangerous in most cases of neuralgia, except
for temporary use; indeed, I have seen so many cases of neuralgia
seriously depressed by the use of antipyrin that I seldom administer it.
Aconitia is sometimes  an excellent analgesic, more especially in tri-
geminal and sciatic neuralgia,  and Duquesnel's and Merck's pre-
parations  are  the best.  These can be obtained  from all  the  large
manufacturing  houses  in the form of hypodermic tablet triturates.
The dose should be -j-^-  grain to start with, given every four or five
hours, and gradually increased until some slight  tingling or numb-
ness is perceived by the patient, and for this purpose it is safe to give as
high as sV.or ~io grain> but it should uever be administered to a person
with arterial, cardiac,  renal, or pulmonary disease.  It  may  be con-
tinued in suitable individuals for weeks, and  to show  how well it is
borne I may cite  the case of a patient who was taking -A^ grain four
times a day for tic douloureux, when he was caught in the terrible crush
upon the Brooklyn Bridge that occurred shortly after the opening of
the structure, and which  resulted in the loss of several lives ;  and yet
his heart was not affected  in any appreciable degree  by the terrible
scene.   Aconite is an excellent analgesic as a  local application, either
alone or in  combination  with other substances, as in the  following
prescription:

      R.—Tr. aconiti rad.  )
          Tr. opii        y......aa gj.  M.
          Tr. iodi        J
  S.—Apply with camel's-hair brush.

But it should  not be used internally for this purpose, because of its
depressing effect.   This is also true of veratrum viride.  Acupuncture
and aquapuncture are occasionally excellent analgesics where the pain
is  localized, and this not only in  hysterical individuals, for  I  have
seen it relieve pain marvellously in certain cases that were in no sense
of the  word hysterical  or even unusually sensitive ; and  patients who
crave a hypodermic will  sometimes be  satisfied with acupuncture or
aquapuucture.  Warmth by means of hot or dry applications is not
so much a reliever of pain as an  aid  to  the  true relievers of pain.
Neuralgic nerves, as a  rule, do  best in  an equable and warm or
moderate temperature.   The best  means of applying warmth is  by
poultices, encasing the body or limb in oil silk  or wool  gauze, or by
the application  to the neuralgic  part of a  handkerchief dipped into
boiling hot water,  quickly twisted perfectly  dry by a stick  in  each
corner, and removed in a few minutes as the heat becomes bearable.
Electricity is of great  value in  some forms  of neuralgia, and per-
fectly useless in others, as will be  pointed out shortly.
  We  will now proceed to  detail the application of these general and
special considerations to  each form of neuralgia.
  In ordinary trigeminal neuralgia the general  health must be care-
fully attended to, and all causes of local irritation should be removed,
but usually, even  after this has been done, some neuralgia will persist. 
190
NERVOUS DISEASES.
This can  be relieved  by aconitia, quinine, either alone or combined
with codeia (the  former in tonic doses, the latter ^or J grain, each
three times a day), and arsenic, either Fowler's solution, 2 or 3 drops
three times daily, or arsenious acid, ^ grain three times a day.  This
has been an effective combination in my practice:

      R. — Quin. sulph........3}.
          Acid, arseniosi......Sr- s-
          Codeia?  .    .    -         •    •     •    •   Sr- viJ-  M
  Ft. pil. no. xxx.   S.—One three times daily, one hour after meals.

   The addition of gr. j-ij of salicylate of soda  to each dose of this
will increase the  analgesic effect without making  it more depressing.
   Electricity in  the form of galvanism or  faradism, generally the
former, is sometimes of use, but  only exceptionally so.   When gal-
vanism is used, the neck electrode (Fig. 67) should  be placed on the
nape of the neck, and the other electrode of Fig. 71 should be placed
upou the affected  nerve-trunk, covering one or more of the tender
points, and a current  of  2 to 5  milliamperes should  be carefully
measured off  and  passed  during  a sitting of three  to five  minutes.
If faradism is used, the electrodes of Fig.  68  should be placed about
two inches apart, and a gentle  current,  sufficiently strong  to be
pleasantly felt  by  the patient,  should be  administered from ten
minutes to half an  hour  at a time, or the  patient may take one
electrode in the hands, whilst the physician takes the other in one of
his and then applies  his fingers gently to the patient's face, using
sufficient current to be gently felt, and to cause a distinct crackling
sound aud sensation.   This  faradic application may be made for
some length  of time,  generally  fifteen minutes, but even thirty
minutes to an hour in the  severe cases.   These electrical  applica-
tions should be  used  every second day at least for a period varying
from four to twelve weeks, according to the severity  of the neuralgia
and the relief that they may give.  The electric air coming from the
static machine is  generally very refreshing  to the patient, but  it is a
feeble agent for  relieving pain  or modifying the  nutrition of the
nerve, whilst  the electric  sparks are either  inert or aggravate the
suffering.
   In occipital neuralgias of the head, however, the treatment is,
curiously enough, quite different, for in them aconitia is  unreliable,
arsenic  is  valuable,  quinine  may be  valuable or  may  aggravate,
whilst electricity, especially  galvanism, is usually  of great value.
The galvanism should be applied by  means  of the neck electrode
(Fig. 67) placed  upon the nape of the neck, whilst electrode Fig. 68
is placed  upon the forehead, and a current gently turned on of 2 to
5  milliamperes, always commencing with  the lowest figure for the
first sitting, and  allowed  to  pass for  from  three to five minutes;
whilst faradism may be applied as when the trigeminus is affected.
   Neuralgias of  the trunk, which are mainly  of the dorso-intercostal
type, are best treated  by means of phenacetine, galvanization  of the
spinal cord, static current in the form of sparks, local  support  by
means of a strong adhesive plaster, liniments, and in severe cases by 
DISEASES OF THE PERIPHERAL NERVES
191
rest of the trunk in bed or on a lounge, the former best.   Quinine in
tonic doses (gr. ij-iij three times daily) usually has an excellent effect
upou these dorso-intercostal neuralgias, especially when it is combined
with moderate doses (gr. ij-iij) of a reliable salicylate of soda.
  Neuralgias of the upper extremity are generally best treated  by
means of aconitia, quinine  in combination with codeia or salicylate
of soda, galvanization of the main nerve-trunks, aud rest of the arm
in a sling, together with such general treatment as may be indicated.
  Neuralgias of the lower extremity, mainly sciatica, are difficult to
treat satisfactorily unless the affected nerve is put completely at rest
by confining the patient to a couch, stopping his walking, and in all
possible ways restricting the use of the muscles of the lower limb, and
this rest must be kept up for a period of from four  to twelve weeks,
according to the chronicity of the case.   To this treatment should be
added salicylate of soda,  arsenic, galvanism, and the static  current.
Injections hypodermically of osmic acid are  occasionally very beue-
ficial, oue to three drops of a one  per cent, solution being used, and so
are aquapuncture aud acupuncture, but these remedies can never be
relied upon.  Another very important  thing in all  cases  of sciatica
is to see that the  patient has a shoe that fits the foot properly, with
a sensible  low heel, a straight inner sole, and wide enough at the
toes to permit the body being lifted on the toes, so  that they will be
spread without bulging over the edge of the sole, and  will give all
the wide base of support and all  the play of muscle in  foot,  toe,  and
leg that Nature  intended.   This  apparently small matter I have
found to be of very great importance  in a number of continuing
cases  of sciatica.
   Visceral neuralgias are best   treated  in the acute paroxysms by
absolute rest aud a sufficient hypodermic of morphine, with  or with-
out atropine, according as  is found best with the patient, and then
afterward  subnitrate  of  bismuth, salol,  and codeia,  or  oxalate of
cerium and codeia, as in the following prescriptions :

      R.—Bismuth, subnit........3 v.
          Codeise.........gr. vj.
          Salol.........3j.    M.
  Ft.  in chart, no. xxx.  S.—One  powder in a wineglass of water, three
times  daily.

      R.—Cerii oxalat.........3).
          Codeise.........gr- vj.
          Salol.........3}.    M.
  Ft.  in pil. no. xxx.  S.—One three times daily.

  To these should be added warmth,  hot or dry.  In ovarian or
uterine neuralgias, gelsemium, 5 to 10 drops of the  fluid extract,
will be found of great value.
  In  obstinate cases of neuralgias that have resisted  all medicinal
treatment, or in that affection of the fifth pair which  is known as
tic douloureux, or when there is any pressure upon a nerve by a neu-
roma, hypertrophied bone,  or callus, it is often advisable to resort
to surgical procedures of  relief.   The removal of a neuroma or of a 
192
NERVOUS DISEASES.
 hypertrophied bone or callus  is, of course, sufficiently simple and
 needs no discussion.   When, however, the neuralgia cannot be traced
 to any gross and removable causes, such as these, nerve-stretching or
 nerve resection or section may occasionally give relief at least for the
 time beiug, and  the  patient may be willing to have the operation
 undertaken with the hope of relief that may possibly last only a few
 weeks, but that may possibly, on the other hand, last a year or two.
 Nerve-stretching  is the  least harmful of all  these  procedures, and
 there is  no question that in a number of instances it has given most
 effectual relief for an  indefinite period.   I have known it to relieve
 sciatica in seven cases for a period of a year or more.   But in the
 stretching of  a mixed or motor nerve care should  be taken not to
 stretch so  much as to  cause paralysis.  The following table of Tram-
 betta shows the amount of force necessary to rupture  the different
 nerves:
      Sciatic (trunk) .
      Internal popliteal (branch)
      Crural   ....
      Median   ....
      Ulnar    ....
      Radial   ....
      Brachial plexus (in neck)
      Brachial plexus (shoulder)
      Infra-orbital
      Supra-orbital .
      Mental   ....

   Symington  saw the sciatic ruptured  in a robust subject by the
 weight of 65  kilogrammes, and in an emaciated girl who had died of
 phthisis with only 32 kilogrammes.  No such force as is necessary
 to rupture a nerve should be employed, and it would be a safe thing
 to keep thoroughly well within the limit, because in three cases upon
 which I have operated  myself I have  seen paralysis of the facial
 result from a force that was entirely incapable of rupturing the nerve.
 In  some cases, where there are spasmodic  movements and where the
 nerve is unimportant, it is well to consider that a motor paralysis
 may be of therapeutic value in putting  the muscles  at rest, aud I
 have recommended it  in some cases with this end in view, and bene-
 ficially,  as the results seemingly proved.  Forcible flexion of the
 thigh upon the body has  apparently at times acted  as  efficiently as
 nerve-stretching, especially  in  sciatica.   The operative procedures
 that have  been done  for the neuralgia  of the trigeminus which is
 known  as  tic douloureux are   nerve-stretching,  nerve-division, or
 neurotomy, the excision of a part of the nerve, or neurectomy, and
 nerve-avulsion. Sometimes the  dental nerves are the source of infra-
 orbital neuralgia, and  then a removal of the segment of the maxillary
 tuberosity  containing  the superior and posterior dental nerves  has
 been recommended.  Carnochan has suggested  that in tic douloureux
 the trunk of the nerve should be resected  beyond Meckel's ganglion,
and that this  ganglion should also be taken out.  Horslev believes
 that  it is better to remove the Gasserian ganglion, aud has shown by
dissection that this gauglion  could be  separated  from the cavernous
sinus.  Horsley's case, in which he operated in this manner, however,
died seven hours after the operation from  shock.   Horsley reports
84 kilogrammes.
52
38
38
27
27
22 to 29 "
16 to 17 "
 2Vy 
DISEASES OF THE PERIPHERAL NERVES.
193
nineteen  cases of operations which  he has done upon the different
branches of the fifth  pair, and in some cures were effected for three
or four years, in others the pain disappeared for a variable length of
time, in some there was no relief at all, and  in  one,  which was the
operation upon the Gasseriau ganglion, there was death.   My expe-
rience has been similar.
   Chipault has collected 50 cases, with the following results :
   Nine fatal results  from operation.  Seven from removal of Gas-
serian  ganglion, 1 from  partial removal, and  1 from intracranial
resection of fifth.
    Excision of Gasserian ganglion.........25 cases.
    Removal of semilunar ganglion.........2  "  '
    Resection of fifth and partial removal of Gasserian ganglion  .      '.  6  "
    Intracranial resection of fifth..........16  "
   Results :  Excision of Gasserian ganglion.
    Improved..............7 cases.
    Recovered..............9  "
    Failed...............7  "
   Results :  Intracranial resection of fifth.
    Improved..............  6 cases.
    Recovered..............4  "
    Failed...............4  "
   Results:  Resection and partial removal of  Gasserian ganglion.
    Improved..............2 cases.
    Recovered..............2  "
    Failed...............2  "
   The  operative methods adopted  iu  cases of removal of Gasserian
 ganglion  were those  of Rose, Navarro,  Park,  d'Artieda,  Doyen,
 Horsley, Hartley,  Krause, and  Quenu.  The methods of Horsley,
 Hartley,  Krause,  and Quenu  are quite similar.  In many of the
 cases reported as improved the improvement was only temporary or
 partial.  Intracranial operation upon this nerve or the ganglion, as
 is evident, is an exceedingly dangerous and uncertain procedure.
   These surgical  procedures are,  therefore,  evidently a last resort,
 and should only be undertaken in  such desperate cases as cannot be
 treated by medicinal means, and no positive promise should  be held
 out to the patient as  to what they  will effect.

                       SIMPLE NEURITIS.

   Definition.   Neuritis is an affection of a nerve-trunk or nerve-
 branches causing, either singly or together, pain, impaired sensation,
 and motor paralysis and atrophy.
   Causes.  The causes of neuritis are—
        Traumatism ;
        Cold;
        Certain diatheses;
        Implication of neighboring organs ;
        Neuromata;
        Adenitis.
   Wounds,  contused or lacerated ;  dislocations,  especially of the
 shoulder-joint; pressure, as by sleeping with the hand under the head;
                                13 
194
NER VO US DISEASES.
 railroad injuries—may all be traumatic causes of neuritis.   Extreme
 contractions of muscles also exceptionally produce it.
   Exposure to cold is a frequent cause of neuritis.
   Gout, syphilis, cancer, leucocythsernia,  smallpox, typhoid, diph-
 theria, and  many other general  diseases would  seem at times to act
 as  predisposing  causes of neuritis, rendering  them  more  liable to
 ordinary exciting causes.
   Pneumonia, pleurisy, meningitis, articular rheumatism, and other
 joint-affections may cause neuritis by an extension of the molecular
 changes to the nerve-sheaths.
   Neuromata  are formations that  are  fully described in a separate
 chapter (Chap. " Neuromata ").
   I have seen a few  cases in which adenitis,  usually strumous in
 character, had seemingly been a  cause of neuritis.
   Clinical  Symptoms.   The  clinical symptoms of  neuritis are
 pain, impairment of the different  sensations, motor paralysis, atrophy,
 and electrical changes.
   These symptoms vary extremely in the different cases, even in the
 mixed nerves, whilst in the  cranial nerves their variation  depends,
 of  course, upon the particular character of the nerve that is affected,
 neuritis  of  the optic nerve leading to changes of  vision and optic
 neuritis; of the  auditory, to  deafness,  loud noises, disturbances of
 equilibrium ;  of the third pair or motor oculi, to strabismus, disturb-
 ances of the  pupillary muscles, etc.    Neuritis  of  the intracranial
 nerves is seldom seen  by itself, but usually in conjunction with the
 intracranial  diseases,  and  occasionally also  w7ith multiple neuritis
 and atrophy from spinal lesions, so that in speaking of neuritis in
 this chapter I shall confine  myself to neuritis of the mixed nerves.
 Neuritis of the  sympathetic  nerve-fibres  is as  yet a  very obscure
 chapter  in  pathology,  and affections which in the past have been
 supposed to be such are resolving themselves into  ordinary neuritis
 in a surprisingly large  number of cases.  ( Vide Chap. " Diseases of
 the Sympathetic  Nervous System.")
   Usually the first symptom  is pain in the affected nerve.  This will
 vary according to the  degree of the  neuritis.   In slight cases the
 pain may be so slight as not to exceed that of an ordinary neuralgia,
 but in the majority it quickly becomes severe enough to cause great
 suffering, although there are remissions, so that  it is bearable during
 the  daytime  and becomes severe at  night,  to such an extent as
 usually to interfere with  sleep.  There soon supervenes impairment
 of sensation and  motility.    The sense of touch and  the  sense of
 pain are usually most impaired, whilst temperature and the muscular
 sense are less  frequently affected, although there are many variations
 from this rule.   The  tactile sense may  be merely  blunted,  or it
 may be absolutely lost.  The  sense of pain in the slighter cases is
 usually but  slightly affected, although the conduction of the painful
 sensation may be considerably retarded.  The  muscular sense and
 the sense of temperature vary extremely in the  amount of impair-
 ment.   Motor paralysis usually comes  on quickly, and is succeeded
by atrophy in  the course of a few weeks.  Trophic changes  in the 
DISEASES OF THE PERIPHERAL NERVES.
195
skin are very constant, producing the so-called glossy skin, and when
this is observed in the fingers they become tapering in shape, which
alteration, together with  the cutaneous glossiness, is almost pathog-
nomonic.   There  may be increased perspiration, or  this may  be
decreased.  Fibrillary  twitchings  of the affected  muscles are also
occasionally observed.  Herpes is not common  in  simple neuritis.
Electrical alteration may be present both to the faradic and galvanic
current, and present the phenomena which have already been described
as the reaction of degeneration (Part  I., Chap. II.).
  Neuritis  may  be either acute, subacute, or chronic.  Its duration
varies exceedingly, and whilst it is in one sense a self-limited disease,
its self-limitations do  not follow  any general law that is at present
known.   There is  no disease that is  more modified by proper treat-
ment.
  In the acute form there are sometimes chilliness or rigor, headache,
insomnia, and slight febrile reaction, but the subacute and chronic
cases have no general symptoms.
  Pathology.   Before entering  into the pathological changes that
constitute a neuritis we  should consider briefly the  structure of a
mixed nerve.  The axis-cylinder is a continuous structure that runs
from  the central to the peripheral  organ.    The motor nerve takes
its origin from  the  anterior  horn of the spinal cord or the motor
nuclei of the medulla oblongata,  and passes out to join with other
filaments going  to the end-plate  that lies  upon the muscular fibre.
The ganglion-cells have  already been  spoken of (page 27), and it is
in the nucleus or  nucleoles of these that the motor nerve takes its
origin.  The termination  in the muscles has been carefully investi-
gated, especially by Gessler,  in  the green Italian lizard and  the
guinea-pig, and  recently (1892) by  Babes and Marinesco.  Gessler

                             Fig. 105.
Normal sciatic nerve of frog.  Obtained by teasing.
states that the motor  end-plate  is essentially the same in the mam-
malia and reptiles, and that it consists of a fine nerve-plexus, between
or under  which—for authors differ  on this very materially—lies a
finely granulated  mass, containing  two kinds of nuclei, the smaller
ones  being granulated and of irregular shape, the larger ones being
oval with double contours and a  nucleolus.  The former are known
as the Scheiden- or Gedstkerne, or, as Ranvier calls them, the noyaux 
196
NERVOUS DISEASES.
vaginaux or noyaux de Varboration, while the latter  are  the Grund
or Sohlenkerne, or noyaux fondamentaux of Ranvier   lo this motor
end-plate, lying upon the muscle, come the medullated nerve-fibres by
a right-angle, losing their medullary sheath as they pass into the nerve-
plexus just described.  The sensory nerve, on the other hand, takes
its  origin in the ganglion  upon the posterior root, and passes down
to the sensory structures of the  periphery to Pacinian  corpuscles,
the tactile bodies, the end-bulbs, and  the  nerve networks (page 30).
From  its point of  origin to  its peripheral  termination there is one
structure of the nerve that  runs  continuously, the axis-cylinder, as
has  already been  said.  This  is  a highly  nitrogenized  body con-
sisting of a number of primitive fibrils arranged longitudinally and
glued together by a minutely granular substance.   Around this axis-
cylinder is a  sheath of  myelin,  a fatty  substance which does not
pass with the  nerve into either  the central or peripheral end-organs,
and which, moreover, is not continuous in its course, but consists of
a series of tubes or segments whose points  of junction are marked
by a constriction in the contour.   Finally, around the  axis-cylinder
and the sheaths of myelin  is a connective tissue covering the sheath
of Schwann, and this is also  segmented, the point  of constriction
being known  as the node of Ranvier.  Occasionally, upon the axis-
cylinder are seen certain  lines which are known as arrow-markings,
or  markings  of Schmitt.  These  were formerly thought to be arti-

                              FlG. 106.
            Section of the human median nerve, magnified 12 diameters.

ficial products, but recently it has been  claimed that they are little
masses of protoplasm, whilst still  others maintain that they belong
to the sheath of Schwann and are connective tissue.   The sheath of
Schwann has a few sparse nuclei.  These different nerves are joined
together by connective-tissue sheaths into buudles,  forming a nerve-
trunk or nerve-filaments. Freely anastomosing capillaries run within
the nerve- and lymph-spaces, aud are to be found within the nerve-
sheath outside of the fibres.   Connective-tissue  cells and fine connec-
tive-tissue fibrils lie between the bundles of nerve-fibres.   An excel- 
DISEASES OF THE PERIPHERAL NERVES.
197
lent idea may be gained by anybody of the changes that occur in
neuritis  by making a section of the sciatic of a frog, then excising
pieces on different days  after the original section, and observing the
changes.
                             Fig. 107.
Section of the same nerve, magnified 22.5 diameters.
  Fig. 108 is a sketch of  such changes  that  were found on  the
fourth day after such  section of a  frog's sciatic.   It  will be seen
that the axis-cylinder  in  some  of these is entirely unaffected, and
that the  medullary  sheath  alone shows alteration, the sheath  of
Schwann in all being  unaltered.  The medullary sheath, as will be
observed, manifests a  tendency to  break up into various irregular
forms.  In Fig. 109, which represents at A the same sciatic nerve on
the eleventh day after section, these changes are seen to be much more
marked, whilst  the axis-cylinder in  all is more  or less affected.   At
later periods, as shown at b, representing the  fifteenth day, these
changes  in the  axis-cylinder and the medullary sheath  increase in
intensity, whilst the connective-tissue sheath of Schwann  becomes
somewhat  opaque,  and  its nuclei, which are ordinarily  sparse and
slightly stained, so that it requires careful focussing to perceive them,
multiply and  imbibe more and more of the coloring-matter.  These
molecular alterations are similar to those which take place in a human
nerve suffering from neuritis, if not identical with them.  The changes
in the myelin are supposed to be due either to a fatty or albuminoid
degeneration or a process of saponification, and there is a diversity of
opinion  as  to whether this  latter is due to active migratory white
blood-globules,  and  furthermore as to whether  the white  blood-
globules may not  be the connective-tissue cells. According  to  the
degree of neuritis, the medullary sheath may be disintegrated in vary-
ing degree or may be entirely absorbed.  It would  seem  quite prob-
able that in all cases the axis-cylinder is affected  in the human nerve,
as the above figures show that it is in the frog's sciatic, although some 
198                    NER VO US DISEASES.

authors maintain that it remains intact, being simply deprived of its
function.   The  numerous nuclei of the altered sheath of Schwann
either come from a segmentation of the original nucleus of the segment,
or are white  blood-globules  or proliferated  connective-tissue cells.

                              Fig. 108.
             Changes on the fourth day after section of a frog's sciatic.

The inter-neural  and peri-neural  connective  tissue may also become
involved in the neuritic process.  Considerable confusion exists as to
what the methods of regeneration are in a nerve that has been afflicted
with neuritis.  By some it is held that the central segment is the part
from which regeneration  begins,  whilst  others maintain that this
commences in the peripheral end, or that new axis-cylinders and
medullary sheaths may develop from the nuclei  in  the sheath of
Schwann.   In some cases  the neuritis affects the nerve-fibres, when
it is  known as parenchymatous neuritis;  whilst  in  other cases the
connective-tissue elements are mainly altered—so-called  interstitial
neuritis; and in still a third class of cases both the nerve-fibres and
the interstitial tissue may be affected together.
   Prognosis.  The prognosis of neuritis is generally good. A recent
writer, Bowlby, states that it  is invariably good, and that all cases
recover; but with this I cannot agree, because it has been my expe- 
           DISEASES OF THE PERIPHERAL NERVES.        199

rience to meet with a number of cases that did not recover, although
I am inclined to believe that proper  treatment will usually effect
a cure if undertaken before the neuritis shows a tendency to become
multiple and affect the other nerves.   In traumatic  neuritis, how-
ever, the  prognosis  may be modified by  the  nature of the trauma.
/
  A. Changes on the eleventh day after section of a     b. Changes on the fifteenth day
               frog's sciatic.                        after section.

A clean cut  across the nerve, for example, must be repaired sur-
gically, or a nerve that is caught in a mass of callus or in an inflamed
joint would have such pressure upon it as to make it impossible to
treat it unless this were surgically removed.  The duration is exceed-
ingly variable.
  Treatment.   The primary necessity in the treatment of neuritis
is to put the affected nerve at rest.   I believe the reason that neuritis
of the upper extremities and the trunk is invariably of better prog-
nosis than  neuritis  of the lower extremities is due to the fact that it
is so much easier to put  the  nerves of the upper  extremity and
the trunk  at rest.   Indeed, most  cases of  sciatic neuritis can  be
handled perfectly with  proper rest, whilst without it  the affection is
usually  very intractable.   When  there is  a neuritis of the  upper
extremities the affected arm should be carried in a sling, the patient
should have  somebody dress and  undress him, and  even in some
severe cases great benefit may be  obtained by putting the patient to
bed for a few weeks.  In neuritis of the  trunk every effort should
Fig. 109.
 
200
NERVOUS DISEASES.
be made to lessen the movements of the trunk-muscles, and this can
be obtained  in a minor  degree  by having the patient abstain  from
walking as  much  as possible, or from horseback-riding,  or  from
bending the trunk backward, forward, or laterally, or by putting on
a strong strip of adhesive plaster,  or  finally by putting the patient
to bed.  Rest  of the lower extremities can only be obtained ade-
quately by putting the  patient in bed, and this  should always be
done  at the  outset; and then, as the disease is  brought under con-
trol, the patient should abstain as much as possible from walking
or standing,  and should, if his means permit  it,  go  about in a car-
riage, or, if this is not  possible, in street cars.   In the early  stage
of a neuritis the pain  is usually the  most  distressing  element, and
this  can be overcome only by opium or some of its alkaloids, in
conjunction with quinine.  There is not the slightest use in wasting
any  time in  this initial pain  of neuritis upon such analgesics as
phenacetine,  autipyriu,  or  exalgine,  or  their  congeners.   Opium,
and  opium  alone—and I  say it  boldly—can  control  this initial
pain.   We  must, therefore,  consider  carefully the  question as to
w7hether our patient  is  of such a  nature that  he is  likely to  form
the opium-habit, and if he is, we must look frankly  in  the face the
question as to whether it is best for him to suffer the pain or run the
risk of forming this opium-habit.  It  has been my experience that
the patient is in no danger unless he is one  of those weak  indi-
viduals whom  I have described  elsewhere (Chap.  " Alcoholism,
Morphomania, etc."), who are prone  to  form habits  to which  they
speedily become abjectly enslaved.  In the many cases of neuritis
that I have treated I have never yet made an opium-eater.   Indeed,
I think there  is some subtle  law  at work here which  preveuts the
person who is in real need of opium  from  becoming a slave to it.
I always use the sulphate of morphine, taking care  that  it is pre-
pared  from a reliable opium,  as most  of the morphine of the shops
is  either from cheap preparations or  has  become stale.  I use it
hypodermically and  commence with  a dose of ^ grain.   Usually
the pain of neuritis is worse  at night or late in the  afternoon, and
this is the time when I give the hypodermic.  If necessary, I increase
the dose of morphine to the point  that will  relieve pain, and I  have
seldom had occasion to exceed f grain at  a dose.  This will usually
control the pain in a week or  two,  and then  the morphine is gradu-
ally  decreased  in quantity.   During  this period  the patient is in-
structed to take quinine, and  the  dose will vary according to the
purpose I  have in view.   If the  general health is poor, I  give 2
grains of quinine three times  a day as a tonic, perhaps adding 2 or
3 grains at the time of the hypodermic.   If the general  health, how-
ever, is good, I give 5  grains of quinine at  the time  that the hypo-
dermic is given, and  I  prefer to administer  it either  in the form of
capsules or  fresh tablet triturates, which latter should always be
tested by the physician by crumbling them between his fingers to see
if they are fresh.  Quinine in  the form of  solution with an acid is
very prone to disagree with the stomach when long continued, and I
have therefore almost abandoned its use.  As the pain comes under 
DISEASES OF THE PERIPHERAL NERVES.
201
control, I withdraw the opium, as  I have said, and  then  begin the
use of the salicylate of soda  in  conjunction  with the quinine, pre-
scribing the former in doses of 2 or  3  grains three times a day.  I
seldom use  larger  doses of salicylate of  soda, because  I  have  not
found that they add anything to the control of the disease, whilst
they are  very apt to depress  the patient.  If the quinine aud  the
salicylate of soda are not sufficient to control the pain, I add to them
moderate  doses  of phenacetine,  5  grains  once or twice a day.   It
should always be carefully ascertained that the salicylate of soda has
been carefully and reliably prepared, and  this should be as carefully
looked after as the quinine and  the  morphine have been.   Exalgine
in my hands has not been a  drug  of much  value.   Antipyrin  un-
doubtedly relieves the  pain better than either phenacetine, exalgine,
or salicylate of soda, but  the  great objection to it is the depression,
and I have for this reason  almost given  it up.   Salophen will occa-
sionally act very well in the gouty cases, in 5 grain doses two or three
times daily.   As the pain becomes a minor matter, electricity may be
used with great advantage, but  it should  never be used before this
period or it will be certain to  increase the pain, often to an unbear-
able degree.   A beginning should be made carefully with the galvanic
current.   I  have given up attempting to localize the current  to  the
affected nerve, because  in  order  to  do  this we must make use of a
very small electrode (Fig. 72), and  this necessarily concentrates  the
electricity upou the  nerve, aud this concentration irritates  it.  I
therefore prefer, when the  neuritis is in the upper extremity, to bend
electrode Fig. 68 over the shoulder, and bend electrode Fig. 69 around
the wrist, and then very gently turn on a  current of 2 to 3 milliam-
peres, permit it to pass  about three minutes, and carefully turn it  off.
Skeptics  in  the  use of electricity need only  try this at the proper
stage in a few patients  suffering  from neuritis  to satisfy themselves
of the  comfort and well-being that will  be experienced  for  from
twelve to fourteen hours afterward.   In a neuritis of the lower  ex-
tremities I also make  use of electrodes Fig. 68 aud Fig. 69, aud
place them so as to bring the whole limb into the  circuit between
them.  If a nerve of the  face is affected, or one  hand  or foot,  the
same principle should  be  made use of in the selection of suitable
electrodes, taking  care  always to select  as  large  ones as possible.
The quantity of galvanism should not be increased  for a week or two
beyond 3 milliamperes,  but if the first  two or three applications do
not irritate the nerve, the sitting may be prolonged  from three to five
or even fifteen minutes.  After the galvanic treatment has  been suc-
cessfully  applied for a  week or two, the process of regeneration can
be greatly aided by also  employing the  faradic battery, care being
taken at first to use a very gentle current, so  that the patient barely
perceives it,  applying it for only three minutes, and increasing  the
length of the sittings and the strength of the current very cautiously.
In some cases even where galvanism is well borne, faradism will not
agree with the patient, and in  such  a case galvanism alone should be
used.  As the nerves become less  irritable,  the sittings with both
currents may be prolonged, and in  some instances  I even allow the 
202
NERVOUS DISEASES.
patients  to apply the  galvanic  current for a half-hour or forty-five
minutes, and the faradic for the same time or even longer.
  In the early stages of neuritis, when the pain is only relatively
well controlled by the analgesics that  have been described, a large
blister applied  somewhere near  the affected nerve, but not upon it,
will usually relieve the pain in  a marvellous way for  a  day or two,
and in a less degree the same effect will  be obtained by cauteriza-
tion near the affected nerve  by a Paquelin cautery or a poker brought
to a white heat.  The cauterization should be done  only by light
stripes, and it is not well to cause more than a  very superficial scar,
because the tissues that are  enervated by a diseased nerve may break
down into a  troublesome ulcer, as I have  seen in  more than one
instance.
  Great attention should be paid to the general  health of the patient.
Anaemia should be carefully searched for by listening for  any anaemic
murmurs in the heart and large  vessels, and perhaps by a microscopic
examination of the blood.   If anaemia is present, iron should be used
in  full doses, and the best  preparations for  this purpose are the
albuminate of iron or the peptonate, the  former in doses of 5j three
times a day,  and the latter in doses of gr. ij-iij three times a day;
or ferratin, gr. iv-viij three times daily, in capsules.  With the iron
should be conjoined abundance  of nitrogenized  food in the form of
meat and beef-tea.  It sometimes will  be found useful in these cases
of anaemia to combine with  the iron  small doses of bichloride of
mercury (-A^  to -Aj  of a grain) three  times a  day (vide  Part II.,
Chap.  III., " Neuralgia ").
  If there is  no anaemia, but the patient's general health is depressed,
tonics of quinine and bark, 2  grains of the former three times a day,
and of the latter the officinal elixir of calisaya, ^ ounce three times a
day, should be administered.    Malt-extracts will usually be found
to  be  of great  use  in this restoration of  nutrition, and  any good
fresh malt-extract that  is  known to contain  a sufficient quantity
of diastase will answer  the purpose.  Occasionally cod-liver oil is
also useful, and when the patient can take  it pure, I prefer to give
a reliable oil  in this way;  but if an emulsion  is used, it should be
made fresh every week or so, and kept in a cold place, best on ice.
Arsenic I have not found to be of very great use in neuritis, although
it often proves of surprising value in neuralgia.
  Surgical procedures are never applicable to neuritis, but they some-
times come into play in the neuralgia that may be  left  after  a neu-
ritis, iu which  event the considerations pro and con are the same as
in neuralgia.
                      MULTIPLE  NEURITIS.

  Definition.  Multiple neuritis is that form which affects different
nerve-trunks or filaments throughout the body or extremities, often
seemingly in  a most capricious manner.
  History.   The first description  of multiple neuritis was  given
by  an American physician,  Jackson,  of Boston, in  1822.  Huss,
describing  chronic alcoholism in 1852, described a neuritis, without, 
DISEASES OF THE PERIPHERAL NERVES.
203
however, being aware of the pathology of what he was describing.
In 1855 Duchenne also made known similar cases under the head of
"general subacute ascending spinal paralysis."   In 1864  Dumeuil
published  his first autopsy; in 1864 Eichhorst, of Berlin, had  the
second  one; and  in  1877 Joffroy published the  third.   In  1880
several cases with autopsies were reported by Leyden, and since then
the literature has become abundant, and has been contributed  to by
Laucereaux, Graiuger Stewart, Mills, and by Starr.
  Etiology.  The causes of multiple neuritis are—
    Toxaemia  from  such poisons as alcohol,  arsenic, lead,  bisul-
       phide of carbon;
    Infection  of such  diseases  as diphtheria,  typhoid, typhus,
       variola, malaria, tuberculosis;
    Cold, dampness, and overstrain;
    Syphilis;
    Sex;
    Age;
    Epidemics.
  These causes are so well known  that they need not be dwelt upon
except those relating to the epidemics of the disease.
  This epidemic type  is very prevalent among the Japanese,  and is
called Kakke, from two Chinese words, " kaiaku," meaning legs, and
" ke," a disease, and  it has been known to the Chinese as far back
as 200 years before Christ, although  it seems to have ceased about
200 years  ago.   In  Japan, however, according to Starr, 14 per
cent, of the men  serving in the army in  1877 suffered from it, and
38 per cent, in 1878.  Dr. Wallace Taylor  tells me that the disease
has diminished since wheat has taken the place of rice in some places,
from which it  would seem that this article of  food bore some etio-
logical  relation to the disease.  Europeans are not affected by it.  It
prevails to some  extent in the islands of the Pacific Ocean, in  India,
Ceylon, the west coast of the Red Sea, Borneo, New Guinea, Brazil,
Cuba, and the Dutch  possessions in the China Sea.  In these  places
it is endemic, occasionally epidemic.
  Clinical History.   The symptoms of multiple neuritis consist
of motor aud sensory  symptoms in the upper and lower extremities,
the special nerves  being rarely affected, and the trophic  symptoms
being marked.   The first symptoms to appear are the sensory ones.
The disease  usually develops with  pain of a burning kind affecting
the feet and hands, and with this are associated numbness, tingling,
or formication.   This pain is usually moderate in degree, but  occa-
sionally becomes extremely severe.  There is also at this time a sin-
gular tenderness  of the nerves and muscles,  and there may be some
hyperaesthesia, and even,  though rarely, anaesthesia.   It is seldom,
however, that the tactile sense is entirely impaired,  and when it is, it
is in areas.   As the disease progresses  there supervenes a  paresis of
the affected  limbs, and the sensory impairment may  become  more
marked, although seldom to any complete extent, there being usually
only delayed transmission of pain and temperature, some dulness of
the muscular sense, and, as I have already said, impairment of the 
204
NERVOUS DISEASES
tactile sense.   The motor paresis, which may have been simply felt
as a  sense of weariness or  fatigue, passes  on to actual paralysis,
usually  in from ten days to three weeks.   Paralysis  may develop,
however,  in  a few  days,  aud  it is probable  that  some cases of
acute ascending paralysis terminating fatally are multiple neuritis.
The paralysis is very capricious in  its anatomical distribution, and
may affect certain filaments in  one nerve-trunk aud leave the others
unimpaired, and thus affect a number of nerve-trunks.   The paral-
ysis is a flaccid one, the tendon-reflexes  are abolished, and atrophy
supervenes in  the course  of a  few weeks.   Electrical alterations
are extremely variable.  In  some cases there is simply diminished
response to galvanism and  faradism;  in  others, complete loss of
response to faradism and  response  to a very strong galvanic  cur-
rent; in others, the response is greater with the negative pole; in
others,  still greater  with the positive  pole; and in some there is
an actual reaction of degeneration.   All sorts of abnormal muscular
deformities may result from the different forms of paralysis, but
a dropped foot aud  a dropped  wrist are the  most frequent, although
the claw-shaped hand and the different forms of talipes are frequently
observed.   As has  been said, vasomotor and  trophic symptoms are
not so frequent as the sensory and paralytic ones.  Temporary oedema
in the feet and hands, coldness and cyanosis, profuse and offensive
perspiration,  glossy skin,  temporary inflammations of joints,  and
bulbous fingers, are  occasionally  observed.
   The onset is usually without fever, or this is slight, but occasionally
there may be  a chill and a temperature of 103° to  104° F., and
this may  persist for several  days.   In other cases  the temperature
may not rise  more than one-half or two degrees.  The pulse is usu-
ally but slightly above the normal, and it is only iu the dangerous
cases that it rises above 120.
   The disease is somewhat more common in males than in females.
   Children are rarely affected,  if at all.   Most cases occur between
twenty  and forty.
   Prognosis.   The prognosis in multiple neuritis is good, although I
have seen a number of cases in which permanent muscular deformity
had been left.  Alcoholic patients in whom the general health has been
shattered  usually become chronic or die, although it is surprising to
see the improvement that will take place in them when drinking has
been  stopped  and the general  health has been built up.  I have in
several instances known such a patient to be so completely paralyzed as
to be helpless in bed, and yet attending to his  business in the course ot
twelve weeks.  Nevertheless, recovery is always much slower in per-
sons who are intemperate or who have been so in the immediate past.
   Diagnosis.   The diseases from which  multiple neuritis should be
differentiated are—
     Simple neuritis;
     Numb fingers;
     Myelitis of the anterior cornua ;
     Locomotor ataxia;
     Acute ascending paralysis of Landry. 
DISEASES OF THE PERIPHERAL NERVES.
205
  Simple neuritis is confined to a nerve-trunk, and the pain is not
burning, but sharp aud stabbing.  This limitation of the paralysis
and the character of the pain alone will serve to make the diagnosis.
  Numb fingers is an affection that was first described  by Putnam,
of Boston, and  is observed in women between forty and sixty, con-
sisting of a tingling sensation in the finger-tips and fingers, or even
the hand, and rendering the movements of the  hand awkward, be-
sides causing a  feeling as if it were asleep.   In some of these cases
there may be a slight degree of anaesthesia and analgesia, but usually
there are no objective changes.
  In myelitis of the anterior cornua, the so-called  essential infantile
paralysis, the affection is purely a motor one, there being no sensory
implication  whatever, and  the muscles affected are almost invariably
limited to a group in one limb, generally in the leg or around the
shoulder  or in  the upper part of the arm.   The entire lack of sen-
sory symptoms  and absence of any tendency to implicate other mem-
bers will usually, therefore, make the differential diagnosis.
  Locomotor ataxia is  a chronic disease, is characterized by sudden,
atrocious, stabbing or lightning-like pains,  which come in very tem-
porary paroxysms and  are  seldom continuous, and there is ataxia,
either preceding the pains or succeeding them ; whilst the muscular
strength is unimpaired, and glossiness of skin, tapering fingers, and
muscular tenderness are absent.  Atrophy of the optic nerve is often
present.
  In  acute ascending  paralysis the  sensory symptoms are usually
entirely lacking, and the paralysis is the salient symptom, beginning
in the lower extremities, ascending in a few days, or even  hours, to
the upper extremities, and often causing bulbar symptoms.   Death
generally ensues in a week or two, sometimes in a day or two.
  Treatment.  The treatment of multiple neuritis should be at first
by absolute rest in bed  in the acute cases, aud iu the chronic ones there
should be such rest for at least a period of one to four weeks.  The
pain can  best be  relieved  by means of warm  applications  and sali-
cylate of soda and quinine.  I shall  never forget the lesson  that I
was first taught as to  the value of hot applications by seeing the
comfort and ease that were given to a youth afflicted with this disease
by immersion of his feet in a tub of hot water.  Swathing the feet in
cotton, over which in its turn should  be placed a strip of gutta-percha
or oil-silk, will give great comfort.   At certain periods of the day,
however, especially toward night, when the pain is apt to be worse,
the patient  may often obtain great relief by putting the feet and hands
in hot water for about half an hour, and then loosely tying around
them a piece of muslin soaked in a mildly  alkaline solution (10 grs.
bicarb, soda to  1 oz. water), with perhaps the addition of some chloro-
form.  Gently rubbing the limbs with oil is often useful also.   Sali-
cylate of soda in doses of 2 to 3 or 5 grains, three or four times a day,
with 2 or 3 grains of quinine at the same time, is generally the best
treatment.  I have  repeatedly observed a  curious  fact  in regard to
treatment to which I have never seen attention called.  Iu several of
my  patients iu  whom the pain  could  not be controlled, and in  whom 
206
NERVOUS DISEASES.
the disease was progressing, removal from the locality in which they
had been attacked to another would often effect a marvellous change.
As my first cases were seen in a malarious, low-lying district, I sup.
posed that there might be some malarial element at play, but I have
since observed the same thing in several other cases in which the dis-
ease had commenced in a non-malarious neighborhood, so that I now
look upon this as a very important  matter iu the treatment, at least
of the cases which we see in and around New York.  If there is an
actual  malarial history, quinine or Warburg's tincture should be used
in sufficient  doses.  In  the alcoholic cases some skill is required in
the withdrawal of the alcohol, and it should always be reduced very
carefully, making use of quinine as a stimulant in its place, and the
doses of quinine should be proportioned to the needs of such a patient,
so that in some cases as much as 5 grains of quinine may be given
every two or three hours, whilst  in others only 2 grains three times
a day may be needed.   If quinine  produces  any cinchonism in the
doses that are necessary to adequate stimulation in place of the alco-
hol, conjoin with it  mild doses of the  bromide of potash, 10 grains
three or four times a day.   When the alcohol is entirely withdrawn,
place the patient upon a malt liquor, either a heavy English or German
beer; and after using  this for some time, taper off with an alcoholic
malt-extract; i. e., a malt-extract  in which the diastase is combined
with alcohol.  When the pain has passed off, galvanism of the affected
muscles and faradism will be found to be extremely useful.  Massage
will often  be of use at this stage, but it should  be very gently done
without any griping whatever of  the muscles, bearing in mind that
its object is only to facilitate the passage of blood  through  the mus-
cular tissue without mechanical irritation of it.  Strychnine, j^j to
■A^ grain,  three times a day, will  be useful in this chronic stage, and
also arsenic, best in the form of Fowler's solution, two or three drops
three times a day.   As improvement goes on and all tenderness dies
away, and the muscles begin to return to their normal bulk, Swedish
movements may be employed in addition.  In the cases that have had
a syphilitic history, iodide of potash in large doses, with inunctions
of mercury should be used.

                      FACIAL PARALYSIS.

  Synonyms : Bell's palsy.   Prosopalgia.
  The symptoms of facial paralysis are an inability to shut the eye,
lagophthalmus, a loss  of power of the facial muscles in the affected
side, so that the naso-labial fold is lost, a puffing-out of the cheeks in
whistling, and sometimes a deviation  of the uvula and  soft palate.
The statements of authors differ very much in regard to the direction
in which the tongue is pointed in  facial paralysis, some maintaining
that it is  put out  straight, others that it  is protruded to  the sound
side, and still others  that it deviates to the paralyzed side.  The truth
seems to be, as Hitzig states, that it is generally put out straight in
the lighter forms, but that in severe and protracted cases it deviates
to the sound side; and if it does, and the angle of the mouth on the 
DISEASES OF THE PERIPHERAL NERVES.
207
paralyzed side is drawn to its proper place, the tongue will straighten.
Very often,  too, there is an alteration of taste on one  side of the
anterior portion of  the  tongue, which,  as we have already  seen
(Part  II., Chap. II., "Taste"), is supplied by the lingual nerve,
deriving its gustatory fibres from  the chorda tympani, whilst the
sense of taste in the  posterior portion of the tongue supplied by the
glosso-pharyngeal  is unaltered.   Reaction of degeneration or lesser
electrical changes are also usually found in the affected muscles.
  The causes of facial paralysis are exposure, a so-called rheumatic
diathesis, disease of the middle ear, traumata, certain febrile diseases,
lesion of the nucleus of the facial in the  medulla  oblongata, in the
fibres  of the facial in the pons, or in the  centre of the facial in the
motor area of the  cortex, and spinal lesions.  The most frequent of
these causes  is  exposure, as to  a high  wind, to the draught from  a
window, to great excesses of temperature, or to bad weather.   It has
been supposed  that  the  rheumatic diathesis—as  evidenced by the
predisposition to rheumatism in  different parts of the body—is also a
cause, but although this does occur,  it is not so frequent as is generally
imagined.   A  frequent cause is disease of the middle ear, such  as
caries of the petrous portion of the temporal bone, or those chronic
middle-ear troubles which are so frequently left as sequelae of scarla-
tina or diphtheria.   Trauma can also be a cause, either from a blow
upon the ear, a fracture at the base, or the pressure exerted upon the
infant's head in difficult or instrumental  delivery.   Certain febrile
diseases may predispose  to facial palsy, such as diphtheria,  variola,
typhus, scarlet fever.  The  lesions of the facial nucleus  of the pons
and the motor area  producing  facial paralysis need  only be men-
tioned in this place as a reminder.   Such spinal lesions as locomotor
ataxia  and Landry's paralysis  are occasionally accompanied by  a
facial paralysis.
  The prognosis will vary greatly, accordingly as  the disease is due
to a peripheral lesion or to a central one ;   in other  words, whether it
is a neuritis  or a neuritis due  to a central  lesion.  The neuritis is
usually of good prognosis.  The degree of reaction  of degeneration
will generally be a guide in the prognosis of these peripheral cases.
If there is but  little alteration  iu  the reaction  of the galvanic and
faradic currents, the  prognosis is excellent,  and the affection will  pass
away in a few weeks. If there is a  partial  reaction  of degeneration—
i. e., the faradic and  galvanic response of the nerve has been greatly
impaired, but not entirely lost, whilst the muscles display qualitative
and quantitative alteration  in the  galvanic reactions  as well as in-
creased response to mechanical excitation—the prognosis  is fair, and
a cure will be  obtained in the course  of two or three mouths.   If
there is a pronounced and  complete reaction  of  degeneration,  the
prognosis is unfavorable, although even  in some of these cases  a
relative cure may be  effected, leaving slight twitching and paresis in
the muscles.   In the cases of lesion of the nucleus of the facial, as
in some cases of  labio-glosso-laryngeal paralysis, the prognosis is
unfavorable.  Iu lesions  of  the  pons the prognosis is  generally un-
favorable, except where the  lesion is in the pons at the  apparent or 
208
NERVOUS DISEASES.
superficial origin of a nerve  and  is only a part of  an intracranial
syphilis  which  is  brought  under  vigorous  treatment  in  the early
stage, when  the prognosis may be fair.   Iu lesions of the motor area
of  the cortex implicating the centre of the facial, the prognosis will
vary according  as it is syphilitic  or not, being fair in the specific
cases that are brought under treatment  in  the early stage, and bad in
almost all others.
                                  Fig.  110.
              Diagram of the facial nerve, its connections and branches.
                          (From Hermann's Physiology.)

F. The facial nerve.     A.  Auditory nerve.
        1. The geniculate ganglion.
          gsp. Great superficial petrosal nerve connecting the facial and Meckel's ganglion.
          ssp. Small superficial petrosal nerve connecting the facial with the Otic ganglion
              and with the tympanic branch of the glosso-pharyngeal.
          esp. External superficial petrosal connecting the facial with the plexus on the
              middle meningeal artery.
          Chorda tympani, joining lingual nerve.
          Nerve to stapedius muscle.
          Communicating branch with the ganglion of the root of the vagus.
          Posterior auricular nerve.
          Branch to the stylo-hyoid and digastric muscles.
        Temporo-facial division! t„„, „„,„   -
            .  ,   , ,.   .    f to muscles of expression.
        Cervicc-facial division ■*
TF.
CF.
V. Fifth nerve,  at. Auriculotemporal branch.
        id. Inferior dental nerve.   I. Lingual nerve.
     MG. Meckel's ganglion.
     OG. Otic ganglion.
     SG. Submaxillary ganglion.
     IM. Internal maxillary artery.
     MM. Middle meningeal artery.
     P. Pneumogastric nerve.
     GP. Glosso-pharyngeal nerve.
        t.  Its tympanic branch (nerve of Jacobson)
   The diagnosis of a  facial  paralysis  is a matter of no difficulty, as
the open eye, the flattened face, and the cheek bellying out when any
marked expiratory efforts are made, are pathognomonic.  But it must 
DISEASES OF THE PERIPHERAL NERVES.
209
be remembered that the  causative lesion  may be peripheral, in the
middle ear, at the base of the cerebrum, or  in the nucleus of origin of
the nerve in the medulla oblongata.   The  course of the facial in the
internal capsule (p.  59),  as well as the  cortical  centre (Plate  I.),
need not be considered in  this process, of differentiation, because a
lesion of either site would not involve the  fibres to the eyelid on one
side, and the levator palpebral superioris would not be paralyzed.   A
peripheral site of  the lesion  may  be diagnosed by exclusion of one in
the middle ear, the cerebrum, or the medulla.  Fig. 110 will show the
relation of the  facial nerve to  the  middle ear.  Fig. Ill gives an
View of the inner wall of tympanum, enlarged. (Gray.)
excellent view of the inner wall of the tympanum.   From these two
figures a clear idea can be obtained of the branches of the facial nerve
and its connection with the middle ear.   A lesion in the aqueduct of
Fallopius, situated  between 3 (Fig. 110), the stapedius  nerve fila-
ment, and 2, the chorda tympani, will cause impairment of the sense
of taste  in the corresponding anterior two-thirds  of  the tongue, as
well as diminished salivary secretion on the same side.  If there is a
lesiou between the nerve-filament to the stapedius (3,  Fig. 110) and
the geniculate ganglion (1), there will also be abnormal acuteness of
hearing—hyperacusis.  Implication of the geniculate  ganglion itself
adds paralysis of the soft palate and distortion of the uvula to the
symptoms.   A lesion above the geniculate ganglion will cause most
of these symptoms—facial paralysis, lagophthalmus, lessened saliva,
paralysis of the soft  palate, and deviation of the uvula; but there will
be no impairment of the sense of taste in the anterior  portion of the
tongue, aud there will probably  be deafness, as the  auditory nerve is
close by; moreover, bone-conduction, as tested by the tuning-fork, will
probably be increased (vide Part  II., Chap. II.).  A lesion at the base
of the cerebrum wrould be certain to involve the auditory (Fig. 36),
would be  likely to  implicate  the neighboring cranial nerves,  and
would be  caused by an intracranial neoplasm, arterial disease, intra-
                                 14 
210
NERVOUS DISEASES.
 cranial syphilis, cerebro-spinal meningitis, or a trauma of the skull.
 Au isolated lesion  of the facial nucleus in the  medulla oblongata
 would  be a clinical  curiosity, as this is generally affected by disease
 involving the nuclei of other cranial nerves, such  as progressive
 muscular atrophy, labio-glosso-laryngeal  paralysis, and occasionally
 Landry's paralysis.  Disease of the pons Varolii (Part II., Chap. I.)
 might also implicate the fibres of the facial.    The  diagnosis of a
 peripheral  lesion of the nerve  must, therefore,  be  arrived at by
 exclusion of disease in  these different regions  through which the
 facial passes in its devious career.
   The  treatment of Bell's palsy will resolve itself iuto a treatment
 of the  lesion causing it.   In the one  case,  therefore,  the middle
 ear  must be treated; in another, the causative lesion  at the base of
 the cerebrum;  in a third, the affection at play in the internal capsule,
 the centrum ovale, or the centre  in the cortex; and in a fourth, the
 neuritis itself, although it should not be overlooked that this neuritis
 must also be cared for even when it is induced  by one of the central!
 lesions.   A neuritis of the facial,  however, is identical with a neuritis
 of other  nerves, so  far as the art of therapeutics is concerned, and
 my reader must, therefore, look to " Neuritis."  As the latter deals
 mainly with the mixed nerves, though, its suggestions for the relief
 of pain may be disregarded.   Fig. 82 will show the motor points of
 the facial.
                           NEUROMA.

   Synonyms: Hyperplastic  neural growths or formations.  Nerve-
 tumors.
   Neuromata are morbid growths upon the  peripheral nerves.  The
 name seems to have first been used by  Odier in  the year 1803.  They
 are classified as—
     Stump-neuromata.
     Painful neuromata.
     Nerve-trunk neuromata.
     Tendril-neuromata.
   Stump-neuromata  are  found in nerves which  have been severed.,
 The first description was given  by Lower in 1669.   All severed
 nerves  have a tendency to become club-shaped  at  the  central end,
although the nerve-fibres are not otherwise altered.   They are found
at various times after section, from two up to many years.
   The painful tubercles (tubercula dolorosa) are small  tumors gener-,
ally lying upon small subcutaneous nerves, circumscribed, movable
in all directions,  very painful upon pressure, and giving rise to neu-
ralgic attacks from cutaneous  irritation.   They were first described
by Cheselden in 1750.
   Nerve-trunk neuromata are, as  the name denotes, to be found upon
the trunks of nerves, and are either single or multiple.
   The tendril or plexiform neuromata consist of a diffuse hypertrophy
of several  nerve-trunks,  branches, and fibrils within a certain  area.
The first description was given by Robin in 1854.
   These different varieties are divided into two  great  classes: true 
           DISEASES OF THE PERIPHERAL NERVES.        211

and false.   The true neuromata consist of medullated or non-medul-
lated nerve-fibre, and between the nerve-fibres is a varying amount
of connective tissue.  Of the false neuromata, fibromata are the most
common, although  myxomata, gliomata, sarcomata, and carcinomata
are  occasionally  met with.  Syphilomata are very rare, except on
the cranial nerves.
  Causes.   The neuromata of the stump are found either in sections
of nerves that have been severed, or after amputations.   The age of
patients suffering from painful tubercles ranges from youth up to the
sixtieth year, although the majority are found between  the twelfth
and fortieth years.  Women  are more  subject to them than men.
Most of them are found about the leg, next around the mammae, less
frequently about the upper extremity, next in frequency about the
head, and seldom in other parts of the body.   The trunk-neuromata
are seen most frequently from the tenth to the fortieth year, although
they are observed occasionally  in  childhood, and even up to the
eightieth year.  There seems to be no difference in the susceptibility
of  the  sexes.  The optic nerve is most  prone to single trunk-neuro-
mata, and after this the median and the ulnar, next the sciatic and
the radial,  although  they are  found in almost all the nerves of the
body in much less degree.   Thus, contrary to what has  been ob-
served  in  painful  tubercles, single  neuromata are found about one
and a  half times more  frequently in the upper extremities thau  in
the lower.   No  explanation has ever been  given of this difference.
 Multiple trunk-neuromata seem to occur more frequently between
the twentieth  aud  thirtieth years, but  nevertheless they have  been
 seen at all periods  of life.   Males are very much more subject to the
 disease than females.   All  the  nerves  may be affected, and there
 seems  to be no  special predisposition for any one, except that the
 spinal  nerves  are  somewhat  more frequently implicated  than  the
 cranial.  The tendril or plexiform neuromata are often  congenital,
 often arise  in childhood, and occur up  to about the thirty-seveuth
 year.   Males are twTice as subject to this form as females.  The  head
 and neck are  most affected.   Other causes  are traumata, cicatrices,
 and neurotic predisposition.
   Clinical  History.   It  not  infrequently happens,  curiously
 enough, that there are no symptoms at all,  especially in  the case of
 trunk,  multiple, and plexiform neuromata.   When symptoms are
 present, they vary  in character according to the nerve that is affected.
 Thus, a neuroma of the optic nerve may lead to impairment of vision,
 of the  facial nerve  to paralysis, the mixed nerves to commingled sen-
 sory and motor  symptoms, such as pain, ansesthesia, and  muscular
 spasms; of the trigeminal nerve, to impairment of the muscles of
 mastication, or pain, or both ; of the sympathetic nerve,  to the vari-
 ous symptoms that lesions of the sympathetic give rise to; and of the
 pneumogastric, to  gastric disturbances.   When the neuromata are in
 superficial  situations they may be felt, and they sometimes give rise
to  tumors  that can be seen, and  occasionally to bead-like  swellings
 when  there are multiple neuromata.  They are sometimes sensitive 
212
NER VO US DISEASES.
upon pressure, sometimes not,  although the painful  tubercles are
almost always painful.
   Prognosis.   The prognosis of neuromata, so far as the removal
of the tumor is concerned, is bad, unless it is in such a superficial
position as to be reached by applications or surgical operation.
   Diagnosis.   The diagnosis of  neuroma cannot be made unless
the growth is superficial, so as to be felt or seen, although it may be
suspected when there is impairment of a nerve-trunk that cannot be
explained in any other way.
   Treatment.  In syphilitic  neuromata  treatment should always
be tried by large doses of iodide and mercury, although I think that
the mercury is better than the iodide in these cases, contrary to what
has been observed in syphilis of the central nervous system.  Iodide
should be  pushed in large doses (gtt.  60 to  200 of a saturated  solu-
tion), or mercury should be pushed to the point of slight ptyalism,
and it should  be used in two ways, namely, by painting  the neuro-
mata, when they are superficial, with the  oleate of mercury (U. S.
and B. P.) once  or twice daily;  and also by inunction of the un-
guent, hydrargyri (U. S. and B. P.), 5j  night and morning. If the
neuroma  is single,  and  situated upou a nerve whose impairment of
function is not of much consequence, it should be excised;  thus, all
neuromata of cutaneous nerves  should be  operated upou.   Neuro-
mata, when lying upon important nerves, however, should not be
excised unless it is possible to do so without seriously impairing the
function of the nerve, and sometimes this can only be determined by
an exploratory incision.  But there is a strong tendency to relapse,
and  then an operation may again become necessary.  All  painful
tubercles should be excised. Plexiform neuromata cannot be operated
on.  In all cases  it  may be necessary to overcome the pain, and this
may be done by means  of analgesics employed internally.   Cauteri-
zation has occasionally cured  painful  tubercles for the time being,
although, as in the  case of operation, there are often relapses; and
the same may be  said of counter-irritation.  In some few cases cau-
terization has  effected  a cure in trunk-neuromata. In 29 cases of
tendril or plexiform neuromata,  gathered by Courvoisier, the results
were as follows:  Cured, 14;  uncured, 4; relapses, 3; death by sep-
sis, 4; result doubtful, 2.  When cauterization is performed, it should
be by means of the  Paquelin cautery, or iron heated to  a white  heat.
Counter-irritation may be by  means  of caustic potash,  or by the
nitrate of silver stick. 
CHAPTEE    IY.
      DISEASES OF THE SPINAL CORD AND  MEDULLA
                         OBLONGATA.

                          MYELITIS.

  Synonyms :  Acute or general diffuse myelitis.  Softening of the
cord.  White softening of the cord.   Transverse myelitis.   Inflam-
mation of the cord.
  Definition.  A diffuse or transverse inflammation, softening, or
sclerosis of the spinal cord giving rise  to  commingled motor, sen-
sory, rectal, and vesical symptoms that are different iu their grouping
from those of the localized or so-called systemic spinal diseases, such
as myelitis of the anterior horns or cornua, locomotor ataxia, or lateral
sclerosis.
  History.   The ancient physicians—among others  Hippocrates,
Aretseus, Galen—seem to have had some indistinct idea of  myelitis,
but not to have been capable of differentiating it in any way.  Until
the  beginning of this century diseases of the  spinal cord were not
distinguished from diseases of its membranes, both being known by
the  terms of rhachialgitis or spinitis.  Hildebrandt (1764-1816) in-
troduced the terra notaeomyelitis.  There is some little  dispute as to
who first coined  the modern term of myelitis, Erb claiming that it
was first suggested  by Klohss  in 1820, whilst Leyden states  that
it is due to Leon  Hardi, although the latter included both spinal and
meningeal affections under this term.  The  first exact description of
what is termed myelitis at the present time was given by Ollivier in
1821, and Abercrombie followed in 1828 with  another fair delinea-
tion of the malady—this, too, although Frank in 1792, Harless in
1814, and Klohss in 1820  had written upon the subject.  Duchenne,
Tiirck, and  Romberg amplified the succeeding knowledge of the
disease by their descriptions of  the different forms of myelitis, both
primary and secondary.   About 1860 may be dated the beginning
of the modern physiological,  pathological, and  histological  study of
the disease, and among the pioneers in this era the foremost has prob-
ably been Brown-S6quard, although a number of important obser-
vations have been contributed by numerous other observers, such as
Oppolzer, Frommann, Mannkopf, Levy, Lockkart Clark, and Gull.
More  recently the school of La Salpetri6re, under the  guidance of
its celebrated master, Charcot, has added enormously to our knowl-
edge of the subject, as indeed it has of many other  nervous maladies;
whilst a great  literature has  grown from the writings of a host of
observers,  prominent among whom are Westphal,  Leyden,  Erb,
Seeligmuller,  Striimpell, Grasset, Liebermeister,  v. Renz,  Gowers, 
214
NERVOUS DISEASES.
Buzzard, Ross, Stewart, Hammond, Spitzka, Seguin, Mills, Mitchell,
and  Wood.
  Symptoms.  The onset may be acute, subacute, or chronic.  AVhen
acute, there may be fever up to  102° or  103°, and the pulse may be
quickened, as to  120 or 130.  Except in children, there are seldom
any  convulsions.
  The symptoms will, of course, vary with the portion of the spinal
cord that is affected.  If reference  is made to page 82, where a de-
scription is given  of the different symptoms  arising  from lesions
of the different portions of the  cord, it will  be seen how great  may
be the variety in the clinical phenomena.   In all cases, however, the
symptoms  are of a commingled motor,  sensory, rectal, and vesical
nature, the particular sensory or motor area that is affected varying
with the locality of the spinal cord affected by the  disease.  Usually
the motor symptoms precede the sensory by a short interval, but it
not infrequently happens that the reverse may be the case.   Usually,
too,  the vesical symptoms succeed  the distinct supervention of the
motor and  sensory oues,  but in this case, too, it occasionally happens
that  the vesical symptoms are the primary ones.   Whether the symp-
toms be  motor, sensory, rectal,  or  vesical, they are apt to  be irrita-
tive  in their nature at first rather than destructive;  for  instance,
slight disturbances of sensation and motion,  or of the bladder or
rectum, first occur some time before paralysis supervenes.   Thus the
early symptoms are apt to  be  some slight  impairment of motion,
some heavy, lead-like feeling of the limbs, which the patient may be
unable for  some time  to distinguish from  fatigue; or  there may be
slight sensory disturbances (parcesthesice), such as furriness  and ting-
ling  in the  fingers  and toes, a feeling as if  ants were  creeping  over
the limbs (formication), or a sensation as  if the fingers or toes had
gone to sleep, or that peculiar sensation of a vibration running up
and  down  the limb,  which is known  by the technical  name of
dysesthesia.   After a period of time,  however, which will  vary
accordingly as the disease is acute or subacute, the  irritative symp-
toms give  place to paralytic ones.   The heavy, fatigued feeling of
the extremities is succeeded  by a downright paralysis, and the various
trifling sensory disturbances are succeeded by impairment  in differ-
ent degree  of the senses of touch, pain, muscular sense,  and tempera-
ture. There is a symptom which is peculiar to myelitis—being seldom
found in the systemic spinal diseases—the cincture or girdle^eelmg.
It consists  of a sensation  about the abdomen, chest, or one of the
limbs as of an encircling, constricting band or string, which will vary
in breadth.  This corresponds to the main focus of the lesion. Above
it there is generally a zone  of hyperaesthesia, answering to the irri-
tated portion of the cord just above the focus ; and this zone can be
detected by the passage of a hot sponge over  it, when  pain will be
felt  instead of warmth.   Paraplegia is  the most  common form of
motor paralysis, although the upper extremities may  be affected in
some exceptional cases.   The  sensory impairment  may vary   from
slight paraesthesia to downright anaesthesia.  As a rule, paralysis does
not occur so suddenly in the acute cases as in the case  of myelitis of 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  215

the anterior horns, although it may be fully established within a day
or two.   In the subacute forms the onset of the paralysis may be
spread over a week or two; whilst iu the chronic cases  it may be
very slow for weeks or even  months.
  The reflexes, both cutaneous and of the tendons, vary according
to the stage and localization of the disease.  Reference to the chapter
"General Motor and Sensory Symptoms" (Part II., Chap. II.) will
make the  reader acquainted with these different reflexes and the
methods of eliciting them.  The knee-jerk is usually diminished or
abolished in early stages, but  it usually becomes exaggerated later on;
and in this latter period the foot-clonus is often obtainable.   The
cutaneous reflexes are generally lessened or lacking at first in the area
of skin innervated by  nerves from the affected portion of the cord,
but they soon become exaggerated, too.
  The electrical  reactions are normal, as a rule, although some reac-
tion of degeneration may occasionally be obtained.
  The duration  of the disease  will vary from a few days to years.
There is one rare form  in  which frequent relapses occur.   The fact
has been overlooked that some of the chronic  cases, lasting several
months to a year and a half, are really self-limited in their duration,
and will recover with little treatment other than  rest and  protection
 from physical strain and exposure, as I have seen in several instances.
  Causation.   The main causes of myelitis are—
      Cold;
      Trauma;
      Muscular strain ;
      Violent emotions;
      Acute infectious diseases;
      Youth and middle age;
      Sex;
      Syphilis;
      Disease of the kidneys ;
      Peripheral neuritis;
      Arsenic;
      Chronic lead-poisoning;
      Chronic alcoholism and lepra ;
      Spinal meningitis;
      Pregnancy.
  Cold  is unquestionably the most frequent of all the causes.  By
it is meant exposure to wet weather and storms.   Feinberg produced
myelitis  in rabbits  by  refrigerating  the  loins with a Richardson
spray-apparatus, some  of the animals recovering, others dying, and
in the latter a myelitic softening was found.  Feinberg also produced
myelitis by varnishing the skin.
  We shall treat of trauma and  muscular  strain  more especially
under the heading of Traumatic Myelitis.
  It is unquestionably the fact that great fright  or auger is capable of
aggravating, perhaps of producing a myelitis.  Leyden tells of a man
who died at the siege of Strasbourg from fright, who had  had a sta-
tionary myelitis  for years ; and I myself have witnessed a  death in a 
216
NERVOUS DISEASES.
case of convalescing myelitis because of the fright produced by another
patient dying iu the same ward.
  Myelitis has been frequently observed after the acute exanthemata,
typhus, acute  rheumatism, puerperal fever, variola, and  bacterial
infection of the spleen.
  Myelitis occurs generally between  the ages of ten and thirty, and
mostly in males.
  There is no question whatever that specific infection is a large
factor  in  the production of myelitis, although a sharp  distinction
must be made, for purposes of treatment, between the myelitis which
occurs immediately from syphilis  and that which  follows a specific
infection as one of its sequelae.
  As  is pointed out at more  length in  the  chapter on  " Keflex
Paralysis," it is a question whether the nephritic disease occasionally
co-existing with myelitis is cause or effect.
  While it has  not  yet been proven that a peripheral  neuritis is
capable of producing myelitis in the  human being,  there can be no
doubt that it does so in experiments on animals,  although  in the
latter the myelitis which results is always purulent, whilst pus rarely
forms during the same malady in the human being.
  Pathology.  To the naked  eye  the cord does not usually seem
much altered, unless the softening is  very pronounced  or  the prolif-
eration of connective tissue has been attended with a shrinkage in
volume.   The cord, however, may be so soft as  to  be actually dif-
fluent; or, on the other  hand, greatly shrunken and hardened.  Of
late years the hardening-methods  have  been greatly improved, and
it is very seldom  indeed  that a cord cannot be prepared for section fit
for microscopic examination.   Microscopically  the cord may present
one of several forms of molecular alteration.  There may be :
   1. An inflammation, generally accompanied by softening;
   2. Softening, without inflammation ;
  3. Proliferation  of  the  interstitial connective  tissue, so-called
sclerosis.
  In general terms it may be said  that the inflammation and soften-
ing are in proportion to the acuteness of the disease, and the inter-
stitial  connective-tissue proliferation in proportion to the chronicity.
But it must not be forgotten that all three processes—inflammation,
softening, sclerosis—may go on simultaneously ;  indeed, small areas
of inflammatory  softening are occasionally surrounded by a connec-
tive-tissue  proliferation, and  in almost  all  cases,  except the very
acute ones, inflammation, with or without softening,  is found  simul-
taneously with connective-tissue  proliferation.   The  softening-pro-
cess is usually divided into three stages, the red, the yellow, and the
gray.  The differences in  color are  due simply to the  amount of
blood  extravasated,  to  the amount of fat produced, and  to the
amount of connective-tissue proliferation.  It must be  borne in mind
that the elements which  are affected in any disease of the spinal cord
are the arterioles and venules, the nerve-fibres,  the nerve-cells, the
connective tissue of the gray and the white matter,  and the mem-
branes.  It must also be remembered that spinal diseases are usually 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  217

attended  by the formation of certain  new elements, such as the so-
called Deiters'  cells,  the  granular fatty masses, and starchy bodies
(corpora amylacea) ;x  nor  must it be forgotten that cysts and cavities
may be formed as the result of myelitic disease.  In the stage of so-
called red softening the vessels are found to be distended with blood-
corpuscles,  frequently surrounded by a gelatinous exudation, and
burst in places; the nerve-fibres may be swollen and disintegrated in
axis cylinder and medullary sheath ; the nerve-cells may be swollen,
broken up, presenting great vacuoles or collections of vacuoles, their
protoplasmic processes destroyed  or  distorted in  shape;  there is
usually a large  number of Deiters' cells and fatty  granular masses,
whilst the pia  mater is often involved in an extension peripherally
    Section of the cord in a case of myelitis, showing the focus of the lesion on the left.
                        Magnified 10 diameters.

of the myelitic process.   In the stage of yellow softening the hemor-
rhagic and hyperaemic appearances are far less marked, having given
place to a  greater abundance of fatty matter.  In  the stage of gray
softening the hyperaemia and  the fattiness have largely disappeared,
whilst the proliferation of connective tissue has become quite marked.
Pus seldom  forms,  but I  have seen  it  in  two  cases of  purulent
meningo-myelitis due  to the  muscular strain  of a  roller-skating
match.   The gray matter  is a  part that  is most  affected, as a rule,
probably  because of its greater vascularity,  and the tendency  to
extension  in  this area is lengthwise, up and down.  Leyden main-
tains that the milder forms have a tendency to dissemination.   The
lower two-thirds of the dorsal cord are most often  affected, although
the myelitis  may affect any  portion.   Besides  the  central  form
1 These corpora amylacea have of late years been shown to be normal products. 
218
NERVOUS DISEASES
located in  the gray matter, the  myelitis may be  diffused on  the
periphery of the cord or it may be one-sided, disseminated (especially
after variola, as has been  described by Westphal) or around the cen-
tral canal (peri-ependymal).
                                 Fig. 113.
Section of the cord in the dorsal region just above the focus of the  lesion, as represented in
                    the last figure.  Magnified 10 diameters.

   The termination of the  myelitic process  may be in—1, regenera-
tion of the tissues; 2, sclerosis;  3, cicatrization; 4, the formation of
cysts.
                                Fro. 114.
Section of the cord in a case of myelitis, showing proliferation of connective tissue aud loss oi
                    nerve-fibres.  Magnified 350 diameters.

   Figs.  112 to 122 will give a good idea pictorially, I  think, of the
changes  that take place iu a case of myelitis.   Fig. 112 is a photo-
micrograph of a section of the cord of a case of myelitis in my prac- 
 DISEASES OF SPINAL  CORD AND MEDULLA OBLONGATA.  219

tice that  commenced  subacutely and terminated fatally after a dura-
tion of some ten months.  In  it is seen, as only a photo-micrograph
can represent,  the initial focus  of the lesion upon the left-hand side
in the lateral column, causing there a gap of substance in the section
Fig. 115.                              Fig. 116.
 Normal cord, showing the relative proportion of     Neuroglia of a normal cord, lateral
nerve-fibres and connective tissue. Magnified 360    columns.  Magnified 360 diameters.
diameters.

which was not due to hardening-methods, as it could be followed up
and down the cord  for  some distance.  The distorted shape of the
cord can be observed, the losses of substance in the posterior columns,
and the sclerotic inflammatory changes that have taken place in the
anterior and  lateral  columns.   Let me say again  that none of these

                              Fig. 117.
     Section of the cord in a case of myelitis, dorsal region.  Magnified 10 diameters.

gaps of substance were artificial,  for  the reason that they could be
followed  up for  some distance in the cord, and that they were sur-
rounded  by evidences  of inflammatory action in the portions of the
cord in which they were found.   In Fig. 113 is seen a  drawing of 
220
NERVOUS DISEASES.
the dorsal region of the  cord  above the focus of the lesion  repre-
sented in the last figure.  The white  areas  represent the places in
which there has been great loss of nerve-fibres, inflammatory changes,
and  proliferation of the  connective  tissue.   In  Fig. 114 is seen a
drawing, magnified 350 diameters, of these sclerotic  portions of the
cord, and  if this is contrasted  with Fig.  115, which represents a
drawing of the  normal cord in the same  region, under about the
same magnifying power, and  with  Fig. 116,  which is a drawing
of a  portion of the neuroglia in the lateral column of the cord, mag-
nified 360 diameters,  it  can easily be  seen  how great has been the
destruction of the  nerve-fibres, how  great has been the increase of
the connective tissue, and how swollen  the vessels are and thickened
in their coats.   Fig. 117 is a  photo-micrograph  of about the same
region of  the cord as Fig. 113, showing as only a photo-micrograph
can,  the distortion of  the cord and  the way in which it is broken
under section, although the  gaps which are here so marked do not
represent  real losses of substance, it  should  be remembered, but are
only due to the tearing of the cord apart under  the microtoue.   Fig.
118  is another  photo-micrograph of the same  cord  in the  cervical
region, showing  the fragility of the  latter, as it has  also torn under
the microtome, and outlining by the  white lines the widespread area
of loss of nerve-tubules, increase of connective tissue, and inflamma-
tion.
                              Fig. 118.
       Cervical region of the cord in a case of myelitis. Magnified 7.5 diameters.

  Fig. 119 is another photo-micrograph of the cord  at  about the
same  region, representing a loss of substance in the posterior col-
umns, which, however, is magnified in the  photograph, and which
was increased somewhat  by section under the microtome.
  In  the ensuing figures, 120 aud  121, are represented the secondary
degenerations which eusued  in this case.  It is a well-known law of
spinal pathology that from  a  focus of  any lesion there is apt to be
a descending and an ascending  degeneration, the latter being along
the course of some motor set of  fibres, the former along the course of
some  sensory set of fibres; in other words,  these degenerations are 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  221

usually in the course of the  nerve-impulses,  so that in the motor
columns they are downward as the motor  impulses pass from within
ontward, and in the sensory columns they are upward as the sensory
impulses pass from without inward.  This law of degeneration, how-

                             Fig. 119.
      Cervical region of the cord in a case of myelitis. Magnified 7.5 diameters.

ever, is by no means invariable, although it is so general as to make
it au excellent guide in tracking the course of fibres and determin-
ing whether they are sensory or motor.   In  this case  with which we

                             Fig. 120.
 Section of the cord showing a secondary degeneration of the columns of Goll after myelitis.
                        Magnified 10 diameters.

are dealing, however,  the degeneration  did  not strictly  follow this
law, as in some  places the degeneration was upward  in the motor
columns aud downward in the sensory, although the main degenera-
tions were in accordance with the rule.  This seeming contradiction 
222
NER VO US DISEASES.
was due to the fact that, in the case here photographed,  the  inflara-
matory changes followed nerve-strands either upward or downward,
whilst the alterations in the nerve-fibres that were due to their being
Fig. 121.
Section of the cord showing secondary degeneration of the columns of Goll after myelitis.
                         Magnified 10 diameters.
Fig. 122.
Section of the cord showing secondary degeneration of the lateral pyramidal column
                 after myelitis.  Magnified 10 diameters. 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  223

cut off from the cells of the gray matter that supplied them with
nervous force (or innervated them) followed the usual course, and
were of the usual ascending and descending type.   As the posterior
root-fibres split into ascending and descending branches on entering
the cord (see Figs. 3 and 12 and p. 31), this also accounts for a por-
tion of the degeneration in the two directions.
  In Fig. 120, for example, a drawing magnified 10 diameters, from
a section  above the  initial focus  of  myelitis, there is  beautifully
marked an ascending degeneration strictly limited  to the columns
of Goll, and marking out perfectly the peculiar wedge-shape of this
fibre-system, represented in  white in  Fig.  121, which is a photo-
micrograph of  almost the same portion  of the  cord.  This latter
figure represents, as only a photograph can do, the appearance under
a low magnifying-power.
  In Fig. 119, which is a photo-micrograph below the initial focus
of myelitis, is  seen beautifully marked  a descending degeneration,
mainly of the  lateral pyramidal columns, although, as will  be ob-
served,  it extends into the  lateral fundamental columns.   At the
 right side of this figure it can be observed how the direct  cerebellar
column has been spared, which does not  show as well upon  the left
side owing to  the imperfection of the  section.   All these  figures
should  be compared  with Figs.  1 and  2,  which show the  normal
columns of the cord.
  Prognosis.  Cases of very acute myelitis are usually fatal, whilst
the subacute and chronic forms will depend largely as to  their out-
 come upon the  circumstances of the patient and the treatment.  In
 every one of the two  latter classes the individual case itself should
 be  a study, aud the  prognosis  should be based upon a number of
 factors, such as—
       Age;
       The severity and acuteness of the onset;
       The progress of the malady, especially in an upward
          direction;
       The localization of the disease in the cord ;
       The presence or absence of bedsores;
       Sphincter-paralysis and cystitis;
       The general health  ;
       The causation ;
       The habits and race of the individual;
       The mental  state.
  Whilst cases of myelitis generally occur  between ten and thirty
years of age, still they may be  met with  at an early age or at an ad-
 vanced  one, and in the latter case this would exert a very unfavor-
able influence.
  A case that  begins with  a widespread paralysis, quickly  superven-
 ing, is of very  unfavorable omen, as has been said.
  A rapidly extending myelitis, especially in  an upward direction
into the cervical centres  of respiration, produciug dyspnoea  and
cyanosis, would be almost invariably  fatal.  The same is true of  a
primarily localized  myelitis in the same portion  of the cord.   The 
224
NERVOUS DISEASES.
lower dorsal cord can be affected most favorably as regards danger
to life.
   The early supervention  of a  bedsore within the  first  week is
usually a very bad omen, though not necessarily so.  But still worse
is the  formation of a  large and rapidly spreading bedsore in the
later periods of the disease.
   Complete and enduring sphincter-paralysis is usually a bad sign,
and so is also an obstinate cystitis.
   It will, of course, be readily uuderstood that the prognosis would
be seriously  affected  by alcoholic or opium-eating habits.   I  have
also frequently noticed  that the lower orders of Germans and Irish
have less recuperative power in myelitis than the other races.  At
the same time I have often observed that  the  more uneducated the
individual is  the more prone he is to become seriously frightened upon
the recognition of a myelitis, especially as the mental  faculties are
usually unimpaired.
   A greatly depressed  individual, whether from mental disease or
anxiety,  is not nearly so apt to make a good recovery as one who is
buoyant  and sanguine.
   Diagnosis.   The  diagnosis  of a myelitis is usually made  with
ease, although  in  the chronic forms care must be  exercised not to
overlook the causative influence of a vertebral lesion, tumor, or an
aneurism.  The  fourfold combination of  motor paralysis, impair-
ment of sensation, rectal  and  vesical  paralysis, oftentimes accom-
panied by cincture feeling, usually differentiates the disease from the
other spinal  maladies,  especially the so-called  systemic ones.  The
latter,  it should  not  be forgotten,  are all  chronic, with the single
exception of myelitis of the auterior horns.
   The diseases from which myelitis is to be distinguished are—
       The systemic spinal diseases ;
       Meningitis;
       Landry's paralysis ;
       Compression-myelitis ;
       Concussion-myelitis;
       Neuritis, peripheral and multiple ;
       Functional paraesthesia;
       Hysteria;
       Reflex paralysis;
       Myelitis of the medulla  oblongata or pons, involving
         the lemniscus;
       Spinal tumor.
   The systemic diseases are locomotor ataxia,  lateral  sclerosis, pro-
gressive  muscular atrophy, and myelitis of the anterior horns.  The
first three are chronic, and the fourth is the  only one which may
be acute.  Myelitis may be distinguished from these by attention to
the following points :   In locomotor ataxia there are stabbing- and
lightning-pains, which are  very severe, very  sudden,  and seldom
come twice in  the same  place;  there is  the  peculiar ataxia, the
atrophy  of  the  optic  nerve, the Argyll-Robertson  pupil, and the
tendon-reflex is often absent.   In lateral sclerosis there is a peculiar 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  225

spastic gait, the exaggerated tendon-reflexes, the foot-clonus, and the
hasty micturition, whilst sensory symptoms and rectal  and vesical
paralysis are lacking.   In progressive muscular atrophy there is the
slow and progressive atrophy of different muscular groups, without
any sensory, rectal, or vesical symptoms.   In myelitis of the anterior
horn there is first the motor paralysis, succeeded by the atrophy of
the paralyzed muscles and the reaction of degeneration, whilst there
are no sensory, rectal, or vesical symptoms whatsoever.
  The most common form of meningitis of the spinal cord is  that
which is seen in  the cerebro-spinal endemics  or epidemics, and in
them  the mental  symptoms,  the  coma,  the  implication of  the
cranial nerves, the retraction of the head, will make the  diagnosis
clear.  In some cases the  cerebral  meningitis may be lacking, and
the disease may be entirely confined  to the spinal membranes, when
the diagnosis may be difficult to make, unless  there is  considerable
pain and spasm.  Occasionally a purulent meningo-myelitis is set up
from  great muscular strain, as I have seen  in two cases of roller-
skaters who had  attempted to  win  a  match  and who had been in
incessant and  outrageous  motion for days.  In such an event the
causation  and the severity of  the  symptoms—pain, spasm,  high
fever, possible delirium or coma—make the diagnosis easy.
  In  Landry's paralysis the onset  is rapid, extending over a few
hours or days; the extension is equally rapid, so  that  the  disease
quickly implicates  the trunk and the upper extremities  after begin-
ning in the lower limbs, the medulla oblongata is usually affected in
some degree, the termination is generally  in death ;  and  there are no
sensory, rectal, or vesical symptoms, or very slight ones.
  In compression producing myelitis, the compression can be detected,
being either a fracture, a tumor, Pott's disease, or an aneurism ;  and
the myelitic symptoms will be mainly localized at the portion of the
cord where the compression is ;  besides, there will be a confused com-
mingling of motor and  sensory symptoms and exaggerated reflexes
that do not correspond to the ordinary picture of a myelitis.
  In  myelitis resulting from  concussion there will be a history of
the concussion upon which the myelitis has supervened within such
a length  of  time  as to  render probable the relation of cause  and
effect sought for.  (Vide Chap.  " Railway Injuries,  etc.")
  Simple  neuritis  of a peripheral nerve  should not  lead to  any
mistake, because the  pain, the motor paralysis, and the  slight  and
glossy-skinned oedema would all be in the distribution of the par-
ticular nerve  affected.  But it is not so easy always at the start to
make a distinction between myelitis  and  multiple neuritis,  although
a few days' observation  should  settle the matter.  In multiple neu-
ritis the pains are always  the  primary symptom,  aud  are usually
very intense;  while in myelitis impairment  of sensation, such as
paraesthesia and anaesthesia, are infinitely more frequent than pain ;
indeed, pain is seldom met with in  myelitis except there  is also a
meningitis.   In  multiple  neuritis  the motor  paralysis does  not
usually supervene until  after several days  or a week of constantly
increasing and often intense pain; whereas in myelitis such a distinct
                               15 
226
NERVOUS DISEASES.
separation in point of time between pain and motor paralysis never
occurs.
   There is a form of functional paraesthesia that comes aud goes for
months and even years, which an incautious observer might con-
found with myelitis.   The lithaemic  paraesthesias—tingling, furri-
ness,  and  numbness in the fingers  and toes—are attended by the
other nervous symptoms of lithaemia, such as tinnitus  aurium, ver-
tigo,  fulness of the head,  gouty or rheumatic habit, etc., and the
absolute lack of  motor or  sensory  paralysis.   (Vide Chap.  IX.,
" Neurasthenia.")
   A hysterical woman might mislead a person for some time, especi-
ally if she be intelligent and have a motive for deception, as is
not infrequently the case where actions for damages are brought.  In
such an event the sensations must be carefully tested, the urine must be
examined for evidences of cystitis, and the subjective symptoms must
be carefully weighed against those  which  are objective.  The subject
is treated at more length in Chap.  IX., " Hysteria."
   Reflex  paralysis  never produces  myelitis, as I have  elsewhere
stated.  (Chap. " Reflex Paralysis.")
   In  spinal tumor there is a chronic course, the symptoms are mainly
localized at the level of the tumor,  intense  pain is present, often
burning and radiating, and there is a marked  immobility of the ver-
tebral column at some point, the latter symptom never being observed
in myelitis.
   Treatment.  The objects of treatment should be somewhat differ-
ent, accordingly as the disease  is of the  acute or chronic type.  In
the former the spinal cord should be put at  absolute rest, and  the
inflammation should be checked as  much as possible.   Unfortunately
there  are no known means of treating the softening.   In the chronic
cases  restriction of the expenditure of energy well within the limit
of fatigue, together with the use of internal or external remedies that
will favorably affect the molecular  changes in  the cord, will make up
the treatment.
   In  the acute cases the patient should be put upon a water- or air-
bed, and care must be taken that the water is kept at such a tempera-
ture as will not chill.  Ergot should  be  administered, either in  the
form  of a reliable fluid extract, 5j-ij, three or four times daily, or
ergotine, gr. ij-v, three times daily.  Belladonna should also be used,
preferably by means of belladonna-plaster, unless a bedsore is form-
ing ;  or atropia sulph. gr. Tl-$, two to four times daily, or a reliable
fluid extract, gtt. j-ij, twice or thrice a day.    Ice should also be ap-
plied  along the spinal column, and the best way of doing this is to
have an oil-silk bag made about two  inches broad and of sufficient
length, aud pack this  with ice.  It  should  be  applied  about  ten
minutes daily, the patient lying on  the abdomen.  For the first three
or four nights quin. sulph., gr. v,  should be given at  bedtime, pre-
ferably in capsules  or tablet triturates, both  freshly made, together
with  potas.  bromide, gr. x-xx;  this  will often be found to have a
most favorable effect iu checking the  progress  of the disease.
  In  the subacute or chronic cases  rest is always an  important aid. 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  227

It will be found best usually to put the patient absolutely to bed for
a week or two at first, then let him up for the latter half of the day,
and so gradually  permit  him  to get about again.   Where this
amount of rest may not be practicable or feasible, it may suffice to
have the patient lie down  several  hours every afternoon, or to have
a business man go to and  from his place of business in a carriage,
and stay in bed on returning home.   Besides rest, numerous reme-
dies may be  employed  externally and internally, as follows: Ergot
may be useful in the cases of recent origin, even although the symp-
toms are very subacute, and in such cases it  should always be tried.
The same  is true of belladonna,  although  in a less  degree.   The
doses should be as they have been given above.  The iodide of potas-
sium has been a drug  of  considerable value  in my hands, but the
dosage should be carefully determined by the presence or absence of
a specific history, as well  as  by the relation of the specific infection
 to the myelitis.   In myelitis that simply follows a specific infection,
 moderate doses  of the  iodide will answer every purpose,  gr.  x-xv
 three times daily.   But where the  myelitis comes on during a period
 of specific  infection, or subsequently to a cerebral syphilis, the doses
 must be much larger, and  should be begun  with grs. xx three times
 a  day and increased quickly until symptoms  of iodism  supervene,
 or until the myelitis begins to yield.   In old specific cases that have
 become accustomed to  large doses of the iodide perfectly enormous
 doses may  be required ; thus, in one case of mine the symptoms did
 not improve until 700 grs. daily were  reached.   In  all such cases the
 saturated solution of  the iodide should be employed, each drop con-
 taining about f gr., and it should be administered  in a full tumbler
 of ice-water, Vichy, or  the Bohemian Giesshuebler.    As  is more
 fully explained elsewhere (Chap. VIII., "Syphilis  of the Nervous
 System"),  I have no  confidence  whatever  in the  use of mercury.
 Strychnine is occasionally  an extremely useful remedy in the chronic
 stages, as first pointed  out by the late Dr. J. S. Jewell,  of Chicago.
 It should be employed  in  large doses, commencing with gr.  -g1^, and
 increasing  gradually to -£% or ^-, but extreme care must be taken that
 the toxic effect  does  not manifest itself in  a sudden or cumulative
 manner, as I have seen it do.  It is best administered by the mouth,
 in pill, solution, or tablet  triturate.  An occasional dose of quinine,
 gr. v, combined with potass, bromide, gr.  xx, at  bedtime,  will be
 found to be of great use iu the more chronic stages of myelitis when
 there is a relapse or when  the disease remains stationary.
   In many cases it is  advisable, for the convenience of the patient
 and to prevent mistakes, to combine these remedies  in one prescrip-
 tion as follows :

     R.—Ergotin.........3}-
         Strychnise sulph.......Sr-j-
         Quin. sulph........3j.    M.
  Ft. in pi), no. xxx.  S.—One three times daily, one hour after meals.

   The  bromide of potash can be added to this, 5 grains for each
 dose, if a  tablet  triturate or compressed  tablet is made, as can be 
228
NERVOUS DISEASES.
done nowadays by any druggist.  The ice-bag, as described above,
should  be applied every other day for a  week  or two at a time.
Counter-irritation along the back is occasionally of use, although its
value has been very much over-estimated.   Of course, it  should be
used with great care until all danger of the formation of bedsores is
past.   Dry cups or the actual cautery, the  latter  either a  Paquelin
or electric cautery, or a poker, should be used, the latter at a white
heat and applied with light strokes.   Electricity is, in my opinion,
the most valuable agent that we  have for  the treatment of the sub-
acute and chronic forms of myelitis, especially in the second  and
third week after the onset.  The galvanic, faradic, and static currents
should  be employed.   Galvanism should  be applied by large elec-
trodes, one (Fig.  67 or 68) in the neck and the other (Fig. 68 or 69)
over the lumbar  spine,  daily  or every other day.   The strength
should  be at first 5 to 10  milliamperes, and the sitting should be
from three to  five minutes; as the patient grows accustomed to the
electricity the current-strength and the length of sitting should be
prolonged until a  current of 15 to 30 milliamperes is attained and
the sitting is prolonged  to ten  minutes.   But the strength of the
current should never be increased to such a degree as to produce any
unpleasant symptoms during  or after the sitting, although much
more electricity can be  given in myelitis than  in  neuritis.  The
faradic  current should be of sufficient strength  to produce  gentle
muscular movement, and should be applied to the different motor
points of the paralyzed limbs.  ( Vide pp. 130 et seq.)  The static cur-
rent will often be of use as an alternative  with the faradic, and the
one will thus frequently stimulate the flagging nerve or muscle which
has failed to  respond to the other.  There is considerable difference of
opinion as to the value of the different natural springs of Europe in
their effect upon myelitis, and the reader who is desirous of inform-
ing  himself  upon this subject had better consult some of the foreign
authors.  In this country I have found  that hot sulphur springs
will very decidedly  benefit some  chronic cases,  but,  as they have a
most deleterious effect upon others, their effect should be tested with
great caution in each individual.  The Turkish  and Russian baths
are, in my  opinion, decidedly dangerous  in myelitis, and I have
abandoned their use.  Massage is a very  uncertain  remedy in this
disease,  and should never be employed except in the chronic cases,
and then empirically.   It should always  be given very gently and
for a short time, and even then its effect can never be counted upon.
Remedies should  be changed from time to  time  in treating cases of
chronic myelitis.  When one  procedure has lost its  effect, another
should  be employed, and the different forms of electricity should be
alternated one with the other.  Change of scene and travel are useful
aids to treatment in such of the chronic  forms  as  have remained
stationary after fair improvement; but any fatigue must be avoided,
and especially high  altitudes or regions of  great barometric changes.
The bedsores should be carefully attended to.  The patient's position
should  be shifted constantly so  as to avoid  pressure upon any one
particular spot.  In sluggish  cases the patient should  be put on a 
DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  229
water-  or air-bed   If there be any  tendency  to  trophic  changes
observed  in the skin, it should  be met by the application of a lotion
of equal  parts  of alcohol aud  water frequently applied  throughout
the day;  or Brown-Sequard's plan of cold water amd poultices should
be tried,  the cold water coming through a douche for ten minutes,
and the  poultice being applied for half  an hour.   When a bedsore
has actually formed, dressing it antiseptically with a solution  of bi-
chloride of mercury, 1 part to  1000, and then coating it over with
contractile collodion will not infrequently relieve small  formations
and hold large ones in check  for some  time.   The  cystitis  which
may ensue  should  be  treated  promptly  by potass, citrat.,  gr. xxx,
every night at bedtime, in a tumbler of water;  or oil of gaultheria,
gtt. x, in sealed capsules, just before retiring.   Some very mild cases
can be alleviated by the use of Vichy, Giesshuebler, or any  of the
other alkaline mineral waters, or the administration of gr. v-x-xv,
sodae bicarb, three times daily  in a full tumbler of water.   If this
does not  give relief, give belladonna in the fluid extract, one or two
drops  twice or thrice  daily, and also boric acid, gr. ^-^, once or
twice daily in a tumbler of  water.   If there is much suffering, the
following suppository will be found to be of value:
     R.—Ext. belladonnas.....gr. iv.
         Iodoform.......gr. xxxvj.
         Opium.......gr. xij.     M.
  Ft. in suppositor. no. xij. S.—One every night at bedtime.

   These  suppositories should be made of fresh cocoa-butter, and  they
should  have  the long  conical shape, and not the blunt one  which is
so difficult  to place well up  in the rectum.  If there is  retention of
urine, soft catheters should be  employed,  but they must  first be dis-
infected in a solution of bichloride of mercury (1 to 1000), and  they
ought to be carefully washed in this after being used.  The catheter
should  never be used by any person who  has not been shown how to
introduce it properly and gently; indeed, its use should  be  avoided,
for it is often very irritating to  the bladder of a myelitic patient, and
I  have on several occasions seen it cause  a dangerous  aggravation of
the cystitis.   In chronic cases, grindelia robusta (fluid  extract,  U. S.),
gtt. xx-xxx, once or twice daily, or the sulphate of strychnia, gr.
■gV ^q three times daily, is often very efficient.
   The  constipation  arising  from  the  sphincter-paralysis should be
treated by means of galvanism applied with one large electrode  over
the lower dorsal spine and  a  rectal  electrode,  or with  the faradic
current applied in  the same manner; but it is far better  to try to
relieve  it by injections  of warm water and soap at  first, and then, if
it persists, by cascara sagrada, either the fluid extract, 5j, once, twice,
or thrice  daily,  or the  solid extract, gr. ij-v, once or  twice daily, or
the so-called cascara cordial, 5j, once or  twice daily; or by the fol-
lowing prescription:
     R.—Ext. aloes      "I                       ^-  ^
         Ext. hyoscyami )                           oj-
         Ext. oucis vomicae  .    .    . '  .    .    .  gr. v.   M.
  Ft. in pil. no. xv.  S.—One every night at bedtime. 
230
NERVOUS DISEASES.
            MYELITIS  OF THE  ANTERIOR HORNS.

  Synonyms:  Poliomyelitis anterior.   Essential  paralysis of chil-
dren.   Infantile spinal paralysis.   Atrophic paralysis of children.
Acute atrophische Spinallahmung.  Spinale  Kinderlahmung.  Par-
alysie atrophique.
  Definition.  A motor paralysis, generally monoplegic, of muscles
that are associated in fuuctiou, followed  by atrophy and electrical
alterations in  them;  cerebral, sensory, rectal, and vesical symptoms
being either absent or temporary in duration.
  History.  It is claimed that Underwood, in England, indistinctly
recognized this disease as far back as  1784; it was better recognized
by Heine, in Germany, in  1840;  but  the  first accurate description
was given by Duchenne (de Boulogne) in 1853.   Charcot, in 1863,
and  Moritz Meyer, in 1868, made it known clinically.    The first
autopsy and microscopical examination were  made by Gombault, in
1873, aud  a very thorough  post-mortem  examination was that of
Cornil and Lepine in 1875.   Since  then many  observations have
established very decidedly the nature of the  pathological changes,
and the  clinical symptoms have  been exhaustively studied.  The
chronic form was first spoken of by Duchenne in 1849-50, and then
more  adequately demarcated  in 1870; and,  in later years, micro-
scopical examinations of  the central nervous  system have been made
by Ross, Aufrecht, Kahler, Vulpian, Provost, Archambault, Daraas-
chino, Sinkler, and Pick.
  Symptoms.  The disease may be acute, subacute, or chronic.  It
has usually three stages,  the initial, the paralytic, and the chronic.
   The initial  stage  may be  febrile or non-febrile.  When there is
fever it  is  extremely variable,  lasting from twenty-four to  forty-
eight hours, several days, or even  fourteen days, being usually mild,
about 102° or 103° F., although it may run  as high as 110°.  The
pulse is usually proportionate to the fever.  Other reflex phenomena,
as variable as the fever  itself, may accompany it, such as delirium,
somnolence, convulsions, with or without loss of consciousness, mus-
cular twitchings, vomiting, headache,  temporary retention of urine,
pain in the loins  and in the limbs that are subsequently paralyzed,
or generalized pains.  Children of four or five years may be able to
locate  the  pain, whilst younger ones will only evidence it by crying
when they  are  touched  or lifted.  These febrile and other reflex
disturbances are most marked in the acute  form, whether in children
or adults; but often  in  the  acute form,  especially in children, the
paralysis may appear without any prodromata whatsoever.  Thus it
is by no means uncommon for a child  to be put to bed apparently m
perfect health, and  to be found  paralyzed  in the  morning.  The
non-febrile  form may be  accompanied or not by the other reflex
disturbances.  The delirium,  stupor,  and convulsions are generally
absent in  the subacute  and chronic  types;  and  in these, as in the
acute forms, reflex disturbances may  be absolutely lacking.  One of
my patients was slowly and completely paralyzed during some four
weeks, in all the extremities and most of the trunk-muscles, without 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  231

the  slightest symptom other than the paralysis.  This initial stage
will, therefore, vary from  hours to weeks or months, accordingly as
it is acute, subacute, or chronic.

                            Fig. 123.
    Myelitis of the anterior cornua, showing atrophy of the leg-type on the left side.

  The paralytic stage.  The onset of the paralysis may be sudden or
gradual.  At first it is usually general, affecting  most of the volun-
tary muscles.   In the course of two or three days, however, there is
a spontaneous recession of the paralysis  from most of the  muscles,
leaving only certain  groups affected.   Occasionally the  paralysis is
limited from the first to certain muscle-groups.  Usually there is a
second and more gradual spontaneous recession of the paralysis dur-
ing several months.  In children the most common form of paralysis
is monoplegia,  most often  of a lower extremity.  In adults,  para-
plegia is most common, usually of the  lower extremities.  Still, it
must be remembered steadily that any of the voluntary muscles may
be affected.   But all the muscles of a limb are not, as a rule, equally 
232
NER VO US DISEASES.
implicated.  In the lower extremities the flexors of the leg, the gluteal
muscles, the quadriceps, and the ilio-psoas are generally spared.  In
the upper extremities it is the forearm- and hand-muscles that gener-
ally remain intact.  The paralyzed muscles of the lower extremities
are usually the tibialis anticus, or the peronei and extensors of the toes.
In the upper extremities the paralyzed muscles may be the supinator
longus, biceps, brachialis internus, and deltoid—the so-called "upper-
arm type" of Remak or Erb; or all the muscles supplied by the radial
nerve  may  be paralyzed, except  the  supinator longus.   Then the

                              Fig. 124.
     Myelitis of the anterior cornua, showing atrophy of the leg-type on the left side.

serratus anticus may be affected, together with  the hinder portions
of the deltoid, the infra-spinatus, and  rhomboids.  Thus, as will be
observed,  of the  five lumbar segments it  is usually the fourth and
fifth that are  the site  of disease in these types;  and of the eight
cervical segments it is principally the fourth and  fifth.   Thus, ana-
lyzing 110 cases of my own, I find that the left leg is most frequently
affected ; next in order of frequency the right leg, theu the right arm
and  left  arm, whilst a  paraplegic  distribution  is  rare, and I have
never  seen a hemiplegia, although it  has been  observed  by  others.
But  the following table of my cases will make plain these and other
details. 
DISEASES OF SPINAL  CORD AND MEDULLA  OBLONGATA.  233
Total number of cases  ....   114
   Males.......69
   Females......45
   Average age, 3 years 8 months ;
   youngest congenital; oldest 18 years.

Mode of onset:
   Sudden......33
   WTith fever......51
   Convulsions.....9
   Gradual (chronic)  ....  3
   Not stated......21

Paralysis:
   Left leg......36
   Right leg......27
   Left thigh......3
   Left arm......9
   Right arm......12
   Deltoid (right).....10
   Deltoid (left).....2
   Paraplegia......15
iology: Diphtheria....	. 9
Fever .....	. 30
Convulsions	. 9
Trauma ....	. 12
Measles ....	. 6
Diarrhoea .	. 6
Scarlet fever	. 3
Mental condition normal

Atrophy:
   Present......75
   Not detected.....2
   Not stated .       .   .    .    .37

Knee-jerk:
   Lost.......39
   Diminished.....30
   Exaggerated.....6
   Not stated......39

Deformity:
   Talipes......15
   Shortening......  6

Sensory symptoms :
   Pain present.....6
   Limb cold......24
   Tact impaired.....3
   Temperature subnormal ...  3

Reaction of degeneration complete   . 24

Reaction of degeneration beginning  .  9

Electric reactions:
   Diminished galvanic and faradic
     response......30
   Not stated......57
114
Fig. 125.
     Myelitis of the anterior cornua, showing atrophy of the leg-type on the left side.

   During the  second week atrophy of the paralyzed muscles is ob-
served, as well as commencing alterations in the  electrical  response.
(Vide-p. 128.)
   The paralyzed muscles are flaccid.   The atrophy is demonstrable by
palpation  and  by the change in  the normal size and contour of the
muscles.  The  electrical changes consist of  diminishing response of the
motor  nerve trunks to faradism and galvanism, and subsequently  of
increasing response of the muscular nerve-filaments to galvanism, as
well as of an alteration  in  the  healthy  polar formula.   During the
first week or  ten  days  an  increasingly strong  faradic and galvanic 
234
NER VO US DISEASES.
current must be applied to'the  nerve-trunks  to cause muscular con-
traction ; and, if the myelitis of the anterior horn be severe enough.
Fig. 126.
Myelitis of the anterior cornua, showing paralysis of the leg-type in the left leg, in which
  the atrophy is masked by the fat of the limb, although the droop of the toes can be seen.
Fig. 127.
  Myelitis of the anterior cornua, showing the upper-arm type on the left side, occurring
twelve days after birth, in which there was absolute paralysis for eleven months, and com-
plete reaction of degeneration. 
DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  235
it may be difficult or impossible to obtain any response to the faradic
or galvanic currents.  However,  the electrical phenomena are differ-
ent with the  muscular  nerve-filaments.   Their response in the first
week or ten days, like that  of the nerve-trunks, is  less and less to
the galvanic and faradic currents ; after this period  the  response to
faradism continues to decrease, as in the  nerve-trunks,  but the re-
sponse to galvanism begins to diminish—i. e., a weaker  and weaker
galvanic current is required  to produce a given muscular  contraction,
and the normal reaction  to the  poles of the galvanic battery com-
mences to alter.  We have seen  that a healthy motor nerve has this
polar formula1 (page 128):

                              Pole.                Circuit.
                             Negative           Closing   =  CC
                                              Opening)   AO
                             Positive               or  y=  or
                                              Closing J   AC
                             Negative           Opening = CO

   From this it is apparent that the  healthy motor nerve responds—
by muscular  contraction,  of course—first and most strongly to  the
negative closing (CC); that  the  positive closing or opening (AC or
AO) requires a stronger current;  and that a muscular  contraction at
the negative opening (CO) is only seen with the strongest currents,
so strong usually as to be painful.   When the muscular nerve-fila-
ments, therefore, show polar change, this is evidenced by AO or AC
being obtained by the same strength of current as causes CC, or even
with less ; or  that CO is obtained with the same current-strength as
is AO, AC,  or CC.  All degrees of change of the  healthy  polar
formula may be observed,  of course; and it is a fair rule, with cer-
tain exception (p. 129), that  the greater the polar change, the greater
the structural alteration.   The contraction of the  affected muscles, it
is also to be noted, differs from that  of healthy muscular fibre of the
voluntary type in being more sluggish and vermicular, thus approach-
ing what is  characteristic of the  unstriped, involuntary  muscles.
This complex series of phenomena, consisting of diminution to farad-
ism and galvanism in the motor nerve-trunks, and of increase  to
galvanism and altered  polar formula in  the  motor-nerve  muscular
fibres, together with the  sluggish muscular contraction,  is known col-
lectively as the degeneration  reaction (Entartungreaction  of the Ger-
mans) (p. 128).
  The deformities which may result  are the different  forms of talipes
known as equinus, varus, equino-varus, and calcaueus, as well as lor-
dosis, or abnormally flexible or contracted joints.  Talipes equinus
and equino-varus result  from  paralysis of the antero-external  mus-
cular group of the  leg, and are the  most common.  Equino-varus,
when it is complicated, is caused  by paralysis of the anterior group
of leg-muscles, together  with the adductors of the foot.   Paralysis

 1 As has already been explained, the positive pole is technically called the anode and repre-
sented by the letter A ; whilst the negative pole is called the cathode, and is  indicated by C.
I he opening and the closing are denoted by 0 and  C. But the reader should carefully read all
that has been said about the diagnostic uses of electricity from page 125 onward, as these elec-
trical reactions, that are really very simple, are apt to be sadly misunderstood.
  Current.
1. Weak
2. Stronger
3. Strongest 
236
NERVOUS DISEASES.
of the calf-muscles alone, which is rare, produces  talipes calcaneus.
Simple paralytic talipes varus is yet more rare.  The condition known
as "pescavus" is not uncommon, characterized by the hollowing of
the sole of the foot and prominence of the instep, and it is attributed
to paralysis of the calf-muscles and simultaneous contraction  of the
foot-flexors—i. c, either of the long flexor of the toe, or the long
peroneus.  Lordosis is caused by partial paralysis of the sacro-spinal
muscles.  When the anterior and internal thigh-muscles are para-
lyzed mainly above the knee, the consequent over-action of the flexors
of the leg on the thigh maintains  the knee partially flexed, the leg
being adducted.  This condition is known as genu recurvatum, and
is generally associated with talipes  equino-varus.  A joint or a limb
may become so flexible as to dangle passively in any direction.  There
has been some difference of opinion among orthopedists as  to whether
the weight of the limb and the approximation of the points of inser-
tion of antagonistic muscles have not been aiding-factors in  the pro-
duction of some of these deformities.
  The bladder may be temporarily affected at the onset of  the dis-
ease ; aud also the rectum, though this is more rare.   Anaesthesia or
retardation  of sensory impressions  may  be temporarily observed.
The paralyzed limbs are generally cold and bluish-looking, the calibre
of the arteries and veins being diminished, and the temperature can
always be felt to be distinctly lessened, the surface-thermometer indi-
cating one or two  degrees less than the normal.  The tendon-reflex
of the quadriceps  is absent or  diminished when the crural nerve is
involved; otherwise, it may be normal or even exaggerated.
  Etiology.   Whilst cases  occur  without known  cause, the causa-
tive factors are usually to be found among the following :
       Age;
       Sex;
       Infection;
       Exposure to cold and dampness ;
       Trauma;
       Muscular or mental strain ;
       Multiple neuritis ;
       Acute diseases;
       Warm weather;
       Syphilis;
       Menstrual suppression;
       Dissipation and sexual excesses.

  Whilst the disease  may occur at any  time  of life, cases having
been  observed at the extremes, alternately, of three months and
sixty-seven years, there are yet two periods of life which seem espe-
cially predisposed to it, viz., the first three years of infancy  aud the
period between the eighteenth and fortieth years.
  In infants  both sexes  seem to be  equally affected,  but in adults
males suffer most.
  There  is a disposition on the  part  of some authors to regard
the disease as infectious because several children have been affected 
 DISEASES OF SPINAL CORD AND MEDULLA  OBLONGATA.   237

simultaneously in one family or in  one village, and also because, as
we shall learn, it is most frequent in the warm months.
  Gowers has  recently reported  a case occurring  with multiple
neuritis.
  It has long been observed that the onset is not infrequent  after
measles, scarlatina, cerebro-spinal  meningitis, dysentery, diarrhoea,
and it has appeared also after parturition and puerperal fever.
  Of 53  cases  collected  by  Seeligmiiller,  27  were in  July  and
August.  In  a  record kept by Dr.  Weir Mitchell  for nine years, it
was noted that cases became more frequent in May, June, and July,
attaining the maximum  frequency early in August, and rapidly de-
creasing in number through August, less rapidly  through September,
until early in October they were as infrequent as in May.
  Cases have been observed during the secondary and tertiary periods
of syphilis.
  Prognosis.  In almost all cases there is  certainly left  an incura-
ble residue of paralysis.  The amouut  of  this will depend upon the
severity of the disease  and the  thoroughness of the  treatment.  It
should not be forgotten that the acute and subacute forms  of the dis-
ease have three periods of recession : First, the spontaneous recession
within a few days of the first generalized paralysis that  may  have
been caused by the shock of an  acute onset; secondly the spontane-
ous recession often observed  in  the first  few months;  thirdly, the
 recession that may be  effected  by early and proper treatment.   All
these recessions may vary in amount.  On the other hand, the paral-
ysis may be progressive in  the chronic forms, aud an approximate
prognosis can only be  framed when it  is  evident that the disease is
not extending.  After  these periods have passed, the data of prog-
nosis are—
   1. The localization and  degree of the paralysis;
   2. The rapidity and degree of the atrophy;
   3. The degree of the electrical changes in nerve and muscle, and
the rapidity  of their supervention.
  It is very seldom that any of  the vital  nuclei of the medulla ob-
longata are sufficiently  affected to cause death, and yet  I have seen
them dangerously implicated during the first few days.  In such a case
the prognosis should be very guarded.   If these nuclei  be not affected,
the rule is that the prognosis is worse the more complete the paralysis,
the more rapid the electrical changes supervene, and the more abnor-
mal they are.  The worst  cases are those in which the paralysis is
complete, and in which  the nerve and muscle undergo  in a few weeks
the typical changes of the degeneration-reaction.   The best cases are
those in which the paralysis is incomplete, and in which there is only
moderate diminution for a few weeks in the response to faradism and
galvanism, without any increased galvanic excitability of the muscle
or alteration in the healthy polar formula.
  Pathology.   Our  views of the  pathology of myelitis of the
anterior horns have undergone considerable modification in the course
of the  last twenty-five  years.   The malady was first regarded as a
functional one, but the autopsies and microscopical examinations 
238
NERVOUS DISEASES.
made by Cornil in 1864, Provost and Vulpian in 1867, Clark in the
same year, Charcot and Joffroy in  1870, Joffroy and Parrot in  the
same year,  and  a number  of others  of the same kind, seemingly
demonstrated that the lesion was a loss or impairment of the ganglion-
cells in the anterior horns.   These  ganglion-cells were found to be
disorganized in varying degree, so that some of them lost their pro-
cesses, became smaller in size, or entirely disappeared.  Of late years,
however, as more autopsies have been made in cases of recent origin,
it has been shown that the lesion  is really a local  or  focal myelitis,
with the usual attendants of a myelitis, such as congestion, softening,
abundance of granular corpuscles,  etc.   The  vessels are generally
gorged  wTith blood, and in a case of Archambault and Damaschino's
the whole of  one anterior horn was fairly flecked,  like a  coarse veil,
with these enlarged capillaries.  The lymphatic sheaths, in such cases,
are filled with granular corpuscles, pressed one against the other, and
containing a nucleus.   Secondarily  to this condition of congestion is
probably the disappearance or  injury of the ganglion-cells.   (Figs.
7, 8, and 9.)   It has been supposed that the anterior and lateral groups
of cells in the  anterior  horns innervate the muscles concerned  in
the flexion and extension of joints, and  that the median  and lateral
clusters preside  over the fine muscular actions of the  hands, fin-
gers,  and thumb,  as  well as of the  ankles and  toes in walking.
In  the  course of a week  or  two changes are found in the anterior
nerve-roots,  of  the nature of a secondary degeneration  of nerves,
also in the motor end-plates, and  finally  in the muscles, these neural
and muscular changes being the familiar ones that have been de-
scribed  as occurring after neuritis  (pp.  175 et seq.).   In the cases
occurring in adults the myelitis is more extended and  not localized,
and there is as yet considerable doubt as to whether  some of the acute
forms of this myelitis of the anterior horns are not identical with the
so-called Landry's paralysis (pp. 224 et seq.).   In  the chronic form
occurring in adults the lesions are iu some  cases confined to the an-
terior horns of the spinal cord ; but it is a question as yet under dis-
cussion  whether  lesions entirely in the  peripheral nerves may not
produce the same symptoms.
  Marie has recently attempted to  explain the one-sideduess of the
lesion by the  peculiar distribution of the spinal arteries.  The an-
terior arterial system is composed  of the anterior spinal artery, which
is formed by the junction in the  superior cervical cord of the two
ascending branches of the vertebral.   This spinal  artery  is in front,
or ventrad, of the anterior  longitudinal fissure, and can be followed
to the lowermost end of the  cord.  During  its course it receives a
certain number of branches  from the  lateral spinal arteries;  audit
gives  off at a right-angle  a series of good-sized branches which pene-
trate the anterior median fissure and constitute the anterior  fissural
arteries  (Fig. 128,  B).  Each one of these penetrates the anterior
cornu on one side and nourishes it with blood, but the peculiarity about
each is that it does not bifurcate, but sends off, as seen  in Fig. 128,
only one maiu trunk, supplying the anterior  horn on the  same side.
At  the  same  time, too, this  branch to the  anterior horn sends  ofl 
 DISEASES OF SPINAL CORD AND  MEDULLA  OBLONGATA.  239

some divisions to the  neighboring white substance of  the antero-
lateral  column.   Marie believes that one of these cornual  branches
of the  fissural artery, known  as the  anterior-root arteries (DD'D",
Fig. 128),  is  the  focus of disturbance in acute  myelitis of the an-
terior horu, and  that this explains the one-sided distribution of the
lesion.   He thinks it probable that  these vessels are affected either
by an infectious embolism or thrombosis. It is true that there are a
number of instances seeming to show that infection may sometimes
cause  this  disease, as  it occasionally  occurs  in limited epidemics;
but the defect in  Marie's theory is  that it does not  explain why the
infection should be limited  to  only one  vessel or set of vessels, and
not extend to all the spinal arteries.

                                Fig. 128.
         Mechanism of lesions of the anterior horn in poliomyelitis anterior.
 A.  Anterior spinal  artery.  B. Fissural artery.   C. Sulco-commissural artery.  DD'D".
Anterior root arteries.  E. Lateral anterior artery.  F. Median lateral artery.  Lesion at M is
from the primary branch of the sulco-commissural artery distributed to the anterior horn ;
whilst the hemorrhage at L is from one of the anterior root arteries, and it extends into the
white substance of the antero-lateral column.

  Diagnosis.  The characteristics of a myelitis of the anterior horns
are the flaccid motor paralysis, which always precedes the atrophy by
a distinct interval, and which is  not  necessarily proportionate to the
atrophy ; the altered electrical reactions ;  the infrequent aud tempo-
rary implication  of the nuclei of the  cranial nerves;  the loss of the
tendon-reflex; the absence of  cerebral, sensory,  vesical,  or  rectal
symptoms, except  temporarily at the onset.   The initial fever may
render a diagnosis impossible at first  from  the  acutely febrile affec-
tions of other origin.
  The acute and subacute forms are to  be differentiated from—
      Acute exanthemata;
      Meningitis, traumatic, from ear  disease,  or cerebro-spinal;
      Meningoencephalitis of childreu;
      Neuritis,  simple or multiple;
      Spinal hemorrhage;
      Transverse or diffuse myelitis; 
240
NERVOUS DISEASES.
        Acute ascending paralysis;
        Lead-palsy;
        Progressive muscular atrophy;
        Joint-atrophies;
        Amyotrophic lateral sclerosis;
        Hysteria.
   In meningitis, traumatic, cerebro-spiual, or  from ear-disease, the
 mental disturbance is  much more marked  and of longer duration;
 the cranial nerves may be seriously implicated, the sensory as well
 as the motor, which never happens in anterior myelitis; there is
 usually, also, the retraction of  the head characteristic of meningitis;
 and  the  paralysis is almost  invariably hemiplegic in  distribution,
 whilst hemiplegia is  extremely infrequent in myelitis of the anterior
 horn; and this hemiplegic paralysis is seldom succeeded by atrophy,
 except very gradually or from years of disuse.
   In  infantile meningoencephalitis the acute  and short fever of
 the  onset, succeeded  immediately  by a  paralysis, might lead to con-
 fusion were it not that, as in the forms of meningitis just described,
 the  paralysis is invariably hemiplegic and without atrophy quickly
 supervening.
   The ordinary neuritis of a mixed nerve, causing  considerable and
 continuous pain, oedema, hot  and  glossy skin, cannot be confounded
 with anterior myelitis.   Chronic  neuritis is distinguishable by the
 disproportion  between  the pain,  on the one hand, and the paral-
 ysis and  atrophy on the other; often, too, by the fact that it is con-
 fined to one nerve-trunk or one branch  of the nerve-trunk.
   In multiple neuritis differentiation is made easy by the infectious
 history, in  some cases  the malarious neighborhood, the continuous
 burning-pains in both lower extremities, the steady progress within
 a week or two of the bilateral  paralysis and  atrophy,  at the same
 time that the  painful symptoms persist.
   Spinal  hemorrhage is  usually attended by more or less persistent
 anaesthesia, often by marked vesical and rectal symptoms, and some-
 times by bedsores.  Should, however, a hemorrhage be  exactly lim-
 ited to the anterior horn, the differential diagnosis might be difficult.
   Transverse or diffuse  myelitis is indicated by such entirely distinct
 symptoms as  marked  sensory and  motor  paralysis,   paralysis of
 bladder and rectum, girdle-sensation, and bedsores.
   In acute ascending paralysis the rapid ascension of the paralysis
 from the  lower to the upper  limbs, then to the cranial nerves, and
 the usually fatal termination,  are  in marked contrast  to the more
 gradual poliomyelitic paralysis, which is seldom fatal, and which is,
 therefore, usually followed by atrophy and the characteristic electrical
 changes.
   In lead-palsy the  exposure  to lead, the characteristic line on the
gums, the preceding intestinal troubles, and the characteristic "wrist-
drop," will make the diagnosis easy.
   In progressive muscular atrophy the atrophy precedes the paralysis,
and  the paralysis is  always closely  proportionate  to the atrophy;
moreover, there is a  much more chronic course than in myelitis of 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.   241

the anterior horn.  Still, progressive muscular atrophy and chronic
myelitis of the anterior  horn are closely allied diseases.   It was
formerly  thought that the distinction was that  in the former  the
motor cells of the anterior horns were  primarily affected, whilst in
the latter it was the trophic cells; but this view has tacitly merged
into the more rational  one that when groups of cells  are diseased
groups of muscles are affected, whilst a lesion  of single cells causes
symptoms in individual  muscular fibrils, especially when the cellular
alterations are chronic.
  In amyotrophic lateral  sclerosis the paralysis and the atrophy are
always accompanied by contractions and exaggerated  reflexes, which
are seldom present in myelitis of the anterior horn.
  It is only necessary to call  attention to the possibility of hysteria
simulating  a  myelitis of  the  anterior horn, because the lack of the
atrophy, the electrical alterations, and an unimpaired tendon-reflex
will demonstrate  that there is no disease of the anterior horn, even
though there  may  be some  doubt as to  the  existence of a motor
paralysis.
  Teeatment.   The objects  of treatment should be—
  1.  To arrest fever and control other reflex disturbances, if there be
any;  2. Possibly to affect the cellular process in the anterior horn ;
3. To affect the degenerating or  degenerated nerve and muscle.
  The febrile disturbance  is seldom  sufficient  to require any active
treatment;  but if it should be,  it can readily  be controlled  by cold
spouging or the cold pack, with or without antipyrin.   The dose of
this drug should vary for children from gr. j-v, once to  thrice daily,
in a little sweetened water.  The other reflex disturbances should be
treated by these same agents, and, if these are  not adequate, also by
the  bromides  and some  mild opiate.   In  children the bromide of
sodium is preferable, because  it  has  the least  tendency  to upset the
stomach.   The dose should be  from gr. v-xx, once to  thrice daily.
It can readily  be given in simple solution in a teaspoonful or two of
water.  Should pain, as is very seldom the case, be  so  pronounced
as to require an opiate, the best combination is that of the sulphate
of morphia with atropia, such as is usually made in the hypodermic
tablets of many of our large drug-firms.  The dose in children should
vary, according to the age, from atropia gr. -g-^-g- and morph. sulph.
gr. -fa to atropia gr. -jwo and  morph. sulph. gr. ■£$.   This had  best
be used hypodermically.
  In  the acute or  subacute  cases sinapisms may be applied to the
spinal  cord at the  onset  of  the disease.   In  chronic cases  a good
effect will sometimes be obtained from the use  of an ice-bag  applied
to the  spinal  column for ten minutes  daily.  This ice-bag can be
made  at home of a piece of  oil-silk, and should be long enough to
reach from the nape of the neck to the lumbar vertebrse, and about
broad enough to cover the vertebral column.  It must be filled with
finely  chopped ice.  Should it produce chilliness, it should be imme-
diately removed;  and should  this chilliness not  disappear with  its
further use, it  should be discontinued.   I have considerable  faith in
the use of ergot in all cases.   Its undoubted efficacy is probably due
                               16 
242
NERVOUS DISEASES.
to its action upon the dilated capillaries.   The fluid extract should be
used  if it does  not disagree with the stomach, and the doses should
vary from  ttlx-xxx three times daily for  children, to 5j-5ss  three
times daily for adults.  Its use should be persisted in for five or six
weeks.   Should the fluid extract nauseate the patient, ergotine may
be substituted, the dose varying from gr. £-£, thrice daily, for adults,
The iodide of potash  is  a  time-honored  drug that seems to  have
met with the approval of almost all the writers for this  disease,
and I am  myself  inclined to affirm  its efficiency,  more especially
in the subacute or chronic stage.   Moderate  doses  only should be
given, from  gr. ij  three  times  daily in a  child, to gr. x-xv in the
adult.  It should  always  be administered, to avoid the acne  and the
stomachic disturbances, in plenty of water, say in a wineglassful for
a child  and in a full tumbler for  an adult; or, better still, for the
latter, in a glass of Vichy or the  Bohemian Giesshuebler.  I  am a
great believer in  the use of quinine in all acute or subacute  affec-
tions  of the  anterior horn.   It may be given in two ways, viz., in
one or two good-sized doses, or continuously in tonic  doses.  In all
acute cases I should strenuously advise one or two full doses as soon
as the disease is  recognized.  In children, according to the age, gr. j-v
will suffice, given at bedtime.   In adults, gr. v-xv should be given
in one  dose  at bedtime.  These doses  should, of course, be larger
with  individuals who  have been  accustomed  to  taking quinine, or
with  those  living  in very malarious districts.   The dose  may be
repeated for one or two  nights, if necessary.  To  lessen the possi-
bility of cinchonism and  further to control the reflex disturbances, it
will be found highly useful to combine with the quinine, thus  given
at bedtime, a full dose of the bromide of sodium or potassium, gr. v-
xxx,  according to age.   The quinine can be administered in capsules
freshly prepared  by a  druggist, in  the soft  capsules  which  have
lately come into vogue, or the tablet triturate.   For children a very
pleasant mode  of  administration is by means of the chocolates of
tannate of quinine, of which the dose, however, should be double
that of the sulphate.
   The  agents capable  of affecting  the  degenerating or degenerated
nerve and  muscle  are galvanism, faradism, massage, and gymnastic
exercises.  Galvanism and faradism should be employed as soon as
the  reflex  disturbances have passed away.   The galvanic current
should  be applied  at least three times a week to  the spinal column,
and also to the nerve-trunks and nerve-filaments  of the  muscles (pp.
112-123 et seq.).   The current should pass for three to five minutes,
and should vary in strength from three milliamperes for  a little child
to ten or twenty or even  more for an  adult.   Faradism should be
applied to the affected nerve-trunk  and  to the muscles themselves in
sufficient strength to cause a general contraction  unless the reaction
to  faradism  is  so diminished  as  to  require  too  painful a  current,
Massage properly  performed may be used with   great advantage in
the latter stage  of  the disease, and should not be begun until the de-
generative process  has reached its limit.   When the treatment  of the
affected muscle  has become  useless, it may often  be  well to ascertain 
 DISEASES OF SPINAL CORD AND MEDULLA  OBLONGATA.   243

whether gymnastic exercises cannot increase the strength of surround-
ing muscles, in the hope that the latter may be sufficiently developed
in strength to compensate the atrophied ones, or whether some device
or operation of the orthopaedic surgeon may not relieve the deformity.

                   LANDRY'S PARALYSIS.

  Synonym: Acute  ascending paralysis.
  This is a form of  paralysis which was described  by Landry in
 1859, and  it is  characterized by motor,  or  almost entirely motor
 paralysis  of the  lower extremities,  then of the  trunk,  then of the
 upper extremities, and then of the neck and face.  The disease runs
 its course in the fatal cases in a period extending over a week or two,
 occasionally in a few days, or even  more quickly.  The paralysis is
 a flaccid  one, usually  attended by muscular atrophy, and generally
 without alteration in the electrical reaction of the nerve and muscle.
 There is usually, as has been said, no impairment of sensation, but
 occasionally there is some slight loss of the sense of touch and mus-
 cular sense.  There is seldom  any febrile reaction, although  some
 cases have been reported in which the temperature has risen to 101°
 and  103°.  The bladder and the rectum are not  affected.  Occasion-
 ally  there is a slight oedema of the feet, profuse perspiration, albumi-
 nuria,  or  swelling  of the  pancreas.   Most  cases terminate fatally
 because of the extension of the disease upward into the medulla ob-
 longata, causing death by failure of respiration  or deglutition, with
 all the symptoms of  ordinary bulbar paralysis.  Some cases,  how-
 ever, are  said  to  have  recovered,  and two noticeable  instances
 have been  reported  by Rendu  and  Schwarz.  In Rendu's  case the
 disease continued to exteud for eleven days, when  the patient was
 greatly embarrassed in eating and breathing.   On the thirteenth dayr,
 however, he began to  improve; by the thirty-first day  he was  able
 to get out of bed, and on the sixty-first day he left  the  hospital.
 In Schwarz's case the disease reached its acme in about  three weeks;
 an improvement began about the fortieth day,  but  the patient was
 not  able  to get  out of bed  in  nearly six months ;  for three years
 afterward,  however, the lower limbs  remained weak.   I  have seen
 recovery  in two  cases of apparent  Landry's disease, the  recovery
 being complete in each case and commencing three and six weeks re-
 spectively  after the onset  of the disease.  Fibrillary  contractions
 are sometime observed.
  The pathology of Landry's disease is somewhat of a mystery.   Of
 late  years  the doctrine of its  being  either  acute myelitis  or acute
 multiple  neuritis, generally the latter, sometimes  the  former, has
 been steadily growing.  Thus Ross has analyzed 93 cases, and has
 reached the conclusion that they were all due to multiple  neuritis,
 whether they were acute, subacute, or chronic.  Nauwerck and Barth,
 Eisenlohr, Centanni, and others have reported cases confirmatory of
 this  opinion; in addition, Centanni has detected a peculiar bacillus
 in the endo-neural lymph-space of almost all  the peripheral nerves,
 although Lewis failed to discover any bacilli in the inoculation which 
244
NERVOUS DISEASES.
 he made from  a fatal case.   Pitres and  Vaillard found the gray
 matter of the  spinal cord  perfectly normal and few alterations in
 the spinal nerve-roots, but all the peripheral nerves were affected to
 such a grave extent that the myelin  had almost entirely disappeared,
 the axis-cylinder being absent  in  many fibres in which nothing re-
 mained but an empty sheath  of Schwann.   The protoplasmic nuclei
 of the fibres  were  generally unchanged,  however, and there were
 none of the active  changes  observed  in the ordinary secondary or
 Wallerian degeneration.  Iwanow found marked pathological altera-
 tions in the cord in two cases.   These were limited to the region
 surrounding the central canal, with extension into the anterior horn,
 and consisted of an exudation  of lymphoid bodies into the tissues,
 as well as of a fibrinous exudate around the vessels and  nerve-fibres.
 There was also  some impairment of  the nerve-fibres and nerve-cells,
 and in places around the vessels some oedema, but no bacteria. Lock-
 hart Clarke, Baumgarten,  and Eisenlohr  found similar conditions,
 Joffroy and Achard have also  found multiple neuritis, but obliterating
 arteritis with it, and  they believe that the  neuritis was  a complica-
 tion or a secondary process.   Sinkler has recently reported a case of
 apparent  Landry's paralysis,  in which  death occurred twelve days
 after the onset, and in which there was shown to be an acute transverse
 myelitis.   Besides these cases in which the  marked evidences of dis-
 ease of the spinal cord and  peripheral  nerve  have been found, many
 others have been reported in which these structures were found to be
 perfectly normal.  It is, therefore, probable that Landry's paralysis
 is due  to acute changes  in the cord and peripheral nerves from the
 action  of some micro-organism as  yet undiscovered, or else that it is
an acute myelitis or an acute multiple neuritis, either idiopathic or of
 bacterial origin.   The  fact that the electrical  excitability of nerve
and muscle is not impaired  for  two or three weeks need not exclude
diseases of the anterior horns or multiple  neuritis, for Immermann
observed a case of poliomyelitis that lasted fourteen days, in which
the autopsy confirmed the diagnosis,  yet the electrical reactions were
 normal; and Schwarz speaks  of a marked multiple neuritis in which
the electrical reactions  were  normal  until  the third week, when a
marked reaction of degeneration ensued.
   The causes of Landry's disease are exposure and the predisposing
effect of such diseases as smallpox, diphtheria, and typhoid ; it occurs
 more frequently in male than in female, and  mainly between twenty
and forty years  of age, but it  has nevertheless been observed in chil-
dren and old persons.
   The diagnosis is  from  myelitis,  poliomyelitis anterior, neuritis,
 and paralytic rabies.  It  must  be  confessed that this diagnosis is a
 matter of considerable difficulty in the acute cases.  So far as we know
to-day, however, Landry's paralysis commences in the lower extremi-
 ties, then implicates  the trunk, the upper extremities, finally extends
to the  medulla, is usually entirely motor, the sensory symptoms being
 either entirely lacking or slight, the electrical reactions also lacking
 or slight, and the bladder  and  rectum unaffected, whilst muscular
 atrophy is either absent or is observed only  in those cases which have 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  245

an unusually long duration.   This group of symptoms will serve to
distinguish the disease from those others which have been enumer-
ated.  It may be, however, that there are acute forms of myelitis,
myelitis of the anterior horns, and  multiple  neuritis, in  which  the
symptoms are identical with those of Landry's paralysis ;  and if this
should prove  to be true, the special designation of the malady will
pass out of use.   Until such time, however, it is well to preserve the
name.  From paralytic rabies  the  diagnosis can  be made  by  the
history of the bite of au animal, perhaps by mental symptoms which
may be present,  or by knowledge of the patient having  been inocu-
lated by the Pasteur method.   (Chapter on  " Hydrophobia,  or
Rabies.'"')
   The  prognosis of Landry's disease is very grave, as most cases
terminate fatally, and it is exceptional for one to recover.
   The treatment should be  by means of the same methods that are
employed in any  acute affection of the cord or peripheral  nerves,
viz., absolute  rest, ergot, iodide of potash, and sulphate of quinine.
The patient should be put to bed and not allowed to rise for any pur-
pose whatsoever.   All noises should be excluded, and all  persons
kept from the sick-room except such as may be necessary to minister
to the patient's wants.   Ergot should be administered in the form of
the fluid extract, one  to two drachms  three or four times  a  day, or
ergotine (gr. ij-v three or four times daily) in case the fluid extract
should disagree with the patient's stomach.  Iodide of potash should
be given in doses of ten to twenty grains three times daily, aud should
be well diluted in a half-tumbler of water.  Belladonna  should be
given in the form of the fluid extract, one or two  minims once  or
twice a day.   The sulphate of quinine should be admiuistered  in tonic
doses, two grains  three or four times a day.  Should  the case  not
terminate fatally, the treatment should be that  of multiple neuritis
or myelitis; for which the reader must turn to the chapters upon these
two subjects.
                   SPINAL HEMORRHAGE.

   Synonyms: Hsematorrhachis.   Hsemato-myelia.   Spinal  menin-
geal hemorrhage.
   Extravasations of blood may occur between the dura mater and the
arachnoid, in  the  subdural space, between the dura mater and  the
bones,  between  the arachnoid and  the  pia mater, or into the sub-
stance of the cord.  The extra-dural hemorrhage is the most frequent,
that into the cord  exceedingly rare.  Spinal or meningeal hemorrhage
may occur at all ages, and the most frequent cause is trauma, although
severe and prolonged muscular  exertion may induce it, and one of
the worst cases I have ever seen was in an individual who had won
the prize iu an  eight- day go-as-you-please walk ;  whilst both varie-
ties are occasionally observed in many hemorrhagic diseases, such  as
purpura, smallpox, yellow fever, and typhoid.   Aneurism is a rare
cause.  The main symptom in meningeal  hemorrhage is usually a
violent pain in the region corresponding to the hemorrhage, and radi-
ating thence upward and downward ; but this is not marked iu spinal 
246
NERVOUS DISEASES.
 extravasation.   It is unnecessary to go into the different symptoms
 at the different levels of the cord, for these can best be studied in the
 table upon p. 82 ; but muscular spasm is a marked symptom in the
 meningeal forms, occasionally causing as general  symptoms as those
 observed in tetanus, although the convulsive  movements are usually
 localized.
   The prognosis is very grave, and death will usually ensue in a few
 hours unless a surgical  operation is done, although cases have been
 recorded in  which  the  symptoms  have decreased, the  patient has
 passed through a period of localized meningitis, and recovered.  The
 diagnosis is  to  be made by the suddenness aud focal localization of
 the symptoms and the  marked pain in meningeal hemorrhage;  and
 in hemorrhage  into the substance  of the cord by the quick onset,
 although the recognition of the latter variety is very difficult, if not
 impossible, which makes it doubly fortunate that it so very seldom oc-
 curs. It is to be distinguished from meningitis, myelitis, tetanus, and
 strychnine-poisoning.    Meningitis  is  much  more  gradual  in  its
 onset.  Myelitis has no such sharp pains, and the symptoms of irri-
 tation are not so marked.  In  tetanus there will be trismus, and the
 onset will not  be so sudden or the pain so severe.  In  strychnine-
 poisoning the paroxysms are much  more extensive.   The treatment
 should consist of absolute rest, venesection  in  robust individuals, or
 leeches or wet-cupping  in those in  whom venesection would not be
justifiable, ice to the spine, ergot  or ergotine, saline cathartics, and
 analgesics.  The patient should be made to lie  absolutely quiet on a
 water- or an air-bed, the bowels should be moved by an enema and the
 bladder emptied by a soft catheter.   The patient should lie  upon the
 face  or the side, so as to  keep the spine high.   Ice should be applied
 throughout the length of the spinal column by means of cracked ice
 put into  a rubber bag or into a home-made bag of oil-silk.  The fluid
 extract of ergot should be freely used in doses of a drachm every two
 or three  hours for the first twenty-four hours, and after that in lesser
 doses. If meningitis results, it should be treated in the same manner.
 If the symptoms progress rapidly, the vertebras should be removed,
 provided the patient's strength is good, and the clot removed.

          DIVERS' PARALYSIS, OR CAISSON DISEASE.

  History.   Attention was first called to this  malady by Hamel,
in 1820,  later by Colladon in  1826, by Triger in 1848, and by  Ba-
rella in 1861.  Since that  time there have been a  number of articles
upon the subject.  The best writings have been those of Smith and
Van  Rennselaer.
  Clinical  History.   The  onset  of  the paralysis  is  generally
sudden  and  accompanied by  giddiness, headache, weakness, and
nausea, occasionally with extreme  pain in the trunk or legs, and
sometimes transiently in  the abdomen, together with vomiting.  In
some cases these are all the symptoms, but in most the lower extremi-
ties are usually paralyzed, together with the bladder and rectum.  The
upper extremities  are seldom or never involved.   The paralysis is 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  247

motor, although there is often an impairment of sensation.  In some
few instances there are swelling, heat, and discoloration of the tissues,
occasionally suppuration.   The skin is cool, of a leaden hue, and
there is often cold and profuse sweat.  The temperature is generally
normal.  Transient attacks occur, characterized by headache, vertigo,
double vision, incoherent speech, occasionally coma ;  but all these are
temporary, unless the coma foreruns death.   Death  may occur very
suddenly, the patients may recover, or  the condition  may become
chronic.
  Causation.  There are three theories as to the causation of caisson
disease, namely—that it  is due to  exhaustion and  cold ; that it is
caused by the evolution of gases ; or that it is the result of congestion.
The objection to the theory of exhaustion and cold is that the atmos-
pheric variations of many climates,  especially that of many parts of
the United States, do not produce a similar disease.   The theory of
the evolution  of gas is twofold.  Bouchard maintains, for instance,
that  the gas which is always normally present in  the intestines is
compressed by the increased air-pressure of the diver's apparatus, so
that its volume varies inversely to the intensity of the compression
—i. e., the volume of the abdomen will become one-fourth if the pres-
sure is four atmospheres, and the abdominal wall will be compressed
against the vertebrae.  In the compression of this abdominal wall, as
by a vacuum in going into the diver's apparatus, the blood accumu-
lates from all other parts of the body into the  abdomen,  producing
in these other parts a great anaemia, and in the abdominal organs a cor-
 responding hvpersemia.   In  going out of the diver's apparatus  the
normal atmospheric pressure  reverses this  process,  aud hence occur
the peculiar pathological appearances of divers' paralysis.  The ob-
jections to this theory are that the symptom of abdominal distention
has not beeu observed, and that hemorrhages which would immediately
 result on the reversal of the atmospheric pressure are infrequent.
 The other gaseous theory is that there is an  abnormal formation of
gas in the blood.  It has not, however, been shown by the experi-
ments in support of this idea that the conditions to which divers are
subjected are exactly the same as  those to which the animals experi-
mented on have had to submit.  Bert, for instance, placed his animals
 under a pressure of from  six to nine atmospheres,  whereas Van
 Rensselaer  states  that workmen in the United States have  never
been in  a pressure  as high  as five atmospheres.  Bert, too, sud-
denly withdrew his  atmospheric pressure, whereas  the workmen in
this  country have the pressure gradually reduced during a  period
of three to eight minutes or more, and death has occurred after a pres-
sure of two atmospheres.   Nor has  any air been found in  the blood-
vessels of any of the sixteen men on whom autopsies have  been made
in this  country.   The theory of  congestion has  involved several
factors :  First, that there was a congestion with black blood ; second,
that the congestion was followed by hemorrhage;  third, that  it was
followed  by  acute  revulsive  anemia;  fourth,  that   comparative
stasis succeeded it.  Analysis of the blood  of people who have been
submitted to different degrees of atmospheric pressure  varying from 
248
NERVOUS DISEASES.
one to ten atmospheres has shown, however, that nitrogen is the only
gas that increases markedly in  the  blood during the increased pres-
sure, that oxygen  increases very slowly, that carbonic acid gas de-
creases very tardily, and that even  up to ten atmospheres the change
is so trifling as not to be sufficient to account for the lesions observed;
and these facts are fatal  to the theory of the  blacky blood as  it im-
plies  a deprivation of  oxygen,  as well as that this  deoxygenized
blood, jointly  with  the congestion,  is the cause of the lesions.  The
theory of a congestion followed by the evolution of  gas  is faulty,
because,  as  we have already  seen, there is no proof that gas is
evolved.   The theory of congestion followed by hemorrhage is open
to the same criticism.  The theory  that congestion is followed by
acute revulsive anaemia  is  met by the  fact that the spinal cord is
almost invariably congested.  Of all the theories, therefore, the only
one left  is that there is congestion followed by comparative stasis.
It has been shown that a sudden cessation of circulation  will cause
as sudden paralysis.  Herter passed a curved needle  through the ab-
dominal  wall  in such a manner  as to include the abdominal aorta
and vena cava, a strong ligature being  carried on this needle; and
compression of the abdominal vessels by this method  produced an
instantaneous  paraplegia.   If  the  compression was  relieved in less
than  three-quarters  of an  hour, the paralysis  rapidly ceased;  but
if it  was continued  for an  hour, permanent paralysis was induced.
Whether stasis, however, must  necessarily coexist with this condition
has not been proved, nor has it been  shown  by any of  these theories
why the  dorsal region of the cord should  be the particular portion
which is affected.  Predisposing causes are obesity, old age, alcoholic
excesses, heart and kidney  disease, or lowered  vitality  of the body
from any cause whatsoever.
   Pathology.  In the cases  of sudden death  the cord has appear-
ances of  softening, and occasionally the brain is congested, or both
brain and cord may seem normal.  Iu  those cases  which are fatal
within a week or two after the onset of the  symptoms, the spinal
cord is congested or softened, and the brain is also hypersemic.  There
may also be serous effusions into the spinal canal or extravasations of
blood upon the dura.   In the more chronic cases, lasting several
weeks or months, similar appearances  are  found in the brain and
cord.   The  other internal organs are also  usually found congested.
Microscopically the lesions are most marked in the lower dorsal region,
greatest in the white  matter rather than in the gray, and either of a
degenerative  nature  or  due to  a  parenchymatous  myelitis.   The
greatest disease is in the posterior  columns and the adjacent portion
of the lateral columns.  If  the cases last long enough, the usual sec-
ondary degenerations are found upward in the columns of Goll and
the direct cerebellar  tract,  and descending  in the pyramidal tract.
Hemorrhages  are not found except upon the dura mater.
   Prognosis.  This is good, as a rule.  The slighter attacks  last
from a few hours to about a week.  Paralysis may continue for hours
or weeks.  The fatal cases are  usually severe from the  onset. 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  249

  Diagnosis.   The diagnosis is very simple, and consists simply of
a knowledge of the manner in which the paralysis occurred.
  Treatment.  The treatment of divers'  paralysis should be that
of an acute  myelitis  (page  225).   Prevention,  however, if it can
be secured, would be the most useful, and  those who are in charge
of caissons should know certain  facts that have been  gained by
experience.   Thus, long-continued work  with  gradually increased
pressure is not harmful.   New  workmen should  therefore be gradu-
ally habituated  to their work.  The pressure should never exceed five
atmospheres, and the workmen should  not be allowed to work over
six hours with  two atmospheres, four hours with three atmospheres,
and three hours with  four atmospheres.  The watch should be short-
ened correspondingly for any increase.  The temperature of the air-
lock will fall very rapidly during  the  removal of the pressure—as
much as seventeen degrees in  four  minutes.   This can  be  avoided.
Intoxicating liquors must be forbidden.  Good sleep, food, and beds
should be given to the men, so that it will  usually be found best to
house them  at  the expense  of the construction company.    Gangs
 should work alternately in the  compressed air and outside.   Corpu-
lent men should not be employed.  The  air-locks should be at the
 top of the shaft, so that the men  may  climb in  the compressed air
 before leaving their work, or there should  be au elevator.  The air in
 the caisson should be pure.   Smith suggests a rough but (he thinks)
 a satisfactory test for the purity of the air, consisting of a  bottle of
 lime-water, through which the  air is passed by  an ordinary flexible-
 rubber syringe,  when an excessive amount of carbonic acid will give
 the water a milky hue, due to the formation of the carbonate of lime.
 Smith also recommends that the following  rules be posted up in some
 conspicuous place :
   1. Never enter the caisson with  an empty stomach.
   2. Use as far as possible a meat diet, and take warm coffee freely.
   3. Always put on extra clothing on coming  out, and  avoid expo-
 sure to cold.
   4. Exercise as little as possible during the first hour after coming
 out, and lie down if possible.
   5. Use intoxicating liquors sparingly; better not at all.
   6. Take at least eight hours sleep every night.
   7. See that the bowels are open every day.
   8. Never enter the caisson if at  all sick.
   9. Report at once to the office all cases of illness, even if they occur
 after going home.

            PROGRESSIVE MUSCULAR ATROPHY.

   Synonyms: Atropine musculaire progressive.  Die  progressive
 Muskelatrophie. Atrophia  musculorum progressiva. Chronic mus-
 cular dystrophy.  Myopathic atrophy.
   Definition.  A chronic muscular atrophy and motor paralysis
possessing these characteristics : The paralysis is almost always ex-
actly proportionate to the atrophy, which is fibrillary, affects sym- 
250
NERVOUS DISEASES.
metrical  muscles  bilaterally,  aud  often attacks widely  separated
muscles successively.
  History.   Our definite knowledge of this subject may  be said to
date from the year 1850, when Aran  wrote his first article, although
muscular  wastings had, of course, been observed  as far back as
Hippocrates.    In a  period extending  from  1853  to 1856  Cru-
veilhier made his  first autopsies, explanatory, as he thought, of the
pathology, but which  have been severely criticised  in later times.
Duchenne followed, in 1854, with a clear-cut description of the disease
in his famous book.  Friedreich published a ponderous and extremely
painstaking tome upon the subject in 1873.  A juvenile form of the
malady was described by Erb in 1884; a facial type of infancy by
Landouzy aud Dejerine in 1885, and a peroneal form in 1886, simul-
taneously by Charcot and Marie in France and Tooth in England.
  Symptoms.  In all cases the muscular atrophy is the prominent
feature of the disease, and  the  paralysis is always  strictly propor-
tionate to the atrophy.  The characteristics of the atrophy are these:
It is chronic;  it  affects the  muscle fibre by fibre,  and  not by a
sudden implication of the  whole muscle, as in acute  myelitis of the
anterior horn; its progress is not  generally among the contiguous
muscles, but  often by a jump over widely separated  ones.- Any of
the muscles of the body may be affected.  As we shall learn further
on, there are cases of spinal origin, and others of peripheral causation.
In the former the anterior cornua of the cord and the motor nuclei
of the medulla may be affected in the same case, the progress of the
disease being either  downward  or  upward.   The muscles supplied
by the cranial nerves would then be affected, together with the mus-
cles of the trunk and extremities.  In the cases of peripheral origin,
however, the muscles  of the  trunk  and extremities are  the  ones
mainly affected, the facial muscles being implicated only in children,
whilst the tongue and larynx always remain intact.  Through many
years neurologists have demarcated many so-called "types" with the
idea of associating them with pathological and prognostic differences;
but no notable success has attended these attempts until within a few
years.  It  is, however, justifiable at the present time to  speak of
these four groups:
       1.  The hand-type;
       2.  The juvenile type (Erb);
       3.  The facial type of infancy (Landouzy and Dejerine);
       4.  The peroneal type (Charcot and Marie, and Tooth).
  1.  The hand-type.   In  this  the  onset is generally in  the right
hand, occasionally in both hands.   The short  muscles of the thumb
and the ball of the little finger are generally first affected—the so-
called thenar and hypothenar eminences.  It is usual for the atrophy
to begin in the abductor  pollicis brevis, and then be observable in
the opponens and adductor.  The complete atrophy of these thumb-
muscles produces a condition to which the name has been given of
" ape-hand"  (Affenhand).   (Fig. 129.)   At  about  the same time,
sometimes a little  sooner, sometimes a little later, the interossei are
implicated, as  is to be seen  from a sinking of the interosseus spaces 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  251

on the back of the hand  and from an  incomplete extension of the
terminal phalanges ; and when this atrophy has attained to a certain
Lirade, it produces, together with the  contraction of the antagonistic

                             Fig. 129.
                           Ape-hand.

muscles, the  so-called  "claw-hand"  (main-en-griffe—Klauenhand).
(Fig. 130.)   Consecutively to the hand-muscles, ofteu after a  long
time—sometimes even after years—the forearm or upper-arm muscles
are usually attacked.  In the forearm it is apt to be the abductor
and extensor  pollicis longus, the supinators, and the flexors.  In the

                            Fig. 130.
                           Claw-hand.

upper arm the deltoid is almost invariably the first to waste, then
the  biceps, aud finally the triceps last of all.   But sooner  or  later
the muscles of the trunk may be implicated, especially the trapezius,
the pectorals, the rhomboids, and the latissimus dorsi.  Atrophy is
infrequent of the cervical or respiratory muscles, or of the diaphragm.
After many years of duration, the bulbar nuclei may be affected, and
then may ensue atrophy of the tongue, difficulty of deglutition, and
death may result from iuanition or respiratory disturbance. 
252                  NEB VO US D IS EASES.

   2.  The juvenile type (Erb).   This form was first described by Erb,
in 1884, and it differs essentially from the hand-type in the location
of its onset, which is almost always in the  muscles of the shoulder
and upper arm, far less often iu the muscles of the pelvis and lower
extremities, whilst, as has just been explained, the hand-type prima-
rily affects the hand-muscles, and only secondarily, often after a long
time,  are the  shoulder- and arm-muscles involved.  The  shoulder-
and upper-arm muscles  most often  atrophied  are:  the  pectorals,
trapezius,  rhomboids,  serrati, latissimus dorsi,  longissimus, sacro-
lumbalis,  forearm-flexors,  supinator  longus, triceps; and  in  the
lower extremities, the gluta>i, quadriceps,  peronei, tibialis anticus,
But this juvenile type of Erb is not so distinct as are the hand and
infantile types.
  3.  The facial type of infancy (Landouzy and Dejerine).   This was
first pointed out in 1885.   It generally begins  with an atrophy of
the muscles of expression.   The face is in repose, the lips protruding,
the brow like ivory, there  is a seeming protrusion of the eyes;  iu
efforts at mimicry the smile is sad,  the movements of the lips are in-
complete, and  the immobility of the lips is in marked  contrast to the
animation of the eyes.  (Fig. 131.)  When the face has wasted, it is
Fig. 131.
                  Progressive muscular atrophy, facial type.

the rule that the muscles of the shoulder and arms are involved next;
but certain muscles usually remain intact, such as the supra-spinalis,
the infra-spinalis, the infra-scapularis, and  the flexors  of  the hand
and fingers.  Exophthalmus is occasionally seen in  this form, as in
Fig. 131.
  4.  The peroneal type (Charcot and Marie, and Tooth).  As stated
above, the French authors described this form in 1866;  whilst Tooth
claims that he  also  called attention to it  at the  same  time.  As is
indicated by the  name which I have given it, it first shows itself in
the muscles  of the  leg;  invading the hand and  then the forearm
several  years afterward.  (Figs. 132 and 133.)  Hoffman and Sachs
have shown that this type is characterized by its heredity, its bilateral 
DISE ASES  OF SPINAL COBD  AND MEDULLA OBLONGATA.  253


implication of the leg- and  foot-muscles, leading to double  club-foot,
the  late  preservation  of  the reflexes  in  it, its  frequent  vasomotor

                 Fig. 132.
Fig. 133.
Progressive muscular atrophy,
     peroneal type.
Progressive muscular atrophy,
       peroneal type.
symptoms, and its occasional tendency to affect the upper extremities,
even causing the claw-hand.
Hand-type.
Muscles of thumb and
   fingers:
  Abductor pollicis
   brevis.
  Opponens.
  Adductor.
  Interossei.
  Lumbricales.
  (Ape-hand, claw-
   hand.)

Arm-muscles:
  Abductor and exten-
   sor.
  Longus  pollicis.
  Supinators.
  Plexors.
  Deltoid.
  Biceps.
JTriceps.
Juvenile type.
Muscles of shoulder
   and upper arm:
 Pectorals.
 Trapezius.
 Rhomboids.
 Serrati.
 Latissimus.
 Longissimus.
 Sacro-lumbalis.
 Flexors of forearm.
 Supinator longus.
 Triceps.

Muscles of lower ex-
   tremity :
 Glutei.
 Quadriceps.
 Peronei.
 Tibialis anticus.
Infantile facial type.
Facial muscles of ex-
 pression.

In shoulder- and arm-
  muscles these  are
  intact:
 Supra-spinalis.
 Infra-spinalis.
 Flexors of hand and
  fingers.
Peroneal type.
Muscles  of the  leg,
 then the  hand  and
 forearm. 
254
NERVOUS DISEASES.
  The preceding table shows, side by side, the location of the atrophy
in each of these four types.
  Of these four types,  it is generally believed that the hand-type
represents the spinal  form of the disease, the juvenile  and infantile
facial types the muscular form, whilst the pathology of the peroneal
types is undetermined.   But it  must be carefully remembered that
Fig. 134.                            Fig. 135.
Generalized progressive muscular atrophy.      Generalized progressive muscular atrophy.
           Front view.                            Rear view.
these statements are only true in a general way, and that our present
knowledge of the disease is insufficient to enable us to base a positive
diagnosis as to the peripheral or central origin upon the muscular
localization of the atrophy.   Indeed, it is impossible to classify mauy
of our cases coming to the clinics under any one of these  four types,
so general is the atrophy, frequently commingled with true or pseudo-
hypertrophy, as in the remarkable case represented in Figs. 134 aud 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  255

135.   This classification becomes additionally difficult  at the begin-
ning of the disease in many cases, as in Fig. 136,|where the supra-
scapular atrophy belongs to no type.
  The course of the disease is gradual, and the duration is from five
to thirty years.   The  chronic and  fibrillary atrophy may not  be
detected for some time, until enough of the muscle has been affected
to alter  the  contour  and  consistence, which  latter  is then found,
upon  palpation, to be softer  and  less resilient  than in a  healthy
muscle.   The  paralysis is  usually proportionate to the atrophy, as
has been already stated.   It  not infrequently happens  that  the loss
of muscular strength  first  attracts  the attention of  the patient, or

                             Fig. 136.
Supra-scapular progressive muscular atrophy.
those interested  in the patient, and then  an examination brings the
atrophy to view.  Fibrillary contractions are  frequently present in
all the types.  These consist of minute movements of the muscular
fibres, and vary in extent  from an  occasional whipcord-like  move-
ment under the skin, likened  by patients to a pulse-beat, to a wide-
spread series of fibrillary  movements that may set a whole muscle
or muscular group  into  tremulous movement.  The electrical alter-
ations may be  those  of the reaction  of  degeneration, or  those of
the so-called "partial degeneration" (page  128), or  the  electrical
reactions may be normal.   If the researches of Gessler upon the
motor end-plates of  lizards and  guinea-pigs should  be applicable 
256
NERVOUS DISEASES.
to human beings, the reaction of degeneration will be in exact ratio
to the amount of atrophy of muscular fibre.   Until within a very
recent time it has been  supposed that a spinal origin was  indicated
by the reaction of degeneration; but this has also been demonstrated
in some recent cases in which careful post-mortem examination could
detect no disease of the nervous system.
   Pathology.  Since the first description of the disease by Aran
in 1850, professional opinion has undergone many changes regarding
its exact pathological nature.  The early French  school strenuously
maintained that the  lesion was in the  ganglion-cells of the  anterior
gray  matter  of the  cord and  medulla; whilst  Friedreich's monu-
mental monograph in 1873 was one ponderous argument in  favor of
the muscular origin of the malady.   At the present day it can be
positively stated that progressive muscular atrophy may be of three-
fold origin :
   1.  It may be due to lesion of the  ganglion-cells  in  the  anterior
gray  matter of the cord  and  medulla ;
   2.  It may be caused by muscular degeneration  alone;
   3.  It may come from simultaneous degeneration of the peripheral
nerves and the muscles.
   The essential change in the anterior gray matter is in the ganglion-
cells.   These undergo various degrees of alteration.  They may be
totally destroyed, so that either  no vestige of  them is visible to a
high magnifying  power, or else only a formless mass of protoplasm
is seen in their place ; or some nucleoli or nuclei  may persist;  or some
cells may have lost all or several of their protoplasmic prolongations;
or the number of the cells may be lessened.   Roger has shown that
the ganglion-cells may  undergo  serious  change  or  even  disappear
after  inoculation of the micro-organism of erysipelas.   Throughout
the spinal cord the anterior horn may have shrunken in volume to
an extent  that will  be visible  to the naked  eye, and  the  medulla
oblongata may also be diminished in size ; not infrequently, however,
neither cord nor  medulla is  of abnormal  size, and the lesions are
only demonstrable by the microscope. The  connective tissue, both
in the spinal and medullary gray matter, is often proliferated; it may
occasionally happen  that the gray matter  of the anterior  horn or
bulbar nucleus becomes converted into a dense fibrillary mass. The
vessels often become enlarged and thickened in their outer tunics, the
intima being seldom affected.  The  cranial  and  peripheral nerves
usually undergo marked changes when their parent gray matter be-
comes affected.  To  the naked eye they usually appear thinner than
normal, more transparent, often  grayish or whitish in hue.   Micro-
scopically, their medullary layer  is seen  to be  more or less affected
in  its continuity  and cousistence, in one case having broken into
irregular  masses  or oil-globules, in another  case being split irreg-
ularly in  places.   The axis-cylinder  may be affected also  in vary-
ing degree.  The affected muscles may  display  au atrophy  alone,
or  an atrophy mixed with  hypertrophy.   So far  as our present
knowledge can enable us to judge, the cases of spinal origin  are very
largely, if not entirely, manifested by  atrophy alone of the primitive 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  257

muscular fibre;  whilst  the  cases of muscular origin, especially  in
children, present  a mixture of atrophy and hypertrophy of the primi-
tive muscular fibres.  Pseudo-hypertrophy—i. e., a fatty accumula-
tion in the sheath of the muscular fibril—may be an accompaniment
of both classes of cases.   Simple atrophy of the primitive muscular
fibre consists of a diminution in size without loss of the transverse
stripping; whilst hypertrophy is an increase in its size.   The sheath
of the fibre, too—the perimysium—is  usually thickened, its nuclei
increased iu size and number.   So-called "vacuoles" have also been
observed, as well as collections of what appear to be giant-cells, con-
sisting of  remains  of muscular and sarcolemmar  nuclei that have
invaded  the true muscular substance.
   Causation.   The most frequent causes  of progressive muscular
atrophy  are—
      Heredity;
      Muscular strain ;
      Trauma;
      Acute diseases;
      Age;
      Continuous  cold ;
      Lower classes;
      Sex;
      Lead-poisoning;
      Syphilis.
   The juvenile and infantile facial types are very largely hereditary,
the heredity sometimes extending  in  the most remarkable  manner
through  several generations.   The hand aud peroueal types are only
occasionally hereditary.
   There can be no doubt  that, next to  heredity, muscular strain  is
the most potent cause of progressive muscular atrophy.  Friedreich
 narrates  case after case of this  kind, and  my experience has tallied
with his.  It is  for this  reason that the right upper extremity  is
 most prone to be affected, especially in those who use this member
 much in manual  labor.
   Trauma needs only to be mentioned, because of its possible medico-
legal bearings.   I have seen several cases caused, in all probability,
by injuries sustained in railroad accidents, and other forms of concus-
sion of brain and cord may act in the same manner.
   Progressive  muscular atrophy has been often observed to follow
typhus,  diphtheria,  measles,  acute  rheumatism,  parturition,  and
cholera; so that these acute diseases must  have some  unfavorable
influeuce upon  the cells of the muscles and the anterior horns.
   Although certain  types, as we have  seen, may appear at  certain
periods of life, the  disease may yet occur at any  age, so  that  this
factor is of relative  subordination.
   Several  cases have been observed, both by myself aud others,  of
the induction of  the disease by  prolonged or  continuous exposure  to
cold of the part  afterward affected.  I  have seen this especially  in
market-men  working in refrigerators, and in ice-dealers.
   It is singular that cases of  progressive  muscular atrophy are seldom
                               17 
258
NER VO US DISEASES.
encountered among the rich or well-to-do classes of our population,
except where there is an hereditary causation.   Its frequency in the
lower classes is  probably due to the greater use of the muscles by
them and to the greater exposure.
   Males  are most  frequently  affected,  probably  because of their
greater exposure to the various causes.
   Lead-poison ing and syphilis are both infrequent causes.
   Diagnosis.   The diseases with which progressive muscular atrophy
is liable to be confounded are—
        Chronic  myelitis of the anterior horn ;
        Peripheral neuritis, simple or multiple;
        Syringomyelitis;
        Atrophic joint-affections;
        Amyotrophic lateral sclerosis;
        Muscular pseudo-hypertrophy.
   In chronic myelitis of the anterior  horns the motor paralysis is
primary, the atrophy is secondary and in proportion to the paralysis,
the spread of the disease  is from muscle to muscle, not from fibre to
fibre, and contiguous muscles  are  usually affected; whilst in pro-
gressive muscular  atrophy the atrophy is  primary, the paralysis is
secondary, the paralysis is strictly proportionate to the atrophy, the
atrophy spreads from fibre to fibre, and widely separated muscles are
involved.
   The diagnosis in simple neuritis of a nerve-trunk  is easy when a
mixed  nerve is affected,  and  when such  symptoms are present as
marked pain in the distribution of the  affected nerve, glossy and
slightly cedematous skin,  heat of the  surface, and  sensory impair-
ment.   But confusion may arise in neuritis of a  mixed nerve when,
as is not  infrequently  observed, the motor fibres are almost entirely
affected.  In such  cases, however, the  paralysis  will be strictly lim-
ited to the distribution of  the nerve and will be primary, whilst the
atrophy will be secondary; and the spread  of  the disease will be
within  the distribution of that nerve, and  not by jumps  to widely
separated muscles.   In multiple neuritis  the onset is often  acute, and
even if it is chronic the burning pains and the sensory impairment
will make the diagnosis easy.  Besides, the endemic, epidemic, alco-
holic, or arsenical causation may be apparent; and in any  event the
atrophy is not primary, nor does the  disease spread fibrillarily from
muscle to muscle.
   The diagnosis can usually be  made  between progressive muscular
atrophy and syringomyelitis.   My reasons for this belief are elabor-
ately set forth in " Syringomyelitis,"  aud  I must ask the reader to
peruse this carefully.
   Iu atrophic joint-affections  the atrophy  is around the joint, and it
is plainly to be seen that the  articular disease has been primary and
the atrophy secondary.
   In amyotrophic lateral sclerosis the  atrophy  and paralysis are
always  accompanied by contractures and exaggerated tendon-reflexes
to a far greater extent than is found at any time in progressive mus-
cular atrophy. 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  259

  In any case of progressive muscular atrophy there  may be a cer-
tain amount of muscular pseudo-hypertrophy ; but this is limited, and
in no case has it the characteristics of the disease to which the name
per  se has  been given of muscular  pseudo-hypertrophy.  In  this
latter affection the hypertrophy is in the  lower extremities, generally
contrasting  sharply with  the atrophy of the upper  extremities.  It
is only in the earlier  stages of pseudo-hypertrophy—when it is first
noticed that the child is defective  in  its  movements—that any con-
fusion should arise.
  Prognosis.  The prognosis of all  forms of progressive muscular
atrophy is unfavorable, although some seeming  cures have been  re-
ported in cases that were  apparently of peripheral origin.
  Treatment.  The treatment should  be by means of galvanism,
faradism, massage, rest, cod-liver  oil, arsenic,  strychnine hypoder-
mically,  generous diet, and occasionally surgical  or orthopaedic treat-
ment.
  The galvanic current should be  applied to the spinal column, and
also to the nerve supplying  the affected muscles, both  to the nerve-
trunks and to the muscular nerve-filaments (pp. 124, 125,  126). The
strength of current should vary from five  to twenty or thirty mil-
liamperes, according to the  effect  upon the particular patient, as
some will do best with the lesser quantity, others with the greater;
but the   painful susceptibility of  neuritis (vide  p. 199) is never
seen in this disease.   The sittings  should  be from five to ten min-
utes, two or three times  a  week.  The faradic current  should  be
applied to the motor nerve-trunks  aud muscular nerve-filaments of
the affected muscles, aud it should be strong enough to be somewhat
unpleasantly felt by the patient.   Both currents should be used in
accordance with the principles that have been  laid down.   Gentle
massage  of the affected muscles should be given  two or three times a
week, and with it the muscles will  often be seen  to increase slowly in
bulk and strength.   Rest of the affected  muscles to the extent of not
straining them  should always  be observed.  I am no believer in
gymnastic exercises in this disease.  Cod-liver oil  should  always be
employed in cases of  progressive muscular atrophy, unless there is a
tendency to pseudo-hypertrophy.   Some  sweet,  fresh oil  should  be
used, preferably pure; but  if an emulsion must be employed, this
should be prepared anew every few days in warm weather and every
week in cold, and  even then  kept  in  the ice-chest.   Arsenic  will be
found to be a useful alterative in  this malady, and may be given  in
the  form of liquor potassae arsenitis, nuij-v, three times a day, well
diluted in a wineglass of water, and taken  after  meals.  If there be
any indication  for  iron, it may be given  in conjunction with this
drug; and the best preparation is  either ferratin, gr. iv-viij, or  the
dialyzed  iron, 3j-ij after  meals, in a full tumbler  of  water, or the
citrate (gr. ij-v three times daily).  A generous and varied diet  should
always be observed.   Surgical or orthopaedic treatment will some-
times overcome a muscular deformity temporarily. 
260
NEE VO US DISEASES.
                     LOCOMOTOR ATAXIA.

  History.   W. Horn, in  1827, was  the first approximately to
describe the disease, and Stanley, in 1840, called attention to the ataxia;
but Todd may be really called the discoverer of the malady itself,
in 1847.  Romberg, in 1851, Russell Reynolds, in 1855, W. Gull,
in 1856 and 1857, followed with  good descriptions  of many of the
symptoms; but that of Duchenne, in 1858 and 1859, was by all odds
the best.  Cruveilhier described the  microscopic appearances of the
cord correctly.   Tiirck was the first one to describe it microscopically.
Leyden and  Friedreich, in 1863, Topinard and Jaccoud, in 1864,
have been followed by scores  of  others since—notably,  Hammond,
Mitchell, Seguin, Spitzka, and Gray.
  Causation.  The causes of locomotor ataxia are :
       Syphilis;
       Sex;
       Trauma;
       Alcoholism;
       Other spinal diseases;
       Chronic ergotism ;
       Chronic arsenicism;
       Heredity;
       Urban population.
  Syphilis is the most frequent of all the causes of locomotor ataxia,
as is now generally acknowledged, although this doctrine was met
by the most furious opposition when  first  maintained by Fournier,
in 1875.   The number of cases  in which an antecedent history of
syphilis  has  been obtained varies in different writers from 30 to 90
per cent.   The most remarkable  confirmation  of this view is to be
found in the  recent observation of Minor, of Moscow, of  the infre-
quency of locomotor ataxia among the Jews, who are singularly free
from syphilitic infection.   I  may say, in  passing, that this present
belief in the  frequent  specific origin  of locomotor ataxia  is a rare
posthumous tribute to the clinical genius of Duchenne (of Boulogne),
to whom we owe the first description of the symptoms, and who espe-
cially remarked the occasional efficacy of iodide of  potash.  But it
must not be  supposed that all the  cases that have had a syphilitic
history are necessarily cases of cerebro-spinal syphilis.  On the  con-
trary, it should be distinctly understood and carefully borne in mind
that most cases are those  in which the  locomotor ataxia has devel-
oped after specific infection, and that these have an entirely different
prognosis and therapeusis from those others in which the symptoms
of locomotor  ataxia are immediately due to cerebro-spinal syphilis.
   It is most  frequent in males, for what reason is unknown, although
it is probable that  the lesser exposure of  the female sex to specific
infection and other causes may account for the difference.
   Trauma is undoubtedly the cause  of some of the severest forms.
One of the worst cases that I ever saw began shortly after a terrible
railroad disaster, in which the patient fell more  than a hundred feet
through a railroad bridge. 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  261

  Alcoholism is more apt to set up the peripheral form.
  Locomotor ataxia may be conjoined with other spinal diseases and
with spinal meningitis, so that its  peculiar symptoms  may be  com-
bined with those of these  other maladies.
  Chronic ergotism, as has been pointed  out by Tiirck,  may set up
locomotor ataxia, as may also chronic arsenicism.
  Heredity is of small importance as  a  causative factor, and  even
then  only indirectly.   Thus  a neurotic heredity of various nervous
diseases may be found in  a small proportion of cases;  but direct in-
heritance  is extremely rare,  except in the  allied hereditary  form
which is known as Friedreich's disease.
  According to  Gowers, locomotor ataxia is more frequent in urban
than  in rural populations  in England ; but  I cannot say that this is
true of America.
  Clinical History.   The  symptoms of locomotor  ataxia may
be divided into three classes, viz., the pathognomonic, the non-path-
ognomonic,  and the symptoms which are merely associated with the
disease.
  The pathognomonic symptoms are:
      Stabbing and fulgurant pains, which are  vagabond, sudden,
         and atrocious;
      Absent tendon-reflex;
      Ataxia, motor and static ;
      The Argyll-Robertson pupil;
      Atrophy of the optic nerve ;
      Ptosis;
      Crises—gastric, laryngeal,  nephritic.
  It  is the association of two or more  of these symptoms that  is
absolutely necessary for  the diagnosis of locomotor ataxia, and  it
may  be said that the association of several of these symptoms is not
known to occur in  any other disease.   The stabbing-pain is  often
described, with  a singular identity of words, as feeling like a  knife
plunged  into  the  limb  and  twisted  around.    It  may  be less,
however, and may simply consist of a sharp pain which  the patient
cannot describe.  The fulgurant  pain is, as the  name  indicates, a
pain  somewhat resembling the  electric  shock passed through the
limb.  Both these  stabbing  aud  fulgurant pains, however, gener-
ally have three  characteristics in common—they seldom can be ex-
pected in any particular  spot (are, therefore, vagabond); they come
and go very suddenly, and  they are very severe—what the French
have called atrocious.   The tendon-reflex of the quadriceps extensor
is almost invariably absent;  but before this can be confirmed a
careful examination should be made upon the bare skin with the aid
of the method  of "reinforcement" (p. 167).  The ataxia  may be
both  motor and  static ; i. e., when  movements are made, or when the
patient is sitting or standing (vide p. 172).  When the lower extremi-
ties are greatly affected, the patient walks with a flopping movement,
bringing the heel down upon the  ground like  a flail; or, in a still
more marked degree, the foot  may be brought down upon the outer
or the inner side.   In the slighter degrees the patient cannot walk a 
262
NERVOUS DISEASES.
chalk-line or a crack in the floor; or, in  the still slighter degrees,
this  may be done with the eyes open,  but not with them shut.
The patient's attention is often called to the ataxia for the first time
by the unsteadiness on a dark night or in a  dark room.  Yet he
can walk very  well if he is  allowed merely to touch  the finger of
some other person.  If seated,  the patient will  fail to hit with his
foot the finger of a person held before him.  If the  upper extremi-
ties are affected, it will be found that the patient cannot, if the eyes
are shut, swing the arm up and hit the tip of the nose with the tip
of the index-finger, or cannot  bring the  tips of  the fingers  of the
two  hands  together quickly and swingingly.   These  phenomena are
known as motor ataxia.  Static ataxia is  failure to  co-ordinate the
muscles so  as to preserve the equilibrium when sitting or  standing,
and  is evidenced by swaying and uncertain movements of the trunk
and  head when the person is sitting  or standing.  The pupil, which
is known as the Argyll-Robertson  pupil, has,  in  its typical  form,
three symptoms-—myosis, failure of response to light, and sluggish
contraction to accommodative movements.  The pupils are usually
minutely contracted, sometimes to such a degree as to suggest  mor-
phinism ; on the other hand, they are sometimes but slightly affected.
The loss of response or  diminished  response of the  iris to light is
probably due to the atrophy  of the  optic nerve, which is a primary
atrophy, and is not accompanied by any signs of retinitis. Its white,
glistening appearance is unmistakable to any tyro in ophthalmoscopy
(Fig. 94).  The ptosis is generally a transient symptom, and usually
unaccompanied by paralysis of any  external ocular muscles.  The
so-called crises are peculiarly violent attacks of pain in the gastric,
laryngeal, or iliac  regions, lasting for hours and simulating organic
gastric, nephritic,  or laryngeal  disease.
  There is no other disease  in  the whole range of medicine which
has so original and marked a  symptom-group  as  locomotor ataxia
when it is characterized by these stabbing and fulgurant pains (which
are vagabond, sudden, aud  atrocious), by the  absent tendon-reflex,
by the motor or static ataxia, by the Argyll-Robertson pupil, by the
optic-nerve atrophy, by the transient ptosis, and by the peculiar crises.
These, therefore, are pathognomonic symptoms.
  The non-pathognomonic symptoms which may be found in  loco-
motor ataxia, but which are often found in other diseases of the nervous
system, are:
       The so  called Romberg-symptom ;
       Anaesthetic zones;
       Joint-lesions;
       Various sensory symptoms;
       Constipation;
       Vesical symptoms ;
       Vasomotor and trophic symptoms.
  The so-called Romberg-symptom is a swaying motion of a patient
standing with the  eyes closed;  but, as it is geuerally  due to a loss of
tactile sense on the plantar surface of the  foot, sometimes to lesions
in the different regions of the cerebro-spinal axis, it is not necessarily 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  263

a symptom of locomotor ataxia.  Not infrequently anaesthetic zones
are found iu the lower extremities in locomotor ataxia, although they
mav be fouud in other forms of myelitis  and in some cases of neu-
ritis.  The retardation  of pain-conduction is evidenced by sticking
a pin or needle  into the patient and then observing that he  feels it
only after a perceptible interval of several seconds or it  may be a
minute.   This is quite a common symptom of locomotor ataxia, but
it is quite as common in many forms of myelitis affecting the sensory
tracts.   Various sensory symptoms may be observed in  locomotor
ataxia, as well as in other  forms of myelitis.  A cincture  or  girdle-
feeling may be felt around the body, as if a cloth or band were com-
pressing the patient round about.  A prick on one limb may be  re-
ferred to the other, sometimes to an identically symmetrical position
(allocheiria); or a prick in one spot may be felt in many places on the
same or on both legs (polyassthesia).  The positive  pole of a galvanic
battery may give the first sensation when the current-circuit is closed,
instead of the negative  pole doing so.   Subjective sensations of cold,
heat, tingling, pins, needles, etc., are often  felt.  Constipation is a
 very frequeut symptom.  The symptoms due to simultaneous disease
 of other portions of the cord are muscular  atrophy of the  muscles
 of the limbs  or truuk, occasionally a lingual atrophy,  or contracture.
   Locomotor ataxia usually^ begins in the lower limbs, and may com-
 mence in the upper ones, although rarely, Dejerine finding one such
 beginning in 101 cases in the Bicetre.
   The disease  is an eminently chronic one in the vast majority of
 cases, although acute cases do occasionally occur, running their course
 in a few months.   The sensory symptoms are usually the first;  in-
 deed, they may last many years before the ataxia supervenes—in one
 case of mine some  twenty-one years.   But the ataxia, it must not be
 forgotten, is  sometimes the first symptom.  The  course of the dis-
 ease is generally slowly progressive.   Long spontaneous  remissions
 were  claimed  by  the  older writers, but it is  extremely doubtful
 whether they  did  not admit many cases which  have since been
 shown to be due to other forms of spinal disease.  The extension of
 the disease is generally upward, so  that the upper extremities  become
 affected  in time; or, if the upper extremities be first affected, the ex-
 tension  is downward.   The ataxia may render the  patient  absolutely
 helpless, unable  to  rise without help, to stand alone, or even to sit
 without support.   Usually the motor strength is in marked contrast
 to the helplessness of the  ataxia, and I have been in the  habit  for
 years of showing my  class a man who  could not stand  alone, but
 whose legs could not be flexed or extended by the  strongest man in
 the room.  Motor weakness is almost invariably the last  of all  the
 symptoms, and many patients die without having displayed it.  Many
 cases  of locomotor ataxia gradually pass into a  form  of dementia
 resembling that of general paralysis of the insane,  but differing from
 it in the slightness  of  the  delusions  and hallucinations, in the lack
 of the extravagant delusions  which  are known as the delirium of
 grandeur, and also in the lack of periods of excitement.   In propor-
 tion as  this dementia  supervenes, the ataxia diminishes, and it  has
 been supposed that this is due to the loss of cortical control. 
264
NERVOUS DISEASES.
   Pathology.   The synonyms of locomotor ataxia, tabes dorsalis
 and posterior  sclerosis, are  misleading in regard to the real patho-
 logical lesion, since this is neither a softening nor tabes, is occasionally
 of cervical and not of dorsal origin, and modern research, as we shall
 see, has  demonstrated  that  the pathological  alterations are  by no
 meaus confined to the posterior column.  Until within about a decade
 locomotor ataxia was thought to be due to implication  of the poste-
 rior columns of the cord and the adjacent gray matter of the posterior
 horns, and  there was a difference  of opinion as to whether these
 posterior columns and cornua were together  or  separately paths of
 sensory conduction.  Then Flechsig's embryological researches map-
 ped out the direct cerebellar  column.  Then Woroschiloff demon-
 strated  that section  of both  posterior columns  and the posterior
 halves of both lateral columns in the lower dorsal region  of the
 rabbit did  not prevent sensory impulses  passing from the hinder
 limbs to  the  motor  structures in the cervical  cord and the brain.
 Three years afterward, in  1877, Gowers wras the  first to confirm
 anatomically what Woroschiloff had observed  physiologically by the
 discovery of the antero-lateral  peripheral tract, which has since come
 to be known as the Gowers  column (Fig. 133), although Westphal,
 Kahler, Pick,  Strumpell, and  Leyden had also partially figured this
 before.   That  this is  a sensory tract  is proved  by the fact that it
 is the site  of  an  ascending degeneration, as is made evident by
 the cases  of tabes dorsalis of Haddon, Gowers, Westphal, and my
 own, and by  Tooth  in  compression-myelitis.    The  objection  of
 Dejerine, that  the degeneration  of this  peripheral tract might be
 due to  meningitis, has been  abundantly disproved, especially by
 Sherrington, who has  found this  column in  the eighth month of
 uterine life, and has demonstrated also that it takes on its medullary
 covering at  a different time  from other strands of the cord.   Bech-
 terew, in  his turn, has  subdivided the Gowers tract into an auterior
 and a posterior portion, and  has been confirmed by Sherrington's ob-
 servations.  In 1885 Spitzka called attention  to a tract which he
 describes  as along the entry-line of the posterior roots of the posterior
 horn on one side  and the periphery of the cord on the other, giving
 to this the name of the  analgesia tract, as he has found it impaired
 in  all cases of  analgesia, and  healthy in others.  According to
 Spitzka,  there is a column of  vertical fibres immediately adjoining
 the gelatinous head of the posterior horn, which  he believes to bear
 the same relation to the gelatinous substance that the ascending roots
 of the fifth pair bear to the gelatinous substance of the tuber ciuereum
 of Rolando, and   this analogy inclines  him to believe that the tract
 may be possessed of trophic functions, although he can affirm nothing
 more positive than that it was healthy in  those cases in  which there
 were trophic disturbances, as well as in that other class  of cases with
 cutaneous lesions directly related to the fulminating-pains.
   Further researches, however, have  shown that there is a still fur-
 ther subdivision of the  sensory columns,  as is delineated in Figs. 1,
 2, 3, and  137, and described on pages 21  et seq.  Moreover, nowa-
days, the  relationship of the ganglion upon the posterior root of the 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  265

sensory fibres has been  very clearly shown (page 30), as well as the
modes of entry of the posterior or sensory fibres into the cord, their
subdivisions into ascending and descending brauches, their  free ter-
mination, and the origin  of still other sensory fibres from the so-
called column-cells of the cord (page 31).  All these anatomical data
have enabled us to obtain a very much clearer idea  of the pathology
of locomotor ataxia.
  In the earlier stages of the disease the Spitzka-Lissauer column,
the anterior root-zone, the middle root-zone, the column of Goll, and
the median zone are implicated in the lumbar region.  (See Fig. 2.)

                             Fig. 137.
Columns of the spinal cord, according to our present knowledge.
In other words, the nerve-fibres  affected are in the Spitzka-Lissauer
tract, the fine fibres coming from the posterior roots, and which some
authors consider to be really collaterals of the posterior roots.  What-
ever they be, these fibres, on entering the cord, pass in a nearly hori-
zontal direction toward the Spitzka-Lissauer column, then they curve
upward to enter the gelatinous substance.   Some of them, however,
continue on with  the larger  fibres of the  posterior roots  and pass
partly into the gelatinous substance and partly into the centre of the
posterior horn.   As these fibres have  but a  short  course  in the
Spitzka-Lissauer column, and  soon leave it, it is easily understood
why the alterations  of them  are principally found  in the  lumbar
cord and, to a  less  extent, in the dorsal.   The anterior  root-zone
receives a large number of its fibres directly from the posterior roots.
They enter the posterior cornua and  disappear in the anterior por-
tions of this, avoiding  the columns of Clark.   There is reason to
believe that this  zone  contains  a  certain  number  of commissural
fibres uniting different  levels of the gray matter.  The middle root-
zone, as has been shown in Fig. 2, has two systems of fibres.  The
first passes  through the posterior columns, enters  the columns of
Clark, or, where these are not present, disappears midway between the
boundary of the anterior aud posterior cornua.   The  second system 
266
NERVOUS DISEASES.
is composed of fibres which, further up, constitute by their union the
column of Goll.   The origin of the fibres of the median zone is not
known.   The column of Goll is  described on page 79.  In  other

                               Fig. 138.
Section from a case of locomotor ataxia, showing degeneration of the columns of Goll
           and Burdach.  Dorsal region.  Magnified 10 diameters.

                             Fro. 139.
 Section from a case of locomotor ataxia, showing degeneration of the columns of Goll and
                Burdach.  Dorsal region.  Magnified 10 diameters.

cases the whole of the posterior  columns between the diverging pos-
terior horns are implicated, as  well as the Spitzka-Lissauer columns;
and  this is what is most frequently seen in the well-established cases,
as in Figs. 138,139,140, which are sections from a  case of locomotor
ataxia that had lasted ten years, and was quite typical in its symptoms.
   Fig. 138 is a photo-micrograph,  magnified 10 diameters, of a sec-
tion of the cord in the dorsal region in which the degeneration of the
posterior columns (columns of  Goll and Burdach) are outlined.  Little 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  267

gaps  are  seen in  the cord, which, however, are entirely due to the
process of hardening.
  Fig. 139 is a drawing from  the lower dorsal region of the  same
cord  magnified 10 diameters, showing very clearly the  degeneration
of the posterior columns (columns of Goll and  Burdach) quite  up  to
the inner side of the posterior cornua, and implicating a portion  of
the Spitzka-Lissauer columns.
  Fig. 140 is a  drawing of a section of the same cord in the cervical
region, magnified  10 diameters, showing the same implication of the
posterior  column,  but not to a like extent, as a relatively less affected
mass is seen toward the posterior gray commissure and running out
like a broad wedge into the posterior columns.

                             Fig. 140.
    Section from a case of locomotor ataxia.  Cervical region. Magnified 10 diameters.

  The  alterations  in the  column  of Clark were first described in
1885 by Lissauer.   As has already been shown, these columns of
Clark consist of certain ganglionic cells and a network of fine nerve-
fibres.  In locomotor ataxia the fibres alone are affected, disappear-
ing to a large extent, whilst the cells remain unimpaired.   Lissauer
is inclined  to believe that the alteration in these nerve-fibres is the
first pathological phenomenon in locomotor ataxia, and in  12 of 13
cases examined by him he found degeneration of the fibres extending
into the column of  Clark from the Spitzka-Lissauer column, and in
two cases of my own degeneration was quite distinct, although I had
uo proof of its being in the early stage.  Lissauer also states that this
degeneration of nerve-fibres is  more accentuated on the internal side
of the  column of Clark, which he explains by supposing that this
receives especially  the posterior root-fibres  coming  from the lower
portions of the cord that are most apt  to be diseased, whilst the
external portions contain  fibres coming  from higher levels.   This
preservation  of the  cells in the column of Clark explains the relative
infrequency of implication  of the direct  cerebellar column, as it is
from these  cells, which  are true  column-cells of the cord, that the
fibres of the direct  cerebellar  tract take their origin.   The  central
canal of the cord is occasionally affected,  and the cells of the epen-
dyma may  be proliferated, occasionally to such an extent as to block
the lumen ;  and in  other cases there is a dilatation of the cord ; but 
268
NERVOUS DISEASES.
it is uncertain whether this is a phenomenon of true locomotor ataxia
      coincidental  occurrence of  gliosis.   These alterations of the
or a
nerve-fibres may be followed up to the nucleus of the column of Goll
Fig. 141.
^1*-.; ,/.>, A*. ,;.*/* i-■:.*.'<
 ■. ;-wrj ^?;>.Tf•r-i-T.v/' K?^« ■;-:>:' • ,;*.-.' ;•.'/ ■'- •--: ^-sT
     '. ,■•' . ;   «■ j-%-*.-  - ©. • •  'V?'
Section of a portion of the cord in locomotor ataxia. Magnified 360 diameters.
and the nucleus of the column of Burdach.   In the medulla oblon-
gata there is often found atrophy of the nuclei of the pneumogastric
and the glosso-pharyngeal.   In some cases the  nucleus of the hypo-
glossal is also affected ; and in others  also the ascending root of the
solitary fasciculus.
Fig. 143.
 Normal cord, showing the relative proportion of
nerve-fibres and connective tissue. Magnified 360
diameters.
 The neuroglia  of a normal cord,
lateral columns.  Magnified 360 diam-
eters.
  The histological character of the lesion consists of a disappearance
of nerve-fibres and an increase of proliferation of the interstitial or
connective  tissue, which is shown  in Fig. 141, a drawing under a
high power (360 times).   This figure should be contrasted with the 
DISEASES OF SPINAL CORD AND MEDULLA  OBLONGATA.  269
connective tissue and the nerve-fibres of the normal cord, as repre-
sented in Figs. 142 and  143, as well as with the  molecular altera-
tions in myelitis, as described upon page 218 (Figs. 114 and 144).

                             Fig. 144.
  Section of the cord in a case of myelitis, showing proliferation of connective tissue and
                loss of nerve-fibres.  Magnified 350 diameters.

  It is a question at the present day as to what is the  exact nature
of these changes  in the nerve-fibres and the connective  tissue.   One
view is that they are all due to a cerebro-spinal  disease of unknown
origin; whilst another is that they consist of secondary degenerations
proceeding from disease of the cells in the ganglion  upon  the poste-
rior root.  There are no  data, however, upon  which to  settle this
question.  Dejerine, Pitres, Vaillard, Oppenheim, Siemerling, Nonne,
Westphal, and Pierret claim that  the disease  may be  occasionally
caused by a peripheral neuritis.  Outside of the two cases reported
by Dej6rine, however, there  is  very great doubt as  to  whether
peripheral neuritis really produces  anything like  the clinical symp-
toms  of true  locomotor ataxia;  indeed, I constantly show cases
in my clinic which might  be taken  for locomotor ataxia, but in
which the distinction can readily be  made, as has  been shown in the
chapter upon neuritis.  In  some cases there is a slight diminution
in size of  the whole cord, especially when the lesions are very pro-
nounced.   Occasionally, also, there is a slight thickening or opacity
of the pia mater  at the level of the  posterior roots;  but the relation-
ship of this meningitis to the parenchymal lesions is unknown.  In
other  instances the implicated columns are of a grayish tint which
makes them easily distinguishable  from  the  neighboring fibres.
Finally, cases  have been reported wherein  the  cord and  periphery
have been absolutely unaltered.
  Diagnosis.   The  diagnosis is a  matter of  ease when  the  full 
270
NERVOUS DISEASES.
 symptom-group is present, viz., stabbing and fulgurant pains, which
 are  sudden,  vagabond,  and  atrocious;  Argyll-Robertson pupil;
 absent  knee-jerk;  motor and  static  ataxia;   optic nerve-atrophy;
 ptosis,  and  the  so-called crises.   But the diagnosis may  become
 difficult when some of these pathognomonic symptoms are lacking.
 There may be said  to be three cardinal symptoms, one of which must
 be  present in order to make  a diagnosis of locomotor ataxia, viz. :
 the  peculiar  pains, the  peculiar  ataxia, or  an absent knee-jerk.
 Upon no one of these alone can a diagnosis be  made, but any one
 of  the  three associated with other pathognomonic  symptoms may
 make the diagnosis certain.  Thus many different combinations may
 be present:
        Pains..........Pupil.
        Pains..........Ataxia.
        Pains..........Optic-nerve atrophy.
        Pains..........Loss of knee-jerk.
        Ataxia..........Loss of knee-jerk.
        Ataxia..........Pupil.

   It  must never be forgotten that  pains closely simulating these
 stabbing and fulgurant ones are occasionally observed in transient
 cases, seemingly of neuralgia or neuritis, and I have known of one
 serious  mistake made in this way.  Atrophy of the optic nerve may
 come, it is well known, from many causes, but a  primary atrophy is
 rare except in this  disease.  The gastric crises are often simulated
 by  functional attacks of gastric neuralgia.
  The diagnosis should be from—
        Neuralgia, especially of the trigeminus;
        Rheumatism ;
        Intracranial tumors;
        Chronic myelitis;
        Lateral sclerosis;
        Disseminated sclerosis ;
        Hereditary ataxia;
        The toxic ataxias;
        Chorea;
       Paralysis of the flexors of the leg;
        Cerebellar disease;
       Cerebro-spinal syphilis.
  As has been said, neuralgia may sometimes have a peculiar stab-
bing or fulgurant pain, which may be severe, sudden, and vagabond,
or it may be difficult to get a sufficiently exact description from the
patient; in either event  the other symptoms  of locomotor ataxia
should be sought for.
  The same remarks are true of rheumatism.
  Locomotor  ataxia may sometimes be mistaken  for intracranial
tumor when the optic-nerve atrophy is observed  and the pain is in
the region of the trigeminus and  associated with gastric crises, so
that the atrophy is regarded as due to a precedent neuro-retinitis, the
trigeminal pain as being of intracranial origin, aud the gastric crises
as being the vomiting of cerebral headache.  But search for the other
symptoms of locomotor ataxia  will make the diagnosis plain. 
 DISEASES OF SPINAL CORD AND MEDULLA  OBLONGATA.  271

  A chronic myelitis may have  many of the non-pathognomonic
symptoms  of locomotor ataxia,  and  may  even have some  of the
pathognomonic ones, if the lesion extend into the  proper portions
of the cord.   In such an  event the non-pathognomonic  symptoms
would either be  the only ones,  or  they would  have preceded the
pathognomonic ones by a distinct interval.
  Lateral sclerosis, pure and simple, would have symptoms of exag-
gerated reflexes and contractures, and  not the pathognomonic symp-
toms of locomotor ataxia.
  In disseminated sclerosis the posterior columns and cornua might
be affected as iu  locomotor ataxia, but then the symptoms of this
latter disease would be combined with the symptoms of disseminated
sclerosis, viz., tremor of the intentional  type, nystagmus,  and scan-
ning speech.
  Hereditary ataxia, so-called Friedreich's disease, is generally  a
disease of youth, and is simply the ataxia without any of the sensory
symptoms.  The diagnosis may sometimes be difficult, and then the
reader had best consult the chapter on " Friedreich's Disease."
  The toxic ataxias, due to brass, arsenical poisoning, ergotism, or
copper-poisoning, may be recognized  by ascertaining the occupation
of the patient.
  The early stage of chorea  is sometimes mistaken for  locomotor
ataxia, because there really is an  inco-ordination of movement.  In
every  such case, however,  stripping the  patient will usually make
plain the quickly begun and quickly ending fibrillary movements of
chorea in the muscles of the trunk, head, and extremities.  In the
chronic and  hereditary forms of chorea  the  differential diagnosis
should be still more easily  made.
  In paralysis of the flexors of the  leg, from neuritis or myelitis of
the anterior horns,  there is a peculiar flop of the leg in walking not
unlike that observed in locomotor ataxia, but there are none of the
pathognomonic symptoms of the latter disease.
  In cerebellar disease the ataxia is of a gently swaying kind, techni-
cally known as titubating, rather than the peculiar flop of the locomtor
ataxia. It is sometimes, however, difficult to distinguish this titubat-
ing sway  from the  static ataxia of locomotor ataxia, but other signs
of cerebellar  disease will  make the  diagnosis plain, viz., occipital
headache,  neuro-retinitis, or some  paralysis.
  Cerebro-spinal syphilis is often  confounded with locomotor ataxia,
and yet it is extremely important to make the diagnosis, inasmuch
as many cases of cerebro-spinal syphilis with symptoms of locomotor
ataxia have been cured, at least to all outward appearance, or at any
rate are much more tractable than cases  which have simply had
syphilis at some  period in the past.  If the  spinal  lesion of this
disease be a secondary degeneration starting from a primary focus of
inflammation or cellular alterations  in the lower dorsal or  lumbar
cord, it would  seem reasonable to assume that  this  primary focus
would  be  the lesion to direct  treatment  to, especially in  the syph-
ilitic cases, and that the secondary  degenerations  resulting  there-
from would  be as hopeless as they are in other diseases of the cord. 
272
NERVOUS DISEASES.
Fournier expressly states that the prognosis is much better in what
he calls a pre-ataxic stage.   If auy case of locomotor ataxia with a
history of autecedeut syphilis has cerebral symptoms, it should be
remembered that  these will probably indicate  intracranial  syphilis,
aud careful examination will bring out the symptom-group  to which
I have called attention of late years (vide Chap. VIIL, " Syphilis of
the Nervous System"),  viz., the quasi-periodical  headache  and the
obstinate  insomnia, or either present alone, ceasing upon the  super-
vention of any convulsive or paralytic symptoms; or else there might
have been  some  mental dulness,  coma,  convulsion,  or symptoms
indicative of a lesion at  the base of the  brain.
  Prognosis.  Almost all  cases of locomotor ataxia can be improved
to the point of great  diminution or cessation of the pains, lessening
of the ataxia to a varying degree that is dependent upon its amount
and duration at the beginning of treatment, and marked bettering of
the general health.   In  other words, most cases can be very greatly
improved, or even practically cured, so far as the arrest of symptoms
is concerned.   We do not know whether this means that the lesions
in the cord have disappeared, or merely that they have not progressed
as in Erb's patient, for this is the only post-mortem on record of an
improved case.
  Treatment.  In all cases of locomotor ataxia it should be carefully
ascertained as to whether or not there has been  a history of  syphilis,
because if there has been, the iodide of potash must be used  in large
doses.  Again and again have I seen syphilitic cases fail to  respond
to the other treatment, and  pass on into  startling results when the
iodide has  been used in the proper way.  In cases in which the
iodide does not agree  well with the stomach, mercury may be used in
conjunction with it.  There is a difference of opinion as to the  result of
mercurial treatment of syphilitic cord lesions by mercury and iodide,
but, if I  may judge  by  my own experience, the iodide is always far
the most reliable.  The latter should be given iu the saturated solu-
tion, commencing  with 20 drops three  times a day, given in a full
tumbler of water.  Sometimes it is best to administer it after meals,
aud  sometimes  immediately before, and  this can  be ascertained by
experiment with the  patient.  It  has  been supposed  that  the dif-
ference is due to the effect of iodide upon the starch in the stomach.
The best method of using mercury is  by means of a mercurial oint-
ment, which  should  be  put into  capsules  which contain a  drachm,
which can then be opened by the patient, and thus there will  be no
danger of exceeding the dose.  A drachm of the mercurial ointment
once or twice a day  will be sufficient in conjunction with whatever
doses of iodide  the patient's stomach will bear.  As these cases of
locomotor ataxia  have usually been greatly discouraged by various
therapeutic experiments,  it  is always best  to put  them to bed abso-
lutely  at  first.  How long  they  should remain there  will  depend
upon the severity of the case. If the patient is  very much exhausted
or emaciated, or has a high  degree of ataxia or  great pain, it may be
well to keep him in bed  for four or five weeks absolutely.   If, how-
ever, neither the pain nor  the  ataxia is  marked, and the  physical 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  273

condition is fair, a week or two will answer;  but this  is a question
which can only be determined by the judgment of the physician.  In
all instances care should be taken to have too much rest rather than
too little.  Whatever the  period of rest be, great caution should be
exercised in  putting the patient  again upon  his feet.  This should
only be done at  first for a half hour or an hour a day, and should
consist merely of allowing him to sit up during that time, instructing
him to lie down immediately when he feels tired.  The pulse should
also be carefully watched, lest the heart may not stand well the strain
of the sudden assumption of an  upright position after the body has
so long  lain horizontally ; and if any cardiac weakness is shown,
a  heart-tonic should be  administered,  the best being  the  sulphate
of strychnia, gr. -fa three  times a day.   Occasionally this drug acts
disagreeably  upon the unstriped muscles of the intestine,  causing
o-riping  and  infrequent small stools.   In  such an  event digitalis
should be given, ten drops of a carefully and  freshly made tincture,
or one grain of the powdered digitalis, either  three  times a day.
The rest  should  be kept up for a period of ten or twelve weeks, to
the extent, at least, of keeping the patient in bed all but about four or
five hours in the day, and during these four or five hours long walks
should be absolutely prohibited.   Massage, if properly  used, will
not only  prevent the  muscles from becoming flabby,  but will  in
 many cases  strengthen them to such  a degree as  to decrease  the
 inco-ordination.   It should be begun in the  second or third week
of treatment.  It must never be severe, however, and it is always
 best to watch carefully the person  giving massage,  to  ste that this
point  is  observed.  How long to  administer it is  a question that
 varies from  case to  case; usually  beginning  with twenty or thirty
 minutes of very gentle  massage, patients will  come to stand forty-
five minutes to an  hour of it, but  in some instances they never can
take more than  a half-hour without extreme fatigue.   The patient
should lie quiet for an hour  to  two hours after each  massage.   It
should be administered  every other day for the  first week or two, and
then daily. Galvanism is  au invaluable agent.  It should be applied
to the spinal column, one pole on  the nape of the neck (Fig.  67), the
 other  on  the lower dorsal  vertebra (Fig. 68), and a  current of  3
to 5 milliamperes should  be passed for three  to five minutes  every
day.  In some cases there is great  susceptibility at first to the elec-
tric current, and it  should therefore be begun with great caution,
although even  in these  cases large quantities may be administered in
time.  In other cases galvanism is  not borne  well at all, and it is a
singular clinical fact,  for which  I have never been able to find an
explanation, that many cases of locomotor ataxia of syphilitic origin
cauuot take  electricity; indeed,  I have seen  two cases get rapidly
worse with very small  currents.  I am not  by any means certain
that the so-called crises are not often  excited  by  the administration
of electricity.  The relief of the pain is sometimes a difficult matter,
but usually  the best  means of  combating them  is  absolute  rest.
^ hen this does  not  answer,  the  following  prescription  may  be
written :
18 
274
NERVOUS DISEASES.
      B.—Quin. sulph.......gr-ij-
          Sodii salicylat.......Sr- J;
          Acetanilide.......gr. rjss.  M.
  Ft. in capsul. no. j.  Mitte xv.  S— One three times daily, after meals.

  Codeia, gr. ±~l, may be added to this if the acetanilide is not suf-
ficient to overcome  the pain, and if the  combination  depresses the
patient at  all, strychnia sulph., gr. -fa, may also be  added.  When
pains continue in spite of these milder anodynes, 10 drops of the
tincture of opium  should be given once or twice a day.  If, however,
the pain is still  uurelieved, resort must be had to hypodermics of
morph. sulph., jr  grain once or twice a day.   It  is always advisable,
however, to avoid this, because no patient is more prone to  form the
morphine-habit than one with locomotor-ataxia ; indeed, all the above
medicines should  be  sent to the patient, and  the prescriptions should
not be put into  his hands,  and  if they are marked, " No  copy, no
repetition," a reliable druggist will not inform him  of their contents,
Even the tincture of opium can  be administered  in the form of a
tablet triturate.   Should the pain still continue, there  is often good
reason to suspect that  the case  is syphilitic to a larger degree than
had  been supposed, and the iodide should be  gradually  increased
until somewhere between 150 and 200 drops of the saturated solution
are given  in  the day.   The application  of the  actual cautery will
often  very  materially relieve  the pain, and it should be applied four
or five times,  but only lightly and superficially.   As  a  further adju-
vant to these anodyne measures the faradic brush will be found useful,
passing a  strong  current  and brushing  it gently over the affected
limbs; also warmth  applied by means of cloths wrung from very hot
water  and quickly applied,  or even  by  poultices.   Suspension  is a
new fad  that  has  certainly effected a temporary  improvement  in all
the symptoms of some cases, often to a wonderful degree, as in one case
of my own where it was tried as the last  resort, and, incredible as it
may seem,  the patient after two suspensions  got out of bed, which he
had not left  for  weeks, and walked down several  flights of stairs!
Yet he died two weeks after.  The suspension-apparatus should be
the ordinary  one  made  by all  instrument-makers, with head-strap
and axillary supports.  Suspension should be very gently and gradu-
ally done, at first for thirty  seconds, afterward, if it has not proved
harmful, for one  or two minutes every  three or four days, and  the
patient should rest  for an hour or two after each suspension   The
atrophy of the optic nerve is sometimes seemingly  benefited by sul-
phate of strychuiue, gr. T^-7 to gr. -fa, three times  a  day,  and con-
tinued for  a week or two  at a time, then  an intermission of several
weeks, when  it may be  resumed again   for a week or two.  The
vesical  symptoms should be treated according  to  the directions
in the  Chapter on  Myelitis (p  229).  The vesical symptoms will
also be benefited  by alkalies, non-nitrogenized  diet, and  properly
selected  clothing  and   underclothing.   Galvanism  will  often be
found  to be  extremely beneficial for  the bladder-trouble, and for
this  purpose the  patient should  be seated  upon a large  electrode,
covered with  a heavy sponge, which should be  dripping  with  hot 
 DISEASES OF SPINAL  CORD AND MEDULLA OBLONGATA.  275

water (p. 121).  This should be placed under the perineum, and the
positive pole  should always connect  with it.  The other electrode
should be  a large  one, and should be placed over the lower  dorsal
spine.   These electrodes  being  placed in position, a gentle current of
2 to 5 milliamperes should  be gradually turned on and allowed to
pass for five  minutes.   This  electrical application should be made
every second day.   The so-called crises often resist treatment very ob-
stinately.   For the  nephritic and laryngeal crises the best treatment is
the internal administration of codeia, gr. \ to \ t. i. d., or every four
hours, or a hypodermic of sulphate  of  morphine  and   sulphate of
atropine.    For the  gastric crises, uux vomica,  bismuth, papain,
codeia, oxalate of cerium, pepsin, and  hypodermics of morphine and
atropine are the means that are most effective.   Moreover, the food
should be light and easily digested, and, if necessary, should be pep-
tonized.   For the obstinate constipation aloetics, with nux vomica or
 belladonna, may be given, or cascara sagrada, as  recommended on
 page 229.

               PRIMARY  LATERAL SCLEROSIS.

   Synonyms: Einfache  spastische Spinalparalyse(Erb).  Tabes dor-
 sal spasmodique (Charcot).   Spastische Spinalishmung.  Primary
 lateral sclerosis.  Spastic spinal paralysis.
   Definition.  So-called  primary lateral sclerosis is  a disease of
 the spinal cord characterized by contractures, exaggerated motor re-
 flexes, and hasty micturition.
   History.   Attention was  first  called to  this disease by Erb in
 1875, and shortly afterward Charcot wrote upou it   Since that time
 numerous contributions  have been  made to the subject.
   Clinical Symptoms.  This is  a chronic affection, and the onset
 is very gradual.  The symptoms  consist of contractures and exag-
 gerated motor reflexes, the combination of the two classes of  symp-
 toms causing  a peculiar  walk kuown as the spasmodic or spastic gait.
 In a pronounced form the contracture  is such as to cause abnormal
 position of the limbs, especially of the flexor muscles, as well as great
 stiffness, and  it can theu be readily detected  in attempting to flex or
 extend the affected limb.  In less degree, however, the contracture
 may not be present to the naked eye, although the patient may com-
 plain of stiffness in the affected limbs.  At this time,  however, its
 presence  can  often be  detected  by the following test: Extend the
 limb fully, tell the patient to  make no resistance whatever, and then
 make a quick, sudden movement of flexion.   If there is a beginning
 contracture, the flexion  will be  met  byr a slight muscular click or
 resistance, which a little experience will easily teach one to differen-
 tiate from voluntary resistance (p. 170).  The exaggerated reflexes
 consist of the knee-jerk, sometimes ankle-clonus, jaw-jerk, and hasty
 micturition.  By this latter symptom, to which attention was  first
 called by Seguin in 1873, is meant a desire  to  micturate that  is far
 less controllable than it  should be  in a healthy person.   In  unusual
 eases the tendon-reflexes of the arm- and hand-muscles may be  also 
276
NERVOUS DISEASES.
found  to be  exaggerated.   The combination  of contracture and
exaggerated tendon-reflexes gives rise to the so-called spastic gait.
The patient walks  upon  his toes and the ball of the foot, scarcely-
touching the heel to the ground, and walks as if upou  stiff bed-
springs,  with a  jerky, jiggery motion that  is  very  characteristic.
Sometimes,  in addition  to  these  peculiarities,  the leg  is trailed
slightly  along  the  ground, the toes  shuffling along  the floor.  It
is a matter of habit in my clinic to  diagnose this walk almost un-
failingly.
  Pathology.  When  the  autopsies in so-called cases of lateral
sclerosis  are examined it is readily seen that the theory that there
is a primary affection of the lateral  pyramidal  columns is scarcely
warrantable.  The first post-mortem was made by Charcot, and the
lesion was found  to be a disseminated  sclerosis.   The second autopsy
was made by von Stofella, and although  the lesion was found  to be
in the two lateral columns in about the area of the lateral pyramidal
column,  the spinal cord was not microscopically examined, and no
mention  was made  of the brain  and  medulla.  Schulz reports five
autopsies ; in one there was a gliomatous tumor in the medulla ex-
tending into the anterior pyramid ; in the second a small sarcomatous
tumor was found between the pons and the crus cerebri ad pontem;
in the third case  there was a chronic  hydrocephalus and no spinal
changes  whatever;  in the fourth there was a pachymeningitis causing
myelitis; in the  fifth there was a transverse myelitis with secondary
postero-lateral sclerosis.  Hallopeau's case had a tumor in the medulla.
Striimpell describes two autopsies ; in the first there was a myelitis of
the upper dorsal region ; in the second there was a hydromyelus
extending  throughout  the  cord.  In  Friedreich's case  there were
numerous cerebral extravasations, multiple sclerotic patches in the
medulla  aud spinal cord, with proliferation  of the neuroglia, aud
many patches of  softening.  Suckling's case was very  evidently one
of myelitis with  subsequent lateral degeneration.   John Hopkins, to
be sure,  reports a case as  having  only a degeneration in the lateral
columns; but he makes no special mention of any examination having
been made beyond the upper portion of the dorsal region.   The only
single case that has been carefully examined and that would seem to
be a case of primary lateral  sclerosis  is one  reported by Dreschfeld
and Morgan.   In this microscopic  sections  of the brain and the
medulla  above the lower portion of  the anterior pyramid iu the
medulla  are said to  have been perfectly normal, and there were no
pathological  changes  observed except in the lateral and  anterior
pyramidal columns.  But one case, out of fourteen reported during
a period  of nineteen years, is certainly  not enough to warrant a path-
ological assumption, and it is very much  more probable that Dresch-
feld has  overlooked some changes in  the upper  portion of the pyr-
amidal tract—possibly such slight ones as have been found in some
cases of  amyotrophic lateral sclerosis  in  the  motor convolutions—
rather than  that there really is a primary implication  of the lateral
pyramidal columns.
  Duration.  The  duration  in cases of so-called  primary lateral 
 DISEASES OF SPINAL  CORD AND MEDULLA  OBLONGATA.  277

sclerosis will depend to  some  extent  upon the causative lesion,
although  in  every  case  that I  have seen it  is  eminently a chronic
disease, one patient of mine having had it for fifty years, since earliest
childhood.
  Prognosis.  The prognosis of lateral sclerosis  is absolutely un-
favorable as  regards improvement or cure.
  Diagnosis.  The diagnosis of lateral  sclerosis from other diseases
is generally  easy enough, and the differentiation is to  be from the
other maladies which are enumerated in "Amyotrophic Lateral Scle-
rosis," immediately7 following.
  Treatment.  The treatment of lateral sclerosis is that of chronic
myelitis, except  that the  exaggerated reflexes can sometimes be mate-
rially benefited by the administration of hyoscyamine gr.  y^- once or
twice a day,  or  the hydrobromate or hydrochlorate of  hyoscine  in
the same doses.   Belladonua also seems to exert a favorable influence
upou this symptom in certain individuals, although it fails utterly iu
others, and the drug should be administered in the form  of a reliable
fluid-extract, one drop once to three times daily, or the sulphate of
atropia, gr. -j-j^ at  the same intervals.

             AMYOTROPHIC  LATERAL SCLEROSIS.

  Synonyms:   Spastische  Spinalparalyse   mit   Muskelatrophie.
Amyotrophische Lateralsclerose.   Sclerose  laterale  amyotrophique
(Charcot).
  Definition.  Amyotrophic lateral sclerosis  is a disease of the
spinal cord characterized by motor paresis, muscular atrophy, con-
tracture, and exaggerated reflexes, without cerebral, sensory, vesical,
or rectal symptoms.
  Duration.  The average duration of the disease is within three
years, but cases have been known to last for ten  and even fifteen.
  Clinical History.   The typical cases usually present three some-
what fairly defined  stages, viz.: First, of paresis ; second, of atrophy ;
third, of contracture and exaggerated reflexes.   But there are many
exceptions to this rule.   The onset is generally in the upper extrem-
ities, sometimes  in one  of the  fingers.   The extension  to the lower
extremities and to  the medulla  oblongata is usually made within six
to twelve months.   Sometimes, however, the onset  may be in the
medulla  oblongata, or  in the lower  extremities.   The paralysis is
purely motor.   The muscular  atrophy is  invariably of the whole
body of the  muscle, and not fibre by fibre, as in progressive  muscular
atrophy.   The  tendon-reflexes  are  exaggerated, especially the knee-
jerks, and  ankle-clonus is ofteu  obtainable; but these symptoms
disappear iu the  later  stages.  The commingled contracture and
atrophy give rise to characteristic deformities, such as the claw-hand,
etc., and  there is generally a fibrillary tremor of the affected limbs,
and sometimes an intentional  tremor, i. e., a tremor caused by volun-
tary movements.  The progress of  the  disease  is gradual.  The
affected muscles usually present some phases of the reaction of de-
generation.   Death ensues from implication of the vital  nuclei in the 
278
NERVOUS DISEASES.
medulla oblongata, from general debility, or from  pulmonary com-
plications.
  Prognosis.   The prognosis is hopeless, both as regards life and
improvement.
  Diagnosis.   The disease is to be differentiated from—
       Progressive muscular atrophy;
       Myelitis of the auterior horn ;
       Ordinary myelitis;
       Postero-lateral sclerosis.
  Progressive muscular  atrophy begins with a fibrillary atrophy of
the muscles, the paralysis is  in proportion  to  this, and there is  no
contracture or exaggerated reflexes  whatsoever;  whilst  in amyo-
trophic lateral sclerosis the  paralysis is usually a  primary symptom,
the atrophy succeeds, is  of  the body of the muscle or muscles, and
not fibrillary, and there  supervene contracture and  exaggerated re-
flexes.
  Myelitis of the anterior  horn in the  child  should  never be con-
founded with amyotrophic lateral sclerosis, for  the  former is always
sudden in onset,  is monoplegic  in its distribution, and affects only a
certain muscular group or groups within that one limb  ; its paralysis
is a flaccid one, and there are no contractures or exaggerated reflexes.
Myelitis of the anterior  horn  in the adult usually begins with motor
paralysis of one  or more limbs or the whole body, reaching  its acme
in a few days, muscular atrophy succeeding within a fortnight, and
the paralysis remains a flaccid  one, contractures and exaggerated re-
flexes very seldom supervening.
  An  ordinary myelitis in its earlier stage might be confounded with
amyotrophic lateral sclerosis, but the progress of the former affection
should render a  mistake impossible, as ordinary myelitis  has pro-
nounced  sensory,  rectal, and  vesical  symptoms,  which are  never
present in amyotrophic lateral sclerosis.
  Postero-lateral sclerosis, or combined  sclerosis—i. e., that form  of
combined myelitis in  which the posterior and lateral  columns are
simultaneously affected—would have superadded to the lateral scle-
rosis the symptoms of locomotor ataxia.
  Pathology.   The lesion of amyotrophic lateral sclerosis always
consists of a degeneration in the lateral and  anterior pyramidal col-
umns and of destruction of ganglion-cells in the anterior cornua  of
the spinal cord and the motor nuclei of the medulla oblongata.  The
implication of the lateral columns is always more marked than that
of  the anterior pyramidal  columns, and sometimes the  latter are
scarcely affected  at all.   The  lesions of the ganglion-cells are the
same  as  are seen in   poliomyelitis anterior, and cousist of morpho-
logical alterations  in  their structure.   Some of the cells disappear
entirely,  some lose their  processes, some become smaller in size, some
are highly  pigmented.   It has been a belief  with many authors that
the cellular alterations in these anterior cornua are due to  precedent
arterial alterations, but  there  has  been no  proof advanced of this
view.  The lesions in the pyramidal columns consist of impairment or
destruction of the nerve-tubules, and proliferation of the connective 
 DISEASES OF SPINAL CORD AND MEDULLA  OBLONGATA.  279

tissue, with  the  occasional presence  of fatty granules and corpora
amylacea.   Inasmuch as the lesions in the pyramidal columns  and
in the anterior horn or the bulbar nuclei are always bilateral, there
has been a suspicion in the neurological mind that the affection  was
of the nature of a secondary degeneration of the pyramidal columns
extending into the anterior horns.   In some cases  there  has been
found to be a marked degeneration of the fibres running  from the
motor convolutions, whilst in the other cases the degeneration has been
traced up into the pons, the crura cerebri, and the internal capsule,
and in still other cases the degeneration has not been observed above
the decussation.   In  none  has  there  been  grave organic disease of
the upper part of the pyramidal tract.  Whether, therefore, the cases
reported  as being  without lesion  above  the  decussation were so
minutely examined as to detect the  slight alterations which others
 have found, is a  question that very naturally arises.   At the present
time we cannot, for this reason, distinctly affirm or deny that the lesion
 in the pyramidal columns is a secoudary lesion,  although the proba-
 bilities are strongly in favor of  its being so.   In many cases of polio-
 myelitis anterior the  lateral pyramidal column has been found  sec-
 ondarily affected ; in many cases of lesion in the cerebrum the anterior
 horns have  been found diseased, although the pyramidal tracts were
 intact.  In several cases of disease in the cerebrum muscular atrophy
 has supervened without intermediate  lesion of the pyramidal tract or
 the anterior horn, or even without lesion  of the  peripheral  nerve;
 from which facts it is easily to be seen that there is  a close connec-
 tion pathologically between the motor convolutions,  the pyramidal
 tract, the anterior horn, the motor nerves, and the muscles.
   Treatment.   As will  be very evident, the  treatment  of amyo-
 trophic lateral sclerosis will in some cases depend upon the causative
 lesion, if that can be diagnosed.  In most cases, however, this is not
 possible, and the treatment must be  experimentally that of chronic
 myelitis.

          THE COMBINED SCLEROSES OF THE CORD.

   Synonyms: Progressive spastic ataxia.   Combined fascicular  scle-
 roses.  Ataxic paraplegia.
   Not infrequently cases are observed with the combined symptoms
 of locomotor ataxia of a mild type and spastic symptoms, with motor
 paresis; and, in 1885, Ormerod analyzed twenty such cases, whilst,
 in  1886,  Grasset collected thirty-three  more,  and, in  1887, Dana
 based a paper upon forty-five.   Since then numerous cases have  been
 reported by different authors.
   The  lesions are  generally in the lateral or anterior pyramidal
 tracts, or both, the cerebellar tracts, the lateral  column  proper, and
 the columns of Goll.  (Fig. 1.)  The dorsal region is  usually most
 affected.   The columns of Goll, the lateral pyramidal tracts, and the
 cerebellar columns are often affected  throughout their whole course.
 The columns of Burdach are sometimes encroached upon in the lower
 or upper parts of the cord.   When the lateral columns are implicated, 
280
NER VO US DISEA SES.
 the disease sometimes involves the column of Gowers, and, inwardly,
 the lateral mixed column.   The long systems of fibres, such as the
 column of Goll, the pyramidal tract, and the cerebellar column, are
 generally affected  throughout  most of their length; and the degen-
 eration usually extends, contrary  to the  Wallerian  law,  in  the
 opposite direction to the course of the normal nerve-sensations or
 impulses; so that it runs downward in the columns of Goll and the
 cerebellar tracts and upward in the pyramidal tracts, being less iu the
 lower levels of the first-named columns and  in the upper regions of
 the latter ones.  In  some cases the  cells of the auterior horns of the
 cord  are implicated, and also the cells of the posterior horns  and of
 the column of  Clark.   There  is, in rare cases, a slight and chronic
 meningitis of the  pia  mater.   The lesions are generally superficial,
 and do not affect  the vital  functions  of the  cord to anything like
 the extent that is  seen  in  ordinary transverse myelitis or Landry's
 paralysis.   In  some of the  cases there is  a commingling of diffuse
 lesions and  degeneration of the tracts that  have beeu named; and
 this is more especially apt to occur  after an ordinary myelitis, giving
 rise to secondary degenerations. The combined scleroses are observed
 in  conjunction with many affections of the  cerebro-spinal nervous
 system, such as general paresis, chronic mania, Friedreich's disease,
 locomotor ataxia,  myelitis, and so-called spastic paraplegia.  It is a
 question whether the disease is a primary one or is secoudary—i. e.,
 whether the degeneration of the different columns is secondary to some
 pre-existing lesion of the brain or cord, or whether they start pri-
 marily and simultaneously in  these  different columns.  It is very
 certain, as we have seen, that such  general lesions as general paresis,
 chronic mania, and myelitis may have  combined scleroses associated
 with  them, and it therefore seems  most probable that the general
 lesions are the  cause and the starting-point of the degeneration in  the
 different columns   Whether any cases are primary is a matter that
 is, to my mind, very questionable,  for a primary disease of the long
 system-fibres of the  cord  has never yet been demonstrated, and, in
 the case of so-called lateral scleroses and locomotor ataxia, the early
 doctrine that the  degenerations observed  in  the different columns
 were  primary has been gradually disproved.   (See Chap. " Lateral
 Sclerosis ")
  As might  be supposed in advance, the symptoms of the combined
 sclerosis  are commingled symptoms  of locomotor ataxia and lateral
 sclerosis, except that the clinical picture is a milder one than in indi-
 vidual cases of either  one of these two  diseases.   The disease is
 chronic, and the onset gradual.  There is first noticed a motor weak-
 ness  of the  lower extremities, usually more pronounced upon  one
 side.   Then the patient begins to show some inco-ordination of move-
 ment, such  as  being  unable to walk  steadily in the  dark, swaying
 with the eyes closed  and the feet approximated, the walk becoming
 unsteady, sometimes tottering.   If at this time the muscular strength
 is tested,  there will be  found  to be muscular weakness, contrary to
 what  is observed in locomotor ataxia.   This ataxia may increase very
greatly in degree.   The sensory and reflex symptoms of locomotor 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  281

ataxia, however, are generally lacking.  There is seldom any of the
lio-htning- and stabbing-pains or much impairment of sensation, and
the tendon-reflexes of the knee and foot, instead of being  lost,  as  is
generally the case in locomotor ataxia, are exaggerated—often greatly,
so that the knee-jerk  is spastic, aud the foot-clonus may  be  readily
evoked.  Gowers believes that a dull  sacral pain is quite frequent,
aud sometimes a similar dull paiu is felt in the legs or in the  spine
after fatigue, and is an  early symptom.  The cincture sensation,  or
feeling of a belt about the waist, so common in ordinary myelitis, is
almost invariably lacking.   The upper extremities are usually nor-
mal, but they  may present symptoms similar to those of the legs.
There is seldom any muscular atrophy.  The sexual power  is  often
impaired at an  early period, and  the bladder  and rectum  are fre-
quently implicated.   There is  sometimes a loss of  the pupillary
reflex to light, and occasionally also to accommodation.  Optic-nerve
atrophy is far  less frequent than in  locomotor ataxia.   The  ocular
 muscles are sometimes affected.   There is no nystagmus.  In  some
 cases slight impairment of articulation has  been  noticed, and slight
 tremulous movements of the facial muscles  without mental change.
 As the disease progresses the motor weakness aud the spastic symp-
 toms increase,  and the case comes to present the picture of a genuinely
 ataxic paraplegia, which is the apt  name that has been given to it by
 Gowers.  Complete paralysis may result.  The malady, as has been
 said, is  a  chronic one, lasting many  years,  aud death occurs  from
 renal disease and the trophic lesious incidental to all forms of myelitis.
   The diagnosis of the combined scleroses  must  be from locomotor
 ataxia, lateral  sclerosis, myelitis, and lesiou of the cerebellum or its
 peduncles.   This diagnosis can  usually be  made with ease.   From
 locomotor ataxia it is to be distinguished by the exaggerated knee-
 jerk and foot-clonus, the former of which is  infrequent and the latter
 unknown in locomotor ataxia, as well as by the absence of the typical
 stabbing-  and lightning-pains of the  latter  malady.   From lateral
 sclerosis it is  to be distinguished by  the marked element of ataxia
 that is observed in the walk, in  the swaying  with the eyes closed and
 the feet approximated, and, when the upper  extremities are affected,
 in the inability to perform finely co-ordinated movements with the
 arms and hands.  From  ordinary myelitis  it is  to be differentiated
 by the  exceedingly gradual  onset, by the  lack of marked sensory
 symptoms, severe paralysis of the bladder and rectum, and the cinc-
 ture sensation; but it should be remembered that  the  disease may
 follow upon a  myelitis, in which case the history will make the matter
 clear.   From  lesion of the cerebellum and its peduncles  it is easily
 distinguished,  because the ataxia of cerebellar disease is  a  peculiar
 swaying and staggering, like that of a person slightly intoxicated—
 so-called titubation; and there will be present symptoms of an intra-
 cranial  lesion, such as headache aud paroxysms of vomiting, whilst
 m some lesions of the  cerebellar peduncles there are semi-rotary  or
 markedly staggering  movements to one side.
   The prognosis of the combined sclerosis, so far as we  now know,
 is grave as regards   the cure,  and most cases continue for many 
282
NER VO US DISEASES.
years, one  of Striimpell's lasting thirty, whilst, on the other haud,
some have  terminated fatally in a few years.  The disease, however,
is  probably, as  has been said, but a mixture of symptoms, and the
future  will probably separate  it into several maladies, so that the
prognosis may undergo much modification.   I am myself inclined to
think, as I have  already said, that many of these cases are really
cases of spinal syphilis.
  The treatment of the  disease should be upon the  same principles
that have  been  laid down when treating  of locomotor ataxia and
myelitis.   The systematic and careful use  of the faradic current of
high tension, as  well as the static current, are spoken of favorably.
In all cases the patient should  be treated thoroughly  for syphilis by
means of the iodides and mercury, as indicated in Chapter VIIL,
" Syphilis  of the Nervous System."

                      SYRINGOMYELITIS.

  Of late  years there has grown up a voluminous literature upon
the symptomatology and the pathology of syringomyelia, which, as
the name  denotes, consists of  certain peculiar  cavities in  the sub-
stance  of  the spinal cord.  This  pathological  condition has been
recognized  for fully two hundred years past, and to it Ollivier pro-
posed the  name above.    There are in reality  two cavities of this
kind within the spinal cord : one termed hydromyelus, consisting of
a dilatation of the central canal lined by cylindrical epithelium; and
the true syringomyelitis, due  either to  an infiltration of the  spinal
parenchyma with  gliomatous cells, or to a peculiar connective-tissue
formation  known  as gliosis.   Either may be congenital or acquired,
Besides these there may  be mixed forms, consisting of hydromyelus
and syringomyelitis—•/. e., congenital and acquired hydromyelus with
congenital  and acquired  syringomyelitis; or there may be a hydro-
syringomyelitis—that  is, there  may be a hydromyelus or dilatation
of the central canal continuous with  a  cavity or  syringomyelitis
extending out into the cord, such as Schaffer and Priesz have recently
described.   Hydromyelus is, as has already been said, a dilatation of
the central canal of the cord.   This, however, is not  always in the
centre  in  the site  of the  fully developed central canal, because the
embryonic  central  canal  is represented  often by a cavity extending
into what  is in later  life the  posterior fissure, which is generally
obliterated in the  process of development, but which  may remain in
adult life  separated from the  canal in  the centre.  Iu such a latter
event, however, this cavity possesses an  epithelial lining, as has just
been stated.   Syringomyelitis  is a cavity entirely outside the  site of
the adult  or embryonic central canal,  never possesses an epithelial
lining, and its site varies in each  case  according to the molecular
causes  leading to  its formation, bearing no  constant relation to the
adult or embryonic central canal.  There has been much discussion
as to the mode of formation of the cavity of  syringomyelitis.  Some
have held that the anterior portions of the posterior columns  have a
peculiar predisposition to pathological alterations, so that in this area 
 DISEASES OF SPINAL CORD AND MEDULLA  OBLONGATA.  283

new formations readily occur in which  the  centre breaks down into
a softened mass  and is absorbed, leading  to  the  formation of the
cavity.  Others  have  maintained that hydromyelus and syringo-
myelitis are  identical—i. e., that the syringomyelitis found in adults
is the remains of a congenital hydromyelus.  This old view of Ley-
den's, however, has beeu abundantly disproved.  Others have asserted
that  both  hydromyelus and syringomyelitis are caused  by the pres-
sure of tumors, especially gliomata, inducing venous stasis and oedema.
But that tumors are not necessary to the formation of such cavities is
proved  by the case of Joffroy and Achard, who in  their turn main-
tain that there is a non-gliomatous form of syringomyelitis;  and this
view has been supported by two cases of Schaffer and  Priesz.  As
has already  been mentioned, either hydromyelus  or  syringomyelia
can be  congenital  or acquired;  that they are identical, however, is
disproved  by  the  histological differences which have  been already
alluded to.  That the  two conditions  may be combined has been
thoroughly proven, especially by the fifth case of Schaffer aud Priesz,
where a hydromyelus of the cervical enlargement was found in  the
same  cord  with a glioma of the dorsal region, the two becoming con-
 fluent at  a  certain level.  In the cases of syringomyelitis due to
glioma  the pathological alterations usually begin with an infiltration
 of small cells, consisting of connective-tissue  nuclei or  embryonic
 cells,  and  at the same  time there is a production of exceedingly fine
 neuroglia, so that the normal elements of the cord are displaced.   In
 the centre of this gliomatous mass there is a tendency to disintegra-
 tion and a cavity results.   These cavities are usually  in the central
 gray  matter  about the commissure, usually extending backward into
 the posterior gray horns or posterior columns, and sometimes extend-
 ing forward into the anterior horns on one  or even both sides.   The
 extent of the cavity upward and downward  in the cord varies, so that
 it may only  be found for a short distance, or it  may extend  through
 the whole cord.  The lower cervical and the upper dorsal regions are
 especially  prone to be affected.   The wall of the cavity  consists of a
 dense connective tissue extending for some distance beyond its mar-
 gins; the  cavity7 itself  is filled with fluid of a serous or hyaline con-
 sistency.  In  the non-gliomatous  cases described by  Joffroy aud
 Achard no  tumor of any kind was apparent, but there was around
 the cavity a  sort of amorphous exudate surrouuding the vessel, often
 infiltrating the whole  vascular  tract.   The neuroglia   of the  white
 aud  gray  substance was displaced and disintegrated by  this exudate.
 This  neurogliar wall  was formed by  greatly condensed fibrillary
 neuroglia, with all the characteristics of an old neurogliar  sclerosis
 which had reached a strong degree of intensity, almost like that of a
 cicatrix, and which the observers considered to be of secondary for-
 mation, as they could  perceive in it  none of the characteristics of
 young  neuroglia or of neoplastic tissue,  such as is  seen iu  the
 periphery  of tumors.   At one  point the  process of disintegration
 of the nervous tissue by the amorphous exudate was plainly observ-
 able.    In this case of non-gliomatous syringomyelia  there was
 noticed an enormous varicose dilatation  of the veins of the pia mater 
284
NERVOUS DISEASES.
(which  has  also  been observed in  the  gliomatous cases), as well as
abundant leucocytes  in  the perivascular  sheaths, which leucocytes
were also observed in the interior of the vessels pressed  against the
internal wall, as if the circulation had been retarded.  The cause of
the stasis of  the circulation is as yet a mystery, although it was at
first supposed that it was due to the pressure of the tumor; but this
case of  Joffroy and Achard shows that it was found in  cases where
there  is  no  tumor.  Rosenbach  and Schtscherbak have produced
such stasis experimentally by compression of the spinal cord,  and
have also observed similar exudates.  Joffroy and Achard think that
in their  case the  relaxation of the  venous circulation was produced
by arterial thrombosis, as they had  found several capillaries affected
with obliterating arteritis.  These same authors call  attention to the
fact that mauy cases of syringomyelitis that have  been  reported as
caused by glioma are really of a nature  similar to their own, and
they maintain that all the scleroses of the spinal cord are  of a similar
nature, and  should be denominated  by the  generic name of gliosis,
meaning by  this  the peculiar histological  formation  described by
Chaslin (vide Chap. IX., " Epilepsy ").   Weigert  agrees with them
to the extent of believing that the presence of a mass of neuroglia
around  a syringomyelitic cavity does not  necessarily signify glioma,
but may be a secondary formation.   Indeed, Joffroy and Achard go
still further  in  maintaining that the presence of a compact and cir-
cumscribed mass of neurogliar proliferation is not necessarily glioma,
because in such cases the structure of the  so-called  tumor is  not
identical with the neoplasms to  which this name has been given;
and Weigert  also  declares that in cerebral  gliomata the neurogliar
fibrillse  are  almost wanting or are much less abundant than in gray
degeneration  or syringomyelia, whilst in this particular gliosis which
we  are dealing with there are certain  characteristics distinguishing
them  from the gliomatous tumors,  such as their development longi-
tudinally, strand-like, as well as their central  softening, with  the
production of a cavity surrounded by a sclerotic and cicatricial-like
wall.   Francotte has observed a case of syringomyelitis  in conjunc-
tion with an  acute myelitis, and Kiewlicz has reported another occur-
ring with a transverse myelitis and  multiple sclerosis.  Charcot has
also seen this affection with  hypertrophic cervical  meningitis, and
Koller, Vulpian, and Simon  have also observed  it in  conjunction
with chronic  meningitis at the points where  the cavity began, whilst
Oppenheim  has found  it also  with meningomyelitis of traumatic
origin, and  Silcock with meniugeal adhesions  of a  general spinal
sclerosis.
  The disease is an eminently chronic one, slowly progressive, some
cases lasting  even twenty  years, but  there are remissions.
  I have been able to count up 167  autopsies.  Upon the symptoms
observed in  these various cases there have  been vigorous attempts
made to offer a symptomatology of the disease  sufficiently precise to
make a diagnosis,  and it  is now quite a fashion in this country to
report  so-called  cases  of syringomyelitis.   Very few  ante-mortem
diagnoses have been made, however, although  recently Dercum has 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  285

reported a brilliant one.  It has already been  stated that the cavity
affects by preference the lower  cervical and the upper dorsal region
of the cord, and by reference to pp.  81 and 82 it will be seen what
groups of muscles are therefore  most  likely  to  be affected.  Iu
this lower cervical  and upper dorsal region  the centre  of the gray
matter is especially prone  to  be involved, and the  cavity extends
out into  the posterior cornua, sometimes  into  the lateral columns.
A priori, therefore, we should  expect that the symptoms of such
a  cavity  would be those  of sensory impairment,  vasomotor and
trophic symptoms, muscular atrophy, occasionally contracture; and
as the cavity is,  as  a rule, predominantly  unilateral,  certain of
these symptoms would prevail more  upon one side.   As a matter of
fact, great stress has  been laid  upon  the sensory,  vasomotor, and
trophic symptoms.  The impairment of sensation, it is claimed, con-
sists of what is termed disassociated anaesthesia; i. e., marked im-
pairment of the senses of temperature and pain, whilst the senses of
tact and  muscular  seuse are either  altogether unimpaired or very
slightly affected.  The vasomotor and trophic  disturbances consist
of cyanosis, coldness, bullous eruptions,  ulceration, abscesses, even
atrophy  and  fragility  of the bony structures, and  a diminution of
perspiration.  It is, therefore, asserted that we may make a diagnosis
of syringomyelitis in any  case of chronic spinal disease in  which
there are  areas of disassociated anesthesia, marked vasomotor  symp-
toms  of  the kind  that have been described, muscular  atrophy of
certain groups of muscles, ataxia, and contracture; these symptoms
being predominantly unilateral and varying  greatly in their  degree
in different areas.  The diagnosis is a difficult one to make, in proof
of which  is the remarkable  fact that Schultze, who has been the most
enthusiastic advocate of the possibilities of such a diagnosis, read  his
first paper upon the subject in 1878,  aud yet, up to the present time,
seventeen years  afterward, he has never  made a single one  before
death.  In especial is it difficult to make a  differential  diagnosis
from  Morvan's  disease  (see " Morvan's   Disease"), in  which the
autopsies so far made  have shown  that  the  lesion is syringomy-
elia, although it is not yet determined whether this  same  symp-
tom-group may not have other pathological  lesions causative of it,
as Morvan himself stoutly believes ; whilst  Hanot has reported a
case of Morvan's disease subsequent to typhoid fever in which  no
autopsy was made, it is true, but yet in which the symptoms followed
the typhoid fever at too quick an interval to permit of the supposition
of a syringomyelitis.
  If the symptomatology, as it has been described, should prove with
time to be accurate, the diagnosis ought readily to be made from such
other diseases as—
      Amyotrophic lateral sclerosis;
      Progressive muscular atrophy;
      Transverse myelitis;
      Disseminated sclerosis;
      Locomotor ataxia;
      Cervical hypertrophic pachymeningitis; 
286
NERVOUS DISEASES.
       Alcoholic paralysis;
       Hysteria;
       Ansesthetic leprosy.
  Amyotrophic  lateral sclerosis and progressive muscular atrophy are
bilateral diseases, and have no  sensory disturbances whatever, and no
trophic disturbances except the muscular atrophy  of the progressive
muscular atrophy.
  Transverse myelitis is  also a bilateral disease, frequently of acute
origin, in which the marked  trophic disturbances causing necrosis
of bone, abscess, and whitlows are not observed.
  In disseminated sclerosis the symptoms  are almost invariably bi-
lateral, and there is a degree of tremor which is not usually observed
in syringomyelitis, whilst the trophic symptoms  are not so great as
in the latter lesion.
  Locomotor ataxia, too, is a bilateral disease, and the  disassociated
ansesthesia has not been  observed in it so far as we now  know, whilst
the  trophic disturbances  are  never of the extent of  those which are
claimed for syringomyelitis.
  In cervical hypertrophic pachymeningitis  the great  pain in the cer-
vical region radiating down into the upper extremities is greater than
is usually observed in cases of syringomyelitis, although occasionally
it may be difficult to make a differentiation from this symptom ; but
in this form of meningitis the trophic disturbances are  never  of the
extent of those  observed in syringomyelitis.
  In certain cases of alcoholic paralysis and hysteria the disassociated
ansesthesia has  been  observed, but in alcoholism  the knowledge of
the causation and the other symptoms, and in hysteria the general
symptoms of hysteria itself, will enable us to make the diagnosis,
although it must be remembered that in syringomyelitis, as well as
in hysteria, there has been  observed a concentration of the field of
vision.
  Iu anossthesic  leprosy there is, according to Leloir,  a prodromic
period, or a period of invasion ; an  eruptive  period, which may be
short or excessively prolonged, and which is characterized by a cuta-
neous eruption  or by an eruption along the nerve-trunks, or,  rarely,
the cutaneous eruption  may be lacking;  third, a stage of nervous
implication.  The prodromic period  has  such general symptoms as
fever, chills, tendency to slumber, painful digestion,  rheumatoid and
neuralgic symptoms, etc., of such marked  intensity that the patient
is usually confined to bed.  The eruptive period is characterized by
macula, erythema, or pigmentary macula.   In  the stage of nervous
involvement there may be well-marked ansesthesia, usually not, how-
ever, so far as we yet know, of the disassociated form, and the trophic
disturbances  may be as  marked as in Morvan's disease.  The diag-
nosis, however, cau be made by attention to the precedent stages.

                      MORVAN'S DISEASE.

  In 1883 Morvan described a disease which he  denominated anal-
gesic paresis with whitlow of the superior extremities, or pareso- 
 DISEASES OF SPINAL CORD AND MEDULLA  OBLONGATA. ■ 287

analgesia of the superior extremities, but to which, in the twelve years
that have since elapsed, the name has come to be given of Morvan's
disease.   He states that he had beeu observing these cases for upward
of thirty years, and his attention was first called to the matter  by
having a patient come to him who had a whitlow for which he  re-
commended incision, and who, much to his surprise, manifested  no
evidence of pain  whatever when the incision was made.  Morvan has
since made a number of communications upon the same subject.  The
malady affects  the upper extremities, being at first localized in one of
them, usually  in the  forearm and hand.   The  first symptoms are
those of neuralgia, the pain being often very severe, and  these are
followed by paresis and analgesia, finally by one  or  more whitlows,
with  necrosis  of the  phalanges.   The disease proceeds in stages.
 When the neuralgic period has lasted for several years, perhaps, the
 paralytic, analgesic, and trophic symptoms  appear, and extend into
 the other upper extremity.  Atrophy of the muscles paralyzed is
 generally observed, or there may be analgesic segments of the limb.
 In 1886 Morvan had reported nineteen cases, four of which  only
 were  in males.   Youth  is a predisposing age, as  in  twelve of these
 cases the  age  was  between twenty and thirty years, and the others
 beyond this.  In six there was seemingly a traumatic origin.   Morvan
 had also seen,  contrary to his first experience, the malady affect the
 lower extremities, although he had never  observed that the muscles
 of the trunk were  affected.  The analgesia  had  sometimes involved
 the whole upper limb, in three  cases  the  corresponding side of the
 neck, the face,  and the scalp to the vertex, and in two cases the trunk
 as far as the last dorsal pair.   Hyperidrosis had also been observed.
 In no case had paresis been witnessed without analgesia, but in three
 cases there was  analgesia without paresis.  In  most of these cases
 disassociated  ansesthesia has been observed, but in some of them
 there has been an impairment of all the four senses of touch, pain,
 temperature, and muscular sense.
   The  only autopsies that have yet  been made are the three  by
 Joffroy and Achard, and in every one  of them a syringomyelitis has
 been found.   Hauot, however,  has   reported  a case as occurring
 shortly after a typhoid fever—years too soon, it would seem, to per-
 mit  of the supposition  of a syringomyelitis  being present.   The
 differential diagnosis has been dealt with fully in " Syringomyelitis,"
 and it is yet a question whether Morvan's disease is a form of syringo-
 myelitis, or whether it may not be due to other causes.

                TUMORS OF THE SPINAL CORD.

   Tumors of  the cord are most frequently syphilitic or tuberculous,
 although parasitic  tumors occasionally  occur, and in  some rare cases
 spinal neoplasms are  congenital.  The tumors  may be  outside  the
 dura, inside this membrane, or in the  substance  of  the cord.  The
 extra-dural forms are lipoma,  echinococci, enchondroma, sarcoma,
 cancer, aud connective-tissue proliferations from osseous disease.  The
 intra-dural neoplasms are chiefly syphilomata, sarcomata, myxomata, 
288
NERVOUS DISEASES.
tubercular, parasitic growths, echiuococci, cysticerci, and fatty growths,
although  the  last  five are rare.   In the parenchyma  of  the cord
syphiloma, glioma,  sarcoma, myxoma, and tubercular tumors occur,
the first two being the most frequent, aud cysticerci are  occasionally
met with.
  The symptoms of spinal tumors should be divided into two classes:
general and localizing ones.   The  general symptoms are pain and
malaise.   The pain is often severe, and varies much in character,
being darting, stabbing, or dull and aching.  Its intensity is usually
great.  The malaise is generally in proportion to the pain, although
in cancers it may be disproportionate.  The localizing symptoms are
those caused by implication of the cord at different  levels, aud of
these the best idea can be gained by a study of the table  on  page 82.
However  much  the localizing symptoms may vary in degree, they
are invariably accompanied by motor and  sensory paralysis and  by
muscular spasm.
  The diagnosis of  spinal  tumors is  a difficult one, and they must
be distinguished from such affections as myelitis, locomotor ataxia,
spinal  syphilis, spinal tuberculosis., neuritis, caries of the vertebral
column, Pott's disease, syringomyelias, and traumata of the cord.
  When myelitis is of the type of poliomyelitis anterior the affec-
tion occurs in a child  usually, and is  purely motor in its symptoms,
consisting of a paralysis of certain muscles in a limb, generally the
arm- or leg-type, with atrophy and reaction of degeneration, and there
are no vesical, rectal, sensory, or spastic symptoms.   When the mye-
litis suspected is a transverse  myelitis, the symptoms are generally
subacute, reaching their acme in a few days or a week, and  not at-
tended by the pain that is characteristic of spinal tumors.
  Locomotor ataxia has only one  symptom giving it a resemblance
to spinal  tumor,  and  that is the pain; but   in locomotor ataxia,
although the pain may be darting, stabbing, and severe,  it varies in
location, is vagabond in character,  and is also  paroxysmal  and not
continuous as in spinal tumor ; nor are there the motor paralysis and
spastic svmptoms which are present in  spinal tumor.  Besides this,
locomotor ataxia  has  an optic-nerve atrophy associated with it in a
certain proportion of cases, which is not usually seen in cases of spinal
tumor.
  Spinal syphilis, it should be borne in mind, may cause a tumor,
and this is generally associated  with symptoms of diffuse spinal
or cerebro-spinal syphilis.  In cases of spinal syphilis I  believe that
there is a great tendency to exaggerated tendon-reflexes,  particularly
of the quadriceps extensor tendon (knee-jerk), and that the paralysis
is either motor or mainly motor, whilst pain is an infrequent symp-
tom;  aud in cerebro-spinal syphilis  there will also be symptoms of
cerebral lesion  which  are  entirely  lacking in cases of spinal tumor.
But if a spinal tumor should be  syphilitic, and  the symptoms of
general spinal implication by the syphilis should be subsidiary, the
diagnosis may become very difficult, and it can only be  made tenta-
tively upon  a knowledge  of the  syphilitic infection, conjoined with
the results of mercurial cr iodide treatment. 
DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  289

  Spinal tuberculosis may give rise to  a tumor alone, or to diffuse
tuberculous infection of the cord, associated with the formation of a
neoplasm.  In the latter case the history of the tuberculous heredity
or infection, with a knowledge of precedent pulmonary implication,
would  aid us  greatly iu making the diagnosis.  If, however, there
should be no positive history of tuberculous infection, and no evidence
of general implication of the spinal cord by tuberculosis, the diag-
nosis may be  made by exclusion ;  in other words, syphilis, caries,
and  Pott's disease must be excluded, when the diagnosis would  lie
between  a tuberculous and some  other form of tumor, and the dif-
ferentiation would be impossible.
  The diagnosis  from  neuritis  should  not be difficult, because  in
neuritis the affection would  be  limited to a single nerve-trunk, or in
multiple neuritis  there would be an acute  or  subacute onset of the
affection, and besides this, the pain of neuritis is not  apt  to  be  so
sharp and lancinating as in spinal tumor.
  In caries of the vertebral column there will be  a greater immo-
bility of the vertebral column than in  cases  of spinal tumor, and
there will not be the pain.  The diaguosis of spinal tumor is often
extremely difficult, however.
  Iu Pott's disease the diagnosis can usually be made  with ease  by
means of the characteristic vertebral deformities, and the history of
rhachitis or tuberculosis as the predisposing cause.
  The diaguosis between  spinal tumor aud syringo-myelitis (which
is often but a form of tumor) can be made by reference to the details
given in the Chapter on " Syringomyelitis."
  Trauma of the cord can be readily diaguosed by a history of the
trauma, with probably the consequent vertebral deformity.
  The prognosis of spinal tumor is unfavorable, except in the syph-
ilitic cases which  have not caused  irreparable structural  mischief,
and whether this  has been done can only  be determined by syphilitic
treatment.
  The treatment of spinal tumors should be by means of the iodide
and mercurials as has been recommended iu Chapter VIIL, " Syph-
ilis of the Nervous System."   If these should prove to have no effect,
an operation upon the spinal cord holds out some chance of relief.

                 TRAUMATA OF THE CORD.

  Traumata of the cord consist of injuries to the cord itself or to
the vertebral column.  When the cord itself has been injured, hemor-
rhage may occur, either extra- or intra-dural, iu the  pia  mater, in
the substance of the cord  itself,  or  the substance of the cord may be
lacerated, aud  this laceration  may  give  rise to myelitis with soften-
ing. Some authors have stated that the cord cannot be injured unless
the vertebral column has  sustained  a  fracture, but  this statement,
which is of great importance in a medico-legal aspect, is incorrect, for
a number of cases have been reported (and I have had several myself)
m which myelitis has occurred from traumatism without the slightest
evidence of  fracture of the vertebra.  This so-called  concussion of
                              19 
290
NER VO US DISEASES.
the cord gives rise to myelitis, and not to the symptoms of so-called
railway spine, for these latter of late years have been shown to  be
really traumatic neurasthenia.  (Chapter XXIL, "Railway Injuries,
etc.")   The symptoms of injury to the cord,  either direct or from
fracture of the vertebrse, are those of myelitis, and these symptoms
will vary in character according to the  level of the cord  that  is
affected, and what the symptoms are can be best realized by a study
of the table on  p. 82.  It must also  be remembered that this is  of
very  great  medico-legal importance.   The symptoms of traumatic
myelitis may not occur immediately after the  injury,  but they may
come on gradually, although in all cases  there  should be a distinct
chronological  sequence.  There is one  symptom, however, that  is
very frequent in traumata of the cord, and that is pain, which may
continue for years—in one case of mine extending over twenty years,
although a very fair recovery was made.   This  pain  may vary in
site according to the  portion of the cord  that is injured, and in the
course of time it usually passes into a neuralgia, which is excited by
changes in the weather, such as the approach of storms, the passage
of storms, or  the period of clear weather (the so-called anti-cyclone)
succeeding storms, or by fatigue or failure of general health;  and  it
often occurs in paroxysms which have no ascertainable cause.
  The diagnosis of injury to the spinal cord or  the vertebral column
is usually made with ease.   In the first  place, there is the history of
the trauma, and  then a careful examination will discover some abnor-
mality in the position of the vertebrse, or some symptoms indicating
disease of the spinal parenchyma.   As these cases so frequently have
a vivid  medico-legal interest aud occupy so much of the attention of
our courts, every case should  be examined with the  most  minute
care.  The patient  should be stripped,  made  to  bend his body in
every direction,  and  the line of the  vertebral column  should be
carefully traced, so  as  to test the mobility of the vertebral column.
Then sensation  should be minutely examined, testing the sense of
touch, temperature, pain,  and  muscular sense (vide  Chapter II.,
" Tests  of  General Motor and Sensory Symptoms").   The condi-
tion of  the bladder should  be carefully inquired into, and also that
of the  rectum.   The patient having  been stripped,  as has been
advised, the muscular groups should be carefully examined for losses
of contour which may indicate  atrophy.  The  skin  of the affected
parts should  be carefully observed so as to  ascertain  whether it
is  unusually glossy,  whether the  fingers or  toes are bulbous, or
whether the  surface-temperature   is  decreased.   The power of
motion  should also be carefully tested by ascertaining the strength
of the  various  muscular groups.   The tendon-reflexes, especially
the knee-jerk, should be interrogated.   When such  a careful and
minute  examination as this is  made  by a  competent observer, no
possible symptoms should escape.   In making  this prolouged series
of tests, such  diseases as traumatic neurasthenia, hypochondria, aud
Pott's disease should  be excluded, and  the possibility of the patient
beiug a  malingerer should be constantly remembered.   In regard to
malingering, however, I desire  to impress  strenuously one fact, 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  291

namely, that  it should  not be assumed, as is  too generally  done,
especially  by  surgeons in  the  employ  of corporations,  that  the
patient  is shamming.  The  importance  of a fair and impartial
attitude in this matter can only be  appreciated  by one  who  has
had large experience in accident-suits.   The diagnosis from  trau-
matic  neurasthenia is made readily enough, for  in the latter  the
symptoms are general and often commingled with an element of hys-
teria, whilst in localized spinal trauma the symptoms are local, and
there is seldom any hysterical element.  In traumatic neurasthenia,
also, there is very frequently a concentration of the field of vision and
a degree of localized, symmetrical, or bilateral ansesthesia, occupying a
segment of limb, and these two symptoms are  not observed in  the
localized traumatic spinal  affection.   In a large number of cases of
traumatic neurasthenia, too, there is no paralysis of motion,  although
 there may be of sensation, but this never occurs with  traumatic myelitis.
 The diagnosis of hypochondria can be readily made by anybody who
 is expert enough in neurological matters to know that no true symp-
 toms of myelitis are  present, and  that the patient  has  the mental
 characteristics of the hypochondriac.   The malingerer can be readily
 detected  by the competent  neurologist who is adept enough to pene-
 trate the sham presentation of a myelitis, many symptoms of which
 cannot be simulated, such  as exaggerated  and spastic knee-jerk and
 foot-clonus,  loss  of  pain-sense,  muscular atrophy,  the  reaction of
 degeneration, and the contractures.   Paralysis of the rectum may be
 claimed, and it  may  be difficult, for  obvious reasons,  to  ascertain
 whether the  patient is telling the truth or not.  To a certain extent
 this is also true of asserted paralysis of the bladder, but it is  some-
 times possible to test this statement by one of two methods.  In the
 first place, it may  be casually inquired of the patient as to how long
 he can retain the urine.  If he states that he can do this for only a short
 time,  it may be possible to engage him  in conversation, or to  keep him
 upon  the wituess-stand for a period long exceeding that which he has
 mentioned.  If, on the other hand, he  asserts that  he cannot pass the
 urine, ask him how long it has been since he last urinated, and if he says
 that it has been several hours before, the insertion of a catheter and the
 determination of the amount of  retained urine will test the truth of
 his remark.   Unfortunately, however, the last of these  methods can-
 not be often employed nowadays, in the State of New York at least,
 since  the courts have  ruled  that defendants in damage-suits have no
 right to a medical  examination of the plaintiff.  Iu the  second  place,
 an examination of the urine may be of value.   If the urine is with-
 drawn  by catheter, and it  presents evidence of a cystitis, this would
 be proof that the  patient's statement of vesical paralysis was  prob-
 ably true.   Let the reader bear carefully in mind, however, that the
 converse of this proposition is not good legal  proof, for it sometimes
 happens that a patient has vesical paralysis, causing retention or
 incontinence of urine, without cystitis.  This test,  therefore, has only
 a positive value, and a very limited negative one.
   The treatment of traumatic myelitis should be the treatment of an
 ordinary myelitis,  unless there is such evident fracture of the  verte- 
292
NERVOUS DISEASES.
bral column as to make it evident that  there is compression, when a
spinal operation  should be done.   Care must be taken, hovvever, not
to operate too soon unless there is such probable compression, for I
have seen a number of cases of  traumatic  myelitis recover without
any surgical procedures.  If it should be thought advisable to resort
to a surgical operation, however,  this should be done as promptly as
it has been decided upon;  for whilst, as I  have  stated, I  have seen
cases  recover without operation, I  have  yet seen  other cases of
indubitable compression left so  long that  irreparable mischief had
been  done  to the spinal  parenchyma,  which  could  have  been
entirely  or largely prevented  by an early operation.  As regards
surgical operation, therefore, cases of traumatic spinal lesion should
be  divided into three classes: those in which there  is indubitable
evidence of  compression, those  in  which  there is no evidence of
compression,  and those in  which the evidence  of  compression is
doubtful.  The  first class should be promptly  operated  upon; in
the second  class of cases an operation is useless;  the third class
should be put under careful treatment for myelitis until such time as
they have ceased to improve, and, when  this cessation of improvement
has continued for a  period of two or three months,  an exploratory
operation should be  done.

           GLOSSO-LABIO-LARYNGEAL  PARALYSIS.

   Synonyms: Bulbar paralysis.  Progressive bulbar paralysis.  Pro-
gressive  Bulbarparalyse.   Paralysie  musculaire progressive de la
langue, du voile du palais,  et des  l&vres.1  Atropine primitive des
noyaux moteurs.
   Definition.   A motor paralysis, with  muscular atrophy, affect-
ing the  motor cranial nerves and  attached muscles, especially the
hypoglossal,  and certain  filaments  of  the facial and the  spinal
accessory.
   History.  As far back  as 1825 Robinson gave  an incomplete
description of this  disease, in a letter to Sir Charles Bell.  But
Duchenne led the way in this, as in  so many  other spinal diseases,
by the first  recognition of it as a clinical  entity in 1861, narrating
thirteen  cases.  Baerwinkel (1861),  Schultz (1864), and Wachsmuth
(1864) located the  lesion, upon  theoretical grounds, in the medulla
oblongata.  But the first autopsies, two in number, were  made by
Charcot  and Joffroy in 1869, and Leyden  made two more in 1870.
Since then a number of microscopical examinations have been made
by Maier, Charcot and Gombault, Duval, Raymond, Pierret, Troisier,
Hayem, Duchenne,  Joffroy, and  Birdsall.
   Symptoms.  The prodromata of  this disease are either  absolutely
wanting, or are  very slight.   When they are present, they may con-
sistof vague pain in the neck and back of the head, slight vertigo,
feeling  of contraction  about the chest and  breast,  and  occasional
dyspnoea.  Krishaber has noticed a  loss of the reflex excitability i"
1 This was the name by which it was first described by Duchenne. 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  293

the pharynx, larynx, trachea, and  oesophagus, although  the  tactile
sensibility was maintained perfectly.  The symptoms are those apper-
taining to a paralysis and atrophy of the tongue, lips, the  lower part
of the face, palate, and finally the larynx and heart.   It  has  been a
mooted question among  the  older authors whether the paralysis or
the atrophy was primary, but, although this is a matter of subsidiary
importance, the atrophy is  undoubtedly the first symptom  in the
majority of cases.
   The lingual affection generally  first attracts the patient's attention
because of some  slight difficulty  of speech.  Upon  examination of
the tongue, it may then  be  found  atrophied, and, if this has pro-
ceeded to a certain degree, the  organ may have a fissured and fur-
rowed appearance,  or may display minute losses of muscular  tissue
on the edges, causing these to be notched  or  creuulated.   Great
atrophy of the tongue is not only visible to the eye by the diminished
size of the organ, but gentle palpation  between the fingers will show
that the muscular tissue has decreased, and that what remains is much
softer than normal.  The tongue is often agitated by minute fibrillary
tremor.   Its usual movements are made with difficulty, so that pro-
nunciation is  impeded, morsels of food  cannot be  swept around the
buccal cavity  with the usual certainty^, aud  deglutition maybe inter-
fered with. It must be remembered, however, that this lingual diffi-
culty of deglutition is something altogether different from that which
may occur when the muscles of mastication are affected.  In pronun-

                             Fig. 145.
Atrophy of the tongue in a case of bulbar paralysis.
ciation difficulty is first noticed in articulating the letter i; then, in
the course of time, r, sh, s, 1, k, g, t, and usually last of all d and n.
Of the muscles of the lip and lower face affected, the orbicularis oris
is usually the first; then in less  degree the  levators of the upper
lip,  the  quadratus  triangularis, levator menti, and the buccinator.
The eyelids are not usually affected—indeed, some excellent authori-
ties say they  never are ; but I have had two cases in which there was 
294
NERVOUS DISEASES.
paresis of both upper lids.  When the  lips and lower facial muscles
are implicated the expression of the face will undergo an alteration.
The naso-labial folds deepen on each  side,  so  that  the patient has a
woe-begone look, and the lower face is immobile, contrasting sharply
with the animation  given to the upper face by the intact muscles of
the eyelids.   Occasionally atrophy is demonstrable to a certain degree
in the lips, but these muscles are normally  so thin and small that it is
usually difficult to determine this point.  The patient finds difficulty
in blowing, whistling, puckering the mouth, kissing, etc., and in pro-
nouncing the lip-sounds, mainly noticeable with  o, u, and a; then
with  p and f, and  finally with b, m, and  w.   The combination ah
seems never to be disturbed.  Later on the palate becomes  affected, and
may be seen to be paretic.  The pronunciation is then altered of the b
and p, which are made to sound like me and we; this can be remedied
momentarily by closing the nostrils with the fingers.  The voice has a
nasal twang.   The laryngeal, respiratory, and cardiac symptoms are
due to implication of the nucleus of the spinal accessory.   It must be
borne in mind, however, that the spinal accessory has  two nuclei, one
in the medulla oblongata, near  the nucleus  of the pneumogastric, and
the other extending down into the  cervical  cord as far as  the sixth or
seventh cervical nerve. (See p. 85.) It is only the upper nucleus, in the
medulla, that is affected in this disease. This has intimate connections
with the pneumogastric, and from it various branches go to the nerve-
trunk of the pneumogastric, to be distributed to the larynx, pharynx,
and heart.   The laryngeal, pharyngeal, aud cardiac symptoms con-
sist of an increasing paralysis of the muscles of these different organs
that is  evidenced:  in  the larynx, by affection of the vocal cords;
in the pharynx, by  the difficulties  of  deglutition  spoken of; and in
the heart, by alterations in  the pulse and  dyspnoea.   It sometimes
happens that the motor nucleus of the fifth  pair is implicated, leading
to paresis of  the muscles of mastication.   When this  is  the case the
disease has an unfavorable prognosis.   The patients are apt to suffer
greatly from  what seems like  profuse salivation.   In the majority
of cases, however,  this increase of the salivary secretion  is purely
apparent, and is due to the paresis  of the buccal muscles preventing
its  retention  within the  buccal cavity in the  normal  manner;  but
occasionally there is a true hypersecretion.
  Prognosis.  The prognosis in  bulbar paralysis is a very serious
one.  It may be questioned whether a  case has ever recovered.  Long
remissions  of the symptoms have been observed by many writers,
and I have seen the disease remain at a  standstill for years, but ulti-
mately death has come.
  Pathology.   The lesion is essentially one of degeneration of the
ganglion-cell of the motor  nuclei  in the  medulla  oblongata.   (See
Plates II. and III.)  The starting-point is usually in  the nucleus
of the hypoglossus; then the nucleus of the facial quickly becomes
affected; and afterward  the nuclei of the  spinal  accessory and the
vagus.   The spinal accessory nucleus here spoken  of is the one
in the medulla oblongata, and not the one which extends into the
cervical cord, as  has already  been stated.  The  glosso-pharyngeal 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  295

nucleus is not always affected, that of the abducens very seldom,
whilst the nuclei of  the  auditory  and the  trigeminus are always
intact, except occasionally in the motor portion of the  latter.   The
olivary bodies are almost always normal, and it  is probable  that
the same is true of the formatio reticularis.  The cerebellar pedun-
cles  are never involved.  The pyramids are sometimes implicated,
aud there may be a descending degeneration of them. To the naked
eye the medulla  oblongata  does  not always display change.   Not
infrequently, however, there are a visible atrophy and a grayish color
of the affected  nerve-roots, generally most marked in the hypoglossal
and  the facial, less  distinct  in the  spinal  accessory, the vagus, and
the glosso-pharyngeal.  The changes in the  muscles are similar to
those found in progressive muscular atrophy.
  In some cases no lesions whatever have been  found in the medulla,
and  it may be  surmised that the symptoms are theu possibly due to
implication of the centres  in the cortex of the cerebrum, although it
must be remembered that this is a mere supposition.
  Diagnosis.   The diagnosis is easily made.   The disease can  only
be confounded with—
      Facial  paralysis;
      The infantile tyrpe of progressive muscular atrophy ;
      Facial tropho-neurosis ;
      Affection of cortical  centres.
  From facial paralysis the diagnosis is easily  made, because iu this
the onset is acute or subacute, the eye is wide open (lagophthalmus),
the tongue is not atrophied or paralyzed,  the affection is unilateral,
and  speech is affected but little and in a different manner.
  In the  infantile type of  progressive muscular  atrophy there  is
atrophy of other than the facial muscles, and the tongue and larynx
are not involved.
  In facial tropho-neurosis there is only a wasting of the face.
  An affection of the cortical centres of the muscles of the lips, larynx,
and  tongue would have such symptoms as aphasia and paralysis of
the  arms  and legs conjoined with it;  besides, there would be the
general symptoms of the various  cerebral  lesions.
  Treatment.   The treatment  must be looked upon as palliative.
It should consist of  rest, some few drugs, electricity, and carefully
prepared food.
  Rest should consist of protection against atmospheric variations
and  total abstinence from mental or physical  exertion.  The cases
in which I have seen long remissions have beeu housed in sunny,
warm hospital wards, where they had the best  of care and  nourish-
ment.
  Some few drugs have been found temporarily useful, such as picro-
toxin (gr. T^¥ once to thrice daily), iodide of potash, and  sulphate
of quinine.  Electricity should be  applied in  the form of both the
galvanic and faradic currents, in the manner that has been described
on page 123. 
296
NERVOUS DISEASES.
              PROGRESSIVE OPHTHALMOPLEGIA.

  Synonym: Poliencephalitis superior chronica (Wernicke).
  History.  The first description of this disease was given by v.
Graefe  in  1868.   Gayet  made his first autopsy in  1875, whilst
Foerster in 1878 located  the  disease  of exterior ophthalmoplegia
in the floor of the aqueduct of Sylvius.   Hutchinson and Gowers
demonstrated  in 1879  the lesion  of  the nerve-nuclei  in a chronic
case,  and  pointed  out  the analogy  of progressive _ ophthalmo-
plegia with progressive bulbar paralysis and progressive muscular
atrophy.   Parinaud, Lichtheim, Erb, and Eisenlohr have also con-
tributed to the subject, but the three most important communications
of late  years  have been those  of  Wernicke, Mauthner, and West-
phal.  Wernicke has described  the disease in his text-book under the
head  of chronic poliencephalitis superior, as the cells of the original
nerves affected are in  the gray  matter of the upper part of the me-
dulla oblongata in the fourth ventricle, the aqueduct of Sylvius, and
the third ventricle (see Figs. 38 and 40), and he  likens the disease
to the myelitis affecting the cells in the anterior horns of the spinal
cord.  The posthumous monograph of Westphal was  published  in
1891, in which the autopsies made by the author are given.
   Definition.  A paralysis, usually bilateral, of the levator palpebrse
superioris and the muscles of the eye, either (1) of the so-called exte-
rior or extrinsic muscles of the  eye, or (2) of the so-called interior or
intrinsic muscles of the eye, i. e., the ciliary and accommodative mus-
cles ;  or (3) both the exterior and the interior muscles simultaneously.
   Symptoms.  The symptoms are those appertaining to a bilateral
paralysis of all the different muscles of the eye, whether exterior or
interior, as well as of the levator  palpebrse superioris.  It  must  be
remembered that the  third nerve—the  motor oculi—supplies four
of the exterior  muscles of the eye  : the internal rectus, turning the
eye inward ; the superior rectus and  the inferior oblique, the two
elevators of the eye; and the inferior rectus, one of the two depressors
of the eye.  This same nerve innervates also the ciliary muscles and
the constrictor  of the  pupil, as well  as  the  levator palpebrse supe-
rioris.  Of the six exterior muscles of the  eye, therefore, the third
pair supplies  four.  Of the other  two, one,  the superior oblique, is
innervated by  the  fourth  or  trochlear  nerve; whilst another, the
external rectus, has the  sixth nerve, the  abducens, going to  it.
Paralysis of the third pair, or motor oculi, is evidenced by ptosis,
great retardation of the movement of the eyeball, and dilatation and
immobility of the pupil.   The ptosis is generally complete, although
it is usually possible for  the lids  to be separated by the contraction
of the frontalis muscle.  If, therefore, this frontalis muscle be pressed
upon strongly by the  thumb, it will  usually be impossible for  the
patient to separate the lids.  There is upward strabismus of the eye,
if the external rectus, deriving its nervous supply from the  sixth
nerve, be unimpaired, and  the  eye cannot be moved  inward.  Up-
ward movement is  impossible,  while the movement downward takes
place, if the superior oblique, supplied by the fourth nerve, be intact. 
 DISEASES OF SPINAL CORD AND MEDULLA OBLONGATA.  297

The dilatation  and immobility of the pupil are due to paralysis of
the sphincter pupillse.  This  pupillary dilatation is not very great;
indeed,  many myopic eyes will present quite as  much.   It may
therefore be  necessary to  determine the pathological  nature of the
dilatation  by comparison with the  pupil  of the other eye, or by
exclusion of any preceding ocular disease.   But the characteristic of
this moderately enlarged pupil is its complete  immobility.   It will
not react to the light, either directly or indirectly, through the other
eye.   Certain fibres of the third pair go to the ciliary and accommo-
dative muscles; i. e., to the sphincter pupillse and tensor of the choroid.
These have, according to Hansen and Volkers, a different origin in
the floor of the  third ventricle from the other fibres of the third pair,
and, as  a  matter of fact, paralysis of them alone is met with occa-
sionally.  In such a  case not only will the moderately dilated and
immobile  pupil fail to react to  light, either directly or indirectly,
but it cannot be made to contract by any convergent movements of
the eye  or by any movement of accommodation.  It has sometimes
happened  that  the muscles  of accommodation are intact, whilst the
sphincter  pupillse  has been  completely paralyzed, or  the pupillary
reaction to light has been lost, whilst its reaction to accommodative
 movements has been preserved,  or  instead of a moderate dilatation
there has been a very great dilatation, or the pupil has become very
 much contracted.  The paralysis of the sixth  nerve, the abducens,
 is manifested by an inward strabismus, due to paralysis of the ex-
 ternal rectus.  Paralysis of the fourth uerve, the trochlear, supplying
 the superior  oblique  muscle, is difficult to  diagnose;  the superior
 oblique draws the eye downward and outward, and inclines the upper
 end of the vertical meridian inward.  But the reader had best read
 carefully the  minute  directions given for detecting paralysis of the
 different ocular muscles given on pp. 154,  155, and 156.
   Headache  may be absent in ophthalmoplegia, although it has been
 intense  in  some cases in which an  implication of the sensory por-
 tion of the fifth pair was either found post mortem or suspected.   It
 has been  noticed that headache will disappear, as in cases  of intra-
 cranial syphilis, upon the supervention of paralysis.
   Nystagmus or nystagmus-like movements are occasionally seen.
 The disease is sometimes seen in conjunction with multiple sclerosis,
 locomotor ataxia, combined  sclerosis, progressive paralysis, aud such
 mental  disturbances as belong to   the psychoses, characterized by
 hallucinatory states of dread,  hypochondria, delusions, and  suicidal
 attempts.  Iu these diseases the ophthalmoplegia may be a prodromal
 or concomitant affection.   The progress  of the disease  is chronic,
 but it may be  relatively so, first  attacking  one muscle or one group
 of muscles, then remaining  quiescent, and again  progressing with
 varying rapidity.  It may be complicated with paralysis of the fifth
 pair,  of the facial, with the general symptoms of bulbar paralysis, with
 locomotor ataxia, with progressive muscular atrophy, or with insanity.
   Causation.  The causes of ophthalmoplegia can scarcely be said
 to be known.  It has  been congenital, or it has developed a few days
 after  birth, in infancy, and also in adults generally between forty and 
298
NERVOUS DISEASES.
seventy.  Syphilis has been found to be a concomitant in a number
of cases.   The  male sex is most often  affected.  Some of the cases
have had a neurotic predisposition.
  Pathology.   The lesions of progressive ophthalmoplegia have
been  found  to  be disease  of the cells in the upper part of the
medulla oblongata  which  give  origin  to  different  nerves  of  the
eyre.  The  cells disappear, and  the nerves  to wfiich they give
origin degenerate through  their peripheral filaments and into  the
muscle.  In other cases  there has been found to be a degeneration
of the muscle- and the nerve-fibres,  whilst the cells  remain  intact.
In  still  other  cases sclerotic foci  affecting the nerves within  the
pous  interrupt  the  nervous conductivity, although  the muscle, the
nerve, and the cell may remain  intact.  In  one  case of Kahler's
there was  an ependymitis with an underlying  sclerosis.   Finally,
in some cases  absolutely no lesion whatever has been found.  But
the most frequent form is that in which  the cells are affected, the so-
called nuclear  paralysis, and the next most frequent form is that in
which the nerves are the site of disease.   When  the cells  are impli-
cated, they are those of the abducens, the trochlear, and the oculo-
motor nerves.   They may be degenerated, vacuolated, pigmented, or
disappear  entirely.  Hypersemia  occurs occasionally,  but  it is  not
the rule.   The ependyma, or lining of the ventricles, is occasionally
proliferated.   But  of all  these phenomena the degeneration  of  the
ganglion-cells in various degrees, the decrease  of  the nerve-fibres
running to the nucleus,  and  the implication of the  surrounding
parenchyma are the most  usual factors, whilst  hypersemia and epen-
dymitis are inconstant.   From this it is evident that most cases are
due to primary disease of the ganglion-cells, and not a hypersemic or
inflammatory process, as is maintained by Guyet, Wernicke, Thom-
sen, and Kowjewkneiff.   As has already been  said, however, a focus
of sclerosis, in the course of the intra-medullary nerve-fibres may be
the sole lesion,  without the cells, nerves, or muscles being affected.
  Prognosis.   The prognosis of ophthalmoplegia is usually serious.
In  acute or  subacute  cases, commencing with great somnolence and
general  muscular weakness,  the result is  usually fatal.  In acute non-
complicated cases improvement may ensue,  or  the  paralysis may
become  stationary, and  sometimes the  latter disappears.  Indeed,
symptoms of bulbar paralysis, if they be  not attended by somnolence,
do not exclude the possibility of cure.
  Diagnosis.   The diagnosis is  easily made.  The only question
that can arise  is as to whether the  disease is complicated by other
affections of the brain  and the spinal cord.
  Treatment.  The treatment of ophthalmoplegia should consist of
rest, tonics, stimulants, and  electricity, as in myelitis.
  The patient  should  be put to  bed, if the attack be an acute one,
until it is positive that the disease is not extending beyond the nuclei
of the ocular nerves.   In  subacute  cases, although it may  not be
necessary to put the patients to bed, they should  be  made  to abstain
from any mental or physical exertion.
  For  further  details  of  treatment,  the  reader  must  consult
" Myelitis." 
CHAPTER  V.
       NEUROMUSCULAR OR MUSCULAR  DISEASES.


             PSEUDO -MUSCULAR HYPERTROPHY.

  Synonyms:  Pseudo-hypertrophic  muscular paralysis (Duchenne).
Myosclerotic paralysis.  Progressive muscular sclerosis.   Atrophia
musculorum lipomatosa.  Lipomatous  myoatrophy.   Pseudo-hyper-
trophie der Muskeln.
  Definition.  Pseudo-hypertrophic muscular paralysis is a chronic
disease, usually causing paraplegia and great increase in size of the

                            Fig. 146.
 Two children with pseudo-hypertrophic muscular paralysis, one (sitting) in the late stage,
                    the other (standing) in the early.

lower limbs, occasionally affecting the  upper extremities in the same
manner,  and without  mental, sensory,  rectal,  vesical,  or atrophic
symptoms. 
300
NERVOUS DISEASES.
  History.   The  disease was first really described by Duchenne,
of Boulogne, in 1858, who denominated it " hypertrophic paraplegia
of infancy," although  Charles  Bell in 1830, two Italian observers in
1838, Partridge in  1847, and Meryon in 1852, had put cases of it
on record.  Since Duchenne's  description of it  in  his famous text-
book, it has  been generally recognized,  but the best essays upon the
subject have  been  by  Gowers  in  1879, Schultze in 1886, and Eay-
mond in 1889.
  Clinical  History.  The disease generally commences in early
childhood  with symptoms of weakness in the lower extremities, to
which attention is first called  by the patient's stumbling or falling
frequently.   As the malady progresses, the gait of the  patient  be-
comes characteristic, with legs  spread wide  apart, shoulders thrown
back, and  waddling;  and it soon  becomes evident that the lower

                              Fig. 147.
   Case of pseudo-hypertrophic muscular paralysis, showing the difference in size of the
               upper and lower extremities, and the helplessness.

limbs are increasing in  size.   If the child is examined at this time,
it will be found that it has a peculiar difficulty in getting up from
the floor upon which it has been placed,  or from a chair, or in going
up stairs.  He first puts his  hands upon his knees, then grasps his
thighs higher and higher, and so, as Gowers  says, by climbing up
his thighs he rises to the erect posture.   Gowers considers this symp-
tom pathognomonic, and I  am inclined to agree with him.  The
muscles will also be found to be increased  in size in varying  degree,
as is shown in Figs. 146, 147, and 148.
   The upper extremities, and also the muscles of the neck  and face, 
NEURO-MUSCULAR OR MUSCULAR DISEASES.      301
Fig. 148.
are rarely affected.  The hypertrophied  muscles are weak, as can be
determined by  testing them in  the proper  way (p. 173).  There
are  no sensory, mental, rectal, or  vesical  symptoms  whatsoever.
There is  generally a  lumbar lor-
dosis, the spine being curved  an-
tero-posteriorly.  The disease is a
chronic one, lasting for many years,
usually terminating,  however, be-
tween twenty and twenty-five, and
seldom continuing until forty years
of age.   Muscular atrophy is fre-
quently conjoined with the mus-
cular hypertrophy, and  it is  not
unusual to find limited or general
atrophy of the upper extremities
in conjunction with hypertrophy of
the lower.  The patient generally
goes on to a condition  of perfect
helplessness.  The boyr represented
in Fig. 148, chubby and handsome
and ruddy as he appears, is abso-
lutely unable to move a muscle of
his  lower  extremities  from   the
trunk  down, and  has  been  for
 years in  this  helpless  condition.
 Whilst the boy in Fig. 147  was
 not, when I saw him  last, quite so
 helpless as this, he still was unable
 to get up from  the floor or a chair
 without  assistance.  When death
 occurs, it  is  the result  of inter-
 current maladies which are greatly
 aggravated by the weakness of the
 trunk-muscles.  Pulmonary affec-
 tions are, therefore, especially dan-
 gerous to these individuals.
   The difficulty in going up stairs
 is mainly due to the paresis of  the
 knee and hip extensors, and the oscillating gait is probably also from
 the latter cause.  As  the patient throws his body laterally, so as to
 bring the centre of gravity over each foot, the weak gluteus medius
 cannot antagozize the  inclination  toward  the leg that is off the
 ground.   The difficulty in rising from the floor is thus explained by
 Gowers: The patient has  not  sufficient muscular strength to extend
 the knees when the weight of the trunk is on the upper extremity of
 the femur, which is then  a lever in which the power, applied between
 the fulcrum and the weight, acts at least  advantage.   He therefore
 places his hands on his knees, and his arms bring much of the weight
 of the upper  part of the trunk on the femur close to the fulcrum,
 between this and  the power, which acts, then, to greater  advantage.
  Case of  pseudo-hypertrophic muscular
paralysis, with absolute helplessness of hy-
pertrophied lower extremities. 
302
NERVOUS DISEASES.
When the knees are extended the body can be raised into the upright
position by the extensors of the hip, or by a push with the patient's
hand.  If these extensors are weak or paretic, the trunk is raised up
by the patient grasping the thighs higher and  higher.  The antero-
posterior curvature  is due  either  to  the weakness of the  trunk-
muscles or to  that  of the hip  extensors, probably the latter, as a
consequence of which there is  an inclination  forward of the  pelvis,
so that the upper part of the trunk has to be held back as a counter-
poise.  The lordosis disappears when the patient sits, and, indeed,
it is then sometimes  converted into a curvature in the opposite direc-
tion.
  The hypertrophied muscles usually are normal in their electrical
reactions until the disease is  far advanced, when there may  be de-
creased response to faradism and galvanism, but never any reaction
of degeneration, so far at least as I have seen, although some French
authors claim that this latter phenomenon occasionally occurs.
  Causation.  The disease is an hereditary one, and occurs princi-
pally in males and in  early childhood.   Some remarkable instances
of the heredity  have been published, as in Meryon's case, in which
eight brothers died from the malady, whilst all the daughters escaped.
Males are much more frequently affected than females.  The disease
first shows itself either when the child begins to walk, or when it is
about four to seven years  of age, in others about the tenth year, and
rarely after this, although cases have  been observed as late  as the
twentieth year.  No other causes than these are known.
  Prognosis.   The  prognosis  of pseudo-hypertrophic  muscular
paralysis is very grave, as no case has ever been cured.
  Pathology.  The lesions of pseudo-hypertrophic muscular paral-
ysis  consist of a proliferation of the connective tissue between the
muscular fibrillse and the muscular bundles, subsequent fatty degener-
ation of this proliferated tissue, aud atrophy or disappearance of the
adjoining  muscular  fibres.  The muscular atrophy is  probably a
secondary process, and results from the compression of the prolifer-
ated connective tissue, although  there has  been considerable doubt
among pathologists as to whether there may not be a primary mus-
cular atrophy in certain of these cases, whilst some  authors actually
classify pseudo-muscular hypertrophy among the  muscular atrophies.
Certainly in many cases, as I have already stated, muscular atrophy
is observed in  the same  individual who presents the hypertrophy.
The atrophy, whether primary  or  secondary, is generally a  simple
atrophy,  the muscular fibres  retaining  their  transverse marking
to a  late period,  as  well as their normal structure,  although in
certain cases there is  a proliferation  of the muscular nuclei, and
granular, colloid, or  waxy degeneration of the myolemma; in others
there is actual hypertrophy of the muscular fibrillre ; whilst in still
other instances  alterations of muscle  and connective tissue in some
portions  of the hypertrophied  limb have been observed, and in
other portions of the same limb simple atrophy,  etc.  In a number
of autopsies which  have  been  made  some  slight affections  of the
spinal cord have been shown, and  it  has been  claimed  that these 
         NEURO-MUSCULAR OR MUSCULAR DISEASES.      303

were in relation with the disease, but they either had been trifling
or else were due to the action of the hardening-agents—so-called
artefacts—or else to defective observation, as  in Pekelharing's case,
which  was first  described as  presenting dilatation of the  central
canal, hypersemia, and diminution  in  consistence of the gray sub-
stance, whilst the ganglion-cells of the anterior horns were supposed
to have either disappeared  or  to be greatly degenerated, until the
sections were examined by Schultze, of Heidelberg, who claims to
have  demonstrated  that they came from a perfectly normal cord,
in which there was  no alteration whatsoever in the ganglion-cells.
Middleton in especial has called attention  to the danger of drawing
conclusions from specimens hardened in alcohol, and  narrates how
he found in one such specimen, as  he  thought, a large quantity^ of
round and irregular  masses  in the spinal  cord, whilst a specimen
from  a section  hardened in bichromate of ammonium was perfectly
normal; nor were even the intramuscular nerve-fibres affected. (See
Pathology, Chap. " Paretic Dementia.")  For these reasons we are
warranted in regarding pseudo-hypertrophic muscular paralysis as a
peculiarly muscular affection, belonging to the class  of the primitive
myopathies.
   Diagnosis.    The diagnosis of pseudo-hypertrophic  muscular
paralysis is easily  made, as  a rule, by the history of the  gradual
onset in early childhood, by the difficulty of the child in rising from
the floor or a chair, or ascending stairs;  by the increased  bulk of
the muscles and their  paresis; and by the  absence  of mental,  sen-
sory, rectal, and vesical symptoms, as well  as by the lack of elec-
trical alteration except in advanced  cases.   The diagnosis should be
from
       Progressive  muscular  atrophy ; and
       A muscular hypertrophy.
   From progressive muscular atrophy pseudo-hypertrophic muscu-
lar paralysis can be  distinguished  by the  fact that  the former  is
 seldom or never paraplegic  in its  onset; that the  atrophy is  first
 observed, and  that even  when  hypertrophy is commingled with
it, it  is only so in  individual  muscles, and is of secondary impor-
 tance.
   Pseudo-hypertrophic muscular paralysis  is differentiated from a
 muscular hypertrophy by the fact  that in the latter rare disease the
 hypertrophy of muscle is attended by a corresponding increase in the
muscular strength,  just the opposite of what  obtains in the disease
that we are considering.
   Treatment.  The treatment  of pseudo-hypertrophic muscular
paralysis amounts to nothing, for the sad reason that no treatment
 whatever seems to be of any avail.   Curiously, too, electricity, which
acts so well in most spinal  and  muscular  diseases, seems in many
cases, if not always, to have an actually deleterious  effect upon  this
 malady.  In the case represented  in  Fig.  147,  for example, if the
galvanic or faradic current  was used  in the  earlier period of the
disease, when  the boy could  still walk, its  employment was always
followed by perfect helplessness for a day or two;  and I have ob- 
304
NERVOUS DISEASES.
 served the same thing in several other cases.   I have not been able
 of late years to  treat a case of  this disease in  the way in which  I
 should like to attempt it, because I have never been able positively to
 promise any relief;  but from a priori reasons I have thought that it
 might be  possible to treat  the affected muscles in such a way as to
 increase the capillary circulation in them, at the same time that  the
 absorbent action of the capillaries and lymphatics might be increased
 by sorbefacients.  I should therefore use massage so gently and  yet
 so efficiently that the blood would be made to pass in increased quan-
 tity through the  muscles  without any mechanical irritation of  the
 muscular  fibre from the hand of the person giving the massage.  In
 my  cases  massage has always given  great temporary  relief, and
 patients have always been eager to have it continued.   Then I should
 give the iodide of potash, in doses of 10  to 15 grains, three  times a
 day, plentifully diluted in a full tumbler of water.  Either with this
 or alone,  I should use mercury in the form of a reliable  oleate, and
 rub this over the affected limb, using a sufficient quantity to produce
 a slight ptyalism.  I should have the massage given twice a day, and
 I should use the mercury once or twice a day.   During  the period
 of active  treatment I should not permit the child to use the affected
 muscles at all, unless they showed some symptoms of returning power,
 and then I should permit voluntary use of the muscles very cautiously.
 Perhaps some one of my readers may have a  chance  to test my
 theoretic views in this terrible malady.


                     THOMSEN'S DISEASE.

   Synonyms: Myotonia.   Tonic spasms in voluntary muscles.
   This disease was  first described in  1876 by  Dr.  J. Thomsen, a
 physician  of Schleswig, who was himself  subject to it, and in whose
 family it  had run for  four generations.   It had been referred  to
 previously by Sir Charles  Bell  and Leyden.   Since  its description
 by Thomsen, a  number of cases  have been reported, and the best
 monograph on the subject is that by Erb,  written in 1886.
   It is a hereditary disease  in the majority of cases, first appearing
 in early childhood, as  soon as the child is able  to make use of  its
 muscles, although lately a so-called acquired form has  been reported
 by Gowers,  under the name of ataxic  paramyotone.   This case was
 in an adult of forty, but I have had under my care one in a child of
 six.   Males seem to be more  frequently affected than females.   Of
 other causes we know very little.
  The symptoms are a stiff and tonic spasm of the muscles, occurring
 upon voluntary exertion.   This gives a peculiar gait to the children,
 which is quickly noticed.   A little patient has  innocently suggested
 for it the  capital  name of  " the wiggles."  Upon any exertion the
muscles become  very  stiff.  Usually  all  the muscles are affected
excepting  those  of the face, tongue, and eyeballs, but  in certain ex-
ceptional cases even these  may be implicated.   Eulenburg, however,
has  recently described what seems to  be an identical disease, which
he calls congenital paramyotone, aud iu which the facial muscles are 
         NEURO-MUSCULAR OB MUSCULAB DISEASES.      305

chiefly  affected, especially the  orbicularis  oris and  palpebrarum, so
that the  patient cannot  speak or open the eyes in the  paroxysm.
Curiously enough, long-continued  rest makes the disease worse, and
the same effect will be produced by cold, heat, excitement, emotions,
or sudden  sensory impressions, whilst  moderate exercise improves
the muscular stiffness. The muscle is usually hypertrophied, although
this is a false hypertrophy, as  it is not conjoined with an  increase of
strength.  The mechanical excitability of the  muscles is  increased,
so that a blow upon them with a percussion-hammer will  produce a
slight contraction of the irritated fibres, which remain contracted for
twenty to forty seconds.   The faradic excitability of the  muscles is
also  increased, a  tonic persistent  contraction resulting.   With  the
galvanic current  applied to the nerve or muscle, single  shocks at
the opening  produce quick contractions.  The muscles  also  show
qualitative change with the galvanic currents, so that the contraction
with the negative pole  at the  closure is equal in strength to  the
contraction with the positive  pole at the closure, or the former may
even be stronger than the latter.  In some cases there are rhythmical,
undulatory contractions  moving from  the negative pole to the posi-
tive pole.
   The pathology  of the disease is  not known, as an autopsy  has
 never  been made, but  the muscles have been excised  or  harpooned
 during life, and examination of them has shown that  they are in a
 condition of enormous hypertrophy of all the fibres and  great pro-
 liferation of  nuclei,  the  transverse striation being indistinct; and
 there are also vacuoles in the muscular fibre aud a slight increase of
 the perimysium.   Dr. George W. Jacoby, of New York, has also
 called  attention to the fact that the fibre is distinctly divided into
 angular  fields, varying  in size, and similar to  the faintly indicated
 Cohnheim fields of normal muscle, and that there is almost every-
 where, as seen with  high power, a  lack  of continuity between  the
 groups of sarcous elements.
   The prognosis of Thomsen's  disease is  grave, inasmuch as we are
 not in a position to say whether a case of the congenital form can be
 cured.   So far, in the thirty odd cases that have been reported, there
 has never been a  cure, but it must be  remembered that our knowl-
 edge  of the  affection dates back only to 1876.  I have, however,
 seen what was perhaps a cure in an  acquired case, with no return of
 the symptoms in  three years.   Patients, however, lead a  fairly com-
 fortable  life,  and  death does not result from the disease itself.
   The treatment  consists simply of learning to avoid  those things
 which have  been found to have an unfavorable influence, as  cold,
 damp air, excitement, etc.  Electricity and drugs  have not as  yet
 proved to be of any value in  the congenital type.  My case, spoken
 of above, was  cured by treatment with  belladonna, rest, and mas-
 sage.  The drug  was given at first one drop morning  and evening,
 then three times  daily.
20 
CHAPTER  YI.
       INTRACRANIAL HEMORRHAGE,  EMBOLISM, AND
                          THROMBOSIS.

   As the symptoms immediately resulting from lesion of the nerve-
strands are almost identical in cases  of hemorrhage, embolism, or
thrombosis, and as the diagnosis between  the  three  must be made
by means of other than purely cerebral symptoms, I have considered
it best to treat these three conditions in one chapter.  Before entering
more immediately into the  subject, however, there should be a proper
understanding of the  way in which  the  cerebrum  is supplied with
blood.   The  researches  of Heubner and Duret have thrown great
light upon the arterial supply of the cerebrum, and the reader should
master all the details of the cerebral circulation  as described on pages
89 et seq.
   Hemorrhage is the most common  of all vascular disturbances of
the cerebrum.  The miliary aneurisms which  were  first described
by Charcot and Bouchard  are by far the most  frequent cause of it.
These little bodies vary in size from a pin's head to a millet-seed,
are reddish in color, and are best demonstrated in a brain by wash-
ing away the  cerebral  substance with a stream  of hot water from a
tea-kettle,  when, with care  and patience, the whole  arterial rami-
fication can be  laid bare.    A  section  of the  cerebrum may show
simply  little  reddish dots, which  an  examination with  a magni-
fying-glass will show to be  larger than an unaltered arteriole.  These
miliary aneurisms are found upon the capillaries, whose diameter does
not exceed that of one-tenth of a millimetre, the so-called capillaries of
the first variety of Robin, but particularly in the capillaries of some-
what larger variety, which are visible to  the naked eye, and which
most anatomists call the arterioles or venules, although Robin desig-
nates them capillaries of the second or third variety.   But they are
also, though  very rarely, found in the  arteries  of the base and the
ramifications of these in the meninges.  According to Andral and
Durand Fardel, confirmed  by Charcot, the parts which suffer most
from hemorrhage are as follows, each part being named in the order
of its frequency :  the  cerebrum  (in which  successively the most
affected are the corpus striatum, the  optic thalamus, the different
lobes of the  cortex, and the convolutions), the  pons, and the cere-
bellum.  There are certain  portions of the brain  in which hemorrhage
seldom occurs, such as  the  tubercula quadrigemina, the crura cerebri,
and the medulla oblongata, whilst it is  scarcely  ever observed in the
cornu ammonis or  the corpus  callosum.   Miliary aneurisms  rarely
occur before  the age of forty, afterward  with increasing frequency, 
      INTBACBANIAL HEMOBBHAGE AND THBOMBOSIS.   307

although cases  have occasionally been reported in  youth and child-
hood, especially one by Baillarger, and of late years there has been
a growing tendency to recognize that infantile hemorrhage, probably
due to this cause, is  much more frequent than  the older authors
supposed.   Next to miliary aneurism, a chronic endarteritis is the
most common cause of hemorrhage ; but it must be remembered that
these two pathological conditions differ from each  other.  Miliary
aneurisms often occur without the slightest atheromatous  disease,
just  as  marked atheromatous disease can take place without the
formation  of miliary aneurisms.   Thus,  in 77 cases collected by
Charcot, miliary aneurisms were found in every  instance,  but 15
(over  one-fifth) presented no  atheromatous  changes, whilst 25  of
them (over one-third) were  but slightly involved  by atheromatous
degeneration ; and the remainder were atheromatous in varying de-
gree.  Miliary aneurisms are the result of a diffuse peri-arteritis  of
the small intracerebral vessels, sometimes associated with  an atrophy
of the walls of the large vessels of the base and the meninges.  This
peri-arteritis leads to  thickening of the lymph-sheaths by prolifera-
tion of the nuclei  of  the latter and  by the  formation of fibrillary
connective tissue.  Alterations ensue in the muscular coat, consisting
of a loss of the muscular  fibres and disappearance of their transverse
 striping;  but this muscular coat is always affected  secondarily, gen-
erally where the alterations in the lymph-sheaths are most pronounced.
 In consequence of  the loss  of this muscular coat  sacculated dilata-
 tion of the vessel occurs  in  places without alteration of the intima.
 Examined under a magnifying-glass,  a miliary aneurism  will be
 found to  consist of  the  lymph-sheath and  intima  fused together,
 whilst the muscular coat  is entirely wanting.   Its contents are fluid
 blood, white blood-corpuscles,  fat-granules,  granular bodies,  and
 amorphous masses.   When  a  hemorrhage  has occurred it is at first
 a dark,  almost black clot, but  sometimes in disease altering the con-
 stituents of the blood, as in pyaemia, it is not coagulated.   The wall
 of the hemorrhagic focus is colored  a  bright red, which is due  to
 capillary hemorrhages.  The gray matter of  the basal ganglia offers
 less resistance than the centrum  ovale to the  hemorrhage.  The clot
 becomes gradually  altered to a dark brown or chocolate color, thence
 becoming  yellowish-red and yellow.   At first the surrounding tissue
 is cedematous and pultaceous.   This hemorrhagic focus may become
 encapsulated by a thin layer of thickened neuroglia, occasionally even
 by the formation of actual  fibrillary connective tissue.   A so-called
 apoplectic cyst  may be formed—i. e., the fibrin of the clot and the
 injured  nervous elements undergo a retrograde fatty metamorphosis
 and are gradually absorbed by the lymphatics, so that a cavity re-
 mains, filled with clear or colored fluid, and surrounded by a smooth
 wall; or the surrounding oedema may extend and cause death.  It is
 often extremely difficult,  however, in  this  last stage to distinguish
 an apoplectic cyst from one  that  has  resulted from  softening.   At
 other times the walls  of the encapsulated clot become approximated
 before the central portions of the clot have been absorbed, and there
 is thus formed the so-called apoplectic cicatrix. 
308
NERVOUS DISEASES.
   Increase of arterial tension may be a cause of cerebral hemorrhage,
although it has never yet been shown that this can  occur in arteries
that are not diseased.   In the general endarteritis which  is  associ-
ated with hypertrophy of the left ventricle and a contracted kidney,
associated with  endarteritis  of the  intracranial  vessels, hemorrhage
is by no  means  infrequent.   Fatty degeneration of arteries is  also
a frequent cause, either alone or by the endarteritis that results in
atheroma, although this latter is more usually an indirect cause by
rendering the walls of the larger vessels rigid, so that the blood streams
into the arterioles without the regulating influence of the normal con-
tractile vascular coats.
   The red softening which was so frequently described by the older
writers, and which was by them supposed  to be a primary process of
softening, is now regarded rather as secondary to the arterial disease.
Intracranial  hemorrhage also occurs in various diseases which lead
to changes in  the tissue of the blood, such as pyaemia,  typhoid, scor-
butus, puerperal  fever, chlorosis, leucocythsemia, pernicious  anaemia,
and icterus.   Heredity also plays a certain part in  causing hemor-
rhage by inducing the tendency to arterial disease, so that it is well
established that certain families have a predisposition  to this condi-
tion.  The short neck, broad chest, and florid complexion, however,
which were formerly supposed to indicate a tendency to hemorrhage,
are no longer  regarded as of any prodromal value; indeed,  it is cer-
tain that no particular bodily type is known to predispose.   Men are
somewhat more affected than  women.  Altitude  also appears to pre-
dispose, as it is more frequent in elevated regions, and I have known
instances in which it has occurred while passing over lofty mountain
chains.  Alcohol also  predisposes by producing fatty degeneration of
the vessels and premature endarteritis.
   Cerebral  emboli may  consist of fibrinous  masses from  the left
cavities of the heart, the aortic  and mitral valves, the arch of  the
aorta, and the pulmonary veins, or from a  thrombosis in the  cerebral
vessels.  After certain acute and exhausting diseases the blood may
become so altered in quality  as to  be  prone  to  coagulate, or, as in
atheromatous  and calcareous disease, the roughened coats of  the ves-
sels may whip up the fibrin.   In certain cases of malaria and inter-
mittent fever the cerebral capillaries may be plugged up by pigment-
emboli.  In other cases they may be obstructed by drops of  fat from
atheromatous  formations in  the larger vessels, or, after injuries to
bone, the fatty tissue of the  marrow may be  carried into the  capil-
laries.   Virchow has described what he calls a lime-metastasis, which
is due to lime being deposited on  the walls of the capillaries when
there is some associated bony disease.
   Clinical Symptoms.   In all cases of cerebral hemorrhage, em-
bolism, or thrombosis  distinction must be made between the  reflex
symptoms and the localizing ones.
   The reflex symptoms are due to the shock which the cerebrum as
a whole sustains from the outpouring of blood of a  hemorrhage, or
from, the plugging of a vessel by an embolism  or thrombosis.  They
consist of loss of consciousness or  coma,  mental disturbances, con- 
      INTRACRANIAL HEMOBBHAGE AND THBOMBOSIS.    309

vulsions, and alterations of temperature.  When there is a loss of con-
sciousness, the onset is a so-called apoplectiform one, and this loss of
consciousness may be  sudden and  complete, or gradual, and in the
latter case it is usually preceded by some abnormal sensations about
the head,  by confusion, difficulty of speech, drowsiness, nausea, or
vomiting.   When the patient is comatose, the face is usually flushed
and swollen, or pale and clammy, the eyes fixed, the  pupils widely
dilated and sluggish, the respiration slow, sometimes stertorous, with
cheeks blown out in  respiration,  pulse generally slow and full, and
the limbs are inert.   In the attack with convulsions the latter are
generalized, or confined to the side that is  afterward found to be
paralyzed.
   The temperature  is subnormal  in almost  all cases, going down
sometimes to 96^°  F., but it rises markedly in the  non-fatal cases
within the first twenty-four hours, aud  in fatal cases may run up to
as high as 108°, although  usually it  oscillates  irregularly between
99° and 100° or 101°.
   Conjugate deviation of the eyes, with rotation  of the head  away
from the paralyzed side and toward the hemisphere which is affected,
often occurs as a temporary symptom.  Alternate conjugate devia-
tion is that condition in which the eyes turn first to one side—gener-
ally toward the  lesion—and  then to  the  other.  It is supposed to
indicate a cortical or  pons lesion;  and it is believed  that the devia-
tion is  toward the lesion when the brain is  affected, and  the other
way wheu the pons is implicated.   The eyes are  usually fixed, but
there is  occasionally slight nystagmus.
   The localizing symptoms will vary according to the location of the
disease,  but  the most frequent site is  in the internal capsule, at the
auterior portion just  around the genu, where the motor fibres come
down from the hemispheres (vide pp. 59 and 145,  and Fig. 35), and
this gives rise to symptoms of hemiplegia upon  the  opposite side of
the body, although  in cases of non-decussation  of the motor  fibres
the  symptoms may  be upon  the same side,  as Brown-Sequard has
 pointed out.   In these cases the patient is afflicted with paralysis of the
 lower part of the  face (see p. 85) and of the upper and lower extrem-
 ities, whilst  the speech  is usually implicated also.   An examination
 of such  a patient will  show that  the naso-labial  fold  upon the
 affected  side  is flattened out, so that the face is drawn to the other
 side, the tongue deviates toward the affected  side, and the arm and
 leg on the same side with the  face are impaired in strength, and in
 certain  cases also in  the  sensations of touch and  pain, more rarely
 in muscular  sense,  least  frequently   in temperature-sense.   The
 tendon and cutaneous reflexes upon this side, notably the knee-jerk,
 are temporarily diminished or abolished,  and this may often be a
 diagnostic sign of great value, especially in the cerebral hemorrhage
 that takes place  with uraemic coma.   Immediately after  an attack
 the  paralyzed limbs  are often warmer and  redder  than  upon  the
 other side, and they may become  swollen from subcutaneous oedema,
 or it may even happen that some of the joints may be subacutely
 inflamed.   Occasionally, though  rarely, the  paralyzed limbs  may 
310
NEB VO US DISEASES.
atrophy.   Iu  the unfavorable  cases  contracture of  the affected
limbs  may gradually  result,  and this  contracture  may  be early or
tardy, coming on  immediately after the attack or  some time after,
In either case this contracture is  a sign of ill omen, but  more espe-
cially so when it follows at an early date.  Even when it comes late,
however, it is seldom  recovered  from.   An acute bedsore may form
in certain fatal cases over  the centre of the gluteal  region on  the
paralyzed side, and is of very evil significance, although  not in my
experience necessarily  fatal.   In  cases of hemorrhage in children the
growth of the whole limb may be arrested.  (See Figs. 149 and 150.)
In the  majority of cases  of cerebral hemorrhage  occurring in this
region  of the internal capsule,  the  symptoms are generally those
that have been  described,  and were detailed  by the older authors
under the name of apoplexy (a name still  retained by the laity),
and which most of the text-books of to-day present under the  title
of hemiplegia—although, really,  hemiplegia can result from hemor-
rhages into so many different parts of the brain that it is  unscientific
to apply the  term to lesion of auy one particular locality.
   When  hemorrhage  occurs  into the convolutions constituting the
motor area (vide p. 139) there is more apt to be paralysis of one
limb (so-called monoplegia), or of the two  limbs,  or of the upper
extremity, with  coincident speech-defect.  As will be seen by Fig.
35, a hemorrhage of the motor  area  sufficient to cause hemiplegia
would  have  to  be spread  over  so large a surface as to make its
occurrence extremely infrequent,  except from trauma.
   Hemorrhage into the occipital  lobe, the lingual or fusiform lobule,
or  the  angular  gyrus, would give rise to symptoms of hemiauopsia
(vide p. 150).
   Hemorrhage  into the  posterior portion of the  first and second
temporal convolutions would cause word-deafness (vide p. 140).
   Hemorrhage into the cerebellum would give rise to symptoms that
are detailed upon p. 149.
   The symptoms, indeed, of hemorrhages  into  the different regious
of the cerebro-spinal  axis  have been  so  fully  considered under
"Localizations," pp. 139 etseq.,  that it  is needless to consider them
again.
   Prognosis.   The prognosis of intracranial hemorrhage  will vary
according to the locality affected and the severity of the symptoms.
When the coma is profound, quickly followed by a rising  tempera-
ture and acute bedsores, the case  will probably have a fatal termina-
tion.  When  contracture supervenes, either early or late, the prognosis
as to recovery from the  paralysis is  bad,  as is also the case when
marked atrophy supervenes in a  few weeks.
   Hemorrhage into the internal capsule is always a serious symptom,
even when there is no rise of temperature or contracture following,
and this is especially so when it occurs in the course of Bright's dis-
ease.   Hemorrhage into  the  cortex is  not  necessarily of  such bad
omen, because of the free anastomosis of the cortical capillaries which
has beeu  described by Heubner and Duret; but even then, when
the hemorrhage  is  into the motor area and is followed  by marked 
      INTBACBANIAL HEMOBBHAGE AND THBOMBOSIS.   311

contractures and atrophies, it is not recovered from.   Of the prog-
nosis of hemorrhage into the cuneus, the occipital convolutions, the
lingual and fusiform lobules, and the angular gyrus (causing hemi-
anopsia), we know very little.  The few cases that have been reported
of hemorrhage into the lemniscus have been fatal, and this is usually
the case with hemorrhage into the pons.   Cerebellar hemorrhage has
not  been accurately studied, because of the difficulties of cerebellar
localization; but of the  cases which have been  studied, most have
resulted fatally.
  Diagnosis.  The diagnosis of cerebral embolism can usually be
made by ascertaining the  causes which can produce cerebral embo-
lism, such as cardiac lesions and pulmonary lesions; but  it may  hap-
pen that an embolus may result from a washed-off thrombus of some
larger intracranial vessel  being carried  to a capillary, and  in such a
case the diagnosis cannot be made.   It  is usually stated in the text-
books that a  diagnosis  between  embolism, thrombosis, and hemor-
rhage can be made  by means  of the  clinical symptoms.   There is
not only  inaccuracy of observation  about this statement, but  also
some confusion of thought.  What the  writers have meant to say is
that the diagnosis can be made in these  three conditions by observing
the onset, which in cases of embolism  will be sudden, and  in cases
of thrombosis and hemorrhage will be more gradual.   But even this
statement is inaccurate.   An embolus, for instance, may  enter a cap-
illary that it  does not  completely plug up at once, so that the onset
of the symptoms may be gradual, or it may fit the capillary so accur-
ately as to plug it up suddenly, in which case the symptoms will be
sudden.  A thrombosis,  on the other hand, may form so  very gradu-
 ally as to produce no symptoms until, by the superimposition upon
 it of layers of fibrin, the final moment  of occlusion of the  vessel has
 been reached, when it may plug up the vessel suddenly and completely,
 and the symptoms would be  sudden also.  A hemorrhage may be
 produced  by a  sudden  or gradual rupture of a  vessel, so that the
 symptoms may be either sudden or gradual.  I have made  a num-
 ber of post-mortems in which I satisfied myself of the impossibility
 of making a  diagnosis between embolism, thrombosis,  and hemor-
 rhage by means of the suddenness or gradualness of the symptoms.  I
 am therefore positive that it is utterly impossible to make a diagnosis
 between the  three conditions  in this way.   Usually, therefore, the
 first thing to be sought for will  be the cardiac or pulmonary lesions
 that might give rise to emboli.  If they are found, and if the onset
 has been sudden, a diagnosis of embolism is probable, although these
 cardiac and pulmonary conditions may  exist without causing emboli.
 If  these cardiac and pulmonary sources of embolism  are absent,
 however, it is utterly impossible to make a diagnosis between embo-
 lism, thrombosis, and hemorrhage, and  all the diagnosis  that we can
 make is between arterial  lesions and other lesions of the brain  that
 might produce similar clinical symptoms.
   The latter conditions are—
       Tumor;
       Fractures; 
312
NEBVOUS DISEASES.
       Thrombosis of the cerebral sinuses;
       Meniere's disease ;
       Cerebral palsies of childhood;
       Intracranial syphilis.
  Intracranial tumors are  very  easily differentiated from  cerebral
hemorrhage, thrombosis, or  embolism, because they do  not  have an
acute onset, are preceded by headache, various  localized paralyses,
changes in the optic disc, and occasionally by mental alterations.
  Fractures of the skull should  never  be confounded with  cerebral
hemorrhage, except in cases that are picked up in the streets without
an  antecedent history.  The hemorrhage of these fractures is much
more apt to be meningeal than into the substance of the cerebrum or
cerebellum.  Usually  the history of trauma, the detection  of frac-
tured bone, the outpouring of bloody serum from the ear in fractures
of the base, etc., are symptoms which will make  the  diagnosis clear.
  Thrombosis of the cerebral sinuses may occur  from  marasmus in
children in the first six months of life after severe  diarrhoea, or in
adults from pysemia, cancer, senile  marasmus, or other  debilitating
causes,  or from diseases  of the cranial bones which may follow
traumata, erysipelas, or furuncle;  but it  is impossible to make the
diagnosis by means of the symptoms alone, although this may some-
times be provisionally done by the conjunction of the symptoms and
the presence of one of these known causes.   Otitis media  or interna
may also be a cause.  The symptoms are varied, and consist of coma,
convulsions, strabismus, contractures, tremors, and paralyses, these
paralyses and  tremors being  either one-sided or bilateral; and these
symptoms  should always be regarded with suspicion when they super-
vene upon diseases of the internal ear.   (See Chap. "Venous  Throm-
bosis.")
  M6ni£re's disease of the   true  type  should never be  confounded
with hemorrhage, although it was frequently in  former  years.  The
loud  noises in the ear, like pistolshots or bells, the partial loss of
consciousness,  the  turning   in  certain directions, and  the absolute
absence of any  paralytic  symptoms  whatsoever, need only to be
studied and  observed  in order to  make the diagnosis (vide Chap.
XV., " Meniere's Disease ").
  The cerebral palsies of childhood are due to many other causes than
cerebral hemorrhage (see Chap. " Cerebral  Palsies of Childhood"),
and it is only  when there is a hemiplegia coming  on after such symp-
toms as we see  in the adult that we  are  warranted in  making  a
diagnosis  of  cerebral hemorrhage.   The  paraplegia,  the  peculiar
contractures, the positions of the limbs, the marked mental symp-
toms, are usually entirely different in their  distribution from what
is seen in the  adult from cerebral hemorrhage.
  Intracranial syphilis  can  in many cases, as I  have demonstrated,
be diagnosed  by means  of the quasi-periodical headache with obsti-
nate insomnia, which ceases upon the  supervention of paralytic or
convulsive symptoms ; and when  the headache and insomnia are fol-
lowed by hemiplegia in an  individual  under forty years of age the
diagnosis  may be  made with positiveness  of intracranial  syphilis. 
      INTRACRANIAL HEMORRHAGE AND THROMBOSIS.    313

In any case of hemiplegia, however, occurring under forty years of
age, syphilis should be  suspected, even though there  has  not been a
history of headache  and insomnia.   In some cases  of intracranial
syphilis, too, the hemiplegia  has  been  preceded  by mental dulness
for  weeks  beforehand  to an extent which is never seen in ordinary
cerebral hemorrhage such as we are  describing.  The  forms of intra-
cranial syphilis which are due to a gummatous meningitis at the base
of the brain are attended by lesions of the cranial nerves, as well as
by paralytic symptoms of the extremities.
  Treatment.   In all cases of cerebral hemorrhage the  patient
should be kept quietly in bed until all symptoms of reflex disturbance
of the cerebrum or cerebellum  have disappeared.  The diet during
this period should be  simple and moderate  in quantity, consisting
mainly of eggs, soups, fish, and milk.  The  patient  should not  be
allowed to rise from a prone position.   If there  is any tendency to
convulsions, moderate doses of the bromide of potash should be ad-
ministered, 10 grains once, twice, or even three times a day.   I have
seen excellent  results from venesection, and I believe that this old
remedy has been allowed to pass into too great disuse,  mainly  in
deference to the prejudice of the laity.  I should have no hesitation
whatever  in taking  ten or  twenty ounces of blood  from a  patient
evidently  full-blooded,  and  who  could therefore bear its loss  well,
because the immediate results are, as  I have said, sometimes  start-
lingly beneficial.  In such a case,  if venesection cannot be performed,
brisk purgation with  saline cathartics, or with croton oil, one drop
given once or twice, will often  be found of advantage, although
neither of these drugs will equal the bloodletting in suitable cases.
As the patient begins to recover from the  reflex  disturbances  small
doses of the bichloride of mercury, -fa grain three times a day, have
seemed to me to be often of considerable value, although, of course, it
is a difficult matter to speak positively about  the effect of this medic-
ament, as the  improvement may have  been  due to natural causes.
In  the same spirit I would commend  the  use of moderate doses  of
iodide of potash, 10 grains three times a day, although I do not  think
that it is as efficacious as the mercury.   Of late years trephining has
been recommended  in cases  of intracranial hemorrhage.   I cannot
say that  I view this  procedure with  any great favor, and this  for
several reasons.   In the first place,  as I  have already stated, it is
often extremely difficult to make  the diagnosis between hemorrhage,
embolism, and thrombosis.  In the second place, the hemorrhage is
most likely to occur into the internal capsule, and it is very difficult
to reach this portion of the brain with  accuracy so as to  hit exactly
the site of the hemorrhage; and even  if this be done,  it is very ques-
tionable whether the puncture with the needle would not inflict more
damage upon the delicate interwoven strands of this locality than the
hemorrhage itself would do.  Should the hemorrhage, however,  be
subcortical in the centrum  ovale between the cortex and the  basal
ganglia, it would  be almost impossible to localize it, and the wild
groping with  the needle, such as we have so much difficulty with  in
cases of cerebral tumor,  would be certain to inflict more damage than 
314
NERVOUS DISEASES.
the hemorrhage  itself.  If, however, the  hemorrhage can be posi-
tively diagnosed in the cortex, I can  see no objection to this method
of relief.   When  the individual  is able to leave his prone position
the paralysis of muscle, if the lesion in the brain has been such as to
cause this, may undoubtedly be favorably  affected by the use of the
faradic current, brushing the electrodes up and down the limbs, pass-
ing a gentle current through the different muscular groups, and doing
this two or three times a week for a period of several months.  This
simple application of electricity cau be done quite as well at the house
by some member of the family with a small faradic battery. General
tonic medication will oftentimes be of use, too—a fact which is often
overlooked.  The best of these is  some of the quinine preparations,
preferably the elixir of calisaya bark. 
CHAPTEE  VII.
               DISEASES OF THE CEREBRUM.

            CEREBRAL PALSIES OF CHILDHOOD.

  Definition.  These palsies consist of hemiplegia, double hemi-
plegia (diplegia), or paraplegia, with mental defect, spastic symptoms,
and atrophy that is generally slight and without marked alterations
in electrical reaction.
  History.   The first  authors  who portrayed what  is nowadays
known as porencephaly  were Braschet,  in  1831;  Lallemand, in
1834; Rokitausky, in 1835; and Cruveilhier, in 1849; although
some of the cerebral lesions of the infant had been described by Reil,
in 1812; Cazauvielh, in 1827 ; and Billard, in  1828.   But the first
accurate description  of paralysis  of cerebral origin in  children was
that of Henoch, in 1842, which was supplemented by Little, in 1853;
Turner, in 1856;  and Von Heine, in 1860.   Heschl formulated the
term " porencephaly," in  1859, to  designate  the losses of cerebral
substance.  From that time to the present day the literature of the
subject has been very abundant, and  the most prominent among the
contributors  have been  Leidesdorf and  Strieker,  in 1865, on the
production of encephalitis in chickens, Tigges concerning encephalitis
in rabbits, Virchow, in 1865, on  congenital encephalitis of a peculiar
nature; Cotard, in his these de Paris, in 1868 ; Kundrat, in his great
book  on Porencephaly,  in 1882; Parrot, in  1883,  on Steatosis;
Striimpell,  in 1844, upon what  he calls Polioencephalitis,  and,
amongst  the  latest  authors, Gaudard, Jendrassik and Marie, Mc-
Nutt, Wallenberg, Knapp, Audry, Gibney,  Gowers,  Osier, Sachs,
and Peterson.
  Etiology.  The causation is by no means certain.  Many attend-
ant or preceding diseases, many circumstances of immediate environ-
ment, and many hereditary  peculiarities, are  ranked  in the time-
honored way among the  causes, without scientific warrant, however,
although each  and all may be factors in  certain  cases, bearing the
same relation  to this class of  lesions that they do to so many other
diseases.   In  this way great stress has been laid upon  marriages of
consanguinity; syphilis and intemperance in  the parents; difficult
delivery; asphyxia of the newborn;  cerebral traumata; infectious
diseases, such as pertussis, typhus, and variola;  abnormal conditions
of the mother during pregnancy; violent vomiting and defective
nutrition.  All these cases are either congenital, having occurred dur-
ing foetal life, or have their onset  in the first three years of life.   The
paraplegiae are generally congenital,  whilst the double hemiplegise
(diplegise) usually occur during the first three years of life. 
316
NERVOUS DISEASES.
   Clinical Symptoms.   In all diseases of the intracranial contents,
whether occurring in the child or in the adult, as has been elsewhere
said,  distinction  must  be  made between  the symptoms which are
reflex and those that are direct or localizing.   For example, a lesion
of sudden onset, such as a hemorrhage, a thrombosis, or an embolism,
may impinge upon the leg-centre of the cortex, primarily causing un-
consciousness or  a convulsion, fever, etc., which symptoms pass off,
and there is detected a paralysis in the leg that has been overlooked
or obscure.   The reflex symptoms  are due  to shock of the whole
cerebral substance from a sudden molecular change, whilst the direct
or localizing ones are caused  by actual destruction of a certain area
of the brain-tissue.   These  considerations, too, apply especially to
the cerebral affections of children, who are more liable to reflex dis-
turbance than adults.
   The reflex symptoms are convulsions, fever, delirium, hebetude or
coma, and emesis.                                               .
   The convulsions are  not pathognomonic.   They may be general,*
or they may implicate one  member, the limbs  on one side, or certain
muscles alone.   They may be tonic  or  clonic.  It has been a grow-
ing doctrine of late  years  that cortical lesions in  the adult are at-
tended by convulsions, while subcortical ones are not so accompanied;
but however true this  rule may be in  adults, it is certainly not so
of children, in whom unconsciousness is  not  infrequently observed
in poliomyelitis or even from reflex causes.  The fever seldom goes
above 101°  or 102°  F., and often  there is no fever at all, although
it must be remembered that in this particular we  must usually rely
upon the statements  of  parents or relatives.   There is generally no
delirium, and when there is, it is slight and  temporary.  Hebetude
is present, as a rule,  and coma is sometimes observed, although both
of these conditions, like fever, may be entirely absent.
   Emesis seldom occurs, although the child may not take food more
because of the hebetude or coma or  the general malaise than from,
nausea.
   The localizing  symptoms will depend upon  the  area of the brain
implicated.
   So far as they have been determined, however, the localizing symp-
toms are paralyses,  muscular wasting,  exaggerated tendon-reflexes,:
contractures, mutism, mental impairment, and speech-defects; al-
though most of the cases have a preponderance of motor symptoms.
   A classification of these  paralyses  by the motor symptoms is as
follows :
       Hemiplegia;
       Bilateral hemiplegia or diplegia ;
       Paraplegia.
  Hemiplegia generally occurs during the first three  years of life.
In such cases the face  is  not always  affected, and when it is, the
upper portion (the eyelids and brow) is not involved.   Figs. 149 and
150 represent a hemiplegia which had its  onset in a boy five years
before the photograph was  taken.  His face is keen and intelligent,
and the only mental defect in his case was that he was good-naturedly 
                 DISEASES  OF THE CEREBRUM               317

uncontrollable and difficult to teach for about two years after the onset;
but since this period he has been as intelligent as the other children of
the same  family—an excellent test, by-the-by, of a child's  mental
stature.

        Fig. 149.                                 Fig. 150.
     (FRONT VIEW.)                                (REAR VIEW.)
Hemiplegic boy of eight, showing difference between right (affected) and left (unaffected)
                       sides five years after onset.

  The name of birth-palsies  has been suggested by Gowers for con-
genital  bilateral hemiplegia  or  diplegia which results from prenatal
causes or accidents occurring through excessive pressure of the brain
m parturition.  Fig. 151 represents such a case, with marked mental
defect, which is very evident in the child's vacant expression.
 
318
NERVOUS DISEASES.
  Paraplegia is usually a disease of early infantile life or is referable
to abnormal conditions of the  mother during pregnancy.  Contrac-
ture of the paralyzed  muscles is  usually present in all these three
forms, few  exceptions  to this rule  being observed.   When limbs
thus affected are subjected to movement, they oppose a soft, wax-like
resistance, slowly yielding, and returning gradually to  their former
position  when the  compelling-force  is removed.  Often there is a
bar-like rigidity of the lower extremities, which is well represented
in Fig.  151.   This can  be easily evoked  by handling the limb,
Fig. 151.
                Congenital diplegia, with marked mental defect.

dangling it to and fro for a few seconds, or  tapping steadily on the
quadriceps tendon.   The extensor muscles are generally less affected
than the flexor.  In many cases the small joints are particularly
pliable, so that the  fingers can be  moved in any direction, either
extended, flexed, or abducted and adducted with extreme facility.  A
lock-like movement will be observed when a  limb is suddenly and
quickly flexed.  (Vide page  169.)  Various muscular deformities
result from these contractures.  As a general thing, the tendon-re-
flexes are exaggerated in the limbs affected, but not to any great ex-
tent.   Varying degrees of mental impairment take  place, ranging
from a slight feebleness of intellect to idiocy of the most pronounced
type.   (Figs.  151  and 152.)
  The wasting of muscles is not so marked as in poliomyelitis anterior,
being more in the form of  arrested development.    One little patient 
DISEASES OF THE CEREBRUM.
319
under my care shows each year a greater difference in the size of the
arms, the affected one being relatively smaller, owing to the fact that
no development takes place in  it,  while  the  other is constantly
growing.  Speech-defects and  mutism are  of  common occurrence.
No marked degree of disturbance of sensation is  usually noted, but
it  must be borne in miud  that in infants and young children it is
impossible accurately to test the sensations.   Defective vasomotor
circulation and lower temperature of the affected limb are of frequent
occurrence.  The electrical reactions are normal, except that there is
a slight quantitative increase to faradism, and also  to galvanism in
some instances.  Weir Mitchell has described in the hemiplegic form,
according to Osier, one case in which post-hemiplegic tremor affected
the entire arm,  twenty-four cases  of hemiplegic chorea  (or hemi-
FiG. 152.
                Face with cerebral palsy of congenital origin.

ataxia), athetosis and mobile spasm  in  six cases.  So-called spastic
chorea and double athetosis have been described in the bilateral hemi-
plegias.  Epilepsy often occurs  in these uufortunate  cases, as, out of
one hundred and forty cases reported by  Sachs, the percentage was
44-^.   There were  forty-one cases  of general epilepsy among  the
hemiplegias, one case of  petit mal, aud nine of the Jacksonian type,
about 50 per cent, in all.   In twenty-four cases of diplegia, one had
Jacksonian epilepsy, and seven  (29  per cent.) had general epilepsy.
Four cases of general epilepsy (about 36 per cent.) occurred in eleven
cases of paraplegia.  The percentage in these cases differs very little
from that given by Wallenberg, Gandard, and Osier.
  Diagnosis.   The diagnosis should be  made from the following
diseases :
      Traumatic meningitis;
      Cerebro-spinal meningitis, of epidemic  or sporadic origin ;
      Suppurative  meningitis;
      Tubercular meningitis;
      Transverse myelitis;
      Myelitis of the anterior cornua;
      Intracranial tumors; 
320
NERVOUS DISEASES.
        Hydrocephalus;
        Reflex hebetude, coma, or delirium.
   A careful history should  always  be sought for in all such cases
 from some intelligent person—the mother generally the best, as hav-
 ing  been constantly with the child  from the onset, unless the disease
 has been recognized by some intelligent physician early  in its course.
 The diagnosis is usually made very difficult by the lack of this precise
 history.
   A diagnosis of traumatic  meningitis can only be  made when the
 trauma is positively known.
   In cerebro-spinal  meningitis  of epidemic or  sporadic origin the
 disease is recognized by the characteristic  retraction of the head, by
 the fact that the disease is known to be prevalent at the time, by the
 ages of those attacked being mostly between one and fifteen, by the
 fact that the paralysis is usually one-sided and  rarely paraplegia or
 double hemiplegia, by less tendency to permanent mental impairment,
 and by marked  tendency to hebetude and coma.
   Suppurations in  the nasal cavities, orbit, ear,  or lung,  or some
 septic condition, mark the presence of suppurative meningitis.  Also,
 a  fluctuating temperature, rigors, or chills are apt to  prevail, and
 there is a peculiar remission in the symptoms.
   The chronicity of the cerebral symptoms and the infrequency of
 an acute onset  will  aid in  the  diagnosis of tubercular meningitis,
 coupled with a  history of tuberculosis in  either the patient or the
 family.
   Children are rarely subject to transverse myelitis, but when it does
 occur it causes  paraplegia,  perhaps bedsore, as well as rectal and
 vesical  paralysis.   There is no  mental impairment,  and usually no
 affection of the upper extremities.
   Myelitis of the anterior  horns, as is indicated by the name, is an
 affection of the anterior cornua of the  spinal cord, causing a sudden
 loss of the  ganglion-cells, characterized  by absence of  knee-jerk,
 flaccid paralysis, atrophy of certain muscular groups, usually in one
 limb, and altered electrical reactions.   It is very seldom hemiplegic
 in the  child, and never doubly  hemiplegic, but necessarily mouo-
 plegic in its distribution.  There  may be a doubt as to the diagnosis
 for a few days  in cases that are marked  by convulsions, hebetude,
 coma, and fever, but the question may be settled  by the ultimate dis-
 tribution of the  paralysis.
   Intracranial tumor  is extremely difficult to  differentiate from
 cerebral palsy.   But  in the  former  the  tendency is  to a greater
 localization of the symptoms, to chronicity, to a greater frequency of
 purposeless reflex so-called cerebral vomiting, and  to neuro-retinitis.
   Hydrocephalus is almost positively diagnosed by the  peculiarly
 shaped head, and is often associated with tubercular meningitis.
   Hebetude  or  coma,  seemingly of a most alarming nature, may
 prevail for  a few days in  children, but will soon disappear, being
 apparently caused by a reflex indigestion or  vasomotor condition.
 In the acute  febrile affections grave conditions of hebetude, coma, or
delirium may often occur, and it is a matter of great  nicety to deter- 
DISEASES OF THE CEREBRUM.
321
mine what proportion is due to implication of the cerebrum and  its
membranes, and how much is reflex from the primary disease.
  Pathology.—Of the numerous  diseases of the infantile brain,
those are well known that are due to a suppurative meningitis occur-
ring from a distinct cause—cerebro-spinal meningitis of the sporadic
or epidemic type and cerebral meningitis of traumatic origin.  Out-
side of these, however, the many pathological conditions affecting the
foetal and infantile brain are involved in great obscurity.   It is not
strange that this should be so.   Almost all these lesions are chronic ;
autopsies are not had until a considerable time after the onset, so
that the  terminal conditions—the post-funereal ones, so to speak—
are the only ones that can be studied, and a bewildering diversity of
opinion necessarily obtains as to the exact nature and origin of the
causative processes.   Nor  has  the clinical expression of these intra-
cranial processes thrown  much light upon the subject.  It  must  be
remembered that the brain  is a  highly complex structure.  In  the
child only gross impairment of motion,  sight,  and  hearing can be
observed, and  even  these  only after a certain age.  The ordinary
forms of sensation, the group of  symptoms included under the com-
mon name of aphasia, the so-called word-deafness, the fine muscular
movements, the more delicate impairments of sight, such as hemian-
opsia, etc., the subjective  sensations  of vertigo,  and the peculiar
noises that are often of so much diagnostic importance  in certain
impairments of hearing—all these are finer functions that cannot be
tested in the child until  it has  attained nearly7 the intelligence of
youth, and they are  entirely beyond  our recognition in  the infant.
Moreover, these old lesions that have  begun in  infancy or foetal  life
do not cause the same localized  impairment of function that they do
in  the adult brain.   Hydrocephalus, hemorrhage,  embolism, and
thrombosis are described  in their respective chapters.  Aside from
these, the following lesions have been observed  in the braius of
foetuses and infants  who had presented during life the clinical symp-
toms of the cerebral palsies :
       Encephalitis and meningo-encephalitis ;
       The so-called polio-encephalitis ;
       The congenital encephalitis of Virchow ;
       Porencephaly :
       Apoplexy of the newborn ;
       Thrombosis of the cerebral veins ;
       Atrophy and sclerosis.
   Encephalitis and meningo-encephalitis generally  begin  in the pia
aud cortex,  and  proceed  with  cellular infiltration  and  sclerosis,
 minute hemorrhages, eventually  atrophy,  or,  more rarely, hyper-
trophy of the  affected convolutions.   The  large  basal ganglia and
even  the spinal cord may be implicated simultaneously in this pro-
cess, but this is to be distinguished from  the secondary descending
 degeneration which may  result  from a lesion  in  the cortex.   The
 onset of  these processes has not  been  studied microscopically.   The
 thick connective-tissue masses  may vary in size  from that of the
 cortical surface  of the whole hemisphere to a mere cicatricial streak.
                                21 
322
NERVOUS DISEASES.
In these sclerotic masses scanty remains of nerve-elements are found.
The connective tissue may consist of a  network, in the meshes of
which are seen scanty openings for  the vessels and  granulated  cells
and nucleoli, or  it  may  be  very dense,  and the openings for the
bloodvessels large  and numerous.  Because of the seeming relation-
ship between the density of  the connective  tissue and  the size of
the vascular openings, because Hayem has found the walls of the
bloodvessels thickened, especially the adventitia, and because Marie
has  found  these  vascular walls  iu  a condition  of  inflammatory
infiltration, with embryonic  nuclei, it has been  suggested that the
vascular lesions were the initiative process ; but  there is nothing to
show whether  or  not they are the cause,  effect, or part of a general
underlying condition.  In the hypertrophic  form  of sclerosis  the
cerebral substance is not infrequently dotted  with  ten or twelve
masses, varying  in size from that  of  a beau to  that of a ten-cent
piece, round or streak-like, or of the consistence of India-rubber,
principally in the  cortex  or in the  central ganglia.  From these
masses  the pia tears easily, but is adherent to the surrounding tissues,
which are  of a reddish color from a markedly  vascular injection.
These masses consist of thick connective tissue, with spindle-cells,
and pass into the  normal tissue without  sharp demarcation.   A
few atrophied ganglion-cells  are found, filled  with  pigment  and
granules.
   In 1884 Striimpell advanced the theory that there was in children
an acute infectious encephalitis of the motor convolutions, analogous
to the acute myelitis of the anterior cornua of the spinal  cord.  This
seems to me to have been one of the most flippant pathological  sug-
gestions ever made in medicine, advanced without the slightest proof
on the  part of its author; and as yet only  one  writer, Ranke, has
adopted this view, and only one clinical observation, probably merely
coincidental, not elucidated by an autopsy, has been cited in support
of it.   The avidity with which the suggestion has  been seized for
discussion and observation, and the large  literature which has grown
up in refutation of it, are pitiable illustrations of the paucity of our
exact knowledge of the pathology of the foetal and the  infantile
brain.  Cotard and Gandard cite seven  cases with the symptoms of
Striimpell's so-called polio-encephalitis,  in  which  the  cortex was
found to be normal, and in which the lesions were as follows:  cyst
in the corpus striatum, cyst iu the  frontal lobe  beneath the cortex,
sclerosis beneath  one lateral  ventricle, clot in  the  internal  capsule,
embolic softening of the  corpus striatum and  surrounding tissue,
hemorrhage into the thalamus opticus  and corpus striatum.   Besides
this, Hoven records a cyst of the  internal capsule, aud in this case
an especially careful examination was  made of the cortex, which was
found to be perfectly normal.   Wallenberg also reports a cyst beneath
the anterior corpora quadrigemina, implicating the crus  cerebri and
the lemniscus, and destroying completely one red  nucleus.  The title
polio-encephalitis is the more unfortunate, as the same name has been
 very properly given by Wernicke to a thoroughly authenticated dis-
ease of the motor nuclei of the medulla oblongata (seep.  296),which 
DISEASES OF THE CEREBRUM.
323
are the true medullary analogues of the anterior cornua of the spinal
cord.
  In  1865 Virchow  described what  he termed congenital encepha-
litis, consisting of little yellowish masses in the white cerebral sub-
stance, and referable,  he  thought, to  interstitial inflammation  of the
cerebral substance, the color coming from fatty granules.   Although
it has been maintained by Jastrowitz that fatty granules  are physio-
logical in  foetal brains, there yet seems reason  to believe that Vir-
chow's description applies to certain infrequent cases.
  Heschl, in 1859, gave the name  of porencephal (jzopo^,11 &  hole;"
and b(x£i}'olov, the brain) to certain exceedingly curious losses of cere-
bral substance in fcetal  and infantile  brains, varying in size from
small cavities to  an entire absence of both hemispheres.   These cavi-
ties are generally full of liquid, and are traversed by filaments forming
light and incomplete partitions.  Substances resembling adipocere are
sometimes found floating in them, or other substances of transparent,
citrou, yellowish, or brown color.   These cavities may open into the
arachnoid cavity, although they generally have a vascular membran-
ous cover, the external face of  which may be colored orange, yellow-
ish, or brownish.  Ordinarily the pia is absent.   Kuudrat maintains
that the convolutions  bordering upon these cavities have a radiating
form in the cases of pre-natal origin.  The adjacent convolutions may
be carpeted with a fine cerebral debris, or may undergo a gelatinous
transformation.  Sclerosis  of the tissues bordering the cavity is very
frequent, and  these walls  often have  a rusty  color, probably from
hemorrhage.   Near the lesion diminution or obstruction to an artery
may be found.   Instead  of the cavities, however, there may be abso-
lute loss of one hemisphere or  both.  The bones may be thinned or
thickened, the skull may be hydrocephalic or microcephalic in shape,
 occasionally the  front is very much flattened and slopes  backward.
 Porencephaly is  generally fcetal in origin, after  this being most fre-
 quent in first infancy, occurring exceptionally afterward.  In fifty-
 seven cases analyzed  by  Audry, thirty-four were probably of fcetal
 origin, thirteen in the first two years of life, nine in the  second in-
 fancy—viz., three in the third year, one at three and one-third years,
 one at seven, one at nine and a half, one at eleven, one at fourteen—
 and one in an adult.   These singular losses of cerebral substance have
 been attributed to an  arrest of  development, extreme hydrocephalus,
 embolism or hemorrhage, encephalitis, and a profound cerebral anaemia.
 Kundrat endeavored  to trace a constant relationship between  vascu-
 lar lesions and the porencephalic  areas, but indubitable  cases have
 been reported demonstrating that this view was not tenable.   A pecu-
 liar gelatinous and  cellular infiltration  seems, in  certain cases, to be
 one of the early stages of the process.  The predisposing and excit-
 ing causes  are but little known, though  traumatism would seem to
 have  been a distinct etiological  factor in several instances.
   The apoplexy of the newborn is regarded by Osier as one of the
 chief causes of the bilateral hemiplegia  or  paraplegia occurring at
 birth, and there can be no doubt that it is a very frequent condition 
324                   XER T Vj US DISEASES.
in newborn children—especially, as Sarah J. McNutt has shown, iu
conjunction with abnormal labor, asphyxia, and convulsions.
   Thrombosis of the cerebral veins  is regarded as a frequent factor
by Gowers.
   It will thus be seen that the pathological behavior of the fcetal and
infantile brain is different from that of the adult one.   Iu the former
we encounter much more frequently meningeal hemorrhages and acute
forms of encephalitis and  meningo-encephalitis, whilst the rapid losses
of cerebral substance of porencephaly are practically unknown at later
periods of life.   Nor should  we find  it surprising  that there is such
easily effected  retrogressive metamorphosis of the  cerebral substauce
in the  infant,  when we consider that  the intracranial contents are the
last portions of  the nervous substance to develop, that they are very
imperfectly developed during fcetal and infantile life, and that their
great relative bulk, badly protected by the imperfectly ossified cranium,
renders them  extremely liable to injury from without iu the  helpless
foetus and in the almost equally helpless infant.  It is a singular fact,
however, that most of  the lesions are in the motor  tract that extends
from the motor convolutions to the muscles.  The course of this motor
tract (pp.  80 et seq.) is through the corona radiata to the internal cap-
sule, thence through the pons to the region of the decussation, where
it divides  into two columns, the  one going down upon the same side
into  the anterior pyramidal columns (columns of Tiirck), the other
crossing to the opposite side to pass down through the lateral pyram-
idal column, thence into the anterior cornua, making direct connection
with the great ganglion-cells,  from which  arise the motor nerves that
emerge along  the anterior roots to  terminate in the motor end-plates
of the muscle.  Although different convolutions are not infrequently
the site of lesion, even as far back as the occipital lobe, the motor
convolutions are pre-eminently affected.   But lesions have also been
found  in the  intracranial portions of this motor tract without affec-
tion  of the convolutions;  thus, as has been already stated, one  of
Gandard's cases had a clot in the internal capsule, with softening and
ecchymosis of the Sylvian fossa ; another had a focus  of softening in
the region  of  the internal capsule; and another a softening of the
corpus striatum  and the surrounding region.   One of Wallenberg's
ca<es had  a hemorrhage in the right optic thalamus and corpus stria-
tum ; and another a cyst  beneath the anterior corpora quadrigemina,
implicating the  pes and  lemniscus and destroying fibres from the
third pair  and red nucleus; whilst Hoven's case had a cyst in the
nucleus caudatus.  These lesions act  more disastrously upon the foetal
and infantile brain  than upon that of the adult, for the evolution of
the former is  seriously  hampered.  The condition  of the spinal and
peripheral  portions  of the motor  tract has yet to be  studied thor-
oughly, although in some cases of spastic paraplegia there is reason
to believe that there is  either  a  descending degeneration  or a lack of
development  of the intraspinal  motor strands.   There cau be  no
question that the motor tract is peculiarly liable to disease in children,
and that the cerebral palsies are the earliest, in point of time, of the
great series of  lesions to which  it is liable  at this period of life 
DISEASES OF THE CEREBRUM.
325
Dividing the motor tract into three portions, the intracranial, the
spinal, and the peripheral, we may classify its lesions in this manner :
cerebral, the cerebral palsies; spinal, myelitis of the anterior cornua
(poliomyelitis anterior);  peripheral, pseudo-hypertrophic paralysis ;
whilst  progressive  muscular  atrophy is sometimes  of  spinal and
sometimes of peripheral origin.  The spinal and peripheral portions
of the motor tract, however, are much  more prone to chronic disease
in children, almost the only exception being the acute onset  of most
cases of poliomyelitis anterior, whilst the intracranial portions of the
motor tract are very liable to acute disease, the chronic lesions being
rare.  The cellular  processes of the spinal lesions have been admir-
ably studied, so that one of the most  certain facts in pathology to-
day  is the disappearance or  injury of  the  ganglion-cells of  the
anterior horn in poliomyelitis and  in the spinal forms of progressive
muscular atrophy.   It is not as yet  quite certain whether the muscular
wasting of the peripheral forms of  progressive muscular atrophy and
the commingled wasting and hypertrophy of the pseudo-hypertrophies
are due primarily to the affection of the  muscle-cells, or are second-
ary to changes in  the anterior cornua  that have not  thus  far  been
detected by the means of microscopical preparation at present in use,
although the evidence is as yet entirely in favor of the former view.
But we are sadly in lack of knowledge as to the exact pathological
nature of the lesions in the intracranial portion  of the motor tract.
Porencephaly, as we have seen, would  seem to be a cellular process
independent of preceding arterial impairment, inasmuch as Kundrat's
opinion, that  the  porencephalic loss of substance is  always in an
arterial range, has been disproved.   The fcetal and the infantile brain
must be subject, therefore, to sudden cellular disintegrations, such as
we see in the anterior horn of the spinal cord in poliomyelitis ante-
rior, although on a  much larger scale, and such as are not seen in the
adult brain except in the rare cases of idiopathic softening that have
beeu described by Wernicke.  Arterial and capillary hemorrhage and
arterial and venous  thrombosis are  also important factors, as we have
seen, but we do not know  what relationship they bear to the atro-
phies, the sclerosis,  porencephaly, or the cerebral porosity of Golgi.
   Prognosis.  The extent of the cerebral lesion, as  manifested in
the contractures,  the paralyses of  motion, the mental  changes, and
the exaggerated tendon-reflexes, will indicate the prognosis.   A care-
ful examination should therefore  be made in each case to determine
the amount of damage done, which  will  be ascertained by these symp-
toms.  Tests of the motor and sensory power of the paralyzed limbs
should be made.   Examinations of the eye and  ear are important.
The tendon-reflexes should be tested and the amount of contracture
ascertained.  Mental tests should  be applied, and the impairment of
cerebral substance resulting from disease should not  be confounded
with the intellectual dulness occasioned  by lack of  mental training
and the  petting  and spoiling usual in  the case of a  paralytic and
helpless child.
   Treatment.   Very little can  be accomplished by treatment in
such cases.   The faradic current is undoubtedly  the most efficacious 
326
NERVOUS DISEASES.
 agent in  the  cases of hemiplegia, especially those taken in the early
 stage, its use sometimes  proving very beneficial indeed.   The case
 represented in Figs. 149 and 150, for instauce, has made an excellent
 recovery, as has been said.   In paraplegia, however,  it has proved
 quite useless iu my hands, and in bilateral hemiplegia it has not been
 of marked benefit.  Osier speaks of massage, with vigorous flexion aud
 extension of the limbs, as having been of great service, but I have not
 found it of  any special use except in the before-mentioned cases of
 recent hemiplegia.  The knife aud apparatus of the orthopaedic sur-
 geon are usually the only relief for the spastic  defects.  In proper
 cases, careful  and special education may greatly  help the mental
 defects.   Surgical operation upon  the  brain is preposterous, both
 on account of its probable  hopelessness in  case the lesion can be
 localized, as well  as on account  of the  extreme difficulty of such
 localization.
                  INTRACRANIAL GROWTHS.

   Etiology.   The causes are—
       Sex  ;
       Age;  _
       Heredity;
       Trauma;
       Nervous strain.
   Males are very much more  subject to intracranial growths  than
 females, in a proportion of about two-thirds of the former.  Most
 of the cases occur between the twentieth and  fortieth year, and more
 frequently after this period than before it.   In children cases are
 rather more rare under eight than after.
   Age seems to  have somewhat of an influence upon  the variety of
 growth; thus children are more prone to tubercle, ynung adults to
 glioma, and sarcoma and cancer occur after maturity.  Gumma is pre-
 eminently a malady of adults.
   Heredity does not play much of a part except in some cases of cancer.
   Trauma is au occasional cause.
   I  have seen  a  number of cases  of cerebral tumor develop after
 great nervous strain, such as  business cares and domestic anxiety,
 and  bearing such  a relationship to these circumstances as to warrant
 me in considering them as true causes.
   Clinical  Symptoms.  In  every case of  an  intracranial growth
there are  two sets of symptoms, namely, the general and the local-
izing.  The former are due to the disturbance of the cerebrum or
cerebellum as  a  whole, whilst the latter are from local  implication
of some portion of the cerebrum or  cerebellum.
   The general symptoms consist of—
       Headache;
       Vertigo;
       Vomiting ;
       Optic neuritis;
       Convulsions ;
       Mental disturbance. 
DISEASES OF THE CEREBRUM.
327
  Headache is one  of the  most constant symptoms.  It may vary
enormously in character, however.   The older writers were prone to
dwell upon the severity of the headache of intracranial growth, but
this has not been borne out by experience.  In one case of ray own,
for  instance, where  a round-cell sarcoma of the size of a hen's egg
involved  the centrum  ovale, and in which the time from the onset
of the  first symptoms  to death did  not extend over two months, the
headache was very slight, non-localized, aud vague ; iu another case of
a still larger tumor  involving the temporo-sphenoidal lobe, in which
the duration was some five months, the headache  was a dull ache, with
sharp  exacerbations of a  few hours' duration,  over one brow; in
another case of  small  cystic sarcoma  of the size of a hickory-nut,
just beneath the  white matter of the left ascending parietal convolu-
tion, the  duration  of the  symptoms being about three weeks, the
headache  was slight until  the  last  week, when  it merged so rapidly
into coma that its characteristics could  not be determined ;  and so I
might  multiply instances of the variability of this symptom.   On the
other hand, I have  known of excruciating pain ; but the rule is that
the headache is not  violent except in the cases of intracranial  syph-
ilitic growths, which, however, as we shall have occasion to see, are
 usually conjoined with a gummatous meuingitis.  In children intra-
 cranial growths  are very1 frequently accompanied by no headache at
 all.  I do not, therefore, thiuk that the violence of  the  headache is
 of any diagnostic  value  iu  intracranial growths,  although I do
 believe that  in  adults some form  of  headache, however slight and
 variable, can constantly be ascertained  by searching inquiry.  Nor
 does the location of the headache usually bear any relation to the site
 of the growth, as  I have  demonstrated over and over again to my
 own satisfaction.  Indeed, with a history7 of fifty cases before  me,  I
 have never yet  found the pain a localizing symptom, except that in
 twelve it  was upon the same side as the lesion, but bore no exact
 relationship to it.  Of course, if the trigeminal nerve at the base is
 affected, there may  be pain limited to the area of distribution of this
 trunk ; but this is  a localizing symptom and not a general  one—in
 other words, it is due to local implication, and not to disturbance of
 the cerebrum as a  whole.   Nor have  I found that localized tender-
 ness is of any more value diagnostically.
   Vertigo as a general symptom—i. e., due to the disturbance of the
 cerebrum as a whole—is generally slight aud  vague, no more than is
 seen in many other diseases of the brain, and indeed it is not nearly
 so apt to  be so severe as in most  cases of lithaemia.   A distinction
 must  be  made here, however, between vertigo as a general symptom
 and vertigo as a localizing symptom, because when it affects the cere-
 bellum, for instance, or the peduncles  of this organ, it may become
 very pronounced in a characteristic  way, which has been spoken of on
 page 149. I should therefore lay down as au  axiom  that pronounced
 vertigo without  the special  characteristics of cerebellar vertigo is not
 due to an intracranial growth, but  is much more likely to be  due to
 lithsemia, some  lesion of the aural apparatus,  perhaps  of the tem-
 poral  lobe, or some ocular strain. 
328
NERVOUS DISEASES.
   In 568 cases tabulated by Jacobi vomiting was noted in only 172;
in 40 cases collected by Knapp it was  observed in only 17; but in
50 cases of my own it was  observed 45 times, and  I believe that,
as in headache, a  history of vomiting or nausea  will be found in
almost  every case.   Like headache, however, nausea  and vomiting
may be excessively variable,  so  that on the one hand it may  be so
persistent  as seriously to endanger life, whilst on the other hand it
may be so  slight as to consist  of nothing more than occasional qualm-
ishness.
   There has been an attempt  made to create a distinction between
optic neuritis and so-called choked disk ; but this does not appear to
be warranted, as in both cases  there is a true neuritis of the optic-
nerve fibres of the  ordinary nature of degeneration.   Great stress is
laid  upon this symptom  by almost all writers, and,  in my opinion,
too much.   According  to the careful examination of cases made by
Knapp, optic neuritis was present in  over two-thirds of the  cases
examined.   Gowers estimates the percentage as four-fifths of all the
cases; Bernhardt found either atrophy or neuritis in 25 per  cent.,
amblyopia in 20.4  per cent, and normal vision  or  normal fundus in
6.8 per cent., 47.8  per cent, of the cases giving no data; Oppenheim
determined the presence of  neuritis on one or both  sides in 82 per
cent, of his 23 cases;   while Annuskee and  Reich  found neuritis
absent in only 5 per cent, of 88 cases.   I cannot agree with this esti-
mate  of the frequency  of optic neuritis, at least  for  practical pur-
poses, for in 20 of my 50 cases there was no neuritis found.  It is true
that in only 30 of these cases of my own were repeated examinations
made of the  retina throughout  the course  of  the  disease, and it is
therefore  possible  that  in the  other patients such a neuritis might
have been  found ;  but for practical purposes my estimate is more apt
to be the correct one, I  believe,  because  but few of us can wait weeks
or months to  make a diagnosis, and the practical question therefore
is as to  how often an optic neuritis is to  be found in the earlier stages
when the diagnosis is obscure, and not as to how often it may be found
when such cases are repeatedly examined through weeks and months
of the duration of the malady, by which time probably the diagnosis
can be made by other symptoms.
   Convulsion, like headache and vertigo, may be both a general and
a localizing  symptom.   When  it is due to disturbance of the cere-
brum or cerebellum as  a whole it is generalized, but when it is due
to implication of a particular portion of the motor tract it is limited
to certain muscles,  to one extremity, or one side of the body.
  The mental disturbance in intracranial growth  is usually slight,
although exceptionally syphilomata (which are generally accompanied
by gummatous meningitis, as has been  said) may give rise to varying
mental symptoms, such as mania, or even general paresis. As a  rule,
however, the mental symptoms  consist of such slight changes of the
mind as to be scouted  by the  patients and relatives, although  they
can usually be detected  by the skilled observer, and consist of some
slight impairment of judgment, some heaviness that can be dispersed
by a conversation  or attracting the patient's attention, by loss of 
DISEASES OF THE CEREBRUM.
329
interest iu the subjects which have before interested him, or by a
tendency to somnolency or coma.  Of these changes, I consider  the
tendency to somuolency as by all means the most important one;
indeed, in  any case of gradually supervening  coma with a precedent
history over weeks or months of vague cerebral disturbance, I should
suspect au intracranial growth, after  excluding  nephritis, diabetes,
and trauma.   I should have a suspicion, too, amounting almost to a
certainty, of intracranial growth  in  a case of recurring  headache,
either slight or severe, with recurring periods of somnolency.  Vari-
ations  in the  pulse, respiration,  and pupils occur  occasionally in
varying degree throughout the career of an intracranial growth, but
none of them is of any special value as diagnostic of such  a growth.
Occasional attacks of pseudo-apoplexy may also  be observed, either
from the growth of the neoplasm  or  from hemorrhages around and
about it; and, of course,  signs of disturbance  of the organism as a
whole are usually present, such as emaciation, auaemia, digestive dis-
turbance, anorexia, etc.  And toward the last the usual signs of dis-
solution common to so many nervous troubles may  appear, such as
vesical and rectal paralysis, bedsores,  irregular respiration,  etc.
   Localizing  Symptoms.   The localizing  symptoms   of  intra-
cranial growths will depend, as a matter of course, upon the  par-
ticular portion  of the cerebrum  or cerebellum  which is affected.
(Vide Chapter I., "Localization of Lesions," etc.)
   Pathology.   Knapp, Starr,  Bernhardt,  and Birch-Hirschfeld
have  tabulated  1139 cases, and to these I can add  50 cases of  my
own, making 1189 cases in all.  An analysis of  these shows that of
the different  forms of intracranial  growths tubercle is  the most
frequent, then sarcoma and glioma, aud next in frequency are gum-
mata, cancer, aud  parasitic  cysts,  whilst the remaining varieties are
rare.   The different forms of  intracranial growths, therefore, are—
       Tubercle;
       Sarcoma ;
       Glioma;
       Gumma;
       Cancer;
       Parasitic cysts;
       Fibroma;
       Osteoma;
       Enchondroma;
       Myxoma;
       Lipoma;
       Angioma;
       Neuroma;
       Adenoma;
       Cholesteatoma;
       Actinomyces;
       Aneurism.
   Tubercle is by far the most frequent  form of  tumor, and is  the
 most  common  iu  children and  young adults.   As has been said in
 Chapter VIIL, " Tubercular Meningitis," in which a fuller descrip- 
330
NERVOUS DISEASES.
tion will be found, there may be either tuberculous meningitis with
tubercular nodules, or the latter may occur alone.
  Sarcoma may develop from the dura, pia, or the brain-substance.
It may be solitary or multiple, beiug flat in  shape, or  fungus-like,
or wedge-shaped, or  it may occur simultaneously with growths in
other parts of the body, when,  it is said, it is generally roundish
in shape.  Internally, the  sarcoma may have hemorrhagic, caseous,
cystic, or fatty formations.   When the usual rouud or spindle-shaped
cells are predominant it is known as a rouud-cell  sarcoma.  When
cysts are present in the tumor it is known as a cysto-sarcoma;  when
the  cells contain pigment  it is a melano-sarcoma; when  there is a
structure in the neoplasm like that  of a lymph-gland it  is known as
a lympho-sarcoma ; and when the fibrous tissue is predominant it is
a fibro-sarcoma.   In my cases  the  most common  form has been the
round-cell sarcoma, next  the  melano-sarcoma, and then the cysto-
sarcoma.  Besides these forms which have been enumerated, there is
a glio-sarcoma, or a mixture of the  pathological elements of a glioma
with the round- or spindle-shaped  cells of a sarcoma; telangiectatic
sarcoma, in which the growth  is very vascular; the plexiform angio-
sarcoma, in which the cells are clustered around an enlarged vascular
plexus; and augiolithic  sarcoma, in which there is calcareous trans-
formation ; but these varieties are rare.   The  round-celled  sarcoma,
the  most common  form, is often confounded with epithelioma if it
arises from the dura and is of the so-called endothelioma type, when
it is usually flat and may grow downward into the cerebrum or out-
ward  into the skull.  Histologically the distinction is usually ex-
tremely difficult, and it is doubtful whether it can really be made.
  Glioma is  usually solitary,  and is most frequent in the cerebrum,
next in the cerebellum, and then  in the pons and surrounding struc-
tures.  It has a tendency  to  recur, although this is slight, and it
may attain a considerable size.  It develops from the neuroglia and
connective  tissue of the central nervous system, and a  reference
to " Syringomyelia," in Chapter IV., will  show that  it has  cer-
tain  peculiarities that are very  apt  to  be  overlooked.   It is pre-
eminently a tumor of the parenchyma, and not of the  membranes.
Outwardly it  may not  show  any  sigus at  all.   It infiltrates the
nervous substance, and there  is  no line of demarcation between it
and the  surrounding healthy tissue.  It may produce  softening or
even cysts, but it does not seem in the  intracranial contents to have
the same marked tendency in this  respect that it does in  the spinal
cord,  probably because  of the different conditions  of environing
pressure.  The sub-varieties of glioma are the telangiectatic, where
there  is an excessive  development  of vessels  ; a fibro-glioma, when
the fibrous tissue is greatly increased ; a myxo-glioma, when mucous
tissue develops within the growth ; aud a glio-sarcoma, when  there
is a large number of  round or spindle-shaped cells.
  Gumma  is  usually only one  of the varied lesions of an iutra-
cranial syphilis, which consists of pseudo-meningitis, an infiltration
of the nervous parenchyma, and  occasional nodules or  distinct out-
growths, which  are called  gummata.  The solitary gumma is com- 
DISEASES OF THE CEREBRUM.
331
paratively rare,  and especially so in children.   The  pathology of
these  growths is  treated of  in  the chapter  upon  " Intracranial
Syphilis."
  Intracranial cancer  may  be primary or secondary, usually the
latter.   When cancer  arises  primarily in the brain  it does so from
the epithelium of the choroid plexuses, or from the epithelium of the
ependyma, and possibly from  the hypophysis or in the transverse
fissure.  When it appears in the skull or in the brain-substance it is
usually secondary to these primary growths of the epithelium or the
choroid  plexus aud the ependyma, or from secoudary growths outside
the skull.   These secondary growths are usually small and rounded
when in the brain-substance, or when they perforate the  skull they
may form one of the fungi hsematoides.
   Parasitic cysts may be caused by echinococci or cysticerci.  When
they are due to the echiuococci, they are the so-called hydatid cysts,
may vary iu size, and be single or multiple, usually lying upon the
brain, causing softening.  The cysts due to cysticerci are of the form
of small fibres, with scolices (i. e., one of the cystic worms) of the
racemus form.
   Fibroma is rare.   It is a rounded growth, hard in  consistence, and
consists of  a  fibrous tissue with  a few cells.   It may, however, be
intermingled  with the texture of a  sarcoma, constituting the fibro-
sarcoma already  mentioned, or there may be calcareous deposits con-
stituting one of the psammoma.   Fibrous thickenings are sometimes
found in the epithelium or the ependyma, and are regarded as being
organized thrombi.
   Osteoma usually proceeds  from the skull,  although it may arise
from the dura,  the falx, or  the tentorium, and it rarely develops
 within the nervous parenchyma.   There may be pseudo-fibroma, or
pseudo-sarcoma may occur.
   Enchondroma arises from the bones of the skull or dura, aud lies
 upon the brain.   It  is cartilaginous in formatiou.  Pseudo-enchon-
 droma may also  occur.
   Myxoma is a soft,  round,  moderately developed growth, and is
 rare, much  more so than  the mixed forms, consisting of the so-called
 myxo-sarcoma and myxo-glioma.
   Lipoma is  extremely rare.
   Angioma is also  rare, much  more so than when it is combined
 with sarcoma and glioma in the so-called telangiectatic varieties.
   Neuroma is also rare, and consists of two  forms: the heterotopy
 of gray or  white  matter  that  has been described by Virchow occa-
 sionally as  of congenital development,  and the  neuroma, which is
 similar to the neuromata  elsewhere found.
   Adenoma is rare.
   Cholesteatoma is also rare.
   Actinomyces usually proceed from  actinomycosis of the face and
 neck through the  occipital forameu, giving rise  to a diffuse puru-
 lent meningitis of the  pia, with a formation of nodules or  even of
 abscess.
   Aneurisms of the large arteries  at the base of the brain constituting 
332
NER VO US DISEASES.
the circle of Willis may be sufficient in size to give rise to the symp-
toms of a neoplasm, but this is rare.
  Diagnosis.   The diagnosis of an intracranial  tumor is usually
not difficult except in the very earliest stages, but occasionally it may
become one of  the  most vexed  questions  in the whole  range of
medicine.   In every case where there is a suspicion a careful history
should be  obtained from some  reliable  person who  has been well
acquainted with the patient,  and it should always be remembered
that the defects of memory or the slight mental changes of a patient
may render him or her a totally  untrustworthy witness.  Headache
should be carefully inquired for, and care should be taken to distin-
guish a headache  that may  have existed throughout the whole of
life, as in cases of  migraine, from one that has gradually or suddenly
supervened.  A^omiting  or  nausea should be carefully searched for,
and we should be careful not  to  be  misled by the  general tendency
of the lay public  to attribute every nausea or vomiting to so-called
" biliousness."   Vertigo is not usually a symptom of much impor-
tance in  intracranial lesions, except  when it has the peculiar  char-
acteristic impressed upon it by  neoplasm of the cerebellum or its
peduncles ;  nevertheless, careful  inquiry should be made for this
symptom, because it will have a  corroborating value in conjunction
with those of more importance.   Iu every case careful and repeated
ophthalmoscopic examination should be made, and by one who is a
skilled ophthalmoscopist.  Fortunately nowadays  ophthalmologists
are so numerous and so skilful that  there are very few communities
in which this examination cannot be faithfully made.  If a patient
should have a  marked headache, with vomiting or nausea, aud also
a neuro-retinitis, the general symptoms will usually  be sufficient to
base upon them a  diagnosis  of an intracranial growth, when proper
exclusion  has been  made of other  conditions which might produce
headache,  vomiting, and neuro-retinitis.   As  a matter of fact,  how-
ever,  it is rarely  that a  diaguosis can be made upon these general
symptoms alone, and it is usually only done by the commingling of
certain of the  general  symptoms with some  of the localizing  ones,
such as have been already detailed.   The diagnosis should be from—
       Nephritis;
       Locomotor ataxia;
       Myelitis;
       Intracranial syphilis;
       Paretic dementia;
       Multiple sclerosis;
       Chorea;
       Lithaemic neurasthenia;
       Lead-poisoning;
       Amaurosis  from tobacco.
  In nephritis  there may be persistent headache, even with somno-
lency, and  the arterial  changes of the disease may give rise to paral-
ysis, which is  usually, however,  of  the hemiplegic form.   I do not
believe that the optic neuritis  of  nephritis can be distinguished from
the optic neuritis of intracranial growth except in  the early stage of 
DISEASES OF THE CEREBRUM
333
great oedema, but not in the  later period of beginning or  complete
atrophic changes in the retina.   But a careful and repeated examina-
tion  of the  urine microscopically, chemically, and quantitatively,
will invariably determine the  matter, although  care  must  be  taken
not to lay uudue stress upon a few casts or a slight amount of albu-
min aloue.
   I have seen cases of locomotor ataxia in which there was persistent
pain about the head, especially in the ramifications of the trigeminus,
accompanied by optic-nerve atrophy, in which  a  mistake had been
made in the diagnosis, but  a careful examination  of the case  would
soon make the matter plain, because of the presence of the character-
istic ataxia, the absence of the knee-jerk, the peculiar pains, and some-
times the trophic changes in the bones.
   Occasionally what are reported as cases of myelitis will be accom-
 panied by an optic neuritis.  Seguin has reported three cases of this
 kind, one of which I attended with him.   Here, of course, the diag-
 uosis can be easily made, because the  paralysis is both sensory and
 motor, is bilateral, may  be accompanied  by  vesical and  rectal im-
 pairment, there is no headache, and no mental  changes whatever are
 observed.
   Intracranial syphilis is often confounded with intracranial growths,
 and the differential diagnosis  may sometimes be impossible.   It can
 be made readily in that form of syphilis described in Chapter VIIL,
 and characterized by the  quasi-periodical  headache, with  obstinate
 insomnia, both of these disappearing suddenly upon the supervention
 of paralysis or convulsion.   In syphilis  of the base, with  implica-
 tion of the cranial nerves, preceded by this characteristic headache,
 the  diagnosis  can usually be  made.   In any case with a  syphilitic
 history, in which there is evidence pointing to a neoplasm, the diag-
 nosis can be made, I think, if the characteristic headache and insom-
 nia have formed part  of the  history.  But in cases of  intracranial
 syphilis that are diffuse in  character, or  in which  the  gumma  is
 merely a part of the general syphilitic infiltration of nervous  paren-
 chyma and  membranes, and in which  there is not a distinct syphilitic
 history, it may be utterly impossible  to make  the  diagnosis.   This
 syphilitic history is, as has been said,  usually very difficult to  obtain
 from women who may be entirely unaware of haviug been specifically
 infected. In  any case, however, of a tumor  implicating  the base,
' even when  there has been no  syphilitic history, I think  that  we are
 warranted  in  suspecting  intracranial  syphilis,  and  we should hold
 our diagnosis in  reserve until a careful trial has been made of large
 doses of iodide of mercury, or both these drugs; although it must
 be remembered that the gumma  may give rise to  considerable de-
 velopment  of connective tissue  in  and around the  tumor, and this
 cannot be affected by either mercury  or iodide, so  that  in  all cases
 these medicines may not determine the diagnosis.  Nevertheless, they
  will usually have immensely more effect up to a certain point in the
  syphilitic tumors than in non-syphilitic ones.
    The symptoms of paretic dementia without doubt occur occasionally
  as the result of intracranial  syphilis. Sometimes  I am iucliued to 
334
NERVOUS DISEASES.
think that these cases will give an earlier history than is typical of an
intracranial neoplasm, but it is undoubtedly a sad truth that in many
instances this cannot be made out, and  then it is impossible to make
the  diagnosis.  This has been shown  by the researches of  Morel-
Lavallee and Belieres.   On the other  hand, it occasionally happens,
though rarely, that non-syphilitic intracranial  neoplasms  will give
rise to symptoms of general paresis, and Knapp has detailed  a very
interesting case  of this kiud.  It  is  fortunate  for  us in the present
condition of our knowledge that this is  rare, as there are no means of
diaguosis.  I have myself, however, never seen such a case.
   Certain cases of multiple sclerosis, when the sclerotic patch is suf-
ficiently localized to cause localizing symptoms, may  cause confusion
to one who is not familiar with the types of nervous disease ; but the
presence  of  the tremor, the  nystagmus,  the stupidity that  occurs
when the sclerotic process implicates large portions  of the cerebrum,
picture a disease that is different from that of tumor, characterized as
the latter is by headache, vomiting or nausea ; and  tumors are apt to
be considerably more rapid in their course than is sclerosis.
   Chorea of the Sydenham type presents no similarity whatever to
intracranial tumor  in its clinical symptoms, although in  both there
may be a neuro-retinitis; but chorea  accompanied or preceded by
paresis or convulsions might lead to confusion iu some cases, although
stripping the patient and detecting  the  tell-tale choreic movements
will clear up the diagnosis.  Huntington's chorea might also lead to
a mistake, but to anyone who is aquainted with the symptoms  of the
disease the mere mention of the fact of such possible confusion should
be all that is necessary.
   In lithaemic neurasthenia (vide "Neurasthenia," Chapter IX.) the '
vertigo is frequently so intense and obstinate as to  cause a suspicion
of intracranial growth ; but the absence of a true  headache and the
presence of a sense of fulness or pressure, the fact that the vertigo is
more intense than in cases of brain-tumor, and that it has not the
characteristics of the vertigo of cerebellar disease, together with the
entire  absence of any localizing symptoms, will  make  the diagnosis
easy.  Some observers claim that  they have seen  optic  neuritis in
cases of lithaemic neurasthenia, but I have never perceived it.
  In lead-poisoning  the  diagnosis  is easily made  by means of the
lead-line on the  gums, the flexor paralyses, the history of an exposure
to lead, etc.
  Amaurosis from tobacco, caused  by optic-nerve atrophy,  might
lead to a mistake, but the entire absence of  the general  or localizing
symptoms of intracranial growth  should make the  diagnosis by ex-
clusion.
  Prognosis.   The prognosis of  intracranial growth is iu the main
unfavorable,  although it may be considerably modified  by three cir-
cumstances :  first, the effect of treatment; second, the question  of its
being of syphilitic origin ; and  third, the feasibility of an operation.
  As a rule,  a fair idea of what the progress of the growth will be
can be obtained  by observing carefully what its progress has been, so
that a tumor that  has progressed very  slowly will  usually  continue 
DISEASES OF THE CEREBRUM.
335
to do so, and vice versa.   Whether treatment materially affects the
course of  a non-syphilitic intracranial growth  is a  matter about
which neurologists are in  great doubt.   Certain  it is that under
vigorous treatment some intracranial growths will not  only be ar-
rested, but will retrograde, and the patient may materially improve.
I have seen this in several instances, and at the present time  I num-
ber among my patients some six or seven who have remained in this
quiescent condition for years, one especially in whom the growth has
made no progress for nearly nine years after  it  had been seemingly
arrested and caused to retrograde.  While syphilitic tumors, so called
gummata,  may attain to a stage of  connective-tissue  proliferation
which  cannot be affected by means of  the anti-syphilitic  remedies,
yet in a number of instances vigorous treatment may cause  a start-
ling  improvement;  so much so that it is my custom  to be very
cautious about prognosis in such cases.   I can recall several instances
in which the patient was  seemingly so  near  death  as to be  beyond
reach of even surgical  help, yet in which  the  symptoms have so
markedly  improved as to constitute a practical cure; i. e., the patient
is able to attend to his or her usual avocations, taking care, however,
not to be subjected  to great mental, emotional, or physical strain.
 More than this, it should be remembered that in all cases of gum-
mata it is  almost impossible to say how much of the symptomatology
 is due to the syphilitic infiltration of the cerebral or cerebellar paren-
 chyma and its membranes,  and  how much is from actual gummatous
 formation; and, therefore,  it is impossible to say as to what is the
 exact pathological nature of the cases in which there is cure.  It is a
 common experience with me to  see cases of intracranial syphilis with
 symptoms that are indicative of a lesion at the base  and that have
 gone no further than  some implication of the crura cerebri and the
 cranial  nerves, particularly the third  pair, become absolutely cured
 and remain so.   The modifying effects of  operation will be fully
 considered in the section upon treatment.
   Treatment.  In all cases of intracranial growth resort should
 be had to vigorous treatment  by means of the iodide and mercury.
 This should be done  even where there is no history of syphilis, both
 because the syphilis  may  have been  overlooked,  especially in the
 female, and  because  it is  not yet positively known whether the
 iodides and mercurials may not modify the course of a non-syphilitic
 growth.  Both in syphilitic and non-syphilitic growths I have much
 more faith in the iodide than in mercurials, for reasons that  will be
 found  fully stated in  Chapter VIIL, under "Syphilis of the Nervous
 System."   The iodide should  be  pushed to  the  point of  iodism,
 about  which directions  are given  in  the chapter just mentioned,
 and if mercury is used it should be made to  produce ptyalism.  In
 all cases  in which, in spite of  treatment, the growth is rapidly pro-
 ceeding and  inducing symptoms which may be fatal  to  life, such
 as severe convulsions and paralysis, or symptoms which may  involve
 great danger  to  structure, as  in  rapidly  advancing blindness, an
 operation  should be  done  promptly if the  tumor can  be reached.
 But I  am firmly convinced that we  usually wait  too  long before 
336
NERVOUS DISEASES.
operating.  There is nothing to gain by delay, except the bare possi-
bility that a tumor may undergo a retrograde metamorphosis; whilst
the danger is that  of an intracranial growth.  I believe, therefore,
that when treatment has been accorded a fair trial an operation should
be  done  immediately.   Early operation  should  become a surgical
axiom in these cases;  and when it does, the rate of  mortality will
be materially lowered.   Tumors of the cortex, of  the centrum ovale,
or of the cerebellum  should  be  operated  upon ; but it is useless to
attempt to reach them at the  base uuless they produce such symptoms
as will probably localize them at the base  of the frontal lobes, when
there will be some impairment of the sense of smell.
  There are certain inherent  uncertainties, however, about an opera-
tion for the  removal of an intracranial growth which should be
carefully contemplated by the surgeon and explained to the patient or
his friends.  In the first place, while we  may be  reasonably certain
in tuberculous or syphilitic tumors as to the real pathological nature
of the lesion, we cannot be  positive until the brain is opened how
much  of tubercular  or syphilitic  meningitis may accompany the
gumma or  tubercle, and therefore we cannot know until this  time
how much relief can  be afforded.  I  have seen  three cases of intra-
cranial syphilis operated upon in which a gumma  was found, but in
which there was too extensive a meningitis to be removed by the sur-
geon's knife, all dying; but  in two of these the tumors were found
to  be  multiple,  the  largest one  having produced  the localizing
symptoms that  had dictated the operation.  In  gliomata, too, the
infiltration of the cerebral or cerebellar parenchyma may be so wide-
spread as to make it impossible to feel sure of eradicating it all with
the surgeon's knife.   My deceased friend, Dr. Frank W. Rockwell,
operated for me many years ago upon a case of this  kind in which
death shortly followed, and in which it was ascertained at the autopsy
that only a small portion of the gliomatous formation had been re-
moved ; and in another case  operated upon  by the same surgeon the
operation was abandoned, after opening the skull, for  this  reason;
very wisely, as the post-mortem examination showed.  Then, too, it
is impossible to tell beforehand as to whether a tumor is cortical or
sub-cortical, and if  it should prove to be the latter, it may be impos-
sible to find it.  Thus, in one case of mine  to which I have elsewhere
alluded (Fig. 22), a small cystic sarcoma lay just  beneath the gray
matter iu  the  ascending parietal  convolution at the junction of the
upper  and  middle  thirds,  but it was not found  at the operation;
and even when the  brain was taken out and  dissected, it was detected
with great difficulty.  The reason was that  it was a round-cell  sar-
coma, with a cystic degeneration in the centre that had given it a rather
softer consistence than the surrounding cerebral substance.  Although
I thought I detected it by palpation at the operation, the surgeon
would not agree with me, and at the autopsy  it was  found, marvellous
to relate, that the probing-needle had gone through it in three dif-
ferent directions without giving us any sense of resistance to the touch,
In another instance in the experience of an eminent neurological col-
league, the tumor was not found  at  the operation,  or at the autopsy, 
DISEASES OF THE CEREBRUM.
337
or, indeed, until months afterward, when the brain had been hardened
in bichromate salts, and  careful dissections made of it, when it was
discovered to  be not  larger than a pea.   I know of several  other
instances of this  kind.  Another danger lies in the fact  that  the
tumor may lie upon the same side as the paralysis of the limbs,  not
upon  the  opposite side,  as  generally happens; and  this is due to
the fact that in such a case only a small proportion of the motor
strands have decussated and  passed  over to the opposite side as usual
—a fact which was pointed out by Flechsig.  Not long ago  my*
friend, Dr. R. H.  M. Dawbarn, operated upon a traumatic  hem-
orrhage that I had  diagnosed, selecting, as  usual, the side oppo-

                             Fig 153.
Tumor of left temporo-sphenoidal lobe, causing hemianopsia, word-deafness, ataxic aphasia,
             hemiplegia, motor oculi paralysis, and convulsions.
site to the hemiplegia.   Finding nothing upon that side, and  the
patient being too much exhausted to go on with the operation, it was
abandoned, and  the autopsy showed that the hemorrhage was upon
the same side as  the hemiplegia, whilst the cord showed but a partial
decussation.  Finally, the growth may be so large or so deeply seated
as to render it  impossible to remove it.  In still other cases  the
lesions may be multiple, as in  one case of mine where a melanoma
of the augular gyrus  caused hemianopsia, and another melanoma of
the internal capsule caused hemiplegia, both sensory and  motor; or,
as in the case represented  in Fig. 153, where a tumor caused word-
                              22 
338
NER VO US DISEASES.
deafness, and also, by the pressure of the distorted  cerebrum, ataxic
aphasia,  third-nerve  paralysis,  and  hemiplegia;  whilst another
tumor, impinging upon the  optic  fibres  as they  entered the rear
portion  of the internal capsule (Fig. 39), caused  hemianopsia.  I
believe,  however, that the size or deep-sea ted ness of a growth should
not stop us from operating on a patient who is certain to die  unless
relieved, because  many cases of this kind have shown that in these
days of  antiseptic  surgery a  patient may  thus  be  snatched from
'out of the shadow of death.  Considering all these  difficulties, there-
 fore, the  question arises  as to what percentage  of success we  can
 expect in operations for  cranial  tumors.   The accompanying table
 is based upon an investigation made for me  by my friend, Dr. R. S.
 Newton:
Total number
 of operations
 for tumor t'>
 September 15,
   1892.
110
 Times failed
to remove tlit
growth when
  found.
Times tumor
not found at
 point of
 operation.
  Times
trephined or
operated for
 relief of
 pressure.
15
Recovered
.  after
removal of
 tumor.
fi3
Number of
 deaths.
42
Percentage
   of
mortality.
38£
  A perusal of this  table will show that out of 110 operations 5
failed to remove the  tumor.  In 7 the trephining was only done to
relieve pressure.   Where, however,  a growth has actually been re-
moved, in  105 cases there were 63 recoveries  and  42 deaths, the
mortality having been 38T2T.  This result is to my mind exceedingly
favorable for brain surgery when we consider that the first operation
upon a brain tumor  was done in 1884,  only six years ago, because
I have no doubt whatever that every year will witness great progress
not  only in our  methods of localization, but  also  in our surgical
technique.   In any  case, however,  it should be remembered  that,
as was first suggested by Horsley in 1890,  trephining for the relief
of tumor may be of  considerable therapeutic value in relieving pres-
sure, even when the tumor is not found or cannot be removed.  Some
of the cases in the above table show  a very  remarkable success from
an  operation done with  such  an end iu  view—much  too favorable,
indeed, I think, to be warranted by the facts, as, in  four cases of my
own, death followed in every instance, although remarkable improve-
ment was temporarily obtained in three  of them.   In one of these
last-mentioned cases—the one represented in Fig. 153—indeed, the
patient lived  four months after the operation was so done, although
he was at the point of death at the time, and considerable improve-
ment was obtained, yet at the autopsy a tumor as large as a hen's egg
was found  in' the depths of the  temporo-sphenoidal lobe; and in
another  case  of  mine, operated  upon three months ago, seemingly
moribund at the  time, there has been marked improvement.
   Whenever the  brain is trephined for the removal of an intracranial
growth the former should  be liberally exposed  by making repeated
openings with a  trephine along a large  arc, and then  cutting with 
DISEASES OF THE CEREBRUM.
339
a saw or  rongeur forceps from hole to hole, elevating the bone and
breaking its back upon the base  of the  arc in  this manner.  This
should be done  because it  is impossible to diagnose  minutely the
exact site of the most pronounced lesion.   A dental engine or electric
motor is much the best instrument to operate with.  When the brain
is exposed the dura and the pia should be carefully dissected away, and,
if the tumor is not found upon the surface, the nervous mass should
be carefully palpated.  If this does not locate the subcortical growth,
a long, fine needle should be carefully inserted at different places and
moved in different  directions.  This  needle,  however, should have
the inserted end  blunt and  rounded, so that it will be more likely to
give a feeling of resistance  when it strikes a tumor.  If this does not
suffice, I can see no  objection whatever to careful incisions, and  I
think that surgeons are very much more afraid of these than  is at
all  warranted by the  circumstances.   It is  only a question of time,
after all, for  the patient to die  if the tumor  is not removed, aud a
few incisions  more or  less can make no  material difference, whilst a
small tumor,  such as a cystic sarcoma, which I have just spoken of,
or a melanoma, would be detected iu  this mauner.  Horsley  recom-
mends that oozing from the  diploe should  be checked by plugging
the bone with a  wax made accordiug to the following directions :

                                                  .   1 part.
                                                  .   4 parts.
                                                 !ia  q. s.   M.


   But it does not seem  to  me that this is necessary, as such hemor-
 rhage from the diploe can be much better controlled by compression
 with an artery-forceps for a few minutes.   Some hyper-cautious oper-
 ators object to opening the  dura should nothing appear after remov-
 ing the bone, but this seems to  me rank nonsense in  these days of
 antiseptic surgery.  It is generally supposed that a subcortical growth
 will be disclosed by discoloration of the  brain or a bulging, but this
 is seldom the case.  All the  bleeding vessels should, of course, be
 ligatured, and a  20 per cent, solution of cocaine may aid in  con-
 trolling the troublesome hemorrhage ; or, as Roswell Park has sug-
 gested, a 5 per cent, solution of  antipyrin.  Surgeons are divided in
 opinion as to the question  of drainage, and Horsley has abandoned
 it; but I have never seen any ill results iu my cases from it.   If no
 tumor has  been  found, a liberal  portion of the bone should not  be
 put back; but if the  tumor  has  been located, of  course  there is no
 objection to putting all  the  fragmeuts into place,  these having been
 kept warm and aseptic  until such time.   I presume, of course, that
 no surgeon would undertake an  operation of this kind without  the
 most strict regard to antisepsis.   1 have seen cases operated upon in
 both ways, and whilst I have never  seen any sepsis  result from an
 operation done antiseptically, in  two cases in which antisepsis was
 disregarded there was not only the most frightful sepsis,  but  in one
 of  them there was the most horrible purulent encephalitis that it has
    R.—Cera? flavse  .
       Vaselini
       Acidi carbolici 1:40
       Cerse albse
S.—Boil before using. 
340
NER VO US DISEASES.
ever been my fortune to meet with upon a post-mortem table.   The
further risks of the operation are  shock and hemorrhage.   The first
of these will depend  upon  such well-known surgical considerations
as the extent of the growth, the length of time consumed in remov-
ing it, and the physical coudition  of the patient; and is, of course,
to be met by the ordinary means.   Hemorrhage to  a fatal extent is
exceptional, although the German surgeon Von Bergmann lays con-
siderable stress upon it.  The convolutions can be reached in accord-
ance with the rules that are formulated under the heading " Cranial
Topography."

                       HYDROCEPHALUS.

   Hydrocephalus may be either subdural or ventricular. The former
variety is known  as external hydrocephalus, whilst the latter is the
internal.   It may be either primary or secondary—i. e., the result of
other lesions of the nervous system ; and it may be of an acute or
chronic type.
   Acute hydrocephalus is  usually caused by tubercular meningitis,
and the fluid may be either subdural  or ventricular.   The effusion
is caused by the meningitis  of the pia, the  lining membrane of the
ventricle,  the choroid plexuses, and the velum interpositum.  Occa-
sionally,  however, the hydrocephalus may be acute  and febrile, and
in these  cases  the choroid  plexuses  have  undergone inflammatory
alteration, there is a granular condition of the lining  membrane of
the ventricles, the surrounding brain-tissue is softened, and the brain
substance is compressed, whilst the external meninges are apparently
healthy.
   Chronic hydrocephalus may be external or internal.   The external
form is usually a  senile phenomenon, and it may occur in many con-
ditions of wasting of the brain or arrested development.   In other
cases without any atrophy  of brain-tissue  the  subdural  fluid  is in
excess, when all that can be detected post mortem is the undue amount
of fluid,  without membranous alteration, the real  causation  being
unknown.  In this external form  there is sometimes a sacculation
caused by adhesions between the dura and pia, and  this  may occur
over a hemisphere or beneath the tentorium, so that there is corre-
sponding  unilateral enlargement of the  skull.  These  cystic forma-
tions are probably of inflammatory origin, and they may be accom-
panied by intercurrent meningitis.  The external form  of chronic
hydrocephalus is congenital or acquired.  The former is  usually of
fcetal development, and its etiology and pathology  are not known,
except that it sometimes seems  to be  hereditary.   It may affect all
the ventricles or the fourth ventricle alone.  In this variety the shape
of the skull is  characteristic, and it becomes more marked after birth.
The fontanelles are conspicuous and bulging, and the bones* are  often
separated at the sutures.  The cranium is generally  disproportionate
in size to the  face and  of a rounded  shape, as in Fig. 154.  The
frontal skull projects, the orbital plates are oblique, and the eyes
look downward and the lower lids overhang them.  The duration of 
DISEASES OF THE (EREBRUM.
341
this congenital hydrocephalus is variable, death usually occurring in
a few months, although  exceptionally the  patient may live on  to
adult  or old age,  probably because the  progress of the  lesions is
arrested and the fluid is absorbed, when ossification of the bones
may be completed  with the  development  of the  so-called Wormian
bones.   The mental and motor  symptoms are persistent throughout
life in less degree, however.  The  acquired form of chronic inter-
nal hydrocephalus may be secondary, being usually  caused  by me-
chanical or meningeal lesion and the primary form.   Obstruction of
the vense Galeni, tumors, abscess, aud meningitis are lesions which
                             Fig. 154.
Case of hydrocephalus.
act by either hindering the return of blood from  the vessels within
the ventricles, or obstructing the passage of fluid out of the ventrcles
through the openings in the membranes of the fourth ventricle,the
foramen Magendie and Merzejewski's apertures on each side of the
roots of the glosso-pharyngeal nerve.   When these latter canals are
blocked by a meningitis, the interchange  of fluid betweeu the ven-
tricular systems becomes disarranged, and the effusion may be confined
to the lateral ventricles.  It must be said, however,  that the pathology
of this form has not  been satisfactorily explained.
  Hydrocephalus may occur without  any of these lesions, and  then
its causation is utterly beyond  our knowledge.
  The symptoms are akin to those of tubercular meningitis of a low
grade, but the distinction can  usually be  made by the fact that the
clinical phenomena are vague and by no means so  distinct as in true
tubercle.  They are extremely variable, consisting  at times of mental
defect, sometimes actual idiocy, whilst upon other occasions there
is a considerable degree of intelligence.  The child is usually unable
to walk, not so  much from lack  of muscular strength as from ability 
342
NER VO US DISEASES.
to co-ordinate.   Convulsions, contractures, fever, and vomiting may
occur.   The  head is not held erect, but  lolls in different directions.
The eyeballs  are restless, the hair is scanty, aud the skin of the head
is thin.   In some cases amaurosis may occur, when usually au atrophy
of the optic  nerve will be found.  Temporal  hemianopsia is  some-
times observed.  In  the adult the enlargement  of the head  is less
common.
   The diagnosis is to be from rickets  and thickening of  the  skull-
bones.
   In rickets  the head is square, the fontanelles do not bulge, and the
other signs of rickets are present.
   Thickening of the cranial bones  is easily distinguished from the
fact that the  progressive enlargement of the head is extremely slow,
and the mind is  generally unimpaired.   I have seen one case in a
man of fifty  who was mentally far above mediocrity.
   No diagnosis can be made between the external and internal forms.
   The prognosis is always grave.
   The treatment is practically nil.   I have never yet seen a case re-
lieved, and the temporary improvement  has  been of slight amount.
The lateral ventricle  can be punctured by the surgeon  according to
the rules laid down on pages 97 et seq.; but this method  is sometimes
fatal in results, aud has never been of much use.  Iu any case where
some  relief was absolutely insisted  upon, I should much prefer to
have a portion of the bone, two or three inches across  and three or
four inches long, removed over one side of the  head when the hydro-
cephalus is unilateral, or over both hemispheres in a bilateral effusiou.
This bone should not  be replaced.  Puncture of the spinal membrane
has been resorted to, and although it is harmless,  it is also valueless.
Compression  of the skull by diachylon-plaster according to the method
of Trousseau has been no more successful at my hands than the punc-
tures.   If it  is desired to resort to  this, the plaster should be one-
third of an inch broad  and  applied in strips from each mastoid pro-
cess to the outer part of the opposite organ from the hair at the back
of the neck to the root of the nose; over the whole head so that the
strips shall cross at the vertex ; a strip three times around the head,
first above the ears  and  eyebrows, and  a little below  the occipital
protuberance. This compression, though, should be carefully watched,
A broad elastic band, however, will exercise  quite as much compres-
sion, it is claimed.

                    HUNTINGTON'S  CHOREA.

   Synonyms:  Hereditary chorea.  La choree chronique.  La choree
vulgaire chez les veillards.   La choree de l'adulte.   Choree clinique
hereditaire.  Corea ereditaria.  Chorea chronica progressiva.
   History.   The first description  of this disease  was given by
Huntington,  a physician of Long Island, and his name has very
properly been given  to it.   We are not as yet sufficiently informed
as  to  the pathology to distinguish  it by any better  title.  As
chronic chorea was but little known previous to Huntington's paper, 
DISEASES OF THE CEREBRUM.
343
I claim for my own country the  merit  that  belongs  to it for this
discovery.  Waters, of Franklin, New  York,  had  remarked the
same disease as far back as 1841 in a letter to Dunglison, and in
1863 Lyon had also observed it; but nevertheless the best description
was that of Huntington, and he was really the first to portray accu-
rately the malady.   Since  that  time a number of cases have  been
observed by different authors—Landouzy, Maclaren, King, Russell,
Sinkler, Ewald, Peretti, Dejerine, Lanois, Huber,  and many others
iu different countries.
   Etiology.  The etiological factors having a certain relationship
to Huntington's chorea are :
       Heredity;
       Age;
       Sex;
       Pregnancy ;
       Rheumatism;
       Emotions;
       Some functional  nervous  diseases, as hysteria, epilepsy, etc.
   Heredity is a very constant factor in Huntington's chorea.  There
 are many communities in different parts of America, to my  knowl-
 edge, in which this  form of chorea runs in certain families, and  inas-
 much as there is a great superstition in regard to it,  it is very difficult
 to obtain much information  about it.  I can  name  at  the  present
 moment at least a  dozen towns within  easy reach of New York in
 which it is very prevalent, and yet in which  it is  nursed as a  dark
 secret.  This heredity has been well established in all the cases which
 have been published in other countries.
   The hereditary progression is apt to be capricious  at times, as it is in
 other hereditary maladies. Thus, in King's case, the  great-grandfather
 was choreic.  He had ten children, only four of whom had this  chorea;
 concerning only three of these four are there very definite details, and
 it is only known that they had  children who were also choreic; the
 fourth  one of these four  had nine  children, eight of whom  were
 healthy, but the  ninth was  choreic; this ninth one  had five  chil-
 dren, of whom four were choreic.   Of these four, three had no chil-
 dren; but the fourth  one had  a  chorea whilst  he was  still young
 himself, and was  cured of it, wheu again  at thirty-five he passed
 gradually into the typical Huntington's chorea.
   Huntington's chorea generally  commences in adolescence, attain-
 ing its  maximum at adult age, contrary  to the chorea of Sydenham,
 which, as we have seen, is  found  in infants, at  which  age Hunting-
 ton's chorea is rare.  The following table of Huet's embraces Hun-
 tington's  observations and  his own :
 10 years .
 10 to 15 years
 20 " 25  "
 25 " 30  "
 30 " 35  "
 35 " 40  "
 40 ;' 45  "

A congenital case
 1       45  to 50 years   ....  7
 2       50  " 55  "    .   .   .   .  S
 1       60  " 65  "    ....  1
 5       65  " 70  "    ....  1
16                               —
13              Total   .   .   .   .66
11
s represented in Fig. 154
From this it will be  seen  that  most cases occur between the thir- 
344
NERVOUS DISEASES.
tieth and forty-fifth years, and this has been confirmed by tabulated
statements of other authors.  Even where  there  is no heredity, the
onset at different ages is the same.
  The female sex are much more prone to Huntington's chorea than
the male, just as is observed in the chorea of Sydenham.
  Pregnancy is a frequent cause of Huntington's  chorea.  Primi-
parse are most affected (and during the first five  months), although
multipara? may be affected who have never had the disease before.
  Rheumatism  is an  infrequent  cause  in  Huntington's  chorea
although it may have been observed in the hereditary history.
  The emotions are frequent causes.
  The relations of Huntington's chorea to other nervous affections
have not been thoroughly studied, but  so far, hysteria iu combination
with it as a personal  or  hereditary antecedent  is  rare.   Epilepsy is
more frequently seen ; migraine is extremely infrequent.
  Clinical History.  The onset is generally  very  gradual and
progressive, but it may be sudden, and in  some  cases, after severe
Fig. 155.                         Fig. 156.
Case of congenital Huntington's chorea.   A case of Huntington's chorea.  One attitude.
relapses of ordinary Sydenham's chorea, the Huntington chorea may
supervene.  The muscular movements  are  entirely different from
those of Sydenham's  chorea.   In the former, as pointed out in
Chap.  IX., under  " Chorea,"  the  muscular  movements consist of
fibrillary contractions that are jerky, beginning quickly and ending 
DISEASES OF THE CEREBRUM.
345
quickly, or others that are not abrupt enough to be called jerky, and
may rather be designated as wavy, as in the athetoid variety.  In Hun-
tington's chorea, however, the muscular movements are of far larger
range than the fibrillary ones of Sydenham's chorea, and whole groups
of muscles are  set into action as  in a voluntary movement, so that
Fig. 157.                           Fig. 15S.
A case of Huntington's chorea.          A case of Huntington's chorea.
      One attitude.                       One attitude.
the patient seems to be posturing and grimacing  almost from eccen-
tricity, and he has a dancing movement, with many queer contortions
of the face and head, the whole picture  at first  exciting ridicule.
(■tigs. 155-158.)   Most of the  muscles of  the  body are generally
affected, and  the disease  is never a localized one.   In  some cases, 
346
NERVOUS DISEASES.
however, the fibrillary movements of the  Sydenham  type are inter-
mingled in slight degree with the dancing aud grimacing ones. The
muscles that are first affected are those of the face, especially of the
mouth, aud after  these the  limb, trunk, and  other  muscles become
affected, although  sometimes all are involved simultaneously.  The
speech is frequently altered in consequence  of the muscular  move-
ments  of the buccal cavity,  pharynx, and respiratory diaphragmatic
muscles.  This  alteration  imparts to the speech  a  nasal, confused,
obstructed, and sticky articulation.   The external  muscles of the eye
are not often affected.  Although most of the muscles of the body are
attacked, nevertheless individual  cases vary as to the muscles impli-
cated,  so that in some it is the extremities,  in others the face, respi-
ration,  and  deglutition;  whilst  in  others  again  there is  a  hemi-
plegic  distribution, or the lower extremities are implicated.  There
is seldom  any impairment  of sensation, and when there is, it is
only some slight dulness of perception of painful  sensations,  which
is probably  due to the mental  enfeeblement.  The special  senses
are not altered.   There  is  usually marked  incoordination, evi-
dently dependent  upon  the  movements, so that the patient brings
the forefinger to the nose in a series of zigzags and fails to hit the
mark,  or cannot walk a straight line, etc.   There is no alteration
in the  response of nerves and muscles to either the galvanic or faradic
currents.  The sympathetic  nervous sy\stem is  not affected, nor the
bladder or rectum, except in a very advanced stage.  The  urine is
unaltered.   There is  almost  invariably  some  mental  impairment,
generally consisting of slight and  progressive dementia, which may
pass on to absolute dementia.   Memory is greatly enfeebled.  At
the onset there is apt to be a great  tendency to depression, although
this is not  a true melancholia, but rather a depression  of spirits,
partly  due to the  disease itself—more largely,  I  think, to  the fact
that this disease is known  to be hereditary  aud  is looked  upon with
extreme dread in families who are subject to it.  Suicide occasionally
occurs, mainly from a well-founded dread of  the  consequences with
which  the patient  is apt to be familiar.  As the  disease progresses,
however,  this suicidal tendency is  apt  to disappear.  At times the
patient is very irritable and subject to violent  bursts of passion.  In
others  there are vague ideas of persecution, and in  others again there
may be  violent and dangerous  outbreaks of mania.  Occasionally
there are hallucinations, especially  of sight.   As the  disease pro-
gresses through many years, the patient  may  become so helpless as
to be  confined  to  the room or  even to  bed,  and  the dementia may
become absolute, although many reach a fatal stage with but slight
dementia and with but slight  impairment of  memory, aud  in some
cases intelligence is not at all  affected.  These mental  troubles usually
supervene long  after the motor troubles have been in existence, but
occasionally the two sets of symptoms are synchronous.  The duration
of the  malady is very chronic, and patients frequently live to be sixty,
seventy, or eighty  years, and even longer.
   Pathology.  The pathology of Huntington's chorea, like that
of Sydenham's  chorea and athetosis, is somewhat obscure.   In one 
DISEASES OF THE CEREBRUM.
347
case of Huber's there  was found to be a cerebral  pachymeningitis.
In one of Macleod's there  was  a  cerebral pachymeningitis and  a
haematoma of the left hemisphere, the latter extending from the pos-
terior  portion of the frontal lobe into most of the parietal lobe;  the
superior parietal convolution, the ascending frontal and  parietal con-
volutions iu their upper part, and some other of theparietal convolutions
being  thickened and atrophied.  In another case of Macleod's seve-
ral tumors  of the dura  mater  were found  in  the left hemisphere
implicating the first and second frontal convolutions, the upper por-
tion of the ascending  frontal and  the ascending parietal, causing a
depression and thinning of the cerebral  parenchyma, but not leading
to complete destruction of the gray matter.  The arteries of the cere-
brum  were also atheromatous, and the cerebrum itself was firm and
pale.  The  spinal cord was normal.  In still another case of Mac-
leod's  there was a pachymeningitis and hgematoma of each hemisphere,
implicating the parietal lobes and the posterior portion of the frontal
lobes, and reaching down to  the fissure  of Sylvius.   The pia mater
was congested and adherent.  The  meningeal vessels  were dilated
and varicose, and  the larger vessels were atheromatous.  The Pacchi-
onian  bodies  were numerous  aud voluminous,  particularly on  the
left.   The cerebrum was abnormally small, aud its convolutions gen-
erally atrophied,  particularly of the superior  parietal lobe.   The
cerebral substance  was  firm  and  congested, and  the perivascular
spaces very  marked.   But  little fluid  was found  in the ventricles.
The choroid plexus contained small gliomatous bodies.  The walls of
the lateral  ventricles  were  red  and  granular, and the floor of  the
fourth ventricle was covered with large and thick granulations.  The
spinal membranes were congested,  but  the spinal  parenchyma  was
sound.  In Maclaren's case the dura mater and the pia were thick-
ened,  the Pacchionian  bodies voluminous ; and  there was subarach-
noid  hemorrhage, covering the  middle  lobe on  the  two sides,  but
most  on  the  left.  There was general atrophy of the convolutions,
abundant fluid  in the ventricles, the cerebral substance was ansetnic,
a focus of softening was found in the centre of the right optic thala-
mus.  The meningeal vessels and the anterior columns of the spinal
cord were congested.   In Berkeley's case there were dilatation and
thickening of the arterioles, small necrobiotic foci around numerous
vessels, amyloid corpuscles  in the  lymphatic  sheath, vacuoles  of
the cord, and  white substance,  varicosities of the sheath of Schwann,
absence  of axis-cylinders of  the nerve-fibres,  and  complete pig-
mentary degeneration  of a large number  of cortical cells with loss
of their processes.  Cellular alterations in  the spinal cord  were
found, the  cellular degeneration being especially  marked  in   the
spinal enlargements, whilst  there  was an antero-lateral sclerosis.
The heart was affected, but  without any case  of old or recent endo-
carditis.  In  Bacon's case there  was a chronic arachnitis, the cere-
brum  was atrophied, and there was much fluid in the ventricles.   In
Vassitch's case no  lesion whatever was  found  in  the cerebrum or
cord.  In Pau's case the  cerebral meninges were found to be pale
and amemic, the cerebro-spinal fluid  was abnormally large, the cere- 
348
NERVOUS DISEASES.
bral parenchyma was pale, markedly atrophied, the  white  and gray
substance being  somewhat  less dense  than usual, whilst there was
softening of the spinal  cord from  the pyramids to the inferior third
of the dorsal  region, so that the  medullary substance of the  ante-
rior half was converted  into  a diffluent pulp, whilst the posterior
half was abnormally  dense and  resistant.   In Charcot's case the
cerebral  meninges were found  to be very adherent in certain places,
particularly in the anterior  and middle lobes, and where these adher-
ences occurred the cortical substance presented a deeply rosy colora-
tion and was resistant to a stream of water.  The convolutions were
very small, particularly the anterior ones, and there was such a large
quantity of fluid in the meninges as to warrant  the term oedema of
the pia  mater.   In  Tissier's case the cerebral pia mater was thick-
ened, slightly  congested, and adherent  in only a few places.  There
were  numerous  foci of softening upon the external face of the two
occipital lobes and the third and second frontal convolutions of the
left hemisphere.   This  softening was entirely cortical, and absolutely
no lesions of the heart or vessels were observed.   From this rSsume
it will be seen that there is nothing about the pathological lesions  to
constitute anything pathognomonic of Huntington's chorea, although
it will be noted  that there has been a disposition to  affect the motor
convolutions and sublying  strands and  the motor  portions of the
basal ganglia.   The  lesions  seem to  be grosser than is the case
in ordinary Sydenham's  chorea,  and constitute  a  marked type  of
meningo-encephalitis.   The relative frequency of meningitis, hsema-
toma, and gross arterial  lesions, such as atheroma, is remarkable when
compared with the infrequency of these in Sydenham's chorea.
  Prognosis. The prognosis of Huutington's chorea is exceedingly
grave, not only because a case has never been cured, but also because
of  the tendency to  mental  impairment and to the heredity being
transmitted.
  Diagnosis.  The diagnosis of  Huntington's chorea is made very
readily.  The characteristic dancing  and posturing  movements and
grimaces, the mental impairment, the peculiar inco-ordination, often-
times the progressive course of the disease and the heredity, all
together make a picture that bears only a faint resemblance to  any
other disease.  The  maladies from which it should be differentiated
are—
       Sydenham's chorea;
       Athetosis;
       Locomotor ataxia;
       Friedreich's disease;
       Paralysis agitans;
       Disseminated sclerosis ;
       Hysterical chorea ;
       Palmus.
  Sydenham's chorea is a  disease of infancy, whilst  Huntington's
chorea is a disease seldom occurring under  the age of fifteen, gener-
ally between thirty and forty-five years of age, and it may  therefore
be practically  called a disease of adult life.   In Sydenham's chorea, 
DISEASES OF THE CEREBRUM.
349
too, the movements are fibrillary, except in some temporarily violent
cases, and  these  fibrillary movements, as  I have  again and  again
said, are jerky, beginning quickly and ending quickly, or the jerkiness
may be merged into  a gradual, wavy movement, as in the  athetoid
variety.
  The  movement of athetosis is  wavy and gradual, usually of the
hand.  Double athetosis may cause a certain difficulty of diagnosis
at times.   It usually dates back to iufancy, however.  These move-
ments are not only more gradual and wavy than the dancing move-
ments of Huntington's chorea, but they are accompanied by rigidity
and contracture of the affected  parts,  usually  leading  to  marked
muscular deformities,  whilst  neither rigidity  nor contracture is
observed in Huntington's chorea.  The mode of progression is also
different.  The patient with Huntington's chorea dances and  postures
and grimaces as he goes, with a suppleness that is very suggestive of
affectation.   The double athetoids, on the contrary, are spasmodic
and stiff in their movements, walking on the point of the  foot, the
knees approach  so that they are knock-kneed, the arms are spas-
modically held against the trunk,  whilst the forearms are spread out
as  if balancing, and  the fingers are affected with the  peculiar stiff,
wavy movement, at  the same time that  the trunk is held  stiffly
with the shoulders thrown back, and the speech, instead of being
thick and explosive, is jerky, high-pitched, scanning, somewhat nasal
and guttural.
   Locomotor  ataxia  may have an inco-ordination  that seems  to an
 inexperienced eye to resemble the inco-ordination  of  Huntington's
 chorea, but  in reality it is  very different.  The case  of locomotor
 ataxia has no choreic movements of the dancing, grimacing type, and
 the inco-ordination is therefore a pure inco-ordination, not due to
 the choreic movements.   In the gait of locomotor  ataxia the heel is
 brought down with a flapping movement.   In locomotor ataxia, toe,
 mental impairment is not  usual, and there is  usually very marked
 sensory impairment of the sense of touch, muscular sense, and pain,
 and the bladder and  rectum are often affected at an early stage.
   In Friedreich's disease the diagnosis sometimes  needs care.  The
 movements  generally affect one  extremity or a segment of an ex-
 tremity, and consist of a sort of instability of position, and not  of the
 dancing movements  of Huntington's chorea,  for  the former small
 muscular movements are not so multiple or various or irregular as in
 the latter disease. The motor inco-ordination is especially prominent
 in intentional  movements, whilst in Huntington's chorea the choreic
 movements diminish with a volitional movement. In Friedreich's dis-
 ease the patient grasps an object in a different way from what he would
 do if afflicted with Huntington's chorea; for in the former the open,
 flat hand  poises, as  it were, for  some  time over  the object before
 grasping it.  In Friedreich's disease the gait is aggravated by closing
 the eyes.  (Romberg's symptom.)
   In paralysis agitans  the characteristic visage and attitude (vide
 Chapter XIII., under "Paralysis Agitans"), the tremor that is so
 entirely different from the  dancing movements   of  Huntington's 
350
NERVOUS DISEASES.
chorea, the slow, wise, deliberate, monotonous speech, easily enable
us to make the diagnosis.
   In disseminated sclerosis the tremor is a tremor, and not a dancing
seemingly voluntary movement, as in Huntington's chorea, whilst the
speech is  scanning, slow, jerky, and entirely different from the nasal
confused, sticky pronunciation of Huntington's chorea.
   In hysterical chorea—chorea  major or rhythmic chorea—as  it is
sometimes called, the diagnosis is easily made.  This chorea manifests
itself in single attacks, as do hysterical convulsions.   The movements
are rhythmical and of great variety,  so  that they may sometimes be
dancing, hammering, swimming, etc.  The attacks are provoked by
compression or excitation of hysterogenic points, and are sometimes
arrested by the same  method, and there may exist such accompanying
symptoms of hysteria as limitation of the field of vision, anaesthesia,
color-blindness, etc.   The picture is therefore a radically  different one
from the  chronic, progressive  Huntington's chorea, with its persist-
ently dancing movements.
   When palmus, or convulsive tic, is localized the diagnosis is easy;
but  when it has extended  and   become  generalized the diagnosis
may need  some  care, especially as palmus may be hereditary.   The
movements, however, are entirely different from those of Huntington's
chorea.  They are  very brusque, rapid, instantaneous.   They have
not  the waviness or  dancing aspect  of  Huntington's chorea.   The
movements are automatic in that the same movements  or order of
movements are  repeated again and  again, and in  this respect they
differ markedly  from the great variety  and semi-involuntariness of
the  movements of Huntington's chorea.  They  are not continuous,
but occur in paroxysms varying in duration.   They can be arrested
by a voluntary effort for a longer or  shorter time, but this effort of
suppression of them is generally accompanied by a feeling of extreme
anguish, after which there is a sort of discharge, as it were, and the
movements become  more pronounced.   By means of this voluntary
control patients affected with palmus  are often able to accomplish in-
tentional acts during which the movements are completely suspended,
whilst in Huntington's chorea there is only a diminution of the move-
ment in performing the voluntary act, or in some cases suspension for
a few seconds of the movements of the muscles that are concerned in
the voluntary action, whilst the other muscles  not concerned in  this
voluntary action are  in motion with the characteristic  movements.
Palmus generally begins at a very early age, in  childhood, or early
adolescence, while Huntington's chorea is exceptional at this period,
and  is a  disease of adults.  In  palmus, too,  there  often is ejacu-
lation or exclamation of entire words, while in Huntington's chorea
the sounds are inarticulate and are  usually produced as in  Syden-
ham's chorea by involuutary movements, such as movements of the
tongue against  the  buccal cavities, the   laryngeal squeaks, etc.  In
palmus, also, there is sometimes observed what is known as coprolalie
—i.  e., an  involuntary repetition  of certain gross words or expres-
sions ; or  echolalie, or echokinesia—i. e.,  involuntary repetition of
certain words which a  patient is pronouncing, or of the gestures 
DISEASES OF THE CEREBRUM.
351
which are made before him.   These phenomena are never observed
in  Huntington's chorea.  The mental  alterations in palmus when
present consist of fixed ideas, of certain emotional fear of places, the
folly of doubt, and of touching, etc., whilst in Huntington's chorea
there is a very gradual dementia  with slight  depression, sometimes
at  the onset, and there are slight losses of memory during the differ-
ent stages of the malady.
   Treatment.   The treatment of Huntington's  chorea is a matter
of considerable doubt.   I am inclined to think that if the malady
were properly treated at the start it  could be controlled ; but the
great dread of it, especially in the hereditary cases, causes the patients
generally to be hidden from observation and sight.   Certainly in the
advanced cases which I  have seen and treated the ordinary medica-
tion  of chorea is absolutely without effect.  I have tried arsenic, bro-
mide, hyoscyamine, even hyoscine slightly, and have never yet been
able to observe any result.  I have never been able to try the electric
currents, but I doubt veiy much whether they would have much effect,
especially as the European observers claim  to have seen none.  Were
I to  have a case  brought to me at the  onset, I should certainly put it
to rest and treat it with arsenic, Fowler's solution, commencing with
two  drops three times  a day, running up to six or eight drops,
with bromide of potash, ten  to thirty grains in the day ; and  then,
if this did  not succeed,  I should try  hyoscyamine  or  hyoscine, T^r
grain once  or twice a day, and apply  the galvanic current carefully
to the spinal column.  I should, howrever, mainly rely upon the rest.
But it must be borne in mind that this is pure speculation, as I have
never been able to treat a  case in  this early  stage myTself, nor have
I  known of anybody else who has.

                          ATHETOSIS.1

   Athetosis was first described by William A. Hammond, in 1871,
 and since that time the  disease  has beeu described by a number  of
 other authors.   He gave it the name because it was  mainl\T charac-
 terized by an  inability to retain the fingers and toes in any position
 in which they might be placed, as well ar. by their continual motion.
 Fig. 159 shows the hands of a patient afflicted with this disease.  In
 Hammond's case  the  affection was  unilateral.   In  1872 Clifford-
 Albutt published the first case of double athetosis—i. e., of athetosis
 implicating all four extremities.  The movements of the fingers and
 toes are slow,  wavy, and gradual, the fingers  having  a tendency to
 separate and  the hands having  a  tendency to  pronate,  whilst the
toes simply have a less tendency to separate,  and  none  to flex
 or extend ; aud  these movements are continuous, so that, as Ham-
 mond says, there  is no fixed  position.   In  some  rare  cases  that
 have been  described by Kinnicutt, athetosis has  neither paralytic
 nor  sensory troubles, although  it is usually marked by some degree
 of imbecility  (Fig. 159); but  in the vast majority  of instances it
i From aderoc, without fixed position. 
352
NER VO US DISEASES.
is conjoined with contracture or paralysis of the affected limb, some-
times with  muscular  atrophy and  hypertrophy, and in  many cases
there are marked  symptoms  of intracranial lesions,  such  as con-
vulsive and apoplectic  attacks, dementia,  and cranial deformities,
The so-called post-hemiplegic chorea is, in my opinion, nothing more
than athetosis.
                              Fig. 159.
Case of athetosis.
  Athetosis is a hereditary disease in a large proportion of cases,
although the heredity cousists rather of a family neurosis thau especi-
ally of athetosis.  It may occur at any time from infancy to advanced
age.   Sex does not appear to  be of much etiological consequeuce, but
prolonged  or difficult labor,  infectious  maladies, traumatism, and
other general causes have seemed  at times to be causative  factors.
  Athetosis may occur from  intracranial and spinal lesions, periph-
eral  neuritis, aud even from  hysteria.  The intracranial  lesions are
not fully understood, and  the autopsies  have  been  rare.  The few
autopsies have been  made  by Hammond, Bernhardt,  Duchenne,
Bourneville, Putnam, and others. There have beeu found pachymenin-
gitis, cerebral and cerebellar asymmetery and atrophy, a slight degree
of disseminated sclerosis, adhesions of the lips of the fissure of Sylvius
to the frontal lobes, whilst Putnam could detect absolutely no cranial
lesion visible to the naked eye, aud Bourneville  has had a similar
case.   Ross, Rolla, and  Massalongo have found  a secondary degen-
eration of the pyramidal columns of the cord,  but Curella and Put-
nam  had nothing  of  this  kind  in their cases,  whilst Bourneville
discovered a  gray discoloration of the internal  portion  of the left
anterior pyramid.  In a case reported by Ringer there was a cyst in the
posterior half or two-thirds of the lenticular nucleus, the cyst lying 
DISEASES OF THE CEREBRUM.
353
in front, immediately without the inner capsule, aud passing obliquely
through the lenticular nucleus.   It  also  involved the whole  of the
white matter lying outside and rather beneath the optic thalamus for
about a half-inch.  G. M. Hammond has also  reported a case  with
tumor of the basal ganglia.  The caudate nucleus  was also involved,
and a few of the fibres passing between the two nuclei of the  corpus
striatum were destroyed. Dr. Hammond is inclined to think that this
is the only real description of the pathology that has been published,
and that, as he stated in his  original article, the seat of the affection
was in the optic thalamus or corpus striatum.  Landouzy and Sturges
found respectively lesions  of the lenticular nucleus and the  corpus
striatum ; but  the other lesions which have been already detailed and
those which are about to  be  described gainsay  this view.   I believe
that the cerebral  lesions  associated with cerebral palsies of child-
hood are often causative of this malady (vide "Cerebral Palsies of
Childhood").  Athetosis  has been observed  in  conjunction  with
locomotor ataxia, always of the bilateral or double form.   It is also
occasionally associated with neuritis, as in Lowenfeld's case, and with
hysteria. Outside of these pathological findings, there is no doubt in
my mind that athetosis is, more frequently than is generally imagined,
a functional disease in the sense in which we apply the term " func-
tional" to  chorea; for, as stated in Chapter IX., under "Chorea,"
there are certain cases in which the movements are athetoid, aud
other cases of  chorea in which athetoid  movements are commingled
with what I  believe to be the true choreic movements, and the cura-
bility of these former is the  same, so far as I have been able to  per-
ceive, as that of the latter.
   The prognosis of athetosis, when  it is organic, is very unfavorable,
for no case has been either cured or ameliorated ;  but, as I have just
said, the prognosis of the functional cases that are generally mistaken
for those of chorea of the Sydenham type is the same as that of the
chorea itself.
   The differential diagnosis of athetosis  is exceedingly easy, because
the movements are not unlike those of any other form of nervous
disturbance.   Even in the athetoid  chorea the waviness and gradual
worm-like character of the movements are readily distinguished from
the quickly beginning and quickly ending fibrillary jerk of the  true
Sydenham chorea.  The so-called cases of post-hemiplegic chorea are
really, as Dr. Hammond  agrees  with me in believing, cases of post-
hemiplegic athetosis.
   The treatment of athetosis, when it is  of the organic type, is  not
known, for as  yet no drug has been found to be of any  value.   It is
probable, however, that the future will show that the athetosis which
is conjoined  with peripheral neuritis will  be relieved  by the same
treatment as that of the neuritis.  In athetoid chorea the treatment
should be the same as that of Sydenham's chorea.
23 
CHAPTER  VIII.
  DISEASES OF THE CEREBRO-SPINAL  NERVOUS SYSTEM
                    AND ITS MEMBRANES.

  HYPEREMIA AND ANEMIA OF THE  BRAIN AND CORD.

  Hypersemia and anaemia of the brain and cord are terms that
are very glibly employed by the general practitioner to explain many
symptoms whose pathology is obscure to him.  But their use by the
neurologist has steadily decreased within the last ten  or fifteen years,
until nowadays it is exceedingly rare to hear  a diagnosis of this kind
made in the neurological clinics; certainly in most of those of New
York it is never made.   Indeed, when, in my Inaugural Address as
President of the New  York Neurological Society, at a meeting held
in May, 1890,1 expressed myself as I shall do in  this chapter, there
was unanimous agreement with my views, with the exception of Dr.
William A. Hammond, whom I  had invited to  be  present.  Most
of the neurological text-books of late years have either omitted any
chapter with these headings, or else have been very cautious in their
statements.
  The symptoms alleged to be those of cerebral hypersemia or anaemia
are headache, flushing or pallor of the face, delirium, vertigo, motor
or sensory paralysis, retinal changes, slight aural symptoms, insomnia,
and myosis.  If these symptoms are examined one by one, the sig-
nificance of each will become decidedly problematical to anyone who
has had much acquaintance with the clinical aspects of cerebral dis-
ease.  Headache, for example, is a very general symptom, indicating
too many disorders  to  be of any service except in conjunction with
other signs, and the statement that it is apt to be localized and wide-
spread in cerebral hypersemia is a pure assumption, of which no proof
has ever been  adduced.   The condition of the capillary circulation
of the face is by no  means  a reliable guide  to the condition of the
cerebral  capillary circulation.   Any  hospital  surgeon  knows that
marked meningeal hypersemia is often  associated with  great facial
pallor  in fractures  of the skull and the attending cerebral  hyper-
semia, just as great  pallor may  exist with many other hypersemic
intracranial conditions, whilst precisely the same  pathological states
may cause vascular  flushing in other individuals.  Delirium, like
headache, is a general symptom  indicative of too many conditions to
be of any value by itself.   The  same remark is true of vertigo. Of
motor and sensory paralyses as symptoms of cerebral hypersemia and
ansemia, it may simply be said that there is not an authentic case on
record in which a simple ansemia or hypersemia has  caused a motor 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.       355

or sensory paralysis.  It is  almost, if not absolutely, impossible  to
distinguish from the normal retinal changes consisting only of slight
differences in vascularity, as every ophthalmologist knows, while the
well-marked  changes  of neuro-retinitis have never  yet  been shown
to have been produced by  cerebral ansemia or hypersemia.   Tinnitus
aurium aud insomnia, like headache, delirium, and vertigo, are symp-
toms that are absolutely worthless by themselves.  Neuritis is said  to
be a symptom of cerebral hypersemia.  It may be, but nobody has
yet made  public  the  proof.  It will thus be seen that,  of all these
symptoms, headache, delirium, vertigo, tinnitus aurium, and insomnia
are general symptoms which only derive a diagnostic value from their
associates, while flushing or pallor of the face is an extremely doubtful
indication of'the  intracranial  circulation; motor and  sensory paral-
ysis  and retinal  changes  are  absolutely worthless as signs, and the
diagnostic value  of myosis is a pure  assumption.   Nor, when we
take these  symptoms together in a group, can we say that they are
indicative  of cerebral hypersemia, because they  are found in  so
many other  diseases  of the  brain.  Hammond  affirms that  cere-
bral hypersemia  can  produce the symptoms of apoplexy, paralysis,
convulsions,  a soporific condition, mania, and aphasia.   But when
we turn to  his chapter on the  pathology of  this  particular form
of cerebral disease we find the statements that the capillaries and
large bloodvessels of the brain  and pia  mater will be found to  be
increased in size; that the white  matter of the  brain is  increased  in
consistence aud density, the  gray  matter is red or even violet in hue;
there is a large amount of subarachnoid effusion, or  even an effusion
 into the  ventricles, and the choroid  plexuses are often  enlarged;  if
 there have been  repeated attacks of cerebral congestion, granules of
 hsematin will be found in contact with  the bloodvessels,  or the latter
 may be unusually tortuous and have minute aneurisms.   Now, I
 submit, this  description is not that  of a  mere hypersemia, but it  is
 a condition of actual structural disease of the cerebral tissue, quite as
 pronounced as can be found in many cases of general paresis of the
 insane, in the severer cases of chorea, or  in certain cases  of intra-
 cranial syphilis, as may be seen by turniug to the chapters upon  these
 subjects;  indeed, it would seem that a  part  of this description—
 that relating to the hsematin and the tortuosity and the aneurismal
 swellings of  the arterioles—is acknowledged to be from the work of
 Laborde upon softening  aud congestion of the brain of the aged,
 written in 1866.   In addition  to this description, Dr. Hammond
 also says that we  will  find this state of the brain described by Calmeil
 in 1826, subsequently given the name of Vetat crible  by Durand-
 Fardel in 1854, and described respectively in treatises upon the in-
 sane and the aged.
   The symptoms of spinal congestion  are said to be: a dull, aching
 pain, increased by the recumbent posture aud by  standing,  if the
 lower cord is affected, but not augmented  by pressure; an occasional
 sensation of heat in the cord ; disturbances of sensibility and motility,
 such as hypersesthesia,  shooting-pains, girdle-sensation,  formication,
 etc.; erections, vesical and  rectal paralysis, diminution of electro- 
356
NER VO US DISE A SES.
muscular reaction, and bedsores. These are the symptoms of myelitis;
aud not only has it never been proven that mere congestion can pro-
duce these symptoms, but there has never been any means demon-
strated  of making  the differential diagnosis.   The  symptoms  of
spinal  ansemia are said to be  manifold.   In one class of cases the
morbid  action  has  been  supposed to  be largely confined  to the
posterior columns of the cord.   In another the  ansemia is supposed
to be  restricted  to  the antero-lateral columns  of the cord.  It  is
admitted by the  writers upon this subject  that post-mortems are
lacking to support these claims, and if the chapter upon " Combined
Sclerosis"  is read, together with  the chapters  upon  "Lateral and
Amyotrophic Lateral Sclerosis," it will be seen that the symptoms of
disease of  the postero-lateral columns of the cord are  perfectly well
known at the present day, so that if any congestion of them had been
capable of causing the alleged characteristic symptoms just described,
it should have been demonstrated by at least one post-mortem.
  The truth of the matter is that our knowledge of nervous diseases
has increased  so rapidly within the last quarter of a century as to
make it a matter of little surprise that the older authors should have
attempted to satisfy their ignorant consciences by dubbing as conges-
tion  or hypersemia  the many  puzzling  symptoms which time has
resolved  into distinct  system-groups.  The most difficult of all
phrases for the average scientist is,  " I do not know."  The disease
must be labelled  at auy  cost, and, once labelled,  it takes many  years
to rub out the  brand.   Meningitis, general  paresis, porencephalus,
cerebral  and spinal  syphilis, disseminated  sclerosis, bulbar  lesions,
poliomyelitis anterior, central or transverse myelitis, syringomyelitis,
progressive muscular atrophy, acute ascending or Landry's paralysis,
locomotor  ataxia, especially in  its  early stages, many forms of neu-
ritis,  focal diseases  of the brain, lateral sclerosis, many forms of
lithsemia and neurasthenia—these  are some of the  many diseases
of which we  now possess a knowledge at which the  general  prac-
titioner of twenty-five years ago  might  well  stand appalled, and
which he may well be pardoned for having supposed  to be due to
some vague form of ansemia or hypersemia.  Indeed, Leyden, writing
in 1875 of essential  infantile  paralysis,  thought it was caused  by a
peculiar congestion of the cord, while Cornil and Lupine had demon-
strated some two years before that  the pathological condition was a
disappearance of the  ganglion-cells in  the  anterior  horns of the
spinal cord, the  autopsy in their case being followed by another one
to the same effect by Gombault  in the  same year as  Leyden's article.
  After this necessarily cursory review, we may  ask ourselves, Can
hypersemia or ansemia of the brain and  cord  be diagnosed ?  I, for
my part, would answer very positively that  a diagnosis is not pos-
sible by  means  of the  nervous symptoms  alone.  In  other words,
the symptoms as I have  narrated them above are not sufficient,  indi-
vidually  or in a group, to warrant a diagnosis of ansemia or hyper-
semia of the brain or cord.   It must be remembered that the brain is
an exquisitely and well-nigh inconceivably complex organ, pulsating
and vibrating with  a  most explosively nitrogenized  molecular life, 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.        357

and reacting to myriad  influences  in  a kaleidoscopic way that con-
stitutes the never-tiring charms of  character, poetry, music,  and the
varied forms of mental activity.  To put our finger on a few slight
changes of temporary nature that  occur in an organ like this, say
that they  are  really due to hypersemia or ansemia, and exclude all
the cellular play, all the  reflex  modifications from the other viscera of
the body,  all the morbific elements that may be circulating in the
blood, all the factors of  temporary  discomfort  that  are to be  found
in the atmosphere, in the food and  clothing, and in the circumstances
of a human  being's environment—even  if this is not impossible, it
has certainly not been done.  If we  have evidence of some  intra-
cranial disturbance, such as those we have already detailed—headache,
delirium, vertigo, tinnitus aurium,  insomnia, flushing or pallor of the
face—and  with  these we  have some concomitant conditions that
would make it reasonable to suppose that there might exist a conges-
tion or ansemia of the brain or cord, then we should be warranted in
regarding  such a diagnosis as probable.   Thus, certaiu cardiac con-
ditions, lesions of the great vessels  of the chest and  abdomen, certain
forms  of hepatic disease, tumors making pressure  upon these great
vessels, a general ansemia,  leucocythsemia, intense mental exertion, or
exposure to  great  heat—these  conditions when associated with the
above-described general  symptoms, would make it probable  that the
general symptoms were due to hypersemia or ansemia as  the case
might  be; but even  then there might not be certainty.   I cannot
conceive, however,  how we are to make a diagnosis  of spinal ansemia
or hypersemia, for I know of no pathological observations that would
warrant on the one baud  the diagnosis by means of the vague pains
that are described  by some  authors,  or, ou  the other, by the symp-
toms of the full-fledged diagnosis which  others would have us place
faith iu.

       THROMBOSIS OF THE INTRACRANIAL SINUSES.

   There are certain  peculiarities  in the anatomy of  the cerebral
sinuses predisposing  them to  thrombosis, and these are their great
 width, the rigidity of their walls,  their triangular  form, their occa-
sional septa, the fact that they are not emptied during inspiration,
and, in the case of the longitudinal sinus, the entrance of the blood
 from the cerebral veins at au obtuse  or  right  angle, so that it is op-
 posed to the current.  These factors  all favor coagulation.   There
 are two varieties of thrombosis in these  veins, namely, primary or
 marasmic, and secondary, infective or inflammatory.
   The marasmic form is  much the least frequent,  and  is generally
 found in the longitudinal sinus, and rarely in either  the lateral or the
 cavernous.  It occurs chiefly in those who have been wasted by ex-
 hausting diseases, and is most frequent at the two  extremes of  life,
 iu the  very young  and the very old.   Exhausting  diarrhoea  is the
 most frequent  etiological factor in childreu, but pulmonary affections,
 both acute and chronic, not infrequently cause it.   Other  supposed
 causes in childreu are respiratory obstruction with consequent dilata- 
358
NERVOUS DISEASES.
tion of the right heart, as from pneumonia, pleurisy, and tubercu-
losis.  It is most frequent toward the end of these diseases or in early
convalescence.  In adults, it may be caused by enteric fever, phthisis,
the puerperal condition, and occasionally by carcinoma in old people.
  Marasmic  thrombosis  is generally confined to the  longitudinal
sinus,  but it may extend to  the  lateral,  sigmoid,  and cavernous
ones and the jugular vein.  The clots are dense, resilient, stratified,
aud do not adhere to the walls of the vein, and  seldom occupy the
whole  lumen of the vessel.   Their  organization is  strong, and they
rarely  disintegrate, although in some chronic cases they may have a
canal sufficient to  permit the  re-establishment of the  circulation.
Great  congestion  of the  meningeal  and cerebral  vessels speedily
ensues, with  oedema, but, of course,  these phenomena depend upon
the site and extent of the clot.   For  instance, if this is confined to
one sinus, part of the blood may still pass by  some of the  tributary
veins.   If the clot, however, is  one of the cerebral veins, great oedema
and congestion  results, and the capillaries  may become turgid aud
burst,  giving rise, with the other  factors,  to  red  softening.  The
ventricles may even become distended with serum, and  sometimes
the retro-ocular tissue becomes the site of transudation, causing ex-
ophthalmos.   The  parietal and occipital lobes are most affected by
secondary softening, whilst the  frontal lobes are least implicated.
  The symptoms of the disease are often obscure, and when present
they depend, of course, upon  the sinus  that is affected.   When the
longitudinal  sinus  is implicated  there is distention  of  the frontal
and parietal veins, with  oedema,  occasional  epistaxis,  frequently
strabismus, tremor of the lower limbs,  contracture,  and rigidity of
the muscles of the extremities  and sometimes also  of those of the
neck and back.   General convulsions, with  unconsciousness, are apt
to occur  in children, whilst in adults their  place is  taken by head-
ache and delirium.   It  is said  that the convulsions are occasionally
unilateral or even  monoplegic.  They  are apt to be intermittent in
character and occur in paroxysms.
  The diagnosis of  marasmic thrombosis  is  not always an easy
matter.  Headaches,  the paralysis of one side of the body or of a
limb, with delirium, somnolence, coma, and oedema aud venous dis-
tention of the scalp of  the parietal and frontal regions, may create a
strong suspicion  of the affection  in adults if  other cerebral  lesions
can be excluded.  (See chapters on " Cerebral Tumor," " Intracranial
Tumor," "BrainSyphilis," " Hemorrhage," " Embolism and Throm-
bosis," and "Meningitis").   In children the tentative diagnosis may
be  made when an exhausting  illness is  succeeded by convulsions,
oedema, and venous congestion of the scalp in the parietal and frontal
regions, epistaxis, and evidences of some localized brain lesion.
  Secondary infective or inflammatory thrombosis is caused by path-
ogenic micro-organisms, and occurs chiefly in  adults, and seldom in
old people or children.   It generally affects one of the dual sinuses,
and usually that one which is nearest  to the seat of the primary dis-
ease.   It is often associated in  this latter stage with meningitis^as
well as with  small cerebral or cerebellar abscesses.   The infection 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.        359

may extend from  some  traumatic lesion of the  scalp or cranium ;
but the most frequent cause is middle-ear disease affecting the sig-
moid sinus.  Pathological lesions  of the face aud head may also give
rise to it, such as anthrax, erysipelas, cellulitis of the orbital cavity,
ulceration in the nasal fossa and pituitary mucous membranes, peri-
ostitis of the jaw from dental caries, inflammation of the tonsils, and
retro-pharyngeal abscess.  The infection may extend to the sinus by
contiguity of tissue, so that  the wall of the vein becomes inflamed,
and this in its turn sets up coagulation and adhesion of the clot to
the inner coat;  or a  small vein  at the site  of lesion may  become
thrombotic, and thus the coagulation with its attendant phenomena
extend to the sinus.  In  some cases pressure on the sinus, as from a
tumor, is said to be the cause, but it is rare.  In infective thrombosis
the endothelium of the vein desquamates, and  the walls become soft,
thick, and so altered  as  to  tear.  Hemorrhage, singular to say, is
nevertheless rare,  because the blood  coagulates simultaneously with
the alterations in the coats of the  vein.  The clot of infective throm-
bosis  soon  disintegrates  and breaks down into  a  greenish-brown
grumous fluid swarming with bacilli.   From  this source infection
may extend in innumerable directions, either through the veins or
through the general circulation or through the coats of the vein into
the neighboring tissues.  The bone near the sinus may become deeply
pigmented, of a dark greenish aud  brownish hue,  and eroded,  the
staining being thought to be due to the action  of the bacillus pyocy-
aneus or some  other chromogenic organism, and these markings on
the bone often photograph the position of the  sinus  very accurately.
In some cases a similar stain may be left upon the cerebellum by  the
lateral and sigmoid siuus, or upon the bones and soft tissues by  the
internal jugular,  posterior  condylar, and  vertebral  veins.  If  the
 infective process  has caused only a  very limited  disintegration, a
formative process can be  established in the wall of the vessel, granu-
lations springing from  the  wall of the sinus  and the adjacent dura
mater, and penetrating  into the osseous erosion on the one side aud
into the lumen of the vessel on the other.   With time, fibrous tissue
will completely obliterate the sinus.   If the granulation-tissue should
be displaced or disintegrated, the infection may  pass through  the
open mouths of the vessels into the general vascular system, so that
cerebral and  cerebellar meningitis of the  pia may occur, and even
pulmonary infarctions,  cerebral  and  cerebellar abscesses  may be
formed.  The  symptoms of infective  thrombosis  are  themselves
rarely sufficient to base a diagnosis on, but this  can usually be done
 when there has been a history of trauma, middle-ear trouble, or some
well-marked  infective cause  such as anthrax  or facial  erysipelas.
Severe headache is an early and frequent symptom.  It may be gen-
eral, or over the region of the  affected sinus, although its value as a
localizing symptom is not always  great.  Vomitiug is frequent.  The
febrile rise is rapid, occasionally to 103° or even 106° F.; but it  has
 marked fluctuations  and is sometimes very remittent.  The  pulse is
small, quick, and  thready, even when the patient is deeply narco-
tized, as by chloroform or ether.  Rigors are frequent, coming earlyT, 
360
NERVOUS DISEASES.
 often repeated,  and in some cases with  a tendency to periodicity.
 They are succeeded  by profuse perspiration, the tongue is dry and
 coated, and there is a heavy, peculiar  odor from the mouth.  There
 is  a  strong  tendency  to diarrhoea,  although  exceptionally there
 may  be constipation.   If the  disease progresses, the symptoms
 may assume the pulmonary, abdominal,  or meningeal  type.  The
 pulmonary symptoms are, first,  dyspnoea, a localized stitch, " prune-
 juice "  expectoration,  and coarse rales,  which are succeeded by
 moist rales.   In the abdominal  type there are  abdominal  pain,
 meteorism, diarrhoea, "pea-soup" stools  of an extremely  offensive
 odor, great  prostration, pale, pinched face, often a bright  blush of
 the cheek, occasionally a rather dark rash, like measles, which does not
 disappear on pressure and is  not raised above the level of the skin;
 but there are no rose-colored spots, and, unlike the disturbance of
 the skin in enteric fever,  the rash is not elevated, does not disappear
 on pressure, and does not come out in  successive groups.  The men-
 ingeal symptoms are the common ones of meningitis (see Chapter on
 " Cerebro-spinal Meningitis"), namely, vomiting, fever, great excite-
 ment, hypersensitiveness,  and agitation, clonic and tonic contractions
 or  paresis of certain  groups  of  muscles, especially of the face, neck,
 and upper extremities, strabismus, retraction of the head backward
 or  to one side,  and delirium.  The  mind is clear,  however, at the
 beginning of the trouble,  although there may be some slight irrita-
 bility.   These three great types, pulmonary, abdominal, and menin-
 geal, may be commingled.   To  them also may be added the symp-
 toms of cerebral abscess.
   Treatment.   The treatment should consist in the removal of the
 cause, if possible, the remedying of the meningitis which may have
 ensued, and of opening the resultant cerebral or cerebellar abscess if
 there has  been any.  The treatment of the meningitis has already
 been discussed in the chapter upon " Cerebro-spinal and Suppurative
 Meningitis" and that upon " Abscess."  The opening of the sinus
 itself and of  the mastoid cells is a matter  of surgery, for which re-
 course must be had to the general or aural  surgeon.

                  SUPPURATIVE MENINGITIS.

  Cerebral  meningitis  occurs in the  different  forms of  tubercular
 meningitis, pachymeningitis, lepto-meningitis, cerebro-spinal  menin-
 gitis,  and hydrocephalus.   Suppurative meningitis is the only men-
 ingitis of which we have auy practical  knowledge besides  these.
  Etiology.   The best  known causes are purulent pleurisy,  ear
 disease, nasal  disease, cerebral traumata, exposure to  cold,  insolation,
 infection, erysipelas, carbuncle, and extension from other viscera.
  Ear disease is probably the  most  frequent of all  the causes of
 suppurative meningitis.  Between  the  ear  and  the  petrous  portion
 of the temporal bone there are many intercommunications by means
 of veins, arteries, and connective tissue.  The latter is a particularly
good avenue for septic extension, as it contains large  branches of the
middle meningeal vein and artery, passing to the mucous membrane 
THE CEREBRO-SPINAL NERVOUS SYSTEM.
361
of the tympanum through the petro-squamous fissure.  Another ex-
cellent  highway for suppurative affections  between the ear and the
base of the cerebrum is the facial nerve, as only a very thin layer of
bone separates it from the tympanic cavity, so that both the periph-
eral and central tract of the nerve may very readily be affected.
  The cribriform plate of the ethmoid may conduct a lesion  of the
nasal bones to the brain, and in  this way cases of meningitis follow-
ing pertussis may arise.
  Suppurative meningitis  may be set up by cerebral traumata, and
in so many instances  there  may be elicited a  history  of cerebral
trauma which the family had entirely overlooked that I am inclined to
regard this as a much more frequent cause than is usually supposed.
  In rare cases exposure to cold  and insolation have been known to
act as causative agents  in suppurative meningitis.
  In some cases erysipelas and  carbuncle are known to have been
followed by suppurative meningitis.
  Cases of suppurative  meningitis have been  observed following
ulcerative endocarditis, septicsemia,  pysemia, croupous  pneumonia,
suppurative pleurisy, acute articular rheumatism, typhus, dysentery,
scarlatina, and smallpox, as wTell  as from suppurative disease of other
viscera by the  passage of the infection through the  lymphatics  or
bloodvessels.
   Pathological Anatomy.  In meningitis  resulting  from nasal
and  aural  disease the base  and lateral  aspects of  the  brain  are
mainly affected, whilst in  the infectious  cases the vertex is  more
implicated.  In the slighter degrees congestion  of the pia may  be
observed,  dotted with  purulent  matter; but there is more or less
thorough  infiltration matting down the pia to  the cortex, cloudy-
yellow or greenish-yellow in color.  Underneath this infiltration will
be found flattened and ischsemic convolutions.   Along the  course of
the bloodvessels this infiltration is most noticeable.   It generally
passes into the ventricles along the choroid plexus, and an increased
amount of cerebro-spinal fluid is observed.   Atrophy of the  cortex
usually results in chronic cases by reason of the membranes becoming
tough and thick and adherent to each other.   Micro-organisms are
revealed by the microscope in these cases, and further examinations
can be had by inoculations with or without culture.  Netter has
recently made  a collection of  forty-five cases of other authors and
twenty-five of  his own.   In  the latter  were found six species  of
micro-organisms—in four, a  streptococcus  pyogenes; in eighteen,
pneumococci;  in two, a microbe resembliug the  intracellular  diplo-
coccus of  Weichselbaum;  iu  one,  a microbe  very much  like the
pneumo-bacillus of Friedlander  ; in one, a short  bacillus of great
mobility presenting most of the characteristics of the typhoid bacillus;
and  in one, certain bacilli that were  very delicate and  flexible.
Netter's observations and those of the authors in  the forty-five cases
collected by himself tallied in the  main.  Netter believes that the
character of the exudation is indicated by the micro-organism causing
it.  For instance, the exudation in which the pneumococci are  found
is greenish and viscous, and, although the affection is comparatively 
362
NER VO US DISEASES.
a benign one, the meningitis almost always coincides with ulcerative
endocarditis.  The exudation was less adherent and of a sero-puru-
lent nature in the cases in which the  streptococcus was present, but
remarkably thick and viscous in those cases containing the bacillus
of Fried lander.
  Symptomatology.  Suppurative meningitis is indicated by coma,
fever, delirium, muscular twitchings, headache, convulsions, paralysis,
and optic neuritis.
  Many forms of cerebral affection are characterized by the symptoms
of delirium, hebetude or coma, convulsions, and  muscular twitchings,
so that they are  not pathognomonic  of this particular form of men-
ingitis.   The degree of fever is usually between 39.5°  and 40° C.
A constant headache, intermitting to some extent, is always present.
Paralysis may vary in its nature according to  the  portion  of the
brain affected, although it is usually  present in the  form of hemi-
plegia.   Optic neuritis is  sometimes seen, when it is of considerable
diagnostic value; but it  is often absent, and in most  cases  is not
generally observed  until  the case is  quite advanced.   It does not
indicate  the character  of the lesion,  however,  but simply indicates
the fact that an intracranial  lesion  exists.  Opisthotonus may even
be observed in some cases, and retraction of  the head usually occurs.
In  some cases the  headache, dizziness, and  some  mental confusion,
resulting  in children  from suppurative  ear-trouble,  may last for
several days, and be entirely relieved  by the discharge  of pus from
the external ear.   In  cases of less degrees of suppurative menin-
gitis, particularly those caused by  ear-trouble, the symptoms  may
commence with  heaviness, sleeplessness, and  slight headache, passing
gradually into the more pronounced stage.
  Diagnosis.   Cerebral  symptoms alone cannot be depended upou
for diagnostic purposes, but the presence of those causes most likely to
occasion this type of meningitis must also be taken into consideration.
When insolation or trauma is known to precede svmptoms of menin-
gitis in  a child,  it may  reasonably be supposed that the meningitis is
of  a suppurative character.   In any  doubtful case a careful  exam-
ination  should always be made of the heart, the lungs, the  nostrils
and ears, and it should be ascertained whether the child has recently
suffered from pertussis, typhus, croupous pneumonia, typhoid fever,
cerebro-spinal meningitis, ulcerative endocarditis, purulent pleurisy,
pysemia, acute articular rheumatism, dvsentery,  scarlatina, or small-
pox.
  The diseases from which the diagnosis should be made are typhoid
fever, tubercular meningitis, and cerebro-spinal meningitis.
  ^ The  diagnosis from typhoid fever may sometimes be extremely
difficult, unless  sufficient  time has elapsed to mark the variations of
temperature, or unless  the cutaneous  or enteric symptoms manifest
themselves.
  ^ The presence or absence  of tubercular history in the family will
aid in the differentiation from tubercular meningitis.
  Cerebro-spiual meningitis, if sporadic or  epidemic, may be differ-
entiated by this fact from suppurative meningitis. 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.       353

  Prognosis.   In cases which follow diseases  of the middle ear or
of the nasal  cavities the prognosis is extremely uncertain, although
many cases recover.  When the disease  occurs by metastasis from
other viscera, there is not only great danger to life, but a still greater
probability of cerebral or motor defects resulting.  But the prognosis
is usually fair in uncomplicated cases.
  Treatment.   The  cause  of  suppurative meningitis will very
greatly indicate the treatment.  Operative procedure should be re-
sorted to in cases of pent-up pus resulting from diseases  of the  ear
or its appendages.  If caries  of the nasal bone exists, it should be
promptly removed, provided  it is  of  a  nature to  permit removal;
but even in such a case it is of the utmost importance that the menin-
gitis itself should be properly treated.   Ergot  is a remedy of great
value, aud should be given in the form  of the fluid extract, every
three or four hours in doses of from five minims to a drachm, accord-
ing to the age.  A few  large  doses of quinine, say from  two to ten
grains, according to the age, will often  prove of  service if the menin-
gitis is subjected to treatment at an  early stage.   But its use after the
early periods has not convinced me of any further efficacy, except as
a tonic.   Doses of from one-twentieth  to one-tenth of a grain  of the
sulphide of calcium, every  hour for a day or two, have seemed to me
to be of considerable benefit.   The restlessness incident to the disease
may sometimes  be relieved by cold applications to the head, or, if
necessary, by occasional doses of the bromides.  I have  never satis-
tied myself that inunctions of mercury—usually of the  unguentum
hydrargyri—are of any especial use, time-honored though they are.

                CEREBRO-SPINAL MENINGITIS.

  History.  Vieussens wrote the first description of cerebro-spinal
meningitis in 1805.   Whether it had  occurred previous  to this time
is unknown, but shortly  after Vieussens'  account  epidemics  of it
were observed in  Europe.   The  first  American cases were seen  in
Massachusetts  in 1806.   Since then there have  been numerous
epidemics.  Thus, between 1816 and 1828 there was an epidemic in
Connecticut, at Middletowu, and another at Vesoule, in France, both
being limited and brief.   In 1828 it occurred in Ohio, in Trumbull
County;  in 1830 at Sunderland, England, and iu   1833 at Naples.
In 1837 it spread from  the south of France over most of the king-
dom, and continued at intervals until 1849, and also extended to the
various places around the Mediterranean, and to Denmark, Eugland,
and Ireland.  In  1842  it  appeared in  the  United States in various
places; agaiu in 1813, and from 1848 to  1850.   Between 1850 and
1854 there was  no epidemic in any  part of the world, but from 1854
to 1860 there was a severe  epidemic in Scandinavia.   Since 1860 it
has appeared in nearly every civilized country,  and it is the opinion
of competent observers that it has  become naturalized in the cities of
the United States, varying  in  severity^  from time to  time.   In  1872
an unusually severe epidemic attacked the city of New York, extend-
ing even to the lower animals. 
364
NERVOUS DISEASES.
  Etiology.  Among the causative factors of cerebro-spinal men-
ingitis are:
       Season;
       Anti-hygienic conditions;
       Contagion;
       Depression of general health ;
       Sex;
       Age.
  The winter season is that in which most cases are observed.  Thus
Lewis Smith states that of 166 epidemics, all but 50 occurred in the
six  months commencing with December; while Hirsch affirms that
57 epidemics in Central  Europe occurred in winter or in the winter
aud spring, 11 in the spring,  5 between spring  and autumn, 4 began
in the autumn and continued  into the winter or into the winter and
the ensuing spring, and  6  lasted the entire year.   But Smith thinks
that in New York City season appears to exert little or no influence
on the prevalence of the disease—because, as he believes, of the fact
that  New York tenements are under better sanitary regulation than
the dwellings  of the European peasantry.
  It is certain that anti-hygienic conditions are favorable to cerebro-
spinal fever, because it  has  been observed most severely  in large
numbers of people crowded together, as soldiers and tenement-house
dwellers.  A  chart prepared by Moreau  Morris, of the New York
Health Board, seems to show that almost all the cases occur in those
portions of the city where the sanitary conditions are bad.
  Although it has often  been impossible to detect the exact relation
of one epidemic to another, yet there is excellent proof to show that
the disease is slightly contagious, and  this was notably shown in the
epidemic of  1872 in New York, where the lower animals  were
affected, and in 1811 in Vermont, when foxes  died of it.
  Depression  of the general  health  from overwork, bad  air, insuffi-
cient  food, privations of soldiers, etc., would certainly seem to pre-
dispose to cerebro-spinal fever.
  There does  not  seem  to be any predisposition of one sex to the
disease, except, of  course, that meu, who  are more exposed  than
women of the corresponding  family, are  more liable to break down
with it.
  According to the elaborate statistics of  Lewis Smith, three-fourths
of the cases  have been under the age of ten years, and the following
are  the figures of the New York Health Board  of the age of the
patients iu the epidemic of 1872 :

         Under 1 year...........125
         From 1 to  5 years   ....              .  336
          "   5  " 10  '•    .........204
          "   10  " 15  "    ...                .  .  106
          "   15  " 20  "    ....            .  .   54
          "   20  " 30  "    .........79
         Over  30 years...........71
                     Total   ........ 975

  Clinical  History.   The onset  is usually sudden, although in
certain rare   cases  there may be prodromal  symptoms for a few 
THE CEREBRO-SPINAL NERVOUS SYSTEM.
365
hours or days, such as chilliness, lassitude, anorexia, etc.   The onset
is usually with headache, emesis, and slight  chill or clonic convul-
sions.  Coma and delirium  usually succeed,  or, in the slight  cases,
simple drowsiness.   The temperature rauges from 99J° to 101°, and
as the disease progresses it may rise to 102°,  and eveu higher, some
fatal cases goiug to 1071°.   The pulse is usually quickened, although
it may sometimes be subnormal.  When it  is increased, it  rises to
110, 120, and even higher.   The face is generally pale, later on it is
flushed, and often the tache cerebrate of Trousseau is observed; i. e.,
a congestion of the skin produced by running the finger across the
forehead, cheek, or ear, lasting for a short time.   The skin may also
present the characteristic appearance  called "goose-skin,"  due  to
papilliform elevations, from contraction of the muscles of the corium;
or it may  be duskily mottled, or there may be  numerous  minute
extravasations, which are occasionally so large as to  be an  inch or
more in size. In some epidemics these appearances are not observed.
Then there is quite commonly herpes, either early or after a week or
two, and erythema  and roseola occasionally occur.   The skin may
either  be dry or perspiring.   The urine is usually normal, or there
may be polyuria, and the urine may contain a small amount of albu-
 min, or  there  may even be cylindrical  casts and blood-corpuscles.
There  is occasionally oedema around one  or more joints.   As the
disease progresses  more  marked  organic symptoms appear.   Of
these, the most common are strabismus and alterations in the pupil,
such as contraction, inequality, feeble response to light, etc.  Inflam-
 matory changes sometimes occur in the media of the eye.  The head-
ache is usually severe, and attention is frequently called to it by the
 patient, who puts the hand  to the  spot with an exclamation of pain.
 Hypersesthesia of the surface of the skin is common.  Retraction of
 the  head is usually marked, and there is frequently also contraction
 of the posterior  muscles of the trunk, abdomen, and lower extremi-
 ties, so that opisthotonus  and  flexion  of the thighs and legs are
 common. These usually occur about the fourth or fifth day, although
 they may supervene as early as the second.  Paralysis of the muscles
 of the extremities is also seen, and sometimes very shortly after the
 onset.   This paralysis may be  of one side  (hemiplegic) or of both
 legs (paraplegic), or even of individual groups of muscles, although
 this last is rare.  Choreic  or choreiform  movements do  not often
 occur.  The respiration is usually not greatly affected so far as regu-
 larity  is concerned, although it may  rise to forty respirations per
 minute.   There is  often mild otitis media,  usually not leading to
 impairment of hearing, and this is generally bilateral.   The dura-
 tion is very variable, exceptional  cases  terminating in  twentyr-four
 hours, others in a week or  two.   When there is recovery, however,
 it generally takes place in three or four weeks, although fatal cases
 may last as long.
   Pathology.  Cerebro-spinal meningitis is a constitutional malady,
 of which the meningitis is simply one of the local manifestations.  It
 is undoubtedly due to a micro-organism.
   The meninges are markedly hypersemic, although the extent of 
366
NERVOUS DISEASES.
this hypersemia varies greatly in different cases—in some extending
over  most of the cerebral  surface, in  other  being  limited to small
areas.  The very acute fatal cases  have not time to pass beyond this
stage.  Usually, however, free exudation is found in and beneath the
pia mater, usually either serous, fibrinous, or purulent.  Softening
and cerebritis are usually observed.
   Prognosis.  About 50  per  cent, of the  cases of cerebro-spinal
meningitis are fatal, aud of 113 cases which I have seen, in 30 there
has followed some irreparable damage to the nervous parenchyma.
Mental impairment is not nearly so apt to result as is paralysis, how-
ever.   Those  cases in which the clinical symptoms denote that the
base of the brain is  mainly affected are those in which  an excellent
prognosis can be drawn, so far as regards the mind;  but even iu
these  the speech-defects aud paralysis of the members  are often so
great as to sentence the  patient, especially if a child, to such a life
of isolatiou and  helplessness as  to make the outlook very serious.
Nevertheless, many cases do recover without either mental or physical
impairment.   The remissions of the  disease are generally ominous.
Unfavorable symptoms are—the occurrence  beyond thirty, a very
acute onset, coma, convulsions,  active  delirium,  high temperature,
numerous petechial eruptions, and continued albuminuria.  Compli-
cations in other organs, either pulmonary or cardiac, are also of un-
favorable prognosis.
   Diagnosis.  The diagnosis of  cerebro-spinal  meniugitis should
be  from simple meningitis and  tubercular meniugitis.   In simple
meningitis the onset is apt to be more  acute, the hypersesthesia and
retraction of  the head are less  pronounced,  and  the  presence or
absence of a prevailing epidemic  will  throw great light upon the
matter. In tubercular  meningitis there is a prodromal stage of several
days,  and it may be preceded by symptoms referable to tuberculosis
elsewhere.
   Treatment.  The  patient should,  of course, be  kept perfectly
quiet, the same attention  being paid to keeping him sheltered  from
disturbing influences as has been recommended in the other forms of
meningitis.   Cold cloths should be placed on the  head,  taking care,
however,  not to have them icy, or not to refrigerate the  patient with
them.   The drugs which are of most use are ergot, iodide, bromide,
quinine, opium, and chloral hydrate.  Ergot is, in my opinion, a very
valuable drug in all forms of meningitis, and I believe that its value is
heightened by the constant use of the iodide of potash and quinine.
The fluid  extract  of ergot should be  used, and it should be admin-
istered  in half-drachm or drachm doses every three  to  five hours,
according to the age of the patient.  If the disagreeable taste of the
fluid extract is objectiouable,  ergotine may be employed in doses of
2 to 3 grains,  every three to five  hours, as before, although I do not
believe that it is nearly as efficacious as the fluid extract.  The iodide
of potash should be given in doses of  5 to 10 grains, three or four
times  a day.   The form of quinine employed should be the tannate
for young children  and  infants, and  the' sulphate for adults, the
former in doses of 2 or 3 grains  three or four times a day, and the 
THE CEREBRO-SPINAL NERVOUS SYSTEM.
367
latter  in  doses of  2 or 3 grains three  or four  times  a day.   Some
authors  speak well of  opium  in this  disease, but  I have  never
been able to satisfy myself of its beneficial effects.   If there are
much restlessness  or  convulsions, or much  delirium, the bromide
of potash should be used, varying, according to the age of the patient,
from 5 to 20 grains, three or four times in the twenty-four hours.
In some cases, where the  treatment  by these  four drugs does not
seem to  quiet the  patient, moderate  doses of opium or  morphine
will be found useful, preferably the sulphate of morphine, hypoder-
mically,  in  doses of -fa to ^ grain  once  or twice a day, or even
oftener.  If in spite of these drugs there is insomnia, the best remedy,
in my opinion, is, first, urethan, 5 to 10 grains at bedtime, in solution
in water, or, if this does not answer, sulphonal, 5 to 15 grains at
bedtime, in the form of a reliable compressed  tablet, which  should
be tested by the physician to  ascertain  that it is perfectly friable.
Besides all these, however, the most careful attention should be paid
to the nursing and to  the diet, which latter should be suitable to the
age of the patient, and always be bland and easily digested.

                  TUBERCULAR MENINGITIS.

   History.  Robert Whytt, in 1768, first precisely described tuber-
 cular meningitis under the name of hydrops of the cerebral ventricles.
   Clinical Symptoms.   The  prodromal  symptoms are usually
 vague.   The children  are  prone to  emaciate, to  be pallid, peevish,
 listless, and lose their interest in  the thousand  aud one things that
 interest  children.   Sleep may be interrupted, and  the child may
 awake complaining of headache in some  one spot.   The tongue may
 be coated, the patient may occasionally vomit, and the vomiting may
 be propulsive or like a regurgitation.   There may be some constipa-
 tion, the urine may dimiuish, and there may be some slight hyper-
 esthesia of the abdomen.  There may also be photophobia or a
 tendency to sleep.   Usually these symptoms increase in intensity, and
 the temperature rises  from 100J° to 101J°.  The pulse, which has
 been slightly  irregular, becomes  much more so.   These  prodromal
 symptoms may last one or several weeks.  Then  more pronounced
 symptoms appear.   Respiration becomes interrupted, and the patient
 sighs deeply and long; the abdomen is retracted ; the  eyes half close,
 giving the peculiar aspect that  is often seen in dying people, and the
 eyeballs may move slowly in a  lateral direction.   One or both pupils
 dilate.   There are sudden flushes of the face in  limited areas, and the
 skin generally presents a red mark when the finger is pressed over it
 or when it is pressed upon the pillow, and  friction  causes a blush
 corresponding to the area rubbed (the so-called Trousseau's mark).
 Then  there may suddenly break upon the scene more marked  evi-
 dences of orgauic  implication,  such as slight twitchings around the
 mouth and eyelids, or a convulsion, usually generalized, followed by
 ptosis, amaurosis, strabismus, or paralysis  of the face or extremities,
 usually unilateral.  In some rare cases the paralysis may affect one
 extremity alone.  The temperature now rises  to 102°, 103°, or more, 
368                   NERVOUS DISEASES.
the head becomes retracted, there is general  perspiration, the pulse
increases in frequency, and so the symptoms may increase until death,
after a period of three or four weeks.   Death is usually preceded by
Cheyne-Stokes respiration.
   Iu some children the symptoms may be much milder, and convul-
sions may not be observed until a few days before death.  In this form
vomiting, headache, delirium, convulsion, are very marked, and it is
said that a tumid abdomen may be present instead of a retracted one,
and the onset may be very sudden.  In other children there may be
so much somnolence from  the  start as to render the diaguosis very
difficult.  Occasionally there is a hypersemia of the retina or tubercles
of the choroid.
   Etiology.  The etiological factors  of tubercular meningitis are
heredity, age, and erythema nodosum.
   A child coming of tuberculous  parents is much  more likely to
have tubercular meningitis than one of healthy parentage, and yet
tubercular meningitis cannot be said to  be hereditary.
   Most cases are observed between the  second and seventh year.
   A number of cases connected with erythyma nodosum have beeu
reported.
   Pathology.   In  tubercular  meningitis the base of the brain is
especially prone to be affected, and that portion  of the base in which
lie the olfactory, optic, and third nerves, and the crura cerebri. (See
Fig. 36.)  Changes may be found wherever the pia mater extends over
the surface of the brain and into the ventricles  The pia at the base,
extending over the quadrangle  that  has just  been described,  is suc-
culent, and looks like wet blotting-paper, very much as it does in
syphilitic meningitis.  Over the rest of the  base of the brain and
over the vertex where the  pia  is more closely approximated  to the
cerebrum,  this membrane  is opaque and  thickened, but it cannot
usually  be detached easily, and it has the same  characteristics in the
choroid  plexuses of the ventricles.   There is  usually exudation of a
serous or purulent or gelatinous character. The ventricles will usually
be found to contain an abnormal amount of fluid, which may be clear
or turbid ; and when this fluid is excessive the  ventricles are enlarged,
and the basal ganglia, the fornix, and the corpus callosum may be soft-
ened.   Tubercles are usually observed,  either  strewn around the ves-
sels, or beaded through the pia like little grains of rice, or isolated so
as to form genuine tumors, which are usually,  however, of small size.
The cranial nerves are implicated to a varying degree in the tuber-
culous  and meningitic infiltration.  A section of the pia mater and
the subjacent cerebral tissue, made after hardening in alcohol and
colored  by Ehrlich's  method, will show marked changes.  The pia
mater will be thickened, often extending like a wedge into the cere-
bral substance.   There is  often  thrombosis of  the arterioles and of
the venules of the pia, obliterating the lumen.   The walls of these
vessels are thickened, often hyaline, surrounded  by connective tissue
and infiltrated with small round cells with distinct nuclei.  Further
away from the vessels  areas of reticulated  tissue will frequently be
observed.  Many bacilli and granulations will be found.   Giant-cells 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.       359

are sometimes, though rarely, seen in  the internal wall of the vessel
and in the surrounding cerebral tissue, and the tuberculous bacilli are
strewn  throughout the vascular walls.  The perivascular  sheath  is
often dilated and filled with lymphatic cells.
  The discovery of the bacterium of tuberculosis was made by Robert
Koch. He first found in the sputa of tuberculosis, in sections of miliary
tubercles, and in tuberculous lesions in many organs, certain fine and
elongated bacilli which colored in a peculiar manner.  He discovered
that they were especially frequent  in  the giant cells.  Koch's obser-
vations have been confirmed by Balmer, Frenzel,  Lichtheim, Gibbes,
Charnley, Smith, Ransom, Herou, Prudden, Shakespeare, Ernst, and
many others.   Although Koch's observations  have been  attacked by
certain  experimenters,  notably by Spina, of Vienna, yet they have
met with general acceptation.   In tuberculous meningitis, however,
other bacteria have been found than those of Koch.  In twelve cases
examined by Babes, in seven there were found  different  microbes,
and  this variety explained, in  his opinion, the  acuteness and the
purulent nature of some cases.   In all these cases there  were also
tuberculous lesions of the mediastinal ganglia, and often pulmonary
lesions  of the same nature.   In  two cases there was a lanceolated
microbe ; in a third there was the ordinary streptococcus of pus ;  in
the fourth there was the staphylococcus aureus ; in the fifth there was
also the streptococcus of pus, and in  the  two remaining cases there
were peculiar  pathogenic bacilli.  In one of these cases there was a
fine bacillus very closely resembling that of tuberculosis, and inocu-
lation of it by trephining into the meninges of the rabbit produced
acute meningitis and death in two days.  In another  the microbe
resembled that of Friedliiuder, and inoculation of it also produced a
meningitis  iu  the rabbit.  In another case there was a tetrahedric
microbe  in the pus, or arranged  in  groups like the staphylococci.
Inoculation of this was negative.  In still another case there was a
peculiar  microbe which developed an unusual colony in agar-agar.
In other cases, however, that were examined by Babes, no microbe
was found except that described by Koch.  In two cases of menin-
gitis caused by purulent otitis Babes has also found a few tubercular
bacilli.
  Prognosis.  The prognosis of tubercular meningitis  is very un-
favorable, and cases rarely recover, if ever.  I  myself  have never
seen a case of  recovery, but a few have  been reported  by different
writers, such as Hahn and Abraham Jacobi, the latter  of whom
claims that he has seen two cases.
  Diagnosis. The diagnosis of tubercular meningitis may be readily
made when the symptoms of a tubercular meningitis supervene upon
tubercular lesious that have previously existed in other organs.  When
however, there is no  history of tuberculosis personally  in  the indi-
vidual, and when the hereditary history is not pronounced, the diag-
nosis between tubercular and  simple meningitis may  become very
difficult.   The prodromal symptoms of gradual change, to which are
superadded symptoms of organic affection of the cerebrum in the way
of convulsions, paralysis of cranial nerves or extremities, the tem-
                               24 
370
NERVOUS DISEASES.
perature rising to  101° and  above, the retraction of the neck, the
half-open eyes, the delirium, the somnolency—all  these make a pic-
ture of an  intracranial affection that can be diagnosed as tubercular
meningitis when other lesions capable of causing similar symptoms
are excluded.   These other lesions are :
       Simple meningitis;
       Syphilitic meningitis;
       Cerebro-spinal  meningitis;
       Tumor;
       Typhoid;
       Trauma;
       Ear disease;
       Ursemia;
       The hydrocephaloid state;
       Mental disturbances  from pulmonary lesions.
   In simple meningitis the onset is more sudden, and the prodromal
symptoms will be wanting.   The temperature is higher, the disease
runs its course more quickly, and there will  be no history of tuber-
culous infection or predisposition.
   Syphilitic meningitis occurring  in an adult will be accompanied
by symptoms  of intracranial syphilis, and in the child with syphilitic
heredity by such well known signs as the characteristic rash, chronic
snuffling, usually beginning soon after birth, collapse of the bridge
of the nose, early enlargement of the spleen, and rapid improvement
with mercury.
   Cerebro-spinal meningitis occurring as au epidemic is, of course,
easily diagnosed.   When it  occurs endemically or solitarily,  the pro-
dromal symptoms  are  short, the  characteristic  eruption  may be
present, and the vasomotor disturbances evidenced by pressure upon
the skin occur earlier.
   Intracranial tumor in an  adult  or a  child will be much more
prolonged,  have more localized symptoms, and will not have any
temperature-rise.
   Typhoid fever, when typical, may be distinguished by the tempera-
ture-curve, but when non-typical  the diagnosis in the first  week or
two will frequently be absolutely impossible.
   Trauma may set up a meningitis or a  hemorrhage succeeded  by a
meningitis, and from this the diagnosis can be made easily enough if
the trauma is known ;  or if not, the onset of the symptoms will
be  quicker and the general history will be more that of a simple
meningitis.
   In every case of meningitis in which the cause is not clear, the ear
should be carefully examined, and any purulent trouble found there
may aid in making the diagnosis plain.
   Ursemia can be  diagnosed  by careful examination  of  the urine,
and in the later stages by a  lack of the organic symptoms present in
a meningitis.
   The  hydrocephaloid state may present so many of the symptoms
of a meningitis that for a time the diagnosis may be in doubt, but
the  history of  some  acute disease, especially some  gastro-enteric 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.        371

trouble, having preceded the brain-symptoms, will  soon make the
nature of the case evident.
  It should always be borne in mind that an acute pulmonary lesion,
especially in a child, may give  rise to mental  symptoms that may
simulate a meningitis, but auscultation and percussion of the lungs
will clear up the diagnosis.
  Treatment.   Although there  is a doubt that has already been
stated whether treatment is of much avail in tubercular meningitis,
yet the very existence of a doubt renders it  our duty to treat care-
fully aud intelligently.   The patient  should be put absolutely at
rest and screened from any disturbance that may impinge upon any
of the peripheral nerves or the  cerebrum.   The  room  should be
darkened, a careful  and tactful attendant should take charge  of the
case, and medicines and  food should be administered with clock-work
regularity, for in dealing with a fatal disease every attention should
be paid to the most  minute details.  The medicines administered
should be the bromides, the iodide  of potash, quinine, and opium.
The best  bromides are either the bromide of potash  or the bromide
 of soda, and  there is usually no choice  between them, although in
 some exceptional cases the  bromide of soda will agree best with the
 stomach.  The bromide of potash should be administered in doses
 that should vary with the age and  the  amount of convulsive dis-
 turbance.   In children 5 to  10 grains three or four times a day, are
 usually sufficient.  In adults 15 to 20 grains  three or four times a
 day should be used.  In case of convulsions  these doses should be
 increased  according to the judgment of  the  physician.  The iodide
 of potash should be administered iu doses varying from  5  grains
 three times a day in children, and  10 grains  three  times  a  day in
 adults, to double or  treble these amounts;  and it  should be  given
 in  a wineglass, or, better still, a tumbler, of water, or perhaps even
 in a glass of Vichy in cases where the stomach  is irritable.   Quinine
 should be given  in the form of the tannate three or four times a day
 in children, and in  the form of the sulphate three  or four times a
 day in adults.   The tannate can be best administered in the form of
 chocolates, which are made up nowadays by most of the manufac-
 turing chemists; and the  sulphate  may be given in  the form of a
 capsule or the tablet triturates, and  never in solution with au acid.
 I am aware that there  is  considerable skepticism as to the value of
 quinine  in any form of meningitis, and yet I am  firmly  of the
 impression that the strength of the patient holds out  better when
 quinine is administered.   Opium is a very valuable agent in calming
 the excitability of the cerebrum.  Iu children it may be used in the
 form of  5 drops of laudanum  once, twice, or thrice daily,  as the
 physician may judge best; in adults, hypodermics of the sulphate of
 morphine, | grain, of the aqueous extract of opium §• grain, may be
 used either by  the  mouth or  hypodermically once,  twice, or  thrice
 daily, as may be iudicated.   In some cases moderately cold applica-
 tions seem to give the  patient great comfort,  whilst in others they
 irritate, and they should therefore be used or not, as may be deemed
 best;  but I disapprove entirely of  the practice of putting ice-bags 
372
NERVOUS DISEASES.
or ice-cold compresses upon the patient's head, for fairly cold appli-
cations will answer every purpose of contracting the arterioles, whilst
ice applications may dangerously lower  the  bodily temperature, aud
thereby seriously  decrease the general  strength.   If there be per-
sistent vomiting, the  subnitrate of bismuth, 5  to 10 grains, with \
or J grain of codeia, will  be found of the most use; or a  mustard-
plaster applied over the epigastrium  from time to time, or pills of
ice or opiates.  In case of cardiac weakness  this should be  met by a
cardiac stimulant, such as  digitalis, camphor, and strophanthus.
Great attention should be paid to the food, and this should  be of the
blandest and most nourishing character  and  suited to the age of the
patient.   If there is persistent vomiting to such an extent  as to
interfere with alimentation, injections should be used.


                     CEREBRAL  ABSCESS.

   Definition.   Cerebral abscess  results from suppurative enceph-
alitis.
   Etiology.  Abscesses  are caused  by traumata, caries of the
cranial bones, nasal disease, intracranial tumors, and occur at times
without any assignable cause.
   Although marked symptoms may not  supervene immediately  upon
a trauma, abscess may follow after  a lapse of quite a  period of seem-
ing immunity.
   Abscess may result from caries of the cranial bones,  notably that
of the  petrous portion of the temporal bone, more particularly when
it is conjoined with ear disease.
   Nasal  polypi  and caries may cause abscess, the former sometimes
causing disease of the frontal lobe  by penetrating the cranial cavity.
   When  abscess  is caused by intracranial tumors  the latter are
always in close proximity to the former.
   Purulent lesions of other organs sometimes coexist with cerebral
abscess, among which may be mentioned ulcerative endocarditis, pul-
monary gangrene,  bronchitis, empyema,  puerperal fever, typhus, var-
iola, scarlatina, and measles.
   Symptomatology.  Only vague  symptoms manifest themselves
at first.   The child may show a decided malaise, complaining and
being peevish, or  marked headache  may occur.  Delirium usually
succeeds these vague symptoms, or they may give place to  hebetude
and coma.  The temperature  does not  usually range high, seldom
going above 101°, and sometimes dropping to 99°.  Convulsions
occur in  most cases.   Vertigo and  headache  are usually  present.
All these symptoms  culminate finally  in paralysis, hebetude, and
coma.  To  sum up, the symptoms progress steadily and slowly, and
the individual manifestations will vary according  to  the location of
the intracranial lesion.
   Pathology.   A localized encephalitis tending to the formation
of pus is the direct cause of cerebral abscess.   A limiting membrane
may or may not  surround it.  Secondary changes  may, of course, 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.        373

take place in the contiguous cerebral tissue.   Except in the pysemic
cases, abscess is generally single.
  Diagnosis.  The  gradual onset and variability of the symptoms,
when conjoined with  nasal or aural disease, should create a suspicion
of cerebral abscess, or when such symptoms occur as a sequel to some
one of the suppurative  or infectious  diseases of which a  history is
obtained, it should be differentiated from cerebral  tumor  or  menin-
gitis.
  Tubercular meningitis is a chronic affection, either resulting from
an existing tuberculosis or from hereditary predisposition.  Cerebral
abscess has a  slow  and insidious  onset  which distinguishes  it from
cerebro-spinal meningitis, and in the latter the retraction of head and
abdomen, and the sporadic or epidemic presence of the disease, differ-
entiate it from the former.   As cerebral abscess and suppurative men-
ingitis are often coexistent and proceeding from the same cause, it is
not always possible to make the diagnosis.
  Cerebral tumor is usually much more chronic than cerebral abscess,
and optic neuritis is  occasionally seen in it, never in cerebral abscess.
  It will  sometimes be possible to make  use of the cerebral ther-
mometer, to which I directed attention about twenty years ago.  But
it must be remembered that  the slight changes of import in rectal
and axillary thermometers are useless in cerebral thermometry,  as
here  from three  to five degrees are necessary to  indicate anything
abnormal.  (See  page 174.)
  Prognosis.   Cerebral abscess is of very grave prognosis.   The
tendency to recovery idiopathically is  so  slight  that an  operation
should never be delayed on account of this probability.
  Treatment.  When cerebral abscess  is  positively  diagnosed an
operation  should at  once be  resorted to.   Reference  is made  else-
where in  this work to anatomical data that  may be used in local-
izing it.  (Vide " Cranial  Topography," page 97.) I have diagnosed
two cases of cerebral abscess  in the centrum  ovale, in spite of the
prevailing opinion that localizing  symptoms alone can be depended
upon for  this  purpose,  and Von Bergmaun has  located one in the
temporal lobe.   The pain  which follows percussion upon the skull
may sometimes localize an abscess, but unless this symptom coincided
with others of localizing  value, I must  confess that I should hesi-
tate to follow this indication.   I have, however, known these symp-
toms to conjoin in several instances.  The localizing process will  be
materially assisted by the use of my cerebral thermometers.   Every
case of cerebral abscess should be operated  upon,  as great relief has
often been the result  of surgical interference. Von Bergmann reports
a case where the  patient had suffered from a purulent discharge from
the right ear for fifteen years, caused by a cerebral  abscess, which was
cured by an operation.

           SYPHILIS  OF THE NERVOUS SYSTEM.

  History.   Syphilis seems to have been known first to the Euro-
pean world about the end of the fifteenth  century, and the earliest 
374
NERVOUS DISEASES.
writer upon its connection with the nervous system is said to have
been  Leo Nicenus.   Ulrich von Hutten first observed the relation
between syphilis, apoplexy, and paralysis.  Massar first called atten-
tion to syphilitic neuralgias, although Paracelsus had previously do-
scribed syphilitic phthisis, diarrhoea, and hydrocephalus.   Astruc in
1740, spoke of syphilis as a  probable  cause of circulatory disturb-
ances in the cranium.  Van Swieteu, Carrere, and Swediaur attributed
many chronic  diseases to syphilis;  but, singular  to  say, so keen-
sighted  an  observer  as  Hunter positively stated  that no brain or
other viscus diseased  by syphilis had ever been seen.  This was in
1787.  The enormous influence of Hunter's dictum paralyzed obser-
vations of this kind for some time, and the discovery by Morgagni,
in 1779, of gummatous tumors of the cortex was entirely overlooked,
and it was not  until the time of the great Virchow  that men uncov-
ered their  eyes and recognized the import of that which lay before
them.  In  1854 Gildemeester and  Hoyack published a description
of occlusion of the right Sylvian artery by a neighboring syphilitic
formation.   Then began  a great strife between Robin and Wagner
on the one hand, and Virchow on the other, as to whether these new
formations were specific pathological products or whether they were
new formations of granular tissue, Virchow maintaining the  latter
position.  The solution of this question was due to the observations
of a Dane, Steeuberg,  in  1860.   Still the subject did  not attract the
attention that  it deserved and that  it  has  since obtained, although
confirmations of Steenberg's statements were contributed by Gries-
inger, Passavant, Wilkes, Weber, and  Wagner. The great work of
Heubner, in 1874, however, conclusively confirmed Steenberg, and
settled the matter beyond the shadow of a doubt, and especially did
the former do this by his  minute description of the peculiar syphilitic
diseases of the intracranial arteries.  Since that time the literature
has become so enormous that,  in a monograph written  some five
years ago, I was able  to  count up five hundred different articles on
the subject  in  the preceding thirty years; and this, as I stated, was
one-twentieth  of the whole Sanskirt  literature, or  of the combined
classical  literature of Italy and Greece.  It must suffice here to  say
that, salient among the  salient, are Koster, Friedlander, Chvostek,
Eichhorst, Greiff, Leyden, Yvareu, Gros and Lancereaux, Charcot,
Hughlings-Jackson,  Taylor,   Moxon,   Clifford Albutt,  Fournier,
Morel-Lavallee, Belieres,  and  finally, in 1887, appeared the complete
and decisive work of Rumpf.
   Etiology.  Syphilis of the nervous system usually occurs in the
secondary and tertiary stage.  Thus, of 150 cases of my own 87 have
belonged to the tertiary stage, whilst 41 have occurred in the second-
ary aud 22 in  the primary stages.  It will thus be seen that, contrary
to the affirmations of those who have limited their observation of
syphilis to the  skin and mucous membranes, the nervous system may
be  affected  at  any  time.   Indeed, the great French syphilographer,
Fournier, goes  so far as to say that syphilis manifesting itself promi-
nently in the  cutaneous  organs and mucous membranes is  of the
benign form, and is  not  so likely afterward to affect the nervous 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.        375

system as is syphilis in which there have been scanty cutaneous mani-
festations ; and this view is confirmed by my own observations as I
have just stated them.  Syphilis may be communicated in various
ways.  Thus, a chancre may be acquired in the ordinary  fashion, or
through the buccal membrane,  through examinations by  a physi-
cian, or through a surgical operation, aud it is even a question as to
whether it cannot be  acquired  through articles of clothing, whilst
heredity is an occasional cause.   Physicians should  bear  all  these
sources of infection well  in mind, and should emancipate  themselves
from  the  traditional idea that it  can only be acquired in the usual
way.   I  have known  several physicians who  have infected them-
selves through examinations of patients or  through  surgical opera-
tions ;  and I also know of numerous cases in which the wife has been
innocently infected through the husband.   For all these reasons, it
is evident that  we cannot  exclude syphilis because of a lack of a
clear history of infection or because  of a  lack of the usual typical
cutaneous manifestations.
   In 150 cases of my own the average age was thirty-five, the maxi-
mum being fifty-two years and the  minimum eighteen;  135 were
males and 15 females.
   Pathology.  Syphilis of the nervous system may affect any por-
tion of it—intracranial contents, spinal cord, peripheral nerves, and
the membranes and bony structures surrounding the spinal cord and
intracranial  contents, as  well  as the  arteries and  capillaries within
them.  The arterial lesions were  first  described in 1874 by Heub-
ner, of Leipsic, whose observations have  given rise  to further and
even  contradictory investigations by Koster,  Friedlander, Baum-
garten, Rumpf, and many others.   Heubner advanced the view that
in  syphilitic vessels the endarteritis  was  peculiar in its place of
origiu, which was in the vessel-less tissue that lies between the fenes-
trated membrane  and the  endothelium,  which two  structures are
 normally so closely approximated that no  intervening tissue can be
 seen microscopically.  In  syphilitic endarteritis, however,  Heubner
 maintains, they are  widely separated by  a new cellular formation
 which consists of a proliferation of endothelial cells, to which, after
 a certain time, there  are added  numbers of peculiar rouud cells, of
 which we shall have  more to  say later.   Heubner very  minutely
 and carefully describes the differences in size of the endothelial cells
 in  health and disease, as well as how to obtain an endothelium that
 has not been produced by the ordinary act of cutting the vessel, and
 it it difficult for anyone who reads his painstaking brochure to refuse
 credence to  his plea for this  peculiar  anatomical site of syphilitic
 endarteritis; nor is it  easy to resist the wish that it were true, as it
 would constitute so valuable a guide  in dubious cases;  but in the
 eighteen years that have elapsed since Heubner first made his views
 public no one has fully confirmed him.  Koster, Friedlander, Baum-
 garten, Huber,  Schottelius, Marchand, and Rumpf  deny that the
 endarteritic  process  starts in the vessel-less structure between the
 fenestrated  membrane and the  endothelium, or  that it  consists at
 first of an endothelial proliferation,  maintaining, on the  contrary, 
376                   NERVOUS DISEASES.
that this endarteritis is due to the outpouring of round cells from the
minute nutritive  vessels of the vessels  themselves—from  the vasa
vasorum—contained in the outer coats, and that the endothelial pro-
liferation is only a part of the general cellular disturbance that takes
place in consequence of this outpouring of round cells.
   The question needs further investigation.   But, however  it may
be decided,  there is no diversity of opinion as  to  the results which
follow the endarteritis.  The vessels may become narrowed in their
lumen by the thickening inward of the fenestrated membrane and the
intima.  They may be entirely occluded from the same cause.   The
inner surface of the intima may become roughened or altered in its
chemical constitution, and a thrombus may form,  which,  iu its turn,
may give rise to an embolus.  It  may even happen, though rarely,
that minute aneurisms may7 be formed from the  wasting of the mus-
cular coat of the vessel, and occasionally there maybe a hemorrhage.
In other words, the syphilitic infiltration may set up an endarteritis,
which usually leads to a narrowing of the  canal of the vessels or to
an occlusion of it, but it  may occasionally induce thrombi, emboli,
aneurism, and hemorrhages.   Around  the vessels will  be found a
number of cells reaching  out  into the  tissue for a considerable dis-
tance, tapering off into the normal tissue and becoming scantier and
scantier as the normal tissue predominates.   The tissue in which these
cells lie is finely granular, and  is  traversed by  bands of connective
tissue.  This tissue is evidently the product of the cellular infiltration,
with slight exudation.  The cells are in  all appearances similar to the
white  blood-cells, but their histological conduct is  peculiar.  They
preserve their vitality for a great length of time in some places, and
when they do undergo retrogressive  metamorphosis it is into caseous
and calcareous products and connective tissue, and seldom into pus-
differing in these  respects entirely from the cells that are found in
tuberculosis, and  acting rather like  the cells of lupus, leprosy, aud
actinomycosis. Virchow classifies them with the granulation-tumors,
Klebs  with  the  infectious tumors, and  Ziegler with the infectious
granulation-tumors.   Rumpf states that  the cells that are near a
vessel are very tardy in undergoing any retrogressive metamorphosis,
and it is only those  that  are  so  far away from a vessel as to be
deprived of their  proper nutrition, either  because  of their distance
or because  of the disease in the  vessel, that undergo degenerative
changes.  It  matters not  what portion of the nervous system is
affected, the changes  are always essentially similar in character, dif-
fering only  in the form  somewhat  according to  the  histological
peculiarities of the tissue affected.   In the  nervous system there is
usually a general  infiltration of all the  different tissues, varying in
degree in different parts.
   To the naked eye these pathological conditions will present different
pictures.  The bones of the skull or  vertebral column may be thick-
ened, or there may be spicular or long  pencil-like formations.  The
membranes  are usually greatly affected,  especially at the  base.  One
of the most characteristic appearances  is the infiltration of the pia
mater at the base as it stretches along over the  quadraugular space 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.        377

that is formed by the pons behind, the tips of the temporo-sphenoidal
lobes at the sides, and the  posterior portions of the frontal lobes in
front. ( Vide Fig. 18.)  Here the membrane will be found to be pul-
taceous, like thoroughly wetted blotting-paper, instead of presenting
the translucent  appearance that  is usual  of the normal pia  mater.
This  is very much  the same appearance as  is presented in  cases of
tubercular meningitis;  and, indeed, as we  shall have occasion to see,
there is no means of distinguishing  between the two except  by the
accompanying history and the accompanying pathological findings.
The membranes are usually adherent, so that the cerebral substance
tears as they are pulled away.  It is  very  seldom, however, that any
purulent formation is observed.   Studding the  membranes in places
may  be found little granulations, and these are often large in size,
constituting veritable tumors.  The cranial nerves  at the base, espe-
cially in the auterior portion that has been  alluded to, are often found
infiltrated by the  diseased membranous  structures,  or surrounded
by them,  frequently both.   In the spinal cord the periphery may be
affected, or  there may be infiltration of the whole  cord, so that the
process would seem to extend to the  cord  either through the mem-
branes or the  vessels.  When the spinal or cranial nerves are affected
there is an intense infiltration of the peculiar cells, with a degenerative
process of many nerve-fibres, or there may be granulations or actual
tumors of the nerves.  In some  cases the nerves attain to au enor-
mous size, and the  bony canals through  which the nerves run  may
also  be  affected by  osseous  infiltration.   Donne found a vibrion
vineola iu the  secretion of chancre in  1837, without, however, attrib-
uting to it any importance.  Hallier,  in 1869, thought that he found
multitudes of  micrococci in the  blood-globules.  In  1872 Lostorfor
saw on the third  day, in  syphilitic blood  preserved  in a  humid
chamber,  small  brilliant corpuscles with minute prolongation, these
becoming larger aud mulberry-shaped ; but it has since been  shown
that  these phenomena  are observed in  normal blood, especially in
cachectic individuals.  In  1878 Klebs found little rods animated by
very  slow movements in the liquid from a chancre, and, cultivating
this liquid in  gelatin, he developed  these  rods  into  agglomerations
forming large  spiral masses, which he called helicomonades.  The in-
jection of this liquid into apes produced circumscribed buccal altera-
tions like mucous patches, and at  the  autopsy of one of these animals
caseous deposits were  found between the  dura mater and the skull
resembling gummata, whilst caseous  patches were seen in the lungs,
the pleura,  the  kidneys, etc.  Other apes were injected by Klebs
subcutaneously  with  fragments  of  chancre,  and at the autopsy
caseous deposits  were found, and the cultivation  of the blood of these
animals again gave rise to the peculiar rods  and the  helicomonades.
Cornil and  Babes,  however, doubt  whether  these caseous nodules
might not have been due to tuberculosis, to  which malady apes  are
peculiarly subject in northern climates.  The next year Klebs con-
firmed these researches, but  it is singular that he was  never able to
obtain these results  from inoculation  in  any other animal than the
ape.  Aufrecht found microbes in  the secretion of condylomata in 
378
NERVOUS DISEASES.
1881.   Birch-Hirschfeld gave a description in  1881 of certain bac-
teria which he had found in chancre, condylomata, and visceral gum-
mata.   They consisted of rods varying in length from one millimetre
to three or five, and were found iu the cells  or  in  the  intracellular
tissue.   In 1882 Martineau  and Hamonic stated that they had
observed a multiplication of rods obtained by culture of fragments of
chancre, and that inoculations  of apes had produced eruptions com-
parable to those of syphilis, such as hard chancre aud the secondary
phenomena.  Letuic (1883) obtained negative results in  inoculation
of the  hog and the rabbit with  the micrococci cultivated from chancre
and mucous patches.   Kobler, Neumann, Bayer, Horand, and Cor-
nevin experimented upon a number  of animals, and arrived at the
conclusion that no animal had yet been found capable of receiving
the syphilitic virus.   Cognard (1884) inoculated  an ape with the
cultivated secretion of a raucous patch, aud, like  Martineau, obtained
an induration at the point of inoculation and a general eruption, but
the objection has been raised that this was probably a species of sep-
ticsemia.  Morrison (1888) has found bacteria  in the  secretions of
chancre and mucous patches.   Tornery and Marcus (1884) have cul-
tivated micrococci.  Koniger has seen bacilli in a case of pulmonary
syphilis, these bacilli  being somewhat finer  and longer than those of
tuberculosis, and not colorable  by Ehrlich's method; but many objec-
tions have been raised to his observations both because  of their lack
of evidence in the results and because of the methods of cultivation
and inoculation ; and the same objections are pertinent to the obser-
vations of Schutz, who claims  to  have found similar bacilli.  Lust-
garten  has  observed, in indurated chancre  and in gummata, bacilli
that were  isolated or in groups, resembling  those  of  tuberculosis.
They were  sometimes somewhat  curved and enclosed  in  tumefied
lymphoid cells, resembling the  bacilli of leprosy and tuberculosis. In
a subsequent communication the same author stated that he  had de-
tected them in  the lymphatic vessels  aud the capillaries.  They are
colorable by a method described by Lustgarten,  who found  them  in
sixteen cases of indurated chancre, mucous patches, and the secretions
of tertiary syphilitic productions, as well as in the gummata of an
infant  afflicted with hereditary  syphilis.  Doutrelepont has seen these
bacilli  described by Lustgarten in  eight cases  of chancre  of the pre-
puce, in one condyloma of the  labia majora, and in five papules, and
he has  observed the greatest number of them in cases of syphilis that
have not been treated.  One indurated chancre without secretion did
not contain them, but they were found in many of the sections. Al-
varez and Tavel have found the Lustgarten bacilli in the smegma
and the desquamation of the humid portion of the genital region, as
well as upon the surface of syphilitic and non-syphilitic ulcerations of
the genital organs, and from this  it would seem  at first sight that
these bacilli may be found under normal conditions; but  the method
employed by Alvarez and Tavel is not  identical with that of Lust-
garten, as the bacillus described by the latter is not colored by simple
colors  or by Ehrlich's method, whilst the microorganisms of Alvarez
and Tavel are;  nor have the  latter  found  their bacilli in sections, 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.       379

Klemperer and  Matterstock have confirmed the observations of Al-
varez and Tavel.  Cornil  and Babes  are undecided as to which of
these authors is right.  Other writers  upon the subject on different
sides of the question have been  Giacomini, Disse and  Taguchi (two
Japanese medical men writing in German), Gottstein,  Leloir, Weig-
ert, Baumgarten, Eve, and Longuard.   As a result of all these  re-
searches  it  may be  stated that the bacilli described by Lustgarten
and Doutrelepont have been the ones that have attracted most atten-
tion ; that the question is not by any  manner of means yet decided;
that the bacilli described by Lustgarten have been found by many in
syphilitic individuals; that the bacilli  similar in  some  respects to
those of Lustgarten are found in normal smegma and the secretions
of the  genital  organs; that the bacilli  of Lustgarten and  those of
the smegma  and the genital organs differ from one another distinctly
in several particulars ;  that there are probably several bacilli in syph-
ilis, two varieties being described by Rumpf; that the bacilli of Lust-
garten  have been found in all  stages of syphilis  and in syphilitic
alterations in many different diseases; that nothing like them has
been found in non-syphilitic individuals except in the smegma or the
genital secretions, and even here there are alleged points of difference.
It would therefore seem as if Lustgarten's bacilli bore some relation
to syphilis.   No one has  as yet succeeded, however, in obtaining any
pure cultures of this bacillus, aud this test is therefore lacking.
   Clinical History.   The symptoms of syphilis of the nervous
system are almost coextensive with the symptoms of all nervous dis-
eases, and it is, therefore, very difficult  to give a clean-cut picture.
In most  cases, however, the symptoms are  either  of lesions of the
intracranial  organs or of  the spinal cord.   Lesions of the peripheral
nerves are rare.   We may, therefore, classify the symptoms of syphilis
of the  nervous  system into those of—
       The intracranial contents;
       The spinal cord;
       The peripheral nerves.
   Intracranial   Syphilis.   In 1887,  and again last year, I called
attention to the  fact that most forms  of intracranial syphilis are
characterized by the following  group  of symptoms,  namely:  a
cephalalgia that is apt to be peculiar in having a quasi-periodicity
that manifests itself in a  tendency to return at a certain time in the
twenty-four hours, most frequently at or toward  night, less frequently
in the afternoon or morning ; marked insomnia, usually at the onset,
lasting a few weeks; a sudden  cessation of the cephalalgia  and  in-
somnia upon the supervention of any paralytic or convulsive symp-
toms. I have been working up this subject for some thirteen years, and
I have a history of 140 cases. These symptoms are usually prodromal
to the various lesions of the cerebrum that may be manifested.   In
some cases,  however, these  prodromal   symptoms  will be  absent,
although it is only in a minority that this will happen.   Whether
preceded or not by these prodromal symptoms, the  lesions of the
cerebrum will  manifest themselves by symptoms of paralysis, coma,
epilepsy, or insanity.  The most usual forms of paralysis are either 
380
NERVOUS DISEASES.
hemiplegia, monoplegia, or paralysis of one or  more cranial nerves.
The hemiplegia may be produced by a lesion of the  cortex, of the
basal ganglia, or of the internal capsule, in none of which will there
be any implication of the  cranial nerves.   Hemiplegia produced by
cortical lesion usually begins by paralysis of the upper or lower ex-
tremity, which  gradually  emerges  into a  hemiplegia.  Hemiplegia
of the iuternal capsule has exactly the same symptoms as hemiplegia
caused by lesion of the internal capsule in non-syphilitic individuals,
as it is  precisely  the same arteries that are affected in  both cases,
although the arterial lesions may differ in pathological details.   The
monoplegia of intracranial  syphilis is  almost  invariably due  to a
cortical lesion implicating one of the centres of the motor area. Paral-
ysis  of one or more of the cranial nerves is produced by a lesion at
the base, and, as has already been said, this lesion is most frequently
found  over the optic, the olfactory, and the motor oculi nerves and
the crura cerebri,  although it may, of course, extend further back
and  implicate the other cranial nerves iu the rear, such as the fourth,
fifth, sixth, seventh, and eighth; and the symptoms will, therefore,
be some impairment  of vision,  such as hemianopsia or blindness,
paralysis of the motor oculi, occasionally of the olfactory nerves, and
possibly of the intracranial nerves behind the third pair.  With
this  paralysis  of intracranial syphilis is frequently conjoined a hemi-
plegia due to implication of the crura cerebri, and as these crura cere-
bri contain the motor  and  sensory nerves that pass to the periphery
of the opposite side, the  hemiplegia will be upon  the side opposite
to the cranial  nerves affected, so that  there will be a crossed paral-
ysis.   Care must  be taken, however, not to  confound  the optic
neuritis  that  may result from a  lesion at  the  base or from various
other lesions of the cerebrum with the hemianopsia  or blindness  that
is caused by direct implication  of the  optic tract.   Syphilitic cere-
bellar disease  is in no wise distinguishable  from ordinary cerebellar
disease.
   Coma is occasionally observed in  syphilis, extending over days or
even weeks.   It differs in  no respect from the coma that may be  pro-
duced  by other intracranial lesions.
   Epilepsy is due to some lesion of the cerebrum, and this may be
either a general or focal lesion  at  the  cortex, at the  base, or in the
substance of the cerebrum.   In most  cases it  is due to a gumma.
The epilepsy is sometimes  accompanied  by  localizing  symptoms
which may enable us to judge of its site, or it may  be without these,
so that it may consist of a convulsion limited to  one arm, one leg,
or to certain groups of muscles, or it may affect both sides.
   The most usual forms of insanity that  are due, in my experience,
to intracranial syphilis are dementia, confusional insanity, and hallu-
cinations.   The dementia is usually of the  character of  paralytic
dementia.   The patient is stupid, frequently with stupid non-logical
delusions of a vague, indefinite character, and he may occasionally
have the characteristic non-logical delusion of grandeur.  The tongue
and facial  muscles  are tremulous, the speech is  tremulous and indis-
tinct, there is the  same characteristic defect in pronouncing certain 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.       381

letters that is observed in paralytic dementia, and the gait gradually
becomes shuffling, tripping, and  uncertain.   At times, too, the face
flushes and  the  mental and physical symptoms become intensified,
this exacerbation lasting  for several days.   The pupils frequently
present the characteristic abnormalities of paralytic dementia. There
is, therefore, no means of diagnosing this dementia from that of para-
lvtic dementia except by the  history of  the earlier symptoms of the
case or of a  syphilitic  infection.   The  French  authors have called
this form of  dementia pseudo-general paresis.   In other cases  there
is a  simple  dementia.  The patient's  expression is silly, he laughs
without cause, he  may lose  his way in going out, cannot recall the
names of  friends  aud intimates, may have some suspicions  of  those
about him, and altogether  acts  in a foolish  and childish way.   In
some cases symptoms of confusional insanity will be present.  The
patient will  be restless, at  times  excitable, muttering, confused, pos-
sessed of vague hallucinations, generally of hearing.  Hallucinations
are occasionally observed with but slight mental impairment. These
are usually hallucinations of hearing, occasionally of smell.
   Spinal  Syphilis.   Syphilis of  the  spinal cord, as has already been
said, usually affects the membranes of the periphery of the cord, and
only exceptionally extends into  the spinal parenchyma, so  that the
clinical symptoms are generally  those of a meningitis.   Any portion
of the cord may be affected,  aud the symptoms will, therefore,  vary
 according to the locality.   ( Vide table on page 82.)  Usually  there
 is a bilateral paralysis of  motion and sensation, with early exaggera-
 tion of the  tendon-reflexes  and contracture, and generally this  is
 quickly followed by  atrophy of the paralyzed muscles.   If the dorsal
 cord is affected, there is apt to be impairment of the bladder and rec-
 tum and diminution or loss of sexual power.
   Syphilis of the Peripheral Nerves. Syphilis affecting the peripheral
 nerves may  cause neuralgia, or neuritis of the simple or  multiple
 type.  Syphilitic neuralgia or syphilitic simple neuritis are not gen-
 erally distinguishable by themselves from  the  non-syphilitic forms,
 and care  must be taken not  to confound the nocturnal exacerbations
 of the simple form for  the nocturnal  exacerbations of  syphilis.
 Syphilitic multiple neuritis is not as yet  distinguishable by itself either
 from the  non-syphilitic form, aud, indeed, the only case of syphilitic
 multiple neuritis that has been reported is that of Taylor's,  in which
 the symptoms were almost identical with those of Morvan's disease.

   Besides these more  usual forms of intracranial  syphilis, spinal
 syphilis, and syphilis of the  peripheral  nerves, there may be different
 forms that it is impossible to classify, and of which the diagnosis can
 only be made by a knowledge of the earlier history or of the syphi-
 litic infection.  Thus, there may be lesions of single cranial nerves;
 there may be focal lesions  in different parts  of the cerebrum and the
 cerebellum,  from arterial disease or  from gummata;  there may  be
 mania or melancholia, or  other forms of insanity;  or  there may  be
 focal lesions in the  spinal cord;  or there may be a diffuse cerebro-
 spinal syphilis, giving rise to a bewildering mixture of symptoms. 
382
NERVOUS DISEASES.
   Diagnosis.    No  one should read  this  section upon diagnosis
without having first perused the sections upon the pathology and the
clinical symptoms, so that a clear idea may be obtained of the mul-
tiplicity of the symptoms and the most usual types  into which this
seeming complex is resolved.
   Intracranial syphilis should  be suspected  in any case of a quasi-
periodical headache returning at a  certain  time in the twenty-four
hours, either at or toward night, less frequently  in the afternoon or
morning, conjoined with  marked insomnia;  and vigorous  treatment
should be begun at this period, for although, as we have already said,
the headache and the iusomnia will disappear upon the  supervention
of any paralytic or convulsive symptoms, yet these paralytic or con-
vulsive symptoms may indicate an irremediable lesion,  whilst the
headache and the  insomnia are of  an  earlier period at which the
progress of the disease can  almost invariably, if not invariably, be
checked.   A  careful inquiry should always be made for this headache
and insomnia, for its  importance is seldom recognized by the patient,
and he may therefore forget to mention it, or, if his memory has been
impaired,  he may have forgotten it; indeed, it is always well to re-
member that patients with intracranial syphilis, like those affected
with other intracranial disorders, are often not aware of their defects
of memory, so that a  reliable history can only be obtained from some
one who has  been in constant contact with them,  best of all a wife, a
sister, or one of the female  sex, for they are invariably far shrewder
observers of symptoms than males.   Any symptoms of lesion of the
intracranial contents that has been preceded by this peculiar headache
aud insomnia should  be suspected to be  syphilitic.  Aside from this,
however, a lesion at the base of the brain, especially at that anterior
portion in which lie the optic chiasm, the crura cerebri, the olfactory
nerves, and the third pair, is usually either syphilitic or tuberculous.
By this I do not mean to say that all lesions of this  particular por-
tion of the base are  syphilitic  or tuberculous, but  simply that the
proneness of syphilis  and tuberculosis to affect  this  site  should be
borne in mind.  Besides this, there are certain other groups of symp-
toms that  should cause a suspicion of syphilis, namely: hemiplegia,
under forty years of  age, convulsions in  an adult, and a comatose
condition  extending over days  or weeks.  Hemiplegia in an adult
under forty years of  age  is  suspicious because such a hemiplegia at
this time of life is most likely to be caused by syphilitic endarteritis
of the branches of the cerebral artery supplying the internal capsule.
Hemiplegia, to be sure, occurs in the child  from several causes un-
connected with syphilis (vide "Cerebral Palsies of Childhood"); and
also after  forty from  the endarterial changes (" Hemorrhages, Em-
bolism, and Thrombosis"); but the age  of the patient in the childish
hemiplegia will  make the differential diagnosis, whilst  in the adult
beyond forty there are frequently evidences of atheromatous arteries,
a hypertrophied heart, and occasionally slight renal lesions indicative
of an interstitial nephritis.  Possible sources of emboli must be ex-
cluded, of course, in the consideration of  such a  hemiplegia, such as
lesions of the heart, of the  lungs, etc.   Exclusion being made, how- 
THE CEREBRO-SPINAL NERVOUS SYSTEM.        383
ever, of the hemiplegia of childhood, of that of degenerative end-
arteritis after middle age,  and of cerebral  embolism, the diagnosis
will generally be that of syphilitic endarteritis.  Syphilis should be
suspected of being the cause of convulsions in the adult which have
not been preceded by convulsions in infancy, and which are not of
traumatic  or nephritic origin, or due  to pregnancy, or  in  an indi-
vidual  subject to migraine.  It is too  much the  custom,  I think, to
regard  convulsions in infancy as harmless aud not  prone to recur.
I have  elsewhere ("Epilepsy") called attention to the  fact that  a
large proportion of the cases of epilepsy in  youths or adults would
be found on careful inquiry to have had a convulsion in early life
that had usually been attributed to  dentition  or  intestinal or febrile
complaints; and of such early convulsions it may be very difficult to
obtain  a history unless the  parents or some other near relatives are
interrogated.   The convulsions occurring in nephritis or in certain
women during pregnancy are too well known  to need  more than  a
bare reference.  Again, it is  a curious fact, to which I have elsewhere
referred ("Epilepsy"), that migraine is interconvertible in certain in-
dividuals with epilepsy, so that most persons who have a  personal or
hereditary history of migraine will be found, upon minute and patient
interrogation, to have had a loss of consciousness or some epileptic-
like convulsions at some period of their life.  If, however, pregnancy,
migraine, nephritis, trauma, and preceding infantile convulsions are
excluded, a convulsion in an adult should give rise to grave suspicion
of  intracranial syphilis.   Syphilis  should  also  be  suspected  when
there is a condition of coma extending over days or  weeks, not trau-
matic, meuingitic, diabetic, nephritic, or from typhoid fever.  It is
not always easy to exclude the coma of meningitis when the symp-
toms are of recent occurrence,  and one must often wait for the char-
acteristic retraction of the head or the temperature-curve.  It should,
moreover, be borne in mind that there may be a meningo-cerebritis
of the middle portion of the ascending frontal convolution, just where
 the centre for the muscles of the neck has been located by Wernicke,
giving rise to a retraction of the head as in ordinary meningitis, and
that this symptom may be due to  a  localized meningitis  possibly
 of  syphilitic origin.  Frankel has  reported  such  a case from  the
wards of the Charite Hospital in Berlin.  The coma of  nephritis, it
 must be borne in mind, is not always of the profound nature that is
 seen where the urine contains large amounts of albumin.   It may be
 light and variable  in  its manifestations, simulating  a profound hys-
terical condition.   I have seen several such cases that were thought
 to be due to meningitis.  Nor will  it do to exclude nephritis by  a
 mere cursory examination of one specimen of  the urine for albumin.
 Several specimens should be obtained ;  best one at morning, mid-day,
 and evening, and  the amount of urea should be estimated; casts,
 blood-corpuscles, and pus should be searched for, and albumin should
 be sought by the finer modern  methods rather than by the  old and
 rough test  of heat  and nitric  acid.   Diabetes can  always  be easily
 ascertained.  Some anomalous cases of typhoid fever may mislead
 one at the start, although the progress of the disease almost invariably 
384
NERVOUS DISEASES.
 makes the diagnosis very certain.   We should therefore suspect intra-
 cranial syphilis if there are present
   1.  Quasi-periodical headache that returns at a certain time in the
 twenty-four hours, most frequently at or toward night, less frequently
 in the afternoon or morning;
   2.  Paralytic or convulsive symptoms that have  been preceded by
 this characteristic  headache and  insomnia, when  the headache  and
 insomnia will have suddenly  ceased  upon  the  supervention of the
 paralysis or convulsion;
   3.  Symptoms indicative  of a lesion at the base of the brain, pre-
 ceded or not by the characteristic headache and insomnia;
   4.  Convulsions in the adult which  have not been preceded by con-
 vulsions in  infancy, and are not  of traumatic or nephritic origin, or
 due to pregnancy, or iu  an  individual subject to migraine;
   5.  Hemiplegia in an  adult  under  forty years of age, even when
 there has been no  preceding headache and insomnia;
   6.  A comatose condition  extending over days or weeks, not trau-
 matic, meningitic, diabetic,  nephritic, or from typhoid fever.
   If  a history of syphilitic infection  has been obtained, this will, of
 course, very materially assist the  diagnosis, but it is frequently very
 difficult to obtain such a history.  Women often do  not know that
 they have been infected,  any more than physicians who have become
 tainted at some  surgical  operation or examination.  There  are often
 many motives for concealment, because an acknowledgment of syphilis
 would materially affect the  patient's interests, or his or her station in
 life.  Then, too, a  hard  chancre  may readily be overlooked because
 of the slight local symptoms, and this has  occurred to some of the
 best syphilographers who have had the patient under constant obser-
 vation from the supposed day  of infection.   In any case, therefore,
 where the above groups  of  symptoms are present, the patient should
 be put upon anti-syphilitic  treatment.
   The diagnosis of spinal syphilis is much more difficult than that
 of the intracranial  affection, so that  in  the former case the diagnosis
 must  rest mainly  upon  the history of syphilitic infection.   Grave
 suspicion  may,  however, be entertained in any  case of  a spinal
 lesion in which there is a bilateral paralysis with early spastic symp-
 toms  and atrophy, and this suspicion will be strengthened when
 there  is a spinal lesion of the dorsal cord with the above symptoms,
 and yet with no  implication, or but slight implication, of the bladder
 and rectum.   Tabes dorsalis has, undoubtedly, in a large number of
 cases a history of syphilitic infection, but yet it cannot be classified as
 a syphilitic  lesion, and it really is only one of the syphilitic sequela.
  The diagnosis of syphilis of the  peripheral  nerves  must rest en-
 tirely upon the history of the syphilitic infection, as no characteristics
 of syphilitic peripheral nerve-lesions are known.
  Diffuse cerebro-spinal  syphilis  may be diagnosed by  the presence
of  characteristic intracranial  symptoms, plus the symptoms of a
spinal affection.
  Prognosis.   The prognosis of syphilis  of the nervous system is
largely dependent upon  the question as to whether the lesions are 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.        385

destructive or non-destructive.  In general terms it may be said that
the prognosis is good  except where actual organic disease has been
set up, or except where the syphilitic infiltration has excited in the
normal tissue the formation of some other structure that is  foreign
to the particular texture.   The infiltrations  of  the nervous tissues
themselves, the gummata, the arterial lesions, are  by themselves re-
markably  harmless.  It is singular to see, as  we often do, how much
and how long the nervous structure will  present evidences of syphi-
litic disease aud yet recover entirely under adroit and vigorous treat-
ment.  Buzzard tells of an artery that had  been almost occluded, tested
by the sphygmograph, and yet it was again made patulous by proper
treatment.  To speak in general terms, it may be said that the symp-
toms of good omen are : nervous syphilis iu its early stage; lesions at
the base of the brain ; spinal lesions without preceding intracranial
syphilis, neuralgia, and the lighter forms of neuritis.  Those of un-
certain prognosis are : long-standing syphilis  of the nervous system;
such forms of  mental trouble as are evidenced by slight confusion,
hallucinations, and mania; spinal lesions with hemiplegia.   Of de-
cidedly  bad omen are :  locomotor ataxia;  pseudo-dementia;  nervous
syphilis in persons whose general health is badly broken ; relapses in
spite of anti-syphilitic  treatment;  nervous syphilis in persons who
bear the iodides badly; syphilis of the  peripheral  nerves that has
existed for a long time, or  that has caused pronounced trophic altera-
tions.
   Treatment.  I have very pronounced ideas in  regard to treat-
ment.   I know of no reason for dogmatism  except considerable ex-
perience, and that is my excuse for my dogmatism.   I have but little
faith in mercury, aud I never rely upon  it alone.  Again and again
have I seen  cases go halting along in the most uncertain  manner
under  mercurial treatment, yret the symptoms have been  smoothly,
gradually, and  certainly removed by the iodide.  Iu several cases,
too, I have  known of death, although  the most  careful mercurial
treatment had  been pursued in enormous doses, and these cases have
been precisely  similar, as far  as one is able to judge of one case by
another in the  practice of  medicine, to others  that I have been accus-
tomed to  regard as of favorable  prognosis under treatment by the
iodides.  But  the  dose of the  iodide which  is administered by the
Germans and French will often be entirely inadequate.  I give the
iodides  until the  symptoms  yield or until  iodism  is produced.   I
make use of the saturated  solution of the  iodide of  potash, each drop
of which contains almost a grain of the salt. I commence with twenty
drops three  times  a day, aud increase  it each day by two or three
drops at each dose, and keep  increasing until  the symptoms yield or
iodism is produced. Should iodism ensue before the symptoms yield,
I pursue one of two methods.  I first increase the dose of the iodide
by about one-third, and rapidly increase each succeeding day. Singular
to say, in some cases this increased dosage will cause the iodism to
disappear, and the larger doses will  be borne  very well.   Should,
however, these  larger  doses still  further increase  the iodism,  I de-
crease to one-half the dose at which the iodism had begun, and con-
                                25 
386                   NERVOUS DISEASES.
tinue this decreased dose until the iodism diminishes or disappears,
when I  again  rapidly increase the dose, and am usually able to go
on without further trouble.   In some few individuals, however, no
amount of care will cause more than a certain amount of the iodide
to be borne, and such cases, as I have said, are usually of unfavorable
prognosis.   In some cases—fortunately, they are rare—even  small
doses of the iodide will produce a cardiac disturbance that prohibits
its administration.  But this last fact should not be confounded with
the phenomenon  that the profession  generally does not seem to be
cognizant of, namely, that  small doses of the iodide, 5 or 10 grains,
will  usually produce  more iodism than the larger doses.  I am per-
fectly well aware that the medical chemist will object that these large
doses of iodide pass  through the body and are quickly excreted by
the urine;  but I am equally well aware, in the  face of this fact, that
these large doses  of  the  iodide  will  cause symptoms to yield that
cannot be made to yield  by less doses.   I have given as  much as
800 grains of the  iodide of potash in twenty-four hours, and  have
seen symptoms disappear with these enormous  doses that would not
yield to  minor ones.  I administer the iodide after meals, and either
in a full  tumbler of ice-water, or in a glass of Vichy, or in a glass of
a Bohemian spring water, the Giesshiibler.  I prefer the Giesshubler
to the Vichy, although it is more expensive, because it is much  more
pleasant  to the taste and  agrees much better with the average stom-
ach.  Moreover, the Vichy water which is put  up in siphons in this
country is artificial, by no means equal in its  effects to the natural
water, and the natural water, either of this country or of Europe,
does not keep so well in bottles  as does the somewhat similar water
of the Bohemian spring.
  But he who  expects to cure  his patient with the iodides alone,
unless  the  case be so grave as to  call for  immediate relief, will be
disappointed.   The human organism must be put in the best possible
condition.  A  generous diet should  be employed.   Freedom  from
care and worry, where possible, should be enjoined, and all strenuous
exertion  of mind  and body avoided.  And let  me say here that in
many broken-down individuals the most satisfactory results may be
obtained from  a conjunction of the iodides with the brilliant treat-
ment that  has been  made  known  by Dr. Weir Mitchell, under the
name of "Fat- and Blood-making"—a therapeutical procedure that,
in my humble  opinion, will  rank in coming  years with the surgical
revolution  inaugurated  by Lister.  (" Neurasthenia," Chapter  IX.)
When the acute symptoms  have been brought  under control, travel
—especially an ocean voyage—will often work wonders.  In every
case that tends to chronicity, staple tonics and alteratives should be
used.
  I have often asked myself, When can a person be considered to be
cured of nervous syphilis? aud I have never succeeded in answering
the question to my own satisfaction.   I know of no data by which
we  can guide ourselves.   I have seen relapses  occur years after the
disappearance of  every untoward symptom, and I  have seen  them
even where  a certain moderate treatment by the iodides had been 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.        387

maintained.  I  usually impress this uncertainty  upon  my patients,
warn them  to be on the lookout for future symptoms, and apprise
whoever may be their attending physician of their possible signifi-
cance, and I enjoin them to keep up moderate doses of the  iodide
for yeaus.  This last precaution I observe the more readily because
I have but  seldom seen any ill effects from the continued adminis-
tration of the iodides, to which  patients usually become accustomed
as they do to commou  salt.  Occasionally it  may  happen that  an
obstinate  pharyngeal or post-nasal  trouble may be induced, or some
unsightly cutaneous eruption;  but, as a rule, these are controllable,
aud in any event they are far preferable to the possibilities of nervous
syphilis.

                  DISSEMINATED  SCLEROSIS.

  Synonyms:   Insular  sclerosis.   Multiple  sclerosis.  Sclerose  en
plaques desseminees.  Multiple cerebro-spinal sclerosis.
  History.  Cruveilhier  mentioned disseminated sclerosis for the
first time in his celebrated Atlas in 1835.   In 1838 it  was also de-
scribed by Carswell.  Tiirck iu 1855, Rokitansky in 1856^ Frerichs
and Valentina  in  the  same year, Rindfleisch and Leyden in 1867,
Zenker, Charcot, and Vulpian in 1862, have since dealt with thesub-
ject, although it does not seem to have been known in England even
in 1868.   The  lesion  in children  was  only  called attention  to in
later years, and the first case seems to have been that of Honemaker
in 1879, although since then a number of cases have been published
by  Unger,  Leube, Charcot,  and  others,  and altogether the best
resumi of the subject in children is that which has been written  by
Pritchard.
  Pathology.   Disseminated sclerosis consists, as the name indi-
cates, of a  number of insulated  islets  of sclerosis throughout the
brain or  the spinal cord, or both.   These  consist of circumscribed
grayish spots,  more or less regular in  contour, sometimes discrete,
sometimes confluent, whilst the surrounding nervous parenchyma has
 uudergone  no  alteration.   These sclerotic patches are found  in the
 walls of the ventricles, in the white substance of the centrum  ovale,
 in the septum  lucidum, in the corpus callosum, in the optic thalami
and corpus  striatum, occasionally in the  cerebellum,  in the medulla
 oblongata, in the pons,  and in the spinal cord.  When first exposed
 to the air these grayish spots take on a roseate tint like that  of the
 flesh  of salmon.  Even the nerves  may  be  affected at their  origin
 from  the brain or spinal cord, and  of the cranial nerves  the  optic,
 olfactory, and trigeminus are most prone to be implicated.  In some
 cases  the patches are raised above the surrounding surface and seem
 as if turgesceut, although sometimes they  cause no alteration  in the
 superficial height of the nervous organ, and are even occasionally
 depressed.   The consistence of these patches is  usually  somewhat
 firmer than that  of the  brain-tissue, and they are sometimes quite
 hard.   In the brain the cortex is seldom  affected, whilst in the  spinal
 cord the patches appear upon the surface, and sometimes the whole 
388
NERVOUS DISEASES.
thickness of the cord is  affected.  Microscopically there is found to
be  a  hypertrophied  neuroglia,  glia-cells,  and  fibrous spider-cells,
and in  the later stages a dense mass of fine fibres and also a certain
number  of fatty granules and globules, probably the remains of the
degenerated nerve-element.   The nerve-fibres are peculiarly affected;
the medullary sheath  undergoes degeneration, but the axis-cylinders
persist  to a  remarkable degree, although they  may ultimately dis-
appear, whilst  all  the vessels are  thickened, and occasionally  the
nerve-cells are atrophied. There is occasionally slight hypertrophy of
the connective tissue of the pia mater, but this  is rare.  What  the
pathogenesis  of the affection  is  we do not know, or whether it is a
primary sclerotic disease or an  outcome of vascular  disease.  Occa-
sionally diffuse sclerosis is  found in conjunction with the islets that
have  been  described.  I believe, however, that the symptoms  of
disseminated  sclerosis can  be  caused  by  other  lesions than those
which have just  been narrated, for in one case of mine which was
so typical that I had lectured upon it for many years, and which I
had in  my hospital wards  for  three  years under daily observation,
there  was found to  be a meningitis of the pia mater, lepto-meningitis
cerebralis, and  in this case there was no history of syphilis, none of
the cheesy nodules of syphilitic  sclerosis,  nor any of the  other patho-
logical lesions of sclerosis.
  Clinical  History.  To anyone who has read this section upon
the pathology of this  disease, it will be apparent that there must be
two sets of clinical symptoms,  namely, general  ones and localizing
ones.   In other  words, there are certain symptoms common to dis-
seminated sclerosis wherever  the site of the patches may be, whilst
there  must be localizing  symptoms due to impairment in function by
the patches of some particular portion of the cerebro-spinal axis.
  The general symptoms are :
       Tremor;
       Slight weakness or inco-ordination ;
       Nystagmus;
       Increase of  tendon-reflexes ;
       Contracture;
       Optic-nerve atrophy ;
       Peculiar speech ;
       Vertigo.
  The tremor  is generally present only when voluntary movements
are made, and  to  this the  name of intention-tremor has been giveo.
The best means  of evoking this is to have the patient take  a glass
of water in his hand and carry it slowly to  his lips, when the  tremor
will appear ; or have him  to write his name upon a blackboard, or
take a moderately heavy book in his hand, or do any other acts that
call for  the exercise of volition.  This tremor, therefore, disappears
usually when the  patient  is at rest.   It is a fine  tremor, usually
somewhat coarser than that of  paralysis agitans, and in many cases
becomes extreme  and coarse when voluntary movement  is made.
Great stress  has been laid upon this intention-tremor as a diagnostic
means whereby we  may distinguish disseminated sclerosis from paral- 
          THE CEREBRO-SPINAL NERVOUS SYSTEM.        389

ysis agitaus, and I think that in the majority of cases this is a valid
distinction, yet in some cases of paralysis agitans the same character-
istics of tremor  may be  observed, whilst in some cases of dissemi-
nated  sclerosis the tremor is also present when the patient is at rest,
although  this last is exceptional.   With this tremor usually goes a
slight inco-ordination,  which  is shown by the difficulty that  the
patient evinces in carrying a glass of water to the lips, or in writing,
although  it is impossible to say how  much of this inco-ordination
is  due to the  tremor  and how  much to  actual  inability,  aside
from the tremor, to make the different groups  of  muscles act to-
gether harmoniously.  With the tremor and inco-ordination there is
a slight paresis, which can be shown by the feeble grasp of the hand,
either in pressing the  physician's hand or in testing by the dyna-
mometer, or in the feeble hold of a pencil or a piece of chalk.  As in
the case  of the  inco-ordination, however, it is difficult to say how
much of  this is from the tremor.
   Nystagmus is a common  symptom, and, like the tremor, it is usu-
ally present only on movement, consisting of movements of the globe
in each direction, generally7 more marked in the  lateral than in  the
upward movement of the eyes, or greatest when the eyes are directed
to one side, but it is rarely  rotatory.  Occasionally a slight weakness
in conjugate movements of the eye is also observed, generally to the
sides.  The tendon-reflexes are almost  invariably increased, and this
exaggeration is  found in increased knee-jerk, ankle-clonus, and  hasty
micturition.
   Contracture is a common symptom.  In slight degrees it may only
be evoked by the methods  to which I  have called attention on page
169, namely, extending the arm or  leg, instructing the patient to let
it go, testing by  gentle movements of flexion and  extension  as to
whether  he  has done this, then bringing the arm  or leg to an  ex-
tended position, aud suddenly, without warning, flexing  the  limb,
 when, if  there is any commencing contracture, a sudden  click-like
muscular resistance will  be experienced  by the hand before the flexion
is  completed.  When contracture is more  pronounced, a rod-like
exteusion and a wax-like resistance that is offered to the hand in
 movements of flexion will make the symptom very evident.
   Optic-nerve atrophy is a frequent symptom, either as the result of
a  primary atrophy or from a patch of  sclerosis on the optic chiasm
 or in the optic nerve, and sometimes it  is associated with impairment
 of vision or even  segmental defects of vision.
   The speech of disseminated  sclerosis is characteristic.   It is jerky
 and scanning or staccato,  so that  the patient hesitates;  there  are
 irregular, jerky movements about the muscles of  the mouth and  the
 tongue, and  the teeth are uncovered iu utterance.   In  my opinion,
 the speech is of more value as a means of differential diagnosis from
 paralysis agitans than the tremor, because in shaking  palsy the speech
 is the very antithesis of the speech in  disseminated sclerosis,  being
 slow, deliberate, seemingly  wise.
   Vertigo is a frequent symptom, although it is not in my experience 
390
NERVOUS DISEASES.
so common as Charcot would have it to be, and it is  rarely accom-
panied by vomiting.
  These are the general symptoms.
  In addition to these there may be localizing ones of great variety
due to the  implication of some part of the brain, cerebellum, spinal
cord, or peripheral  nerves by a sclerotic patch.   An attempt has
been made  to distinguish betweeu  the cerebral symptoms and the
spinal  ones, but this can  only be  done by means of the localizing
signs and not by means of the general ones.   It is useless to attempt
to catalogue the different localizing symptoms, because  they are as
various as are the functions of the nervous system.  None of the
general symptoms have been explained by the localizing of patches,
with the possible exception of the optic-nerve atrophy.  In general
terms,  it may be said that if a sclerotic patch implicates the motor
tract, it will cause  paralysis.   An increase in the tendon-reflexes and
contracture, it must be borne in  mind, however, is not evidence of an
implication  of the  lateral columns, as some observers have stated, for
these symptoms  are found when the lateral columns are not affected.
In very few cases, as we  have stated, is the gray matter of the cor-
tex affected, so  that when there are  lesions referable to this gray
matter, such as  dementia, as a rule disseminated  sclerosis should be
excluded except in children.   If the cerebellum is affected, the char-
acteristic symptoms of cerebellar disease will be added to the general
symptoms.   If  there is a sclerotic patch destroying the functions of
certain spinal areas, symptoms of  impairment of such areas will be
present, and the  most frequent of these seems to be some of the symp-
toms of locomotor ataxia, such as loss of the knee-jerk and marked
ataxia, which are  probably due to the implication of the  posterior
columns by a sclerotic islet.  The duration of the disease is indefinite.
Thus,  I have known one case to last fifteen  years, and another to
terminate in two years, whilst Gowers speaks of one that lasted only
a year and three-quarters.  The disease may gradually progress to
great helplessness without actual paralysis, or there may be  a sudden
apoplectoid attack, or the patient may die of failure of respiration.
The nutrition is usually unimpaired throughout.   When the disease
occurs in children, it has  certain peculiarities that are not so often
present in the adult.   Thus, the sudden onset  is most common, and
this  may succeed a convulsion.  Strabismus is frequently an early
symptom.   A low standard of intelligence is the rule.  Convulsions
were observed in more than half the cases.  Contracture is uot nearly
so frequent  as in the adult.  Tremor and  ataxia, however,  are quite
as constant in the  child as they are in the adult.
  Etiology.  The etiological factors which bear a certain relation-
ship to disseminated sclerosis are :
       Age;
       Sex;
       Heredity;
       Exposure;
       Emotions;
       Trauma;
       Febrile disease. 
THE  CEREBRO-SPINAL NERVOUS SYSTEM.        391
  Most cases are found between the  ages of twenty and thirty-five
years, but the disease also occurs in children, and Dr. W. B. Pritchard,
chief of my clinic at the New York Polyclinic, has collected from the
literature more than  fifty cases in  children, rangiug  from  fourteen
months to fourteen and a half  years.
  The disease appears to be much more common among adult females
than males, although in children the sexes are about equally divided.
  Heredity is a frequent cause.  The most remarkable proof of this
was  observed  by Pelizseus, who observed the transmission of the
disease  through  successive  generations,  the  symptoms  manifesting
themselves in the male  members of the family only;  but instead of
the direct heredity of disseminated sclerosis, there  may  be  simply a
general neurotic heredity.
  Exposure  to cold,  and especially  to  damp  cold, has frequently
seemed  to be a cause.
  The  emotions are  potent factors,  as  in  paralysis  agitans ;  thus
Spitzka saw a  case develop from fright in  a  cigarmaker, and Wilson
narrates the history of a child one year  old who was  thrown into a
convulsion by having a goose  thrown at  her, and after the convul-
sion the disease developed.
  Trauma is a frequent cause also.
  Febrile disease, such as scarlet fever, measles, pertussis, diphtheria,
smallpox, and typhoid are frequent causes iu childhood, and Sparks
has even seen a case developing after  herpes zoster.
  Prognosis.  The prognosis of disseminated sclerosis is hopeless.
I am sorry to  say that no case of cure has ever been recorded.
  Diagnosis.  The diagnosis should be from :
        Paralysis agitaus;
        Chorea;
        Hysteria;
        The metallic tremors and alcoholism ;
        Lepto-meningitis.
   From paralysis  agitaus the diagnosis  in  the typical  cases can  be
 made with ease.  This will  be seen  by the following parallel  pro-
gress :
          Paralysis Agitans.                       Disseminated Sclerosis.
  Age over forty.                         Age under thirty-five, or even in a child.
  Tremor usually present only upon voluntary     Tremor usually present both  upon  move-
movement,                           ment and when the patient is at rest.
  Speech slow, deliberate, wise, monotonous.     Speech jerky, tremulous, scanning.
  Attitude characteristic: head bent  some-     No attitude at all.
what forward, shoulders held stiffly; walk
shuffling and stiff.
  Bread-crumbling position of the fingers.       No special position of hand.
  Nystagmus rare.                        Nystagmus frequent.
  Optic-nerve atrophy rare.                 Optic-nerve atrophy frequent.
  Impulse to go forward, or go faster and faster     No impulse to go in any direction.
forward, or to go backward or laterally (pro-
 pulsion, festination, retropulsion, lateropul-
 sion).
  Exaggeration of tendon-reflexes and con-     Exaggeration of tendon-reflexes and con-
tracture rare.                          tracture frequent.

   These signs in  the two diseases  will  make, as  I  have  said, the
diagnosis easy in a typical case; but in a  non-typical case, or in a case
that  stands at the  borderland between the age  of thirty-five and
 forty, the diagnosis may be very difficult indeed. 
392
NERVOUS DISEASES.
   In the ordiuary cases of Sydenham's chorea the diagnosis should not
 be at all difficult, because there is no tremor, and the muscular move-
 ments are jerky, quickly beginning and quickly ending, or wave-like
 in the athetoid variety.   Iu some late cases of chorea, however, that
 have resulted from improper treatment  of the original attack or the
 relapses, there may be a  mixture of choreic movements and muscu-
 lar spasm (not  contracture) that may at  first sight cause confusion
 but the lack of true tremor and the other symptoms of the disease
 will  soon make the matter clear.
   In some cases of hysteria, especially if it be associated with tremor
 and  hysterical  paralysis of  slight degree, there may be some confu-
 sion  at  first, but the  history of the  case  and the lack  of  the many
 symptoms of disseminated sclerosis will afterward prevent continued
 confusion upon the subject.
   Metallic tremors of lead, copper, and mercury are entirely lacking
 in the characteristic symptoms of disseminated sclerosis, so that the
 mere mention of this  fact should prevent error of diagnosis.
   In alcoholism  the  history of continuous drinking or of a recent
 debauch, and the absence of nystagmus, intention-tremor, exaggerated
 knee-jerk, optic-nerve atrophy, etc., are sufficient.
   Lepto-meningitis cerebri—that is, meningitis of the cerebral pia
 mater—is, as I  have seen in one case of my own which I have already
 cited, quite capable of causing the typical symptoms of disseminated
 sclerosis.  In my case, however, there was a marked dementia that
 supervened within a year after the onset  of the  disease, and if this
 should  prove to be true of cases that may be observed in the future,
 it will be a valuable means of differential diagnosis.
   Treatment.   I am sorry to say that the treatment of dissemi-
 nated sclerosis amounts to  nothing.  I have never yet  succeeded in
 doing more than causing some palliation of the tremor.   For this
 purpose I  find the bromide of potash  and  hyoscyamine the  best
 drugs.   The bromide of potash should be given in doses of 10 grains
 twice or three  times  a day, in  conjunction  with Tfo grain of the
 hyoscyamine of the crystallized form once or twice a day, as may be
 fouud necessary to mitigate the tremor.  For the other  symptoms I
 have  never found anything of value, although I have patiently tried
 galvanism, faradism, ergot,  iodide of potash,  mercury, nitrate of sil-
 ver, and hydrotherapy.

                       LEAD-POISONING.

   Lead  can be  carried  into the human  body in many ways—by
 means of the mouth, the skin, and the lungs; and when taken into
 the body it can be stored up in surprisingly large quantities, so that
 as much as two  grains have been found in the brain in  a fatal case.
 The sources of poisoning are  innumerable.  The  workers  in  lead-
 factories are most frequently affected, as well as many other artisans,
 such as painters, plumbers, type-setters, type-founders, glaziers, glass-
grinders, etc.  The occasional sources of lead-poisoning are of  late
years  not nearly so numerous as they were a decade or more ago, but, 
           THE CEREBRO-SPINAL NERVOUS SYSTEM.       393

nevertheless they occur.   Thus, preserved  fruits,  vegetables, acid
fruits cooked in glazed earthenware vessels, shot left in wine  bottles
after cleaning,  snuff packed in lead paper, hair-dyes, cosmetics, and
flour ground in defective mills sometimes still induce the toxic effects
of lead.   From  Marshall's experiments, it is probable  that  the
absorption of lead is  gastric, and not intestinal; but the most  ex-
haustive series of experiments upon the effects of lead have been
those of Prevost aud  Binet.   Beside the clinical  symptoms which
are familiar to  most observers, they have shown that there are diminu-
tion and alteration of the red  blood-globules without increase in the
white corpuscles, albuminuria, fatty degeneration, occasional pericar-
ditis, with at times grauulo-fatty changes in the myrocardium and
segmental degeneration of the peripheral  nerves.  Investigation  has
shown that the lead accumulated in the muscles and in the  kidueys,
and that this was always in proportion to the length of time  during
which the animal had been taking lead.   It was also found abun-
dantly as phosphate in the  bones, the relative  proportions  of  the
mineral  and organic constituents of the  bone  remaining unaltered.
The liver  generally contained  but  little lead in cases of prolonged
administration, although the quantity might be increased temporarily
after each dose; but it never accumulated  in the liver as it did in the
kidneys.  Only small quantities were found  in the muscles,  spleen,
nerve-centres, eyes, lungs, heart, pancreas, genital organs, and blood.
Blyth, examining portions of the bodies  of two persons dying sud-
denly from lead-poisoning, extracted from the liver ^ grain of sulphate
of lead, from one kidney about y1^ grain, from a cerebrum about a
grain and a half, and from a cerebellum about J grain.  Putnam  has
examined the urine of eighty-six individuals, both  healthy and suf-
 fering from lead-poisoning, and has arrived at some rather remarkable
conclusions.  He finds that the urine of persons in  perfect  health is
almost free from lead ; but that in neurasthenia and epilepsy a small
 minority have lead in the urine; that the lead increased in propor-
tion as these nervous symptoms were associated with organic disease ;
that among the cases with organic disease  lead  was found most con-
 stantly in chronically diseased teeth, extending generally along a row,
 hut sometimes limited to  individual  teeth; that those having least
 cachexia were  those in which lead  was not present; but that none
 was found in progressive muscular atrophy.
   The symptoms of  lead-poisoning are  the so-called  cachexia, the
 so-called  lead-line on  the  gums,  colic,  pains, paralysis, cerebral
 symptoms,  hemiplegia, and hemiansesthesia.
   The so-called lead-cachexia consists of anaemia, due to actual dimi-
 nution in the principal blood-corpuscles, as well as to impairment of
 muscular strength.  Fever is very seldom present, and only in slight
 degree.  The  lead-line  is an irregular bluish-black line along  the
 gums at the junctiou with the  teeth.   Lead  colic is too well  known
 to need more than a  bare mention.   It is accompanied by vomiting,
 slight changes  in the pulse, and constipation.  The pains are either
 vague or referable to the muscles of the joints, sometimes conjoined
 with tenderness of the muscles, with  slight sensory symptoms, such 
394
NERVOUS DISEASES.
as tingling,  very rarely  with anaesthesia.    Motor paralysis, with
atrophy, is a most frequent symptom in the case  presented at our
clinics.   Thus, in 75  cases observed  at  the  New York Polyclinic
this  muscular paralysis aud atrophy  were present 69  times.  The
typical  paralysis is that  known as  " wrist-drop."   It is  due to
an inability to extend the fingers, sometimes all the fingers, some-
times only the two middle ones, or the first and second.  The long
extensors are the muscles primarily affected.  But at  this time, it
should  be remembered, the distal  phalanges can  be  extended, as
Duchenne has shown,  by the interossei and lurnbricales.   Extension
of the thumb is also generally impaired  or lost, although its meta-
carpal bone can  be extended.  The extensors of the wrist next become

                              Fig. 160.
Case of lead-paralysis affecting the extensor muscles.
affected, and the wrist-drop then becomes complete.  These different
muscles are affected in varying degrees  in different cases, sometimes
first upon the  radial, sometimes upon the ulnar side.  As Duchenne
has shown, the wrist can nevertheless in  some cases at  this period
be  extended when  the fingers are strongly flexed, which is due to
the fact  that  the extensor carpi ulnaris or  radialis is unaffected.
The affected muscles, therefore, are in  a  range  of distribution of
the musculo-spiral nerve, but the supinator longus, supplied by the
same  nerve, generally is  not impaired,  nor is the extensor of the
metacarpal bone of the thumb.  The  paralyzed muscles are usually
atrophied,  the atrophy sometimes coming first,  but generally the
paralysis.  These affected muscles are usually altered in their mus-
cular  reaction.   There is sometimes  the ordinary degeneration of
reaction, sometimes merely a  slight  diminution in response to fara-
dism.  Erb and Gowers have  seen a slight reaction of degeneration
preceding the  onset of the paralysis, the positive  closing contraction 
THE CEREBRO-SPINAL NERVOUS SYSTEM.        395
being  more marked than  the  negative  closing, and  a continuous
tetanic contraction being produced during the passage of the current.
I have never seen this.  Besides these muscles of the lower  arm,
some of those of the upper arm and shoulder are occasionally impli-
cated, most frequently the deltoid, sometimes the biceps, brachialis
anticus, and triceps.  Paralysis of the legs is rare, but I  have ob-
served it in several instances, and the muscles affected are the peronei,
supplied by the peroneal nerve, aud the long extensors of the  toes.
In some rare cases there  is a  general  paralysis.   In  the cases in
which the atrophy precedes the motor paralysis, there is often a very
close simulation of progressive muscular atrophy, more especially as
fibrillary twitchings are found.  Muscular cramps occasionally occur,
generally in the legs.   Tremor  is sometimes also observed.  Lead-
poisoning sometimes has a purely local effect, causing impairment of
sensation and occasional paralysis.  The cerebral disturbances consist
of convulsions, delirium,  coma,  hemianesthesia,  hemiplegia,  and
chronic mental disturbances, the  latter most commonly taking the
form  of melancholia, sometimes simulating general paresis.  These
cerebral symptoms, however, are exceptional.  AVhen  such general
symptoms  as convulsions,  delirium,  and coma are observed,  their
onset  may  be acute  or preceded  by  such prodromata as vertigo,
tinnitus aurium, and sleeplessness.  The convulsions mayr be epileptic
in form, or of the types of hystero-epilepsy  or  catalepsy.  When
there  are delirium and  convulsions,  a condition  of  coma usually
supervenes, but, although deep, this coma is not complete.   A rise of
temperature from 100° to 101 J°, or even 102°, is sometimes observed
in conjunction with this symptom, and death may occur.   Hemiplegia
and hemianaesthesia are usually transient.   The mental disturbances
that have been mentioned  are chronic.  Ocular  symptoms are  occa-
sionally observed in lead-poisoning, such as inequality of the pupil,
amblyopia, bilateral amaurosis, or the ocular affections which usually
go with hemianesthesia, such as concentric limitation of the field of
 vision and  loss of color-sense.  Optic neuritis is by no means infre-
quent in cases  of acute lead-poisoning, and when there is a cerebral
implication there may be a simple atrophy.
  The most frequent pathological lesions  found in cases of  lead-
poisoning are those of neuritis, especially iu  the intramuscular nerve-
fibres, although the changes are also found  in the nerve-trunks.   In
some  cases the neuritis begins iu the medullary sheath ; in others there
is the ordinary degeneration of the nerve-fibres, such as is  seen after
section of the nerve; and  iu still other cases the neuritis affects the
nerve-segments,  which are separated by normal portions  of nerve.
Changes will appear in the  peripheral portions of the nerve external
to the anterior  roots, although occasionally the latter  are affected.
The posterior roots are almost invariably normal   The fibres of the
atrophied muscles present the usual appearance of muscular atrophy.
As  a  rule,  the  spinal cord and brain are unaffected,  but in  some
cases the cells of the auterior horns have been atrophied, or spots of
softening have been found in the anterior horns and the surrounding
brain-matter, or there has  been a thickening of the vessels of the 
396
NERVOUS DISEASES.
cord or a proliferation of the  connective  tissue, whilst in the brain
slight meningitis (especially of the pia mater) and hyperaemia of the
dura mater have been found.
  The diagnosis of cases of lead-poisoning can usually be made with
ease.   The characteristic lead-line around the  gums, the wrist-drop,
the lead-colic, and the history of the exposure to lead will usually
suffice.   It must, however, be remembered that wrist-drop may occur
from arsenical poisoning and  from the effects of silver.  In cases of
arsenical poisoning, howTever, there is often an ataxia with impairment
of sensation, and in cases of poisoning by silver there is the character-
istic discoloration of the skin, and almost invariably the poisoning has
been because of the medicinal use of the metal.   If there is no history
of exposure to lead, however, the diagnosis may be a matter of some
difficulty, but a rigid investigation of the patient's environment will
make the case plain.  When there is simulation of progressive mus-
cular atrophy from lead-poisoning there may be considerable trouble
in reaching the correct diagnosis.   In all doubtful cases examination
of the drinking-water and of  the urine should be made.
  The prognosis of the nervous symptoms of lead-poisoning are gen-
erally good.   All the cases that come to my clinic recover, and I have
never seen cases in private practice  that did not do the same.
  The treatment of  lead-poisoning should be by means of the iodide
of potassium, salines, tonics, electricity, aud rest in the severe cases.
The iodide of potassium, in doses of 10 to 15 grains three times a day,
is an invaluable drug in  increasing the excretion of lead by the urine
in some unknown combination.   Some authors warn us against using
the iodide in large doses  when there are acute symptoms, in the fear
that the toxic effects of the lead  should be  increased  by its sudden
passage from the tissues and into the blood.  I have  never seen any
such result in an experience of over twenty years.  The  best saline
is the  sulphate of magnesia, and this should be used to produce one
or two free movements, and then only as a laxative.  It should never,
however, be  used to the point of depressing or weakening the patient,
as is too often done.  It  should,  moreover, be  remembered that the
excretion of the lead is not the only object of treatment, but that the
human  organism, weakened by its presence,  must be sustained.  In
all cases, therefore,  tonics should be made use of for  a few weeks,
and the best of these is iron, preferably the dialyzed  form, the albu-
minate  in doses of one drachm three times a day in a cup of water,
or the peptonate, in the form of compressed tablet, three to five grains
three times a day.  The  iron can  usually be  advantageously given
with tonic doses  of  quinine, two grains  three  times  a day, or the
elixir of calisaya.  In cases of colic, morphia  should be used hypo-
dermically to relieve the pain, and usually the morphia will act best
when combined with atropia.   The galvanic or faradic current is of
invaluable service iu treating  paralysis, and should be applied to the
affected nerves in the manner indicated upon pages 123 et seq. 
CHAPTEE   IX.
                      THE NEUROSES.

                          EPILEPSY.

  Synonyms :  Latin, Morbus sacer seu comitialis.   French, l'Epi-
lepsie.  German, Fallsucht.  Spanish, Mai caduco.
  Definition.   The  term  epilepsy,  from  i-dajutftdva), " to seize
upon," means convulsions that are either tonic or clonic, of one limb
or of several or of the whole body, with or without loss of conscious-
ness; or loss of consciousness of a certain character ;  or certain phe-
nomena that are supposed by some authors to be the equivalents of
the convulsive or comatose symptoms.
  History.   Epilepsy was known as far back as the time of Hip-
pocrates, but it  was ill defined, and the knowledge  of the clinical
symptoms and the nature of the various forms has been the work of
the writings of the last twenty years, largely synchronous with  the
great development that has taken place in this time in our knowledge
of cerebral  localization aud the diseases of  the  brain, cerebellum,
spinal cord, and peripheral nervous system.
  Clinical Symptoms.  The main types of epilepsy are—
       Grand mal;
       Petit mal ;
       Convulsive movements without loss of consciousness;
       Vertigo;
       Double consciousness;
       Hystero-epilepsy;
       Procursive epilepsy;
       Laryngeal epilepsy.
  The symptoms of the typical attack of epilepsy are a sudden loss
of consciousness, a sharp automatic cry, a fall, a series of tonic mus-
cular movements of short  range which are  quickly succeeded  by
general clonic convulsions, these latter  lasting for several seconds or
minutes, when the patient becomes partially conscious, being half-
dazed, and then gradually merges into  what seems like a deep sleep,
but is really a return to unconsciousness, this  quasi-slumber  being
generally an hour or more in duration.   This type  is known  as grand
mal, or major epilepsy.   The deviations from it, however, are innu-
merable.  The most frequent non-typical group of phenomena consists
of a loss of consciousness, either without convulsive  movements, or
with very slight ones.   This is  known as petit mal, or minor epi-
lepsy.  Or there may be convulsive movements of the fingers alone,
particularly where the heredity is dying out  in a family; or there
may be a sensation of vertigo, which, indeed,  very frequently occurs 
398
NERVOUS DISEASES.
 in the  individuals between the grand mal and petit mal attacks; or
 there may be  other  sensations which are called aurce ; or there may
 be conditions of double consciousness, as it is called, in one of which
 a person may lead his usual life and  in  the other lead a totally dif-
 ferent one.  The most frequent of all these is either the grand mal
 or  the  petit mal.  The  color of the face in  these attacks is  very
 variable, being sometimes  pale and sometimes suffused.   It should
 always be remembered that statements regarding  this color of the
 face are very unreliable, as the  onlookers are generally too much
 disturbed emotionally to  be accurate observers.  The physician him-
 self seldom  sees  an  attack,  even  if he  be  the resident  of a  hos-
 pital;  thus, while it would tax my memory for  me to recall the
 thousands  of cases  I have treated in  twenty years of professional
 life, I could easily count up all those  that I have  observed  during
 the attack  itself.
   In some cases there is  a queer combination of  hysteria and epi-
 leptoid  symptoms, varying from the pronounced  hysterical attack to
 the  frightful  cases which  are illustrated in  the writings given out
 from the great Parisian hospital of La  Salpetriere; but these are
 seldom, if  ever, seen  in this country, and what we American  physi-
 cians call hystero-epilepsy, and what the English physicians designate
 by the  same name, is of a very much  less  sensational nature than
 what the French describe.  True hystero-epilepsy rarely begins with
 a cry or change of color in the face,  but generally with the tonic
 convulsive movements of true epilepsy\   These are  followed  by the
 period  of  so-called   " clownishness,"  characterized  by all sorts of
 bizarre  movements,   opisthotonus, distended abdomen, grimaces, etc.
 Then succeed a  series of passionate attitudes, with  delirium.  It is
 claimed, too, that ovarian compression  will cause the  symptoms to
 cease, but this has not been so generally in the cases which I have
 seen. All these types of hystero-epilepsy,  however, are different from
 the true epilepsy in the admixture or predominance of purposive or
 seemingly purposive  movements instead of a rigidly tonic or clonic
 movement of  a shock-like character,   whilst  opisthotonus,  a non-
 epileptic symptom, is occasionally observed in them.
  Procursive epilepsy has been recently described  by Mairet, and
 consists of  ruuniug  movements forward, but otherwise  presenting
 the usual phenomena.  It may alternate with ordinary epilepsy, or
 precede or  merge  into it.
  The  so-called  laryngeal vertigo is  unquestionably  a  variety of
 epilepsy, and the term vertigo  should be discarded, because, as is
 stated under " Vertigo,"  this latter term should be reserved for sub-
jective sensations of  loss  of equilibrium, with either no impairment
 of consciousness or very slight implication of it.  Laryngeal epilepsy
 has not as  yet been described in children, but it probably will be in
 the course of time.    It  consists  of a  slight loss  of consciousness,
 occasionally with  light touic or clonic  movements, and the exciting
 cause is some laryngeal, tracheal, or  bronchial  affection, such as
 laryngeal tumors, asthma, etc. Those cases which have been reported
 so far have  ceased after the cure or removal of the seeming cause, 
THE NEUROSES.
399
but the  histories have not been extended over a sufficient length of
time to exclude the possibility of  recurrence.
  Certain dream-like states  may precede the typical  manifestations
of epilepsy, or take their place.  They are simply degrees of impair-
ment of consciousness.   Of the latter, the condition of double con-
sciousness is the most marked.   One patient of mine, a lad of four-
teen, would wander for days about the lower quarters of New York,
sometimes earning wages in some light occupation, without arousing
the faintest suspicion in those about him,  until some fine morning he
would return to his normal condition and then quietly wend his way
home.
   Falret has spoken of another equivalent of epilepsy which he calls
the larvated  epilepsy (epilepsie larve).  This  may consist of an out-
break of hysterical insanity, usually of mania, or, as I have occasion-
ally seen it, an attack of violent  migraine or of great irritability of
temper.  Falret claims that iu  these cases there is  never any petit
 mal.  Hughlings-Jackson, however, calls attention to the fact that
 many cases of petit  mal are so slight,  consisting only  of a very
 momentary impairment of consciousness, with some slight muscular
 twitchings about the face and eyelids or  even of the fingers, that
 they may readily be overlooked by the friends of the patient, whilst
 the impairment of consciousness, hovvever slight, prevents the patient
 from himself recognizing them,  so that any  symptoms  following
 these might  be thought to  be  actual  equivalents,  whilst they are
 really attacks of petit mal  succeeded by the phenomena that  have
 been mentioned.
   The epileptic insanities are treated in another chapter of this book.
   Our  conceptions of epilepsy will be greatly simplified if, at the
 outset, we recognize the indubitable  fact  that epilepsy is but a symp-
 tom, just as  is a cough or fever, so that epilepsies  may be divided
 into those that are due to recognizable organic disease, those that are
 reflex, and those that we may call idiopathic.
    The  clinical characteristics of the idiopathic form  of the ordinary
 grand mal or  petit  mal will occupy us for the present.   This has
 certain features which  are  of great importance from a therapeutic
 and occasionally from a diagnostic standpoint, and  salient among
 these characteristics  are the nocturnal recurrence of some, the quasi-
 periodicity of others, the association with  migraine, and the temporary
 response, usually in a favorable way, to slight changes in the environ-
 ment or the  treatment.   The nocturnal  recurrence of epilepsy may,
 however, readily be overlooked, and  should always  be suspected in
 a child who is hereditarily predisposed  to the malady or who wakes
 in the morning exhausted and pale.  Some eleven years  ago I first
 called attention to the  quasi-periodicity of many epilepsies.  Many
 epileptics will  have  a recurrence  of their attacks at certain  times.
  Ihus, females are more especially subject to it at or about the men-
 strual period, while in others it will recur at certain  times of the
 mouth  or at  certain  intervals, these periods of relief sometimes last-
 ing for mouths, and in some rare cases even years.   I shall indicate,
 in the  proper place, how this quasi-periodicity may  be  utilized  for 
400
NERVOUS DISEASES.
therapeutic  purposes.   Some eleven years  ago I called attention to
the association of epilepsy with migraine,  not kuowing until some
time after the publication of Fere's book  in 1890 that he had done
me the honor to reproduce the history of my case in  that great work
upon epilepsy, and  that  Tissot, Parry, and Living  had previously
observed  the same  association.  In these  cases epilepsy alternates
with migraine, the migraine disappearing when the epilepsy appears,
and the epilepsy returning when the migraine disappears.  By this I
do not mean to say that all cases of migraine are subject to epilepsy,
but I do mean to say that there is a very close relationship between
migraine and epilepsy, and in some  cases the relation is so close as to
permit of this alternation ; indeed, almost  all cases of migraine will
be found at some period of their lives to have had a loss of conscious-
ness, with or without convulsive movements, although generally this
fact  is strenuously denied.   But this association of migraine and
epilepsy is of considerable therapeutic significance, as we shall see.
Epileptics, as is not generally known, are very readily influenced by
slight changes in the environment and  in  the treatment.  This was
first observed as far back as 1828 by the great Esquirol, at the head
of the Salpetriere,  who divided his epileptics into  groups, putting
each group  upon a different medicine,  and one group upon a dis-
guised placebo ; they all improved for a certain length of time, they
all relapsed  at about the same time, and  each  medicament had as
much effect  as the  placebo, and no more.  In addition  to  this, I
have pointed out again  and again, until my neurological brethren in
New York  now twit me for my7 persistency in calling attention to
the matter, that epileptics will do well for  a  time upon any change
of treatment, whether that treatment be medical or surgical, whether
it consist  of cutting  off the prepuce, removing the clitoris, extirpating
the ovaries, doing operations upou the male or female genitalia, using
the hot iron  or moxa, cutting the eye-muscles, or even, as I have
done myself, etherizing the patient and cutting a piece of skin out
of the buttock.   I have even seen  improvement effected in a patient
for months by mere change  of locality, as in one patient of mine
coming from a distant  city in Illinois, who had no attack for eight
weeks while she was in this  city, although  she  had  been having
three or four paroxysms  in a day before coming here, had  the same
number when she went back  home, and received nothing but a few
placebos from me whilst here.  I  know of another  inveterate epi-
leptic whose fits were banished for  months  after she had fallen down
a flight of  stairs into  a  vat  of hot water, not  returning until the
process of cicatrization was completed.   These epileptic attacks are
very prone to recur in variable spells—either every day, often several
in a day for weeks, perhaps  months, and then spontaneously disap-
pearing for  a different length of time, to recur  again and again in the
same old  manner.  I point this out in almost every  epileptic that I
lecture upon at the New York Polyclinic.
   Most epileptics, as I have shown, have large and variable  pupils.
Marie and  Musso  have attempted  to show by measurements of the
pupil that my statements upon this  point were erroneous, but the 
THE NEUROSES.
401
very variability of the pupils  renders their measurements question-
able.  By this I do not mean to say that the pupils are not large and
mobile in other diseases, but  simply desire to call attention to the
fact that this  peculiarity does  exist iu epilepsy.   A trained eye can
readily detect the fades in most epileptics, although it is impossible
to describe its fleeting traits and photography is not yet far enough
advanced to  portray  it,  probably  because the expression is  most
marked when the  patient is not directing his attention to any one
point, so  that when the muscles of the face are  on the alert, so  to
speak, in the  taking of a photograph, this peculiar expression disap-
pears.  I think, however, that I could make a diagnosis of epilepsy
in most cases  by the fades alone.  In the inveterate cases which have
been for  a long time  under treatment  by the bromides it is much
more marked, of course, and at this period the accompanying restless-
ness, the  pallor, the acne, the coated tongue, and the peculiar breath
will greatly aid  in the diagnosis.   The temper of most epileptics is
extremely irritable, aud especially is this the  case in children whose
malady has procured for them ill-advised license.
  The epilepsies of organic origin or of probable organic origin are
as variable as are the functions of the  brain.  Hughlings-Jackson
first called attention to a variety in which the  convulsive movements
were localized in one or more  limbs, and this  has come to be known
as Jacksonian epilepsy.  It has been found in many  instances  to be
due to recognizable gross organic disease of the cortical motor centres
or  the underlying motor  tract.  Procursive epilepsy is believed  by
Mairet to be due—upon what grounds we shall learn  later on—to
cerebellar lesion.   Epilepsy may be found among the symptoms of
almost any disease of  the  brain or spinal  cord,  and it  may also be
present with  tumors of the brain  or cord, the  different forms  of
cerebral and  spinal meningitis, hemorrhages of the brain, traumata
of the brain aud cord, etc.
  Etiology.   The following factors seem to  bear  some relationship
to epilepsy:
       Age;
       Sex;
       Heredity;
       Migraine ;
       Organic brain, spinal, or peripheral lesions  ;
       Traumata;
       Lesions or impairment  of function of non-nervous organs;
       Hysteria;
       Malnutrition.

  Gowers has analyzed 1450 cases as follows  :

         Under 10 years.....
         From 10 to 19 years  .
              20  " 29   "    ...
              30  " 39  "    ...
          "   40  " 49   "    ...
          "   50  " 59   "    ...
              60  " 69  "    ...
              70  " 79   "    ...
                                26
422 cases.
665  "
224  "
 87  "
 31  "
 16  "
  4  "
  1 case. 
402
NERVOUS DISEASES.
   It is  not generally known that, as I have  been for  years in the
habit of pointing out in my lectures, many cases of idiopathic epi-
lepsy will begin with a fit in early infancy, after which no convulsion
may occur in a  year or years, when the attacks will again appear
and at this or some later period the case will become  one of well-
marked  epilepsy.
   In Gowers's 1450 cases the  percentage of females was 54.6, aud
males 46.4.  There was a hereditary history in 36.6 per cent.
   The association of migraine with epilepsy has already been spoken
of, as well as the  connection  with organic brain and spinal lesions
and traumata.
   In some rare cases epilepsy may be caused by diseases of the heart
and of the  kidneys, occasionally by impairment  of function of the
gastro-intestinal organs, rarely of the lungs, and  very rarely, indeed,
if ever, of the genitalia.
   The association of hysteria  and epilepsy is by no means frequent.
   A fact of immense practical importance, and one that seems to have
been  almost universally overlooked, is that profound malnutrition
may be a cause of epilepsy,  so that with  the restoration of the gen-
eral health  the epilepsy will disappear.   In  one case of mine a cure
was maintained  for  nine years, in another for eight, in another for
four, in another for three, and in another  for five, and in none of
these was there any hereditary predisposition.
   Pathological Anatomy.   Epilepsy, as  I have said, is merely
a  symptom, and  in every  case it is a  question as to what it is a
symptom of.   From  a pathological  standpoint  we may therefore
divide epilepsy into two great classes, namely :  epilepsy from rec-
ognizable organic  disease;  second,  epilepsy  which  we may call
idiopathic.
   The organic lesions causative of epilepsy are : tumors of the brain
and cord ; meningitis, either tubercular, cerebro-spinal, suppurative,
or from disease of the  ear, or by metastasis from other organs; the
cerebral palsies of childhood, such  as  hemiplegia, double hemiplegia
(diplegia), or paraplegia, and due  to  such lesions as porencephalitis,
embolism or hemorrhage from  the cerebral arteries, thrombosis of
the cerebral arteries  or veins ;  lesions  of the cerebellum ; sclerosis of
the brain and cord, either of the type of multiple sclerosis or of other
forms ;  syphilis of the nervous system ; and diseases of the peripheral
nerves.
   We know very little about the pathology of the idiopathic forms.
The old theory of vasomotor spasm producing cerebral ansemia or
hypersemia  is  now  almost entirely discarded  by neurologists, as it
ought to have been long ago, for there has absolutely never been any
logical proof of it whatsoever.   It is undoubtedly true that ligature
of the carotid artery and great hemorrhage are capable of producing
epilepsy; but it has never been  demonstrated  that  the profound
ischaemia—not anaemia, as it  is so often incorrectly termed—thus
produced was  present  in every case  of  epilepsy, and  on the con-
trary there  are  many experiments and facts going to show that the
cerebrum of epileptic human beings  and animals is  not vascularly 
THE NEUROSES.
403
altered to any marked degree.   Vulpian, for example, has examined
the brains of guinea-pigs artificially rendered epileptic, aud has found
that they are neither hypersernic nor ischemic during an attack.  The
deductions as to the cerebral  circulation that are drawn by certain
authors from the facial circulation are unwarrantable, as the latter is
by uo means an index  to the former, for it often happens, especially
in cerebral traumata, that the face may be deathly pale at the same
time that the cerebral meninges are in a condition of profound hyper-
semia. The same remark also applies to the proof that would be drawn
from the condition of circulation in the retina.   In some cases of idio-
pathic epilepsy a sclerotic condition will be found in  the brain ; in
others au old focal meningitis, especially in the pia mater;  whilst in
many no lesions at all are visible.  Sclerosis of the cornu ammonis as
a probable cause of epilepsy has caused a great  diarrhoea of words, but
it is by  no means  constantly found, and even when it  has been, it
has never been shown whether it was a  coincidence or  an  effect
rather than a cause.  Barthez and Rilliet have laid great  stress upon
a peculiar variety of sclerosis to which  they have given the name of
tuberous or  hypertrophic, and in which the convolutions are found
elevated, studded  with  round  or  ovoid  tuberosities irregularly dis-
posed upon the convex portions of the convolutions, rarely in the
fissures, the size varying, but sometimes attaining that of a large nut.
These nuclei do not affect the white  matter,  the gray matter of the
cortex, or the  central  nuclei, the basal ganglia being  alone affected.
But this variety of sclerosis is open to the same  objections  as  those
which have  been dwelt upou in regard to the sclerosis of the cornu
ammonis.  Chaslin examined five epileptic brains at  the instance of
 Fere, and found what he called  neurogliar sclerosis in four of them.
 In  this  condition  the  convolutions are  macroscopically shrivelled,
 small, hard,  smooth, or slightly roughened, the pia mater not being
adherent, or otherwise  abnormal, the pathological alteration extend-
 ing in a very variable manner over the surface of the  cerebrum with
 large intervening normal portions sometimes reaching  to the medulla
 oblongata or to the cornu ammonis.  In  only one case  was one of the
 olivary bodies seen to be thus affected.   A microscopical examination
 of the fundamental lesion has  demonstrated that it is essentially due
 to a  number of rough fibrillse  of an  uncertain  length  which  had
 invaded  the cerebral   tissue,  especially the  gray cortex.   In the
 author's  own  words,   " In  the  normal  state  the  first layer of the
 i^ray  cortex  contains certain so-called spider-cells, whose prolonga-
 tions  are scarcely visible.  In this condition, on the contrary, this
 first layer is formed by a bundle of fibrils arranged  nearly parallel
 to the cerebrum, and   it can  be distinctly seen  to originate  from
 numerous cells with hypertrophied prolongations.  In the  prepara-
 tion which I am  viewing at this moment there  is a place  where
 this transformation invades all the layers, but leaves intact numer-
 ous nerve-cells and vessels.   It can be seen, moreover, that these
 fibrillse  in a certain space form in the depth of the cortex a network
 of nodal points, in which lie the cells  of the neuroglia.   Finally,
 and I would call attention  particularly to this fact, this first layer is 
404
NERVOUS DISEASES.
studded in places by large compact bundles, which are evideutly
formed from these fibrillse.  I would observe, in  passing, that the
vessels which remain do not  present a trace of inflammation, there
being simply, in certain points, a hyaline transformation of the capil-
lary wall."  Chaslin  espouses certain views of Ranvier, and main-
tains that a distinction should be made between the connective tissue
of mesodermic  origin and  the  neuroglia, which is of epithelial or
ectodermic  origin; the latter embracing the  Muller's fibres of the
retina, the fibres and cells of the neuroglia in the spinal cord, and the
slightly differentiated  prolongations of the  spider-cells in the brain.
This peculiar  neurogliar sclerosis, which he described for  the first
time, is, he claims, entirely distinct from a sclerosis of the  connec-
tive or mesodermic tissue, as the peculiar fibrillse distinctly emanate
from the neuroglia-cells, whilst the  non-adherence of the pia mater
and  the relative integrity of the vessels are indirect proof in the uanie
direction.  He has also given histo-chemical proof of these assertions.
These  fibrillse  in the bundles resist, in sections made after  immer-
sion in bichromate, the successive action of a 40 per cent,  solution of
potassa for  ten  minutes, as well as washing with water and  concen-
trated  acetic acid, whilst they remained  colored red by the picrocar-
mine used after washing in water, and they can be preserved thus in
formic glycerin.   When the connective tissue, however, is treated in
this  manner it swells and decolorizes so  that in a section of the spinal
cord the pia mater will be  swollen and decolorized whilst the neu-
roglia  is intact.   Moreover,  after the action  of alcohol diluted to one-
third these fibrillse remained colored  by the carmine when subjected
to acetic acid, whilst  all other forms of the connective tissue of the
body were decolorized.  So definitely and so judiciously is this patho-
logical  distinction  of  Chaslin's given that it merits  attention.  The
author believes that this neurogliar sclerosis is the same as that which
has  been found in the cornu  ammonis  and in  the  olivary bodies in
the same cases of epilepsy ; but if it is, certainly his localization of it
in the  first layer of the cortex gives it an importance and  possibility
that were never  inherent to any former descriptions.   Bevan Lewis
has described certain  striking degenerative  changes observed in the
cells of the second  layer of the cortex, and in some cases this has
been found to affect all the layers, even  including the series of spider-
cells.  These are described in detail in the  chapter  upon the " Path-
ology of Insanity."
  Our  knowledge of the modus operandi  of epilepsy is  not much
more definite than our  knowledge of  the  exact  pathology.  The
medulla oblongata was  the  portion of  the  nervous system that the
older writers held to be most  concerned iu  the production of symp-
toms.   Van der Kolk  believed that  the  nuclei  of origin of the
hypoglossal nerve in the floor of the fourth ventricle were always in
a condition of induration which was proportionate to the  amount of
tongue-biting that  had been  observed in the attacks.  But this was
the airiest of theories, and  is scarcely worthy of mention, much less
of sober discussion.  Theu Nothnagel  asserted that in the  floor of
the fourth ventricle there was a certain area which he called the con- 
THE NEUROSES.
405
vulsive centre (Krampfcentrum), and  that  irritation of this caused
epileptic convulsions.  He regarded this area as the vasomotor cen-
tre of the medulla  oblongata.   The location of this area coincides,
according to Wernicke, with the lateral motor field of the tegmentum
in the pons, the lateral portion of Frtg in Figs. 42, 43, 44, and 45,
its lower boundary being formed by the pons, its  upper boundary
not having been determined.  A simple section will suffice as irrita-
tion, and the deeper the section the  more are the lower extremities
convulsed,  and the  nearer  the  section approaches  to the  corpora
quadrigemina the more violent and generalized become the convul-
sions.  Complete section of this region did not produce convulsions
nor death by bleeding.  Owsjannikow has demonstrated, however,
that this area of NothnagePs is the point of termination  of the so-
called long nerve-strands in which run the  fibres of the upper and
lower extremities, possibly concentrating  at  this  point in  a collec-
tion  of  ganglion - cells; so that Nothnagel's  observation simply
added another fact  to  our  knowledge  of the  various  focal lesious
capable of causing  epilepsy.  During the latter years in which our
knowledge of the functions of the cortex has received so tremendous
an impulse  from the experiments of  Fritsch and Hitzig facts have
accumulated tending to demonstrate  more  and  more clearly  that
epilepsy in a large number of cases, if  not in all, is  due to  direct or
indirect excitation of the cortex or of the nerve-strands leading from
the cortex to the peripheral  structures, and Nothnagel's observation,
viewed in the light of these  later facts, only demonstrating the exist-
ence of a  centre subsidiary to  that of the motor cortex, but similar
in kind.   It has  been  shown again  and again that electrical  or
mechanical irritation of the  motor centres can cause  convulsive seiz-
ures of tonic and clonic nature with loss of consciousness, and it has
also been  demonstrated that  the same effects can be produced by the
same irritation of the  nerve-strands underlying the cortex.  Duret
has produced the most  widespread convulsions also by irritating  the
cerebral  membranes, more especially the dura mater.  But we must
remember, too, that  epilepsy can be produced  by such extracranial
lesions as diseases of the spinal cord, of the peripheral nervous sys-
tem, of many of the non-nervous viscera, by alterations in the blood
such as are to be found in albuminuria and malnutrition, and by the
action of  many toxic agents  aud various febrile conditions; so  that
it would  be a matter  of large assumption to  say that in all  these
various conditions the  cortex of the brain alone is the part affected.
The truth probably is that the epileptic manifestations are due to a
peculiar  molecular condition of the motor tract which runs from the
motor convolutions  to  the peripheral  motor structures aud muscles.
We are in entire ignorance of this exact molecular  condition, as we
are  in entire ignorance of the exact molecular condition producing
chorea, or neuralgia,  or tetanus, or hysteria, or any one of the differ-
ent  functional nervous diseases, and  we shall probably  remain  in
such  ignorance until in the ripeness of time we shall possess such
instruments of precision as  will enable us to see the molecular play
in the living  brain  and spinal cord, or until we shall  have  so 
406
NER VO US DISEASES.
advanced in our methods of preparation and staining of the different
constituents of the nervous system that we can detect such slight cel-
lular alterations  as  have thus far entirely eluded our vision.  There
are many childish metaphysical theories that presume to explain these
cellular alterations, but they are simply laughable in the present con-
dition of our knowledge.   Whatever this altered molecular condition
may be,  there can be no question that it finds its  expression in epi-
lepsy through the motor tract running from the motor convolutions
to the motor structures,  the muscles of the periphery.  When muscles
are convulsed  theyr can  be  convulsed only  by direct excitation of the
muscle itself, or of the motor tract leading from the muscle up to the
motor convolutions, or of these  convolutions themselves.  But some
varieties of epilepsy are evidently due to an excitation that extends
into this motor tract from some part of the nervous system beyond
it.   Some cases, for example, present such symptoms as hemianopsia,
word-deafness, aphasia, or the propulsiveness of propulsive epilepsy,
indicating a lesion in the corresponding centres of the cortex or cere-
bellum or their underlying  nerve-strands, and autopsies have demon-
strated the correctness of this view; wyhilst the epileptic convulsions
that are observed from lesions of non-nervous organs, diathetic con-
ditions, and  the action of toxic agents, must be from direct implica-
tion of this motor tract.
   Idiopathic epilepsy, therefore, is a  neurosis,  like neuralgia,  mi-
graine,   hysteria,  and chorea, and  it  is  exceedingly questionable
whether the sclerotic and cellular changes that  have been  found are
not effects rather than causes.
   Diagnosis.  The reader should fix in his mind firmly the fact that
epilepsy is a symptom,  and that therefore  the burning question of
diagnosis is to determine of what epilepsy is a symptom.  We should
always seek to ascertain, therefore, whether it is the symptom of any
organic  disease, such  as lesions  of the brain,  spinal cord, or of the
peripheral nerves; whether  it accompanies the cerebral  palsies of
childhood ; or whether it bears a distinct relationship to heart disease,
marked gastro-intestinal disturbances, nephritis, or  malnutrition.
   When all these organic  lesions have  been  excluded the epilepsy
may be  said to be idiopathic.   Its diagnosis  should' not then be a
matter  of difficulty.  The convulsions consist of unconsciousness,
with tonic or clonic  movements,  or simply of loss  or impairment of
consciousness, either  without  convulsions  or  very  slight convulsive
muscular movements,  and  the differentiation need only be from hys-
teria and simulation.
   True hysterical attacks have not the same sharp  loss of  conscious-
ness that occurs in epilepsy, and  hysterics do  not, therefore, fall  and
bruise themselves or bite the  tongue as do epileptics.   Moreover, the
movements  of hysteria  are more volitional and of wider range, so
that the patient  rolls and turns herself  in  bed or assumes various
attitudes, whilst in epilepsy the muscular movements are limited in
range, consisting  only of limited  flexions or  extensions  or simple
rigidity of short duration with a slight tremor.  It should not, how- 
THE NEUROSES.
407
ever, be forgotten that true epilepsy may be conjoined with true hys-
teria in the so-called hystero-epilepsy.
  The simulation of epilepsy is extremely rare in this  country, ex-
cept in certain prisons where  it is  known that the patient afflicted
with this disease might be transferred to more desirable quarters in
a hospital or an  asylum for the criminal insane.   In Europe it is
said to be frequent among those desiring to  escape military service.
A number of attempts have been made by different authors to deter-
mine symptoms  that are absolutely pathognomonic of epilepsy, but
these  have all  been failures.   Marc  thought that holding some
asafcetida under the nose would not increase the paroxysms of a true
epileptic, but this has  beeu disproved.   Voisin has laid great stress
upon the peculiar characteristics of the pulse during, before, and after
the attacks of epilepsy, but these have  beeu  found to exist in other
conditions, and F6r§ has demonstrated that they were absent in  cer-
tain epileptics, and varied very little  in others.  Among the Eng-
lish thieves there is a  class known  as " dummy chuckers," whose
business it is to simulate a convulsion in  a crowded  place and thus
permit their confederates to rifle the pockets of the sympathetic by-
standers.   One of this  undesirable class  honored  our  American
prisons with  his  presence for  a  number of years, and I have fre-
quently had him "chuck a dummy"—as simulating an epileptic con-
vulsion is called in the thieves' parlance—for  my class; and I must
confess that when this  simulation is artisticalby done  the fraud can-
not be detected except by close and repeated observation,  when the
unchanged color of the face, the undilated pupils, the lack of the long
sleep afterward, and  the tendency to  overdo the clonicity  or the
tonicity of the convulsions or the  bleeding of the  tongue (which is
generally cut beforehand with a sharp knife),  may  throw  light upon
the matter.
   Prognosis.   It is  as  yet undetermined what shall constitute a
cure of epilepsy.   In some cases entire immunity from attack may
extend over a period of ten, fifteen, or  even twenty years, whilst a
convulsion in infancy may not be followed  by any further attacks
for many  years, when a series of them may set in.    Sometimes
remissions of several years may occur, as I have  known in my own
practice, even as loug  as six or  seven  years.  In  other and less
favorable cases  the life of the patient may be made more pleasant
aud useful by a  lessening of the  frequency and  violence  of the at-
tacks.   In some cases, however, no improvement can be effected by
any means now known  to the medical profession.   Grand mal may
be  improved in most cases, but in only  a few of  them can a cure be
effected in the sense iu which I have spoken  of it.  Experimenta-
tion by treatment of a month or so is the ouly way in which it can
be  ascertained what proportion of improvement can be effected.  The
relatives of the patient should always be informed that  continuous
treatment for years must be kept up to secure even au improvement.
I have never yet seen a case of petit mal materially affected by treat-
ment, except those that occur from malnutrition aud the formation of
ptomaines from an acute indigestion.   The prognosis of  the  milder 
408
NER VO US DISEASES.
 degrees of hystero-epilepsy is usually excellent  if proper treatment
 and control can be afforded  the patient.   Cases associated with mi-
 graine may also  be  greatly improved by treatment, and those of
 peripheral origin  usually improve under  treatment, -although  a con-
 vulsive tendency is generally apt to cling to the  latter.
   Treatment.   The treatment of epilepsy will vary somewhat in
 the  different varieties of the disease.   Cases  caused by removable
 intracranial lesions should be operated upon if the localization of the
 latter can be made by our present  knowledge of the subject.  The
 cortex of the cerebrum and the cerebellum, the centrum ovale of the
 cerebrum, and all of  the subcortical tissue of the cerebellum may be
 easily reached by the surgeon, and our knowledge of cerebral  locali-
 zation will be a reliable guide  to him.   The nature of the  lesion,
 however, should be determined before any operation is attempted. In
 the hemiplegias, single or double, and in the paraplegias constituting
 the so-called palsies of childhood it would be folly to operate, as they
 are due to the cerebral losses of  substance known as porencephalitis,
 to  hemorrhage, to arterial  or venous  thrombosis, or sclerosis and
 encephalitis, which usually proceeds from preceding  arterial trouble.
 In cases of well-defined tumor an operation should  always be per-
 formed.   An operation is eminently practicable  in cases  of abscess,
 if it  can  be localized in an  accessible area.   In cases  of epilepsy
 caused by cerebral trauma  the  scalp should be  carefully shaved,
 careful search made for the  cicatrix or depression  of the skull, and,
 if either is detected, trephining should always be done, for in many
 cases slight  adhesions of the  membranes have  been removed with
 excellent results.   Trephining is a harmless procedure under  proper
 antiseptic precautions, and may disclose conditions which otherwise
 could not have been brought to light.  It is exceedingly questionable,
 however, whether  the epileptic habit can be cured by an operation of
 any kind.  Thus, Dr. E.  G. Mason  has collected for me 44 cases
 operated on by different surgeons, and the results were as  follows:
    Cured................2
    No improvement..............10
    Death due to operation.............3
    Improvement, return of fits: malignant brain disease......1
    Cases in which there was a cessation of fits one year after  operation, but in
       which bromides were used...........2
    Temporary improvement; time of observation, however, not given ...  3
    Cases in which time of observation after operation is sufficient to make them
       of value in statistical tables...........23
               Grand total............44
 (This table can be found in Dercum's System of Nervous Diseases, Art. '' Epilepsy ".)

  If  peripheral irritation exists in cases of  epilepsy, the irritant
 should be removed, even though the improvement obtained should be
 only temporary, as even this may be a valuable adjunct to the treat-
 ment  by medication.  An adherent prepuce or phimosis  should be
 rectified.   An irritable  clitoris should be treated  either  by careful
application of nitrate  of silver (a 60 per cent,  solution), or by sooth-
ing applications.   If  vaginitis exists,  it should be  carefully treated.
Marked errors  of ocular  refraction  should be  remedied, but the 
THE NEUROSES.
409
removal of the insufficiency of ocular muscles is, in my opinion, quite
useless.   If a laryngeal  tumor exists, giving rise to the symptoms
of so-called  laryngeal  vertigo  or  epilepsy, an  operation  should be
resorted to for its removal.   In all these  cases surgical treatment
alone should not be relied upon, as it is very difficult to eradicate the
epileptic tendency when once established.
  Parents are too apt to spoil and pet  their children when afflicted
with hysteria or epilepsy, and as a result the little  patients  come to
have even less than the usual feeble self-control of childhood, and too
often manifest almost savage tendencies.  Careful and firm measures
should be adopted in such cases, either by the aid of a trained nurse,
or in a thousand ways that may suggest themselves to the good sense
and tact of the physician or  parents.   Moral treatment in  cases of
this kind is often most surprising in its effect for good.
  Migraine  should be carefully treated if it  exists in conjunction
with epilepsy.  Full directions for such treatment will be found in
Chapter IX., under " Migraine."
  If upon  inquiry a tendency to  periodicity is discovered, at such
periods the patient should be kept  quiet and special care paid to the
medication.   In many cases  where  this periodicity is manifested I
put the patient to  bed  during the time of the expected attack, and
either increase the  quantity of  the drug beiug administered, or  add
to the medication.   In nocturnal cases a dose at bedtime may be all
that is necessary.   In some of these  patients the attacks may be
diverted from their usual period of  recurrence, so that they may occur
at some other time  in the month, or  an attack may come in the day-
time.  In such cases continuous treatment should be kept up, simply
paying attention to the periods  in the manner indicated.
  The bromides, without doubt, constitute  the most  valuable means
of treatment at our disposal.   Unless the idiosyncrasy of the patient
prohibits it, they should be given  in large  doses.   In some epileptic
patients the bromides are badly borne,  but,  as  a rule, they will bear
well all that it may be necessary to administer.  In some exceptional
cases the disease seems to be aggravated by the use of a bromide;
in others  an ounce may be given without ill effect;  whilst in a few a
collapse will be produced by a dose of  10  grains.  Taking all these
facts into consideration, my plan  of treatment  is as follows :  The
dose of the bromide of potassium is at first 10 grains  three times a
day, unless the attack is markedly periodic, in which cases I admin-
ister the bromide in proportionately large doses.   My usual prescrip-
tion is as follows :

       R.—Potass,  brom.......3ss.
           Aquae........^iv.   M.
  Ft. sol.  S.—Teaspoonful three times daily, after  meals, in half-tumbler
of water.

Unless improvement  is manifest, or bromism has taken place, I in-
crease the dose to 15 grains three times a day, after about a week of
treatment by the smaller dose.  I still further increase the dose to as
much as 30 to 40 grains daily, in case the patient bears the bromide 
410
NERVOUS DISEASES.
well, but does not improve.   If the manifestations of epilepsy do not
lessen, but symptoms of bromism are seen, I conjoin with each dose
of the bromide of potassium 5 grains of the bromide  of sodium, as
in the following prescription :

      R.—Potass, brom.......,?ss.
          Sodae brom.......3ij.
          Aquae.......§iv.     M.
  Ft. sol.  S.—Teaspoonful three times daily, in half-tumbler of water.

This  combination of the two bromides will often increase the effect
upon  the  disease without increasing the constitutional effect of the
drug.   This  dosage should  be continued, if the patient has  beeu
satisfactorily brought under its  control.  If relapses  occur, or  im-
provement ceases, I try change of scene, a laxative, a brisk cathartic,
or a combination with the bromide treatment, as already described, of
borax, belladonna, or hyoscyamine.  These  latter meaus I use for a
short time only, gradually discontinuing their use.   These are  em-
bodied in the following prescriptions :

      R.—Potass, brom.  j                        ^  5SS
          Sodae borat.   j
          Aquae........3™-  M.
  Ft. sol.  S— Teaspoonful three times daily, after meals,  in half-tumbler of
water.

Or,
      R.—Potass, brom.  "I                        ^  *ss
          Sodae  borat.   j             •    •    •       5  •
          Bellad. ext. fld........3ss.
          Aquae........|iv.  M.
  Ft. sol.  S.—Teaspoonful three times daily, after meals,  in half-tumbler of
water.

   The hyoscyamine should be given alone, in tablet triturate (gr. y-^y
night and morning);  Merck's  preparation should be  used.  The
loss of uvular  reflex has  beeu thought by some authors to be of
great importance, aud the  ability to  tickle the patient's  throat with
a feather  without  causing him to gag is taken  as an indication that
sufficient bromide has been administered.   In my opinion, this is of
little value, as I have known cases to grow worse when this reflex
had been abolished, aud I have seen  improvement in others where
the reflex was  still present, aud in still others the bromide has been
well  borne in  increasing doses  even though the reflex had ceased.
The bromide of potassium  and the bromide  of  sodium  are the only
ones  of which I  make use, as the bromide of ammonium has not
proved of any use in my hauds, except occasionally as au adjuvant.
The acne, which  is sometimes considerable, has been usually  over-
come by moderate doses of Fowler's  solution of arsenic—gtt. lj-ujj
three times daily, in  a  wineglass  of  water.   It  has  been my experi-
ence  that cases which  are  not benefited  by the bromide treatment
will fail to improve under any other, the only exceptions being some
few cases that will do well  with borax when the bromide has failed. 
THE NEUROSES.
411
Gowers' maximum-dose  treatment  is occasionally very useful, espe-
cially in alternation with the treatment just detailed.  This consists
of doses of 2 or 3 drachms  of bromide of potassium every second
or third morning, increasing the dose to  4 drachms every fourth
morning, and 6 drachms or an ounce every fifth morning, these doses
being given after breakfast in a tumblerful of water, as, if they are
not well diluted, epigastric pain aud vomiting  may be caused.   He
does  not increase  the dose  beyond that which  produces transient
lethargy and dulness.  There is  great variability in the  susceptibil-
ity of patients to  the doses,  some being unable to bear  more than 4
drachms, whilst in others, as I have myself observed, no unpleasant
symptoms will be produced by the administration of an ounce.   The
maximum dose should be  reached in two or  three weeks, and re-
peated three or four times, gradually reducing the  doses so that six
or seven weeks will be consumed in the treatment, when the patient
may be  left without treatment for several weeks  or even months,
although I have never  seen such long periods  of immunity as Dr.
Gowers claims.
   Belladonua, except as  an adjuvant, has not proved of much use in
my hands.   The dose should be  1 or 2 minims of the fluid extract
three times a day, carefully  watching the effects  of the  drug.  In
some cases 10, 20, or 30 grains  of borax  thrice daily, well diluted,
is of as much efficacy as  the bromide treatment, though not generally
so. The borax treatment (gr. 10 to 20, three times daily, in  half-
tumbler of water), however, should be carefully  tried in all  cases
where the  bromides fail in  effect, or disagree with the patient.
   In the last  few years, however, the salts of strontium, the lactate
and the bromide (gr. 10 to 20, three times daily, in  half-tumbler of
water), have  been spoken of  as having considerable value iu the
treatment of epilepsy, the dose being the same as  that of the  bro-
mides.   I have not, however, had any extended experience with them,
and can, therefore, only  mention  the fact.   Nitrite of amyl is some-
times useful iu arresting au  attack which  has  been preceded  by an
aura or warning of sufficient length to permit it to be used, but this
seldom occurs ; indeed, I have almost abandoned the use of the drug.
The zinc preparations, which were so much in vogue twenty years
ago, have beeu of very little  value in my cases.

                         MIGRAINE.

   Synonyms:  Hemicrania.   Sick headache.
   Migraine is a very frequent affection.   In the  typical  form the
symptoms, as the name  indicates, affect one side of the head; but
there are many variations  from  the type,  and the most frequent is
that the pain commences  in a certain spot,  most  frequently  over
the eyebrows or the  vertex.   Usually the onset  is  gradual.    The
patient wakes in the morning with a certain feeling of lassitude and
uneasiness  about the head that  experience has  shown  to be  pro-
dromal.   As  the day goes on, this feeling  merges from discomfort
into actual  pain, and this develops until  the afternoon or evening, 
412
NERVOUS DISEASES.
then  reaching its  acme, when the  pain becomes severe,  at times
almost  unbearable,  and  culminates  in  one or  several  attacks of
vomiting, after which it gradually diminishes  to terminate sud-
denly or  gradually.  The  face may either be flushed or  pale, the
pupils dilated or contracted.  In the non-typical forms, however, the
pain  may  vary very  greatly in  severity and  duration.   Thus, in
some there may be  simply  a feeling of uneasiness which  may last a
whole day or several days, or only a  few hours.   In some, too, there
is no vomiting, and its place may be taken by nausea, or even this
may be lacking.  The attacks usually return with a certain irregular
periodicity, most frequently within the month.   In women  they are
especially prone to bear some relation to the menstrual period, coming
either before, during, or after it, and this does not necessarily denote
any uterine trouble.  Migraine bears a curious relationship to epilepsy.
In almost every case that has been subject  to  migraine throughout
many years there will  be found to have been some loss of  conscious-
ness at some  time, which may have only been called a fainting-fit.  In
others, however, there may occasionally be a true loss of consciousness,
conjoined with muscular convulsions  of the  true epileptic type.  In
still  others the migraine may regularly alternate with epilepsy,  so
that  when one is present the other is absent, and  vice versa.  This
latter form is comparatively rare.   The attacks generally first appear
in adolescence or early adult life,  and usually continue until late in
life,  often gradually passing away  as old age approaches.   Individ-
uals  who are subject to migraine are often subject to alternations of
curious functional  disturbances.   Thus, one patient may have,  in
place of the  migraine  or after it,  a continuous depression of spirits
that  has none of the other symptoms of  melancholia, such as insom-
nia, post-cervical ache, or suicidal tendency, or the fades;  or another
may have a  persistent tachycardia, or another  may be possessed  of
a persistent general  restlessness and  nervousness or irritability.  In
some patients subject to migraine life is  passed in  a constant round
of migraine  and its alternating nervous conditions.   Patients who
are subject to migraine  have  no mental  impairment;  indeed, I
think that most of the patients whom I have  observed were  above
the normal in their mental capacity.   I could name from  memory a
formidable list of distinguished  public men—lawyers, physicians,
artists, inventors, authors, and others of high intellectual stature—
who are afflicted with  migraine, and in whom the disease  in no wise
impairs the  mental capacity  except  that at the time of severe man-
ifestations the patient  is sometimes temporarily confused, and even
in some extreme cases  slightly dazed.   A number of years ago I
was  concerned in the trial of a very important will case, and one of
the leading counsel was to my knowledge subject to violent attacks
of this malady.  One  morning  upon going to court, when the legal
gentleman  whom  I have mentioned was to commence an important
examination  of me as a witness, I immediately perceived that he was
very  pale, that his pupils  were  dilated, and that he  was slightly
dazed.  I at  once recognized the fact that he must have had a severe
attack of migraine the night before, and  that he was in no condition 
THE NEUROSES.                     413
to  enter upon the intellectual  sword-play necessary for the  day's
work, and I called  one of the other counsel to me, stated the fact,
and upon  another plea had  the  court adjourned for the day, after
which I found out that my friend had  been up all night, as  I had
supposed, with a violent attack, and  that  he  was scarcely  conscious
of what he was doing.   The next day, however, he took his place,
and went as brilliantly through the fray as could have been expected.
I cite this as  a striking example of what is occasionally observed.
In certain cases of  migraine there is  impairment  of vision,  which
may consist of slight dimness or irregular blurring, or even of hem-
iopia, and these may  sometimes  persist for  several days  after  the
attack,  but that they are functional may readily be determined by
the history of the case.
   The  chief cause of migraine  is heredity, and I have  discovered  a
singular fact, namely, that the heredity  is mainly through the mother.
It may, however, come through the father, although this is rare, and
much more so than to see it descend through both father and mother.
I have  never seen a case that was not hereditary—i. e., in which there
was not either a heredity of migraine or epilepsy, or some neurosis.
The exciting cause  may be fatigue, the emotions, and any cause that
may depress the general health.
   The  pathology  of migraine is unknown.  It is in my estimation a
neurosis—that is to say, a temporary disease that is not accompanied
by gross lesions.    It stands midway  between a  neuralgia and an
epilepsy,  and it may be  called a neurotic neuralgia or a neuralgic
neurosis.  There has been, for  many years, a question as to whether
it was  of vasomotor origin, and an  attempt  was made to base this
 upon the coloration  of the face; but as  this hue varies very greatly in
different  cases, and as there has  been no proof whatsoever  of the
vasomotor origin, this theory remains a  pure theory, worthless for
any practical purposes.
   The prognosis of migraine is excellent so far as regards life or a
tendency to pass into other  nervous affections, for I have  never
 known a case to die from it, or to pass  into any  other  nervous dis-
 ease, except in the very exceptional cases of alternation with epilepsy.
 Iu this conjunction  it must be remembered that the occasional losses
 of consciousness of which I have spoken  are of no consequence, and
 should not be  for a moment regarded as true epilepsy.  The prog-
 nosis as regards the cure, however, is extremely doubtful,  for whilst
 these cases can often be greatly benefited, I have never known of one
 being cured.   They occasionally die  out, however, in middle age.
   The diagnosis  of migraine is  very  easy, because it is an affection
 that recurs with an  irregular periodicity,  with a  gradual or sudden
 ouset,  consisting merely of a gradually developiug paroxysm of pain
 around the head,  generally unilateral at the outset, that  culminates in
 severe  or agonizing pain  which  may be accompanied  by nausea or
 vomiting.   In certain  cases, however, where the  health has been
 very much depressed, it  may recur so  frequently and so violently as
 to lead to a suspicion of an organic trouble, so that  there may  be  a
 question  of brain tumor;  but this  can readily be excluded  by the 
414
NERVOUS DISEASES.
irregular periodicity of the affection, by the isolated  attacks, by the
lack of retinal changes, by the lack of any paralytic  symptoms, and
by the absence of any mental impairment.
  The treatment of migraine should be directed  to the amelioration
of the disease itself, as well as to lessening the suffering of the  indi-
vidual attacks.  The individual attacks cannot be cut short by rem-
edies administered at the time.  This may be laid down as an axiom.
They can, however, often  be mitigated considerably.  The best of
all drugs, in my opinion, is antipyrin, and five  or ten grains  of it
administered every hour or two until the pain lessens will generally
act like a charm.  This  should be  administered in  water or in the
form of tablet triturate or  compressed  tablet.    The  objection  to
antipyrin, however, is that it is very apt to depress, and inasmuch
as this is a recurring disease, the  habit of taking  antipyrin is a
dangerous one.  Next to  antipyrin, bromide of potash  in  doses  of
ten,  twenty, or thirty grains at the outset of the attack is  the best
drug, and this should be administered in solution, being  given in at
least a tumblerful of water.   It is not  nearly  so depressing as the
antipyrin, and  the danger of taking it in recurring attacks is usually
very small, except in unusually asthenic  individuals.   It should be
determined what dose will give relief, and this  should be adminis-
istered promptly as soon as the attack has commenced,  best of all early
in the morning, when the  first prodromal symptoms are  observed,
and  a second dose may possibly need to be given  during the day.  If
the pain is agonizing, antipyrin may  be given in conjunction  with
it;  but, as I have  said, this should  be done with caution, and the
drug should  not be placed  in  the patient's hands  for indiscriminate
use.    In some few cases, unfortunately  exceptional, large and re-
peated doses of a  slightly  alkaline  mixture will cut short an attack,
and  this may be done by the spirit of Mindererus, half an ounce
every hour or two in a wineglass of water, or a glass  of Vichy with
a pinch of baking-soda in it every hour or two.   Iu  my experience,
however, these alkaline mixtures may act well in one  or two attacks,
but  seldom in  more than  this.   They are worth trying, however, at
times.  Gnarana (ext. guaranse fluid., gtt. x to xx, in water) is occa-
sionally an excellent remedy, but it  is not  nearly so reliable in ray
experience as  bromide or antipyrin.   Peppermint,  applied  exter-
nally, often gives great relief for a time.   Use should  be made of the
oil of peppermint  on a piece of absorbent  cotton, care being taken
that it does not  blister  the skin;  or  the menthol pencils are very
convenient, brushed lightly  over the skin.   Phenacetine, in tablet-
triturate  form, is often a famous drug  for  giving transient  relief,
and the dose should be five  grains every hour  until  relief  is given,
or fifteen grains have been administered.  It does not depress much,
as a rule, but  it is  not so reliable as antipyrin.  Occasionally a full
dose of Huxham's tincture, 5ss-j, will abort an attack.  Hare recom-
mends a pill  containing  acetanilide, gr. ij, camphor monobromate,
gr. \, and citrate of caffeine, gr. \.   It may be well  to try one after
another of  these remedies  in a difficult case,  as  the  reaction of
patients is  extremely variable.  In some very severe and agonizing 
THE NEUROSES.
415
cases resort  must be had to a hypodermic of the sulphate of mor-
phine (gr. ^  to I);  but this  needs  careful consideration, and  should
never be administered  except by the physician.   If the pain recurs
in such violent paroxysms as  to prostrate the patient, causing cold-
ness of the  extremities and rapid pulse-beat,  and  this cannot  be
controlled by antipyrin  and bromide,  hypodermics of morphine
should  be unhesitatingly administered, for unless the habit of the
pain is  thoroughly  broken  up it cannot be controlled afterward.
For this reason it  will usually not  be necessary to administer the
hypodermic  in more than a few attacks  until such  time as the pain
has again been  brought within bearable limits  and recurs without
other grave  nervous  disturbances, after which  resort may again  be
had to  bromide, antipyrin, guarana,  the  salines, etc.  During these
severe attacks the patient should be placed in bed, and warm appli-
cations—best, of hot  bottles—should be applied to the hands and
extremities.   Not only is this application of heat very grateful to the
patient, but  it lessens the pain.   In  every severe case the action of
these special remedies may be aided by keeping the patient in bed,
quiet, with the room  darkened, although this extreme measure may
not be necessary in the mild  attacks.   In some slight cases the attack
may be cut short if, at the time of the first prodromal symptoms, a
dose of bromide, 20 to  30  grains,  is  taken, and  the patient then
lies down in bed  for a few hours, with or without sleep,  the room
being darkened and  noises  being  carefully excluded. In the treat-
ment of the disease itself other remedies are needed.  The best one,
in my opinion, is cannabis  indica, and  this is best  administered in
the form of the extract, of wdiich ^ to ^  grain should be given three
times a  day continuously for weeks or  months, as in the following
 prescription :

        R.—Ext. cannab. ind.  ,.....gr. vj.
    Ft. in pil. no. xxiv.  S.—One three times daily.

   I believe that cannabis  indica acts  as  well in  migraine as the
 bromide does in epilepsy,  aud it should  be as continuously used.
 With the cannabis indica it  may often be found useful to administer
 a dose  once a day, generally at night after the evening meal; of the
 bromide of potash, 10 to 15 grains, although in many cases the ex-
 tract of cannabis indica alone will suffice.   Although the bromide is
 recommended as being of value in the treatment of migraine when used
 continuously, I cannot say that this has been  my experience, because
 I have found that it is not nearly so reliable as  the cannabis indica;
 moreover, I am decidedly  opposed  to continuous doses of the bro-
 mides in any case wherein it is undesirable to impair in the slightest
 degree  the  patient's intellectual  faculties, for I  do not believe that
 any living human being can continuously take the bromides without
 having a subtle loss of the highest intellectual capacity—losing, as it
 were, the fine blush of the mind.   I have spoken of this more par-
 ticularly in  the  section upon "Epilepsy."  Indeed, so much value
 do I attach  to the extract of cannabis indica,  that if relief is not ob-
 tained  in a severe case of migraine  by its  use, I should advise that 
416
NERVOUS DISEASES.
resort  be had  to  other measures than the bromides.   In the first
place,  the  general health should be carefully attended to.   If there
is any  ansemia, this should  be overcome by the use of  iron in full
doses, and it must always be remembered that the dose of iron varies
very greatly in the different ferruginous preparations.   The dialysed
iron, either  the ordinary dialysed form or Dree's albuminate of iron
should  be  administered in  drachm doses three  times  a day after
meals,  and this should  be administered in a cup of water, and not in
a tumbler, because the  dark hue of the iron is  in some fastidious in-
dividuals apt to produce a sensation of nausea if seen in a transparent
vessel  like  a tumbler, whilst it can be  pleasantly taken in a cup.
This is  a  matter of small clinical detail that often makes a great
difference.   The peptonate of  iron and  ferratin are the  best prepara-
tions, however; the former in doses of  3  grains three times daily, in
the form of compressed tablet, and of the latter gr. iv-viij, in cap-
sules.   If the ansemia is pronounced, the citrate of iron and quinine,
3 to 5  grains three times a day in pill or tablet-triturate form, is an
excellent remedy,  although in some cases in which the ansemia has
very greatly depressed  the general health  it will  be  advisable to ad-
minister one of  the preparations  of iron  that  I have  mentioned in
conjunction with  2 or 3 grains of the sulphate of quinine in tablet
triturate, pills, or  capsules.   In some cases of ansemia in which there
have been marked  hepatic symptoms, or in which there is a yellow-
ness of the  skin and conjunctiva, the iron will have a much better
effect if it is not only conjoined with quinine, but also with the mer-
cury, and a perfectly reliable preparation of the latter is the bichloride,
of which fa to -fa grain should be taken three times a day, either in
solution, tablet  triturates, or  pills.  This is another small  clinical
detail that is of considerable value in my opinion, and its therapeutic
importance  is probably due to the fact  that in increasing the hepatic
secretions it also increases the blood-corpuscles iu some subtle way.
I am  perfectly  well aware that mercury is said to decrease the num-
ber of the  red corpuscles, and yet I have again and again observed
the clinical  fact, of which  I can  give  no explanation.  In addition
to these medicinal  measures for the relief  of ansemia the  patient
should  take large quantities  of nitrogenized food, eating savorily
prepared hot  meat at least  three times a day, and in extreme cases
using  the  equivalent of a  pound of beef made into  beef-tea or a
beef-extract;  sometimes, also,  bullock's blood  that can be obtained
from any slaughter-house, and that  can  be frozen into chunks, which
are by no means unpleasant to eat after the patient has overcome the
prejudice.   Besides this, the expenditure of energy should be cut off
by restricting the  amount of exercise, and keeping the patient in bed
until late in the morning, or even until noonday.  This latter meas-
ure, however, will not be necessary except in  extreme cases.  If there
is  lithsemia, the treatment  should  be  something entirely different;
but lithsemia should not be  diagnosed  from the presence of a small
amount of uric  acid, or from a  few oxalate  of  lime crystals  in the
urine,  but  rather  from the  fact that  the patient  has  beeu known
to be takiug entirely too much  food  or has passed gall-stones, or 
THE NEUROSES
417
because the urine is constantly loaded with large amounts of uric acid
and the amorphous urates.   I have seen many cases of ansemia mis-
taken for lithsemia.   In every doubtful case it is  an excellent rule
to apply a stethoscope to the heart  and the large vessels coming off
from the heart, and I have more than  once seen the attending phy-
sician by whom I have been called in  consultation perfectly amazed
at detecting loud blowing ansemic murmurs in a case that had been
treated for lithsemia.  If there is  true lithsemia, however, the treat-
ment should be begun by a moderate dose of calomel, say 3 grains,
with 15 grains of the bicarbonate of soda, given at  bedtime, and  if
this has not acted the next morning before breakfast, a  slight saline
laxative should be given, such  as  a wineglassful or  half-tumblerful
of Hunyadi, or 2 drachms to \ ounce  of the  sulphate of magnesia.
Either an acid or an alkali should  be administered  for a week or ten
days.  The best acid, I think, is the dilute nitro-muriatic, of which
the dose should be 20 drops three times a day after meals in a wine-
glass of water, as follows :

      R.—Acid, nitro-muriat. dil......gj.
         Aquae.........§ij.  M.
  Ft. sol.  S.—Teaspoonful after meals in a wineglass of water.
   In some cases, however, an alkali will do better  than an acid, and
 I know of no means of determining  this except  by that of actual
 experimentation.   The best alkali is a glass of Vichy or Giesshiibler,
 with a pinch of baking-soda in it,  three times a day, an hour or two
 after meals.   The bowels  should be kept open, but  not more  than
 one natural movement in the  day should be maintained, and  it  is
 sometimes a considerable study as to how this  should be done.  A
 glass of Hunyadi may answer, or  it may be necessary to administer
 the cascara sagrada, 2 grains of the solid extract  in pill-form, or a
 drachm of the fluid extract.  This remedy varies very greatly in its
 effect in  different persons, and  it should be determined by observa-
 tion what the  necessary dose should be, for it  may  be  necessary to
 give 2 grains of the solid extract  or  a drachm  of the fluid extract
 three times a day, or even to treble or quadruple  the dose, and the
 great advantage  of the  cascara sagrada is that  this increase of the
 dose when necessary is not accompanied by any griping or other un-
 toward symptoms.   In  some cases the best laxative is this:
      R .—Ext. aloes      )                        - ^ ^ •
          Ext. hyoscyami j                     -ay
          Ext. nucis vomicae   .    .    .    .    .    . gr. v. M.
   Ft. in pil (argent) no. xv.  S.—One daily after dinner.
   If in lithsemia the alkalies or the acid cause slight depression, as
 they are very apt to do, -fa to -fa grain sulphate of strychnine should
 be administered with them, and a favorite formula of mine is :

      R.—Acid, nitro-muriat. dil......3j.
          Strychnise sulph.......gr. J.
         Aquae.........^ij.  M.
   Ft. sol.  S.—Teaspoonful after meals in a wineglass of water.
                               27 
418
NEBVOUS DISEASES.
  For further details of more pronounced cases of lithsemia the reader
should turn to the section  on " Neurasthenia."   If, in  spite of this
attention to  the  general  health, the attacks keep  recurring, great
relief may often be obtained by overcoming any error of refraction.
In  some cases where there is no great error of refraction, but in
which there is exophoria, the use of  prisms or even cutting the mus-
cles of the eye is  often followed by great  relief.  Although I have
never seen  a case of  migraine cured by such means, I have  yet seen
many cases in which recurring serious  attacks were broken  up and
the disease  made to travel along in a very bearable manner.   Travel
and change of scene  are often of great benefit in cases of migraine
that have become severe.

                            CHOREA.

  Synonyms: St. Vitus's dance.  St. Anthony's dance.  St. Guy's
dance.
  Definition.  Chorea is a functional nervous disease characterized
by involuntary or mainly involuntary fibrillary movements consist-
ing either of a jerky twitch that  begins quickly and ends quickly, or
of a wavy, undulating movement.
  History.   Various  functional phenomena of the nervous  sys-
tem have been called chorea,  although  they have borne very slight
resemblance  to what the neurologists  of  the present  day call by
this name.  Thus the  real dance of St.  Guy  or  St. Vitus, which
has also gone under the names of the  dance of St. Modesti or St.
John, choremania, orchestromania,  chorea magna, chorea German-
orum, epilepsia saltatoria, or dance plague  (Tanzplage;  Fleau de la
danse),  was an epidemic prevalent at various times since the end of
the fourteenth century, the first appearance  of  it having been de-
scribed  in  1374, although Hecker claims that it was no new disease,
as it was well known in the Middle Ages.   Men and women would
form circles hand-in-hand and dance for hours  together until they
swooned or a state of exhaustion ensued, very much as is the custom
in the  ghost or Messiah  dance  of  our North American Indians.
They would  then  suffer greatly from tympanites, which was gener-
ally quickly  relieved by abdominal compression with clothing or by
thumping  and trampling upon the abdomen.  Vivid hallucinations
generally accompanied these attacks, usually of a religious character,
so that the heavens would seem to open and  they would see the
Saviour enthroned with the Virgin Mary.   The attack would often
commence  with sudden  loss of consciousness  and the patient would
fall to the  ground, but would usually spring up to begin  the dance
with strange contortions.   In 1374 this  epidemic spread from Aix-la-
Chapelle all over the neighboring Netherlands, and thence to Cologne
and Metz.  The communities were absolutely disorganized.  In
Cologne the number of the dancers amounted to five hundred, and
in Metz to eleven hundred, all classes of the community taking part
in the revels—peasants from their plows, mechanics from their work-
shops, housewives from their homes, girls and  boys leaving their 
THE NEUBOSES.
419
parents, servants their masters, beggars and idle vagabonds seeking
their profit  in  the  general disorder ; aud it was four months before
the Rhenish cities  were able to gain control of the disorder accom-
panying the epidemic, although even  then this went creeping on.
This was called St.  John's dance.   When it broke out again in  1418
in Strasbourg  it was denominated St. Vitus's dance, because the
legend  ran  that St. Vitus, just before he suffered martyrdom with
other early Christians in the time of Diocletian, had prayed to God
that he would  protect from the daucing mania all those who should
solemnize the day of commemoration and fast upon its eve, and that
a voice issued out of heaven saying that his prayer was accepted ; so
that St. Vitus became  the  patron saint  of those afflicted with the
dancing plague, as St. Martin, of Tours,  was at one  time of those
suffering of smallpox,  St.  Anthony   of  those  suffering with the
" hellish fire,"  and  St. Margaret of puerperal women.  Paracelsus, in
the beginning of the sixteenth century, was the first to make an in-
telligent examination of this disorder from a medical standpoint, and
to recommend  treatment, which consisted of harsh means, strict fast-
ing, severe chastisements, immersions in  cold  water, and various
nauseous compounds of the  wonderful quintessences  of that day.
The disease appears then to have declined, and very little of it seems
to have been  known in the  sixteenth century.  The great English
physician, Sydenham, gave the first accurate description of what we
nowadays call chorea, usually giving  it also  his name.   So true to
the life, indeed, was his portrayal of the disease that nobody has ever
surpassed it, and subsequent observation  has merely amplified our
knowledge of it.
   Clinical History.   Chorea consists of the following varieties:
       Sydenham's chorea;
       Athetoid chorea;
       Violent chorea;
       Chorea of pregnancy;
       Paretic chorea;
       Post-hemiplegic chorea;
       Post-hemiplegic and post-epileptic chorea;
       Chorea with loss of consciousness;
       Chorea with rapid pulse and rapid  respiration ;
       Chronic chorea.
   Chorea is manifested by certain  characteristic fibrillary movements
which  are varied somewhat in the Sydenham and in the athetoid
form.  In  the former  they consist of jerky, twitching movements,
the jerk beginning quickly and ending quickly, whilst in the latter
the action of the muscular fibrillse is  less abrupt and  jerky, and is
more wavy, approaching in  miniature the gradual  movement which
has been observed  in cases of athetosis, whence the name athetoid.
In both forms  the movements are only  partially under the control of
the will, to the extent that the patient  can make them stop for a
short time, and in some cases they cease during sleep.  The fibrillary
character of the movements is their salient characteristic,  for in no
other disease  do we see anything exactly like it; and it is for this 
420
NEBVOUS DISEASES.
reason also that simulation is possible, because the individual fibrillaa
of muscle are not under voluntary control, although the bodv of the
muscle itself may  be.   These fibrillary movements can  be  best
observed  by the examiner  taking the patient's hands in his own
allowing  them  to  rest palm  downward lightly  on  his  upturned
palm, or removing the shoe and stocking, placing the  foot in his lap,
and  observing the toes;  or  by stripping the  patient and carefully
watching the muscles of  the trunk.  The face does not usually con-
stitute a  good place for examination in the obscure  cases.  Where
the choreic movements are  slight, much patience  must be exercised
in these examinations, and  I have  held the  hand of a patient  for
ten minutes before  being   rewarded by the characteristic twitch.
The distribution  of the chorea may be throughout all the muscles,
although there is  a  tendency to oue side being more affected than
the other.  The initial attacks generally occur in children at the age
of nine,  and in 250 cases of my own the ages ranged  from two to
twenty-eight.
  The proportion of the sexes was as follows : females, 160; males,
90.
  In violent chorea the movements are either of the ordinary Syden-
ham or athetoid form, and become violent, or they are violent  from
the onset.  In this variety the movements preserve the jerky or the
athetoid  character—generally the former—but are far beyond the
fibrillary range, affecting the  whole body of the muscle, though in  an
automatic and involuntary way that is beyond all effort of simula-
tion.   So violent at times are the movements  that the patient must
be strapped in bed, or else someone must  be placed on either side  of
it to prevent his being thrown out.
  In  certain cases of chorea of the Sydenham type there are losses
of consciousness similar to those of the petit mal of epilepsy, without
any convulsive movements, however, so far as  I have  seen.  I have
never seen this variety, with loss of consciousness, alluded to by any
writer, and believe myself to be the first to describe it.   It may  be
important  or unimportant, according to  the tendency of the chorea
with which  it is associated.   If the chorea has the tendency to de-
velop,  of which I shall speak  in a few  minutes, the  losses of con-
sciousness may become very frequent, prolonged, and accompanied  by
convulsive movements  of tonic or clonic character, and  the patient
may die  in convulsions, with the symptoms  of an acute encephalitis
or meningitis.   I have seen this  in two  cases, but only two of this
type which have had a marked developmental tendency.   If, how-
ever, the chorea shows no tendency to develop, or but a  slight ten-
dency, the losses of consciousness are harmless, and will invariably
pass off under no further treatment than that addressed to the chorea.
This has been my experience in six cases.
  There is another  peculiar form of chorea to which I have never
seen any allusion  made by writers upon this subject, namely, chorea
suddenly developing after a slight attack of articular rheumatism,
and associated  with  rapid pulse and rapid respiration.   The his-
tory of the three cases which I have seen has been this :   A slight 
THE NEUBOSES.
421
articular rheumatism had  appeared,  lasting only a few  hours, and
so evanescent that it might well have escaped the observation of a
careless diagnostician.  In the  course of twenty-four hours a slight
choreic movement  began,  aud the respiration and pulse grew to be
rapid, the  former running up to  30  or 40, the  latter to  120 or 130
or 140.  Careful auscultation revealed no organic lesion of the heart
or lungs.   The chorea showed a marked tendency to develop  rapidly,
so that the movements increased greatly in intensity from  day to day,
and at the same time the tendency to develop manifested itself in the
heart- and lung-beats, so that iu a few days the choreic  movements
aud the pulse and  respiration made a dangerous triad of symptoms,
the choreic movements, however, not developing in anything like the
proportion of the increase in the pulse and respiration.   In one of
my cases  the  chorea ceased, but the pulse and respiration increased
in rapidity, and the child died in the  course of a week, a  pericarditis
appearing  in the last forty-eight hours.   In the other two cases the
chorea never became very violent—never  so marked,  for instance, as
in many cases of violent chorea, even at the onset, and yet the chil-
dren died, neither  of them developing endocarditis  or pericarditis.
No autopsy was permitted in either of the three cases.
   The chorea of pregnancy is a rare  disease, and I have never seen
a case of  it.   It is  said, however, to be  very  fatal, the percentage
running as high as 33 per  cent.
   Chronic chorea is nothing more, in my estimation, than Sydenham
or athetoid chorea  or a violent chorea that has not  been properly
treated, so that the originally slight  fibrillary movements have had
superadded to them muscular movements of greater length, often
with local spasms and contractures.
   The course of a chorea  is very inadequately understood by most
physicians.  Its duration is usually six weeks, this being the average
computed in 250 cases of my own.   But choreic  movements invari-
ably continue  for  months or years  after a so-called cure,  and the
question of what is a cure is to a large extent  an arbitrary matter.
If patients are carefully examined  as I have directed, it will be found
that slight movements can be detected  long after the parents sup-
pose that a cure has been effected, and the continuance of these slight
movements is  the  cause of so many of the odd grimaces which we
see in adults as remnants of a  chorea in childhood.  Every year
there is a tendency to relapse, for Weir Mitchell and Sinkler have
shown that the greatest number of cases of chorea occurred  in those
months in which there are the largest number of cloudy days, the
greatest amount of snowfall, and the greatest amouut of barometric
disturbance,  whilst  high or  low barometer seems  to  have no effect
upon the disease.   In addition,  they  have shown that the proximity
to the centre of the greatest barometric disturbance of a storm has a
direct causative influence upon chorea.  I can confirm these observa-
tions of Sinkler aud Mitchell.  It is well known, for instance, that
a cyclone travels in an ellipse, being  preceded by cloudy sky, foggy
weather, aud some slight barometric disturbance, whilst it is succeeded
by what is known  technically as the anti-cyclone, which is  a period 
422                   NEBVOUS DISEASES.
 of blue  skies, light clouds, bright sunshine, and little  or  no wind.
 Now, I have found that some of these choreic patients are  most dis-
 turbed by the approach of the storm, whilst others are most  disturbed
 by the passage of the storm itself, and still others are affected the
 most during the period of anti-cyclone, or relapses may occur at these
 times.
   Another important feature of the natural history of chorea is that
 certain  cases  have a  tendency to develop, 25 cases  among 250 dis-
 playing  this characteristic.  The cases which develop begin usually
 with pronounced symptoms and rapidly develop in a few  days into
 violent  chorea; but  not infrequently the onset may be  by slight
 symptoms of the minor type, and in a few days or a couple  of weeks
 the  development may be into a violent form.   This developmental
 tendency should always be borne in mind, because much blame may
 attach to a physician if he has not forewarned the parents  that this
 is one of the possibilities; and, moreover, a case which  seems harm-
 less at the beginning may become transformed into one of very serious
 import.  And especially should the tendency to develop be cautiously
 considered in the cases  beginning with slight losses of consciousness
 and  in those accompanied by a rapid pulse and respiration.
   Causation.  The causes of chorea are—
       The seasons;
       The  emotions;
       Trauma;
       Articular rheumatism;
       Malaria;
       Imitation;
       Heredity;
       Eye-strain;
       Pace.
   The effect of the seasons and  barometric disturbance has been
 fully alluded to in the clinical history.
   It is a very common thing to find that the emotions play a great
 role in the causation of chorea, and of all the emotions,  fright is the
 most potent.
   Trauma is one of the less frequent causes of chorea, but  yet cases
 indubitably proceeding from this have been observed by me.
   The role of articular rheumatism in the  causation of chorea has
 been very much overestimated, and the idea that was  formerly so
 prevalent that chorea was a rheumatic disease is entirely untenable,
 Thus articular rheumatism was a cause in only 18 cases out of 250
 of my own observation, whilst 16  had functional cardiac disturbance
 and  22 valvular disease.
   I have seen several cases of chorea with the typical malarial fever,
and  evidently caused by it, and these have  usually been  of short
duration, ceasing upon the removal of the malaria.
   Imitation has often been observed as a cause of chorea, especially
by Mitchell.
   Heredity is often of importance in chorea as an etiological factor.
   In a circular letter that was sent out by Dr.  Mitchell a number of 
THE NEUBOSES.                     423
years ago  to  physicians in the Southern States, it was shown  that
chorea was a very infrequent malady  in  the  negro race.   Whether
this applies also to other races, I do not know.
  Pathology.   Although certain cerebral changes  have been  well
described in the chronic and  fatal cases, as well as of the disease  in
animals, there has never been any approach to a description of the
pathological  alterations that  would explain  the movements of the
ordinary cases  of chorea of the Sydenham  and  athetoid  types.
Hyaline degeneration  in the  nerve-cells  of the central ganglia has
been found by Meynert and Elischer.   The capillary embolism  pro-
duced by Angel Money by injections into the carotids of animals has
not been verified in other cases.  Eisenlohr in one case of congenital
chorea  found a  sclerotic mass at the level  of the  third  cervical
nerve, and alludes to  a similar pathological find of Schultz's.   The
best description of a fatal case of chorea is that given by Dana of a
cerebrum, medulla, and spinal cord from a male patient of  eighteen
who had  had choreic  movements of the Sydenham type  for  over
twelve  years.  There were chronic lepto-meningitis of the cerebrum,
diffuse  and varicose dilatations of the small arteries, especially of the
deeper subcortical capsule; degenerative changes in the arterial wall,
but no  arteritis;  the  white  matter was  honeycombed  with greatly
dilated vascular lymph-spaces, and the cortical  walls in  most regions
were normal.  The severest  changes, vascular, interstitial,  and de-
generative, were  in the under surface of the temporal  lobes, in the
internal capsule and the adjacent parts of the corpus  striatum (espe-
cially the lenticular nucleus), and the optic thalamus, and in this region
varicose nerve-fibres were observed.  In  the pons Varolii and in the
medulla a much less marked phase of the same conditions was found,
and there  was also a certain amount of cellular degeneration in some
of the cranial-nerve nuclei and a slight increase  in  the  connective
tissue of the pyramids. In the spinal cord the pia mater and the
cord were slightly congested, the latter especially in the lateral tracts,
and there was a double central canal.   In Dana's valuable paper upon
this subject 200 autopsies are collected, made  upon  patients dying
with acute or chronic  chorea, but in only  39 of these  was there a
satisfactory account of the condition of the nervous system.  From
this it would appear that after death from chorea various lesions have
been found in the nervous centres, such as congestions,  extravasations,
embolism, and softening, and that heart-lesions are  very  uniform.
Of these 39 cases there were 25 of Sydenham chorea, uncomplicated
with insanity or other serious disease.   In 16 there are  said to have
been intense cerebral hypersemia, peri-arterial exudations  and  erosions,
softened spots, minute  hemorrhages, and occasionally embolism, the
changes being most marked in the lenticular nucleus and inner parts
of the thalamus.  In only a few  cases was  the cord  affected some-
what similarly.   In one case there was absolutely no change found,
although Dana thinks some lesion was overlooked or a mistake made
m some way.  In one case only the corpus striatum  and cord  were
examined, and in them there were foci of softening; and in three cases
the brain was pultaceous, the lymph-walls were disintegrated and full 
424
NER VO US DISEASES.
 of micro-organisms.   In six cases minute hyaline bodies were found
 chiefly in the lenticular nucleus.   In two  cases of subacute chorea
 with insanity there was great cerebral congestion with  thrombosis
 and minute hemorrhages.   In  five  cases of chronic chorea of the
 Sydenham  type lasting  from four to twelve years there  were found
 dilatation and  thickening of arterioles, with  necrotic and erosive
 changes, degenerative changes in  nerve-cells,  varicosities of nerve-
 fibres, old spots of sclerosis, and hyaline bodies, and a somewhat less
 implication of the spinal cord. In the dog a number of cases of chorea
 have been reported after section of the spinal cord, and some similar
 cases  have been  reported  by Weir  Mitchell  in  the human being.
 In  1875 Gowers examined  the  spinal cord of a choreic dog, and
 could  find no alterations; but two years afterward, in conjunction with
 Sankey, he demonstrated that certain limited areas of the cord were in-
 filtrated with small lymphoid cells.  Putnam, however, could find no
 such alterations in two kittens which had been artificially made choreic.
 In one of these no changes whatever could be found  in the nervous
 centres, but in the second there was a marked injection of the blood-
 vessels, and the ganglion-cells of the spinal cord and brain would not
 take up  the  staining-fluid, and could not be examined satisfactorily
 even in glycerin.   II. C. Wood has examined the spinal cords of four
 dogs, three being killed while still able to go about.   Two of them
 suffered from typical rhythmic chorea, one from chorea with move-
 ments exactly simulating  those  of a  child, associated  with great
 weakness.  The fourth animal died of the disease after having com-
 pletely lost control of his  hind  legs.   In each of these there  were
 numerous lymphoid cells in the gray matter, but very few, if any, of
 them  in  the white  matter.   In only one dog was any  connection
 traced  between these  cells  and  the bloodvessels, and in this  one
 instance there were some cells in the perivascular spaces, but there
 was no such outpouring of leucocytes as was found by Gowers  and
 Sankey.  Wood maintains, however, that  these lymphoid cells are
 found in  the normal cord.  In Wood's  dogs the ganglionic cells in
 the cord were profoundly affected, and he states that  the inability of
 the ganglion-cells  to take up  the staining-fluid  is present only in the
 earliest alterations in the cell. The cellular changes were  greatest iu
 the groups  nearest the spinal  canal and just posterior to it, whilst the
 lateral groups of very large cells which are seen in the dog's spinal
 cord were not so profoundly affected.   In the first-named group the
 cells had been transformed into  irregular,  globous-looking masses,
 without sharp outline, and imbibing the staining-fluid very slightly.
 No granulations, no nuclei, no processes were present.  These masses
 evidently represented the cells in the last stages of degeneration,  and
 were of various sizes.   The cells in the lateral  group were distinctly
 altered.   They took the staining very faintly;  in a large proportion
 of  them no nuclei could be found, and in many about one-fourth of
 their contents  were occupied by  a large mass of definite outline,
 free from granular contents, seemingly a vacuole.  Of all the absurd
theories that have been passed around from  text-book to  text-book
and by word of mouth, the most absurd is that proposed  by Broad- 
THE NEUROSES.
425
bent and Tuckwell, of minute embolism of the cerebral arteries as
explanatory of chorea.  In the first place, these minute emboli of the
cerebral vessels are extremely rare;  in the second place, as Octavius
Sturgis has succinctly pointed out, none  of the symptoms of cerebral
embolism are present in chorea, such as  the sudden vertigo or head-
ache, pain with faintness or sickness, hemiplegia, mental impairment,
ansesthesia or aphasia, or a fatal termination  by way of sudden coma.
An attempt has been made of late years  to show that chorea was due
to some infection, and Richter has found cocci in the blood  in  one
case, Donkin rod-like bodies in another, and Berkeley has thought
that the pathological findings in another case were similar to those of
diphtheria;  but proof of this view is yet entirely lacking.
   Differential Diagnosis.  The characteristic twitch of Syden-
ham's chorea and athetoid chorea—the quickly beginning and quickly
ending fibrillary jerk or the fibrillary wavy movement—is never seen
in any other disease than chorea, whilst  the  muscular movements of
larger range of  violent  chorea also have  this quickly beginning and
quickly ending or twitchy character.   In  chronic chorea, however, the
movements may lose these characteristics and become intermingled
with anomalous movements and with muscular spasms or contract-
ures, but here a history of the antecedent  chorea will invariably make
clear the diagnosis.   In all examinations, however, of patients who
are suspected of chorea, not only should  the toes and fingers be care-
fully aud patiently examined, but the patient should be stripped so
that the muscles of the trunk may be brought into play.  Especially
should this examination be carefully made in cases where there are
slight losses  of consciousness, or where there is a grunting or subdued
sound  that is present when the laryngeal muscles are affected, con-
stituting the so-called laryngeal chorea, which is really an  ordinary
chorea, however, with implication of the laryngeal muscles.
   Chorea should be differentiated from—
       Organic  cerebral disease;
       Epilepsy;
       Disseminated  sclerosis;
       The fibrillary tumor of progressive muscular atrophy;
       Hysteria.
   The differentiation from organic  cerebral  disease may become at
first  sight a matter of  difficulty iu  cases where paresis is  an early
symptom or where there  are  slight  losses of consciousness, but the
detection of  the fibrillary movements is  all  that is  needed  to make
the diagnosis.  Sometimes, too, the difficulty  of speech, which is not
infrequent in choreic children, may cause a suspicion of organic cere-
bral disease,  but the movements make the matter plain.
   The cases of chorea which are accompanied by slight losses of con-
sciousness are rare, and therefore generally cause great uneasiness, but
upon search the choreic movements will  be found.
   Disseminated  sclerosis,  as has been shown in the chapter on this
subject, is not infrequent among children, and the tremor may be con-
founded with that of chorea; but the choreic movement is, as I have
said, twitchy, quickly beginning and quickly ending, or wavy, whilst 
426
NERVOUS DISEASES.
the tremor of sclerosis is a continuous  series of very fine muscular
oscillations;  moreover, the nystagmus, the scanning speech, and  the
other symptoms of sclerosis are entirely wanting in chorea.
  The fibrillary tremor of  progressive  muscular atrophy may be
confouuded with chorea, but the former is generally a feeling as of a
pulse-beat under the flesh, is much more continuous and rapid than
the fibrillary movements, and has none of the twitchiness or abrupt-
ness of beginning or ending, besides which the atrophy that is present
is never observed in chorea.
  The tremor of hysteria may be confounded with chorea, but if it
be borne in mind that choreic movements do not constitute a tremor,
as has been  again and  again insisted  upon,  the diagnosis can be
readily made, whilst chorea is wanting in the limitation of the field
of vision  and in the sensory phenomena of hysteria.
  Prognosis.  Cases of chorea with losses of consciousness that
display a  tendency to develop are usually dangerous cases, as I have
said, as the only two which  I have seen terminated fatally; but the
cases of chorea with losses of consciousness  that  show no develop-
mental tendency have the prognosis of ordinary chorea without these
losses of consciousness.   The cases of chorea beginning after a slight
attack of articular rheumatism with rapid pulse and rapid respiration
are, if I may judge by my three cases, always fatal.  A case of chorea
beginning after articular rheumatism of any kind is apt to be more
serious than  if occurring without it, but most  of them recover;
indeed, I have never seen  a fatal case except where  the articular
rheumatism had developed cardiac lesions that were themselves  fatal.
Most cases of chorea which we see  are those of the Sydenham or
athetoid type, and these have an excellent prognosis so far as death
is concerned, but have a serious prognosis so far as relapses are con-
cerned and so far as a tendency may  be left to certain awkward ges-
tures and grimaces.   Thus of 250 cases of mine, 108 had relapses.
These  relapses,  as I have said, are prone to recur in the spring and
the autumn,  but they generally recover ;  i. e., the choreic movements
become slight  or  almost die away,  and the malaise and  disturbed
general health of the child disappear.
  The chorea of pregnancy has a fatality of about 33 per cent., and
is, therefore,  a serious form.   Chronic chorea is  a very intractable
form, and cures are infrequent,  and this is also the case with electric
chorea.
  Treatment.   The treatment of  chorea should be  by means of
cutting off the expenditure of energy, with good food,  arsenic, iron,
cimicifuga, cod-liver oil, and electricity.
  All  cases  of chorea  occur in  children  of energetic minds and
bodies, so that  I  am  accustomed to say  in my  lectures  that it is
rather a back-handed compliment for a child to have  chorea, as I
never saw a fool of a child afflicted with this disease; indeed, it would
seem  that all these children  are those who are making large drafts
upon their reservoir of energy, and  certainly the effect of rest upon
the disease is proof of this  theory.   I put all my little patients to
bed at once unless the chorea  be very slight in type, and even then I 
THE NEUROSES.
427
cut off their expenditure of energy to some degree.  In  most cases
I put them to  bed for the first week, taking  care that their room
shall be sunny  and properly ventilated  and  heated.   It must  be
borne in mind that confinement to bed does not mean the same abso-
lute rest for a child that it does for an adult, for the former will  at
the best be  seizing a thousand pretexts for getting out  of bed, and
will be in constant  motion whilst  in bed.  Yet this relative rest is
very important.  Moreover, it should be remembered  that the repug-
nance of a  child, and  generally of the parents, to rest in  bed is  so
great that as much  of  it as possible  should be obtained during the
first  attack, for it will generally be difficult to obtain it to the same
extent in future ones.   After I have kept a child in  bed for a week
and it has begun to improve, I permit it to get up at noonday for the
second and  third weeks, and then I permit it to rise, say, at ten o'clock
in the morning; but during all  this time I insist that it shall be put
to bed by seven o'clock in the evening.  For a mouth or two more I
do not permit the patient to rise until ten o'clock or to stay up later
than seven, and during the whole  of the period that it is under treat-
ment I forbid walking for any  distance,  although I may permit the
child to take a ride of about an hour in fine weather in the sunny por-
tion of the day.   This  is about the  amount of rest that I should order
in an ordinary case of  minor type; but, of course, this will have to  be
far greater in the violent cases or those of severe type. As soon as a
child has been put  to bed I commence the administration of arsenic,
preferably Fowler's solution, in three-drop doses three  times daily
after meals, in  a small tumbler of water, and I increase  the dose
every two or three  days by a drop until there supervenes some slight
puffiness of the eyelids, some loss of appetite  or  disturbance of the
stomach, or some  distinct paleness of the  conjunctiva.   Usually
these symptoms will  appear  when  the dose has reached  seven  or
eight drops three times a day.   I  never push it beyond this, because
I  have satisfied  myself that the larger doses of arsenic which have
been so much vaunted are not only of no greater effect upon the dis-
ease, but that they are often  harmful by upsetting the digestion and
producing a condition  of arsenical cachexia.   Some  ten years ago I
treated all my cases of chorea with large doses of arsenic, giving  to
some as much as sixty drops iu the  course of the day, but I found
that  my results were no better than those  that were obtained by Drs.
Gray and Tuckwell, of Oxford, England, by simple  rest and good
food without any arsenic at all, aud  since that time I have satisfied
myself that the full effect of arsenic can  be obtained by the smaller
doses, and that while the drug has an undoubted effect upon chorea,
this is not a lasting one and is not enhanced by toxic doses.   When
I have reached the dose that  produces the slight symptoms  of which
I have just  spoken, I rest contented  if the patient has markedly im-
proved ; but if I think the patient should improve still more, I then
begin the simultaneous administration of iron, using the dialysed iron,
thirty to sixty drops three times a day after meals in  a cup of water,
or Dree's liquor of  the albuminate of iron in the  same doses, or the
peptonate of iron, gr. iij three times  daily, in a compressed tablet. The 
428
NERVOUS DISEASES.
other forms of iron have not seemed to me to have anything like the
effect of these three preparations.   I was  led  to  this simultaneous
use of iron and  arsenic by an accident.   I had  given one of my
patients such large doses of arsenic that arsenical cachexia was very
marked, and in order to overcome it  I  used large doses of iron as
an antidote, when to my surprise  not only did  the arsenicism disap-
pear but the choreic movements rapidly improved.   This led to my
further use of the two drugs simultaneously, and for several years I
was  much puzzled to understand how it  was that two medicines
that were mutually antidotal  could have such  an excellent effect in
combination, until  I  came across  the writings  of a German writer
demonstrating that iron has a calmative effect  upon muscular fibre
much the same as arsenic has.   With the iron and the arsenic I
conduct my patients to the end  of the treatment, although iu some
children cod-liver oil may  also be given with advantage in the colder
months of the year in our climate if their stomachs will take it without
disturbance.   I  administer the oil  preferably  pure, a  drachm three
times daily, after meals ;  but if the children prefer, I give it in a per-
fectly fresh emulsion, which should be prepared  every week and  kept
upon ice.  It is very rarely that I have met with a patient who cannot
take arsenic, but this will happen sometimes, aud when it does I use
iron either alone or in  conjunction with cimicifuga, of which I prefer
the fluid extract, ten to fifteen drops three times  a day ;  but a careful
trial of the latter in my clinic has shown conclusively that it is not
equal to arsenic in controlling chorea.  After the patient has gotten
over the more acute symptoms, galvanization of the spinal cord with
a current of 3 to 5 milliamperes every second day at sittings of five
minutes each will often be found to be of excelleut effect. (See p. 108.)
In some slight cases of chorea I  have found  that a change of air,
either from the city to the  mountains  or  seashore,  or vice versa, will
have a startlingly good effect, so much so that it can often be relied
upon to do quite as  much as the  rest will do.   When these little
patients are confined to bed I  take care, as already said, that the room
shall be sunny and well ventilated, and in addition have them  take
an air-bath every day  for an hour in pleasant weather, by having all
the doors shut and the windows open, so that they shall be flooded
with air without draught, taking care, of course, that they are properly
wrapped up.  I also take precautions that my patients shall be brought
to me every spring and autumn, the moment that any relapse is noticed,
and usually these relapses can be treated either by medication of iron,
arsenic, cod-liver oil, or cimicifuga, with  only  slight cutting off  of
energy, as by keeping them in bed till ten o'clock and sending them
to bed at seven, and often  without any particular rest at all.  I take
care also that their idiosyncrasies as regards barometric disturbances
shall be studied intelligently,  so that if they are disturbed by storms
—either in the approach, passage, or after-period—they shall be kept
in the house during these  times, or, perhaps, put temporarily upon
small doses of arsenic.  The food  of these  little patients should  be
varied and nourishing to  the highest degree that is compatible  with
their age, and I have never seen great benefit result from any special 
THE NEUROSES.
429
system of diet.  Good milk, eggs, the amount of meat that is  suit-
able to their age, with fruits and vegetables in their  proper season,
constitute all that is necessary.
  Chronic chorea is a very intractable disease, as I have stated, and
while I have cured some few cases of it by absolute rest in bed and
the administration  of arsenic  and  iron  and  galvanization of  the
spinal  cord, I have yet seen many cases that relapsed in spite of all
treatment.   In those cases which I  have cured,  however, the treat-
ment  in  bed has been  for  a  period of two  or three months, with
daily gentle massage and gentle faradization of the whole body so as
to prevent the ill effects of this prolonged recumbency.  The cases of
chorea with rapid pulse and rapid respiration  should be kept in bed
from the very start, and whilst moderate doses of arsenic are admin-
istered, digitalis should  also be given, a drop  of  the  fluid  extract in
a teaspoonful of wild-cherry bark, although as my three cases have
terminated fatally  I cannot very well say much about the treatment.
Electric chorea  I  have never  seen cured, although  I  have seen it
much improved by the same treatment as that which I have spoken
of in chronic chorea.

                  PALMUS (THE TWITCHES).1

   Synonyms:  The Jumpers.   Latah.   Miryachit.   Tic  convulsif.
   In  1880, Beard,  of New York, called  attention to a malady that
he had observed among the Jumpers  of Maine.  In  1884, Ham-
mond  published an account of an  affection  known  as miryachit, a
similar disease of Siberia.  In 1883, Mr. O'Brien (cited by Grilles de
la Tourette) depicted a similar nervous affection of the Malays.   In
1885,  Gilles de la Tourette published  an elaborate description  of
what was undoubtedly the same affection under the heading of "A
Study of a Nervous Affection characterized by Motor Inco-ordination
with Echolalie  and  Coprolalie," meaning by  these two latter words
a  tendency to  imitation and  to the use of indecent words.   Beard
found  that the Jumpers of Maine did whatever it was told them to
do.  Thus, one who was sitting in a  chair with a knife in  his hand
was told to throw it, aud he  threw it so quickly that it stuck  in a
house opposite;  at  the  same time he repeated the order to throw it
with a cry of alarm  not  unlike that of hysteria or epilepsy.  He
also threw away his pipe, which he was filling  with tobacco, when  he
was clapped upon  the shoulder.  Beard rehearsed the  first  part  of
Virgil's iEnid  aud  the first part of the first line of  Homer's Iliad,
with which the illiterate Jumper could not have been familiar, and  he
repeated the sound  of the words as they came to him, in a quick sharp
voice, at the same time that he jumped, or threw something, or raised
his shoulders, or made some other violent muscular motion.  O'Brien

 1 The different names which have been given to this disease, as indicated by the above syn-
onyms, have seemed to me meaningless or un-English; thus, all the cases do not jump, and
the name oi jumpers, therefore, describes a symptom that is frequently absent; latah and miry-
achit are Malaysian and  Russian names respectively that convey no meaning to the Anglo-
Saxon and Latin races, whilst tic convulsif or convulsive tic would be confounded in most
minds with tic douloureux, which has had a time-honored pre-emption of the word " tic." I
have, therefore, sought for a new name which should describe the main symptoms, namely, 
430
NEBVOUS DISEASES.
was conversing with an elderly and respectable  Malay woman, and
kept up the conversation for  about ten minutes without suspecting
anything.   Suddenly a friend who had accompanied  him took off
his coat, and immediately the patient  began to undress herself, and
would  have stripped herself completely  if he had not interposed,
although all the time she was disrobing she was violently angry at
the  outrage to her sex,  calling him an abandoned  hog and begging
O'Brien to  kill  him.   O'Brien speaks of a  cook on a steamer who
was carrying his child in his arms one day on  a bridge  over the
river, while at  the same  time a sailor  carried a log of wood in like
manner; the sailor threw his  log of wood  on an awning, and amused
himself by causing it to  roll  over the cloth, and finally let go the
cloth, letting the wood  fall to the bridge; the cook repeated every
motion with his little boy, and  killed him on the spot.   Gilles de fa
Tourette shows that these cases have a peculiar motor inco-ordination,
consisting  of muscular movements somewhat resembling  those of
chorea, but  differing from them  in the fact  that they are not con-
tinuous.
   The  tendency to repeat words, so-called echolalie, and the tendency
to indecent conversation,  so-called coprolalie, are generally attendant
symptoms, but not always.   In some of these cases there  is  also a
tendency to  persistent and fixed  ideas, or even a slight delusional
condition, with fear of places (agoraphobia) or folly of doubt.  Since
the writings of Beard, Hammond,  O'Brien, and Gilles de la Tourette,
a number of cases have been described by other authors, and I have
seen several myself.  All Tourette's cases (nine in number)  began
early in life, most of them between eight and nine years, one at four-
teen, and one at sixteen.
   My own  observations have  taught me that this disease, studied by
the European authors entirely among  the hopeless inmates of idiot
asylums and in chronic  cases, is by no means infrequent in relatively
subacute and slighter types in the population at large.   I have seen
a number of cases among the patients who have come to my office.
These are divisible into the following types :
        Facial palmus;
        General palmus;
        Acute palmus;
        General palmus  with pseudo-melancholia.
   Facial palmus constitutes by all odds the most frequent type.  It
consists of sudden, instantaneous, shock-like movements of lightning-
like rapidity, that go to make up a sudden  wink or  twitch of one
cheek, occasionally of both, or of the brow.   This series of move-
ments is generally followed by a second series, that, however, is much

the twitching, as distinguished from muscular movement of diseases, with  which the malady
is likely to be confounded. The word o na^bc is a good old Greek word used by Aristotle to
describe  twitching or palpitation  of the heart,  and I have simply Latinized it into palmus,
which medical men will have no occasion to  confound with the Greek word 6 ndlfivg, " the
king," the more especially as the accent is on the first syllable in the latter, whilst, follow-
ing the Greek derivation, it should be on the  last syllable in my Latinized "palmus." The
adjective is palmodic, from the Greek 7rw?i[xudng, 
THE NEUBOSES.
431
weaker,  and  sometimes even by a third.   Sometimes the head is
retracted or drawn  forward, or one shoulder is elevated.  In the
majority of the cases the winking is bilateral, but the other move-
ments just named are usually unilateral.  I am inclined to think that
this is a much more common affection than is generally supposed, or
even than could be gathered from  my own  observation, because  I
have a  strong suspicion  that most  of  the cases of so-called chorea
that  are treated  by oculists are really cases of facial palmus.   It is
undoubtedly true that in a large proportion of these cases errors of
refraction will be found, but what the  percentage is I cannot say,
because  all of my cases have not been examined for this  defect, and
even if  they had been they are not  sufficient in number to be satis-
factory.  But whether  this  error of refraction is one of the attend-
ant symptoms of the disease, or whether it is a mere coincidence, I
cannot undertake to say.   I have never yet been able to see in four
cases any improvement in the disease result from the mere correction
of refraction, although  I am inclined to think that in some individ-
uals this correction, together with the use of arsenic, has a beneficial
effect.   In  two  cases I have  seen a very distinct improvement ob-
tained by the relief of disease of the turbinate  bones, but this gain
was only temporary in  effect.   The cases which I have seen of this
facial palmus have been of long duration,  usually  commencing in
early childhood and invariably in those whose heredity is neurotic,
although not necessarily to a marked degree ; in other words, I have
seen it occur at the one extreme, as illustrated by a female  now under
my care who is thirty-one years of age, and whose maternal aunt has
been  insane, whose  sister had a similar trouble, and whose brother
had chorea; whilst, on the other hand, I have observed it in several
cases of young children, varying from six to ten years of age, in
whose family, as would  be shown by careful questioning, there had
occurred some slight nervous troubles.
   The cases of general  palmus which I have seen answer very accur-
ately to the  description that was  given of  convulsive  tic by La
Tourette, except that I  have not seen in them any coprolalia, nor
the inco-ordination of  movement that  this author speaks of.  They
consist  of intermittent, sudden, shock-like  movements of different
muscles of the body.   In the face  these may be repeated, as  in the
facial palmus, twice or even three times; but there is not the same
tendency to repetition  in the other  muscles  affected.   What I sup-
pose would answer to a description  of echolalia has also been seen in
these cases, although it, I think, is rather sensational and exaggerated
to liken it  to an echo,  for the inarticulate noise is rather a grunting
or squeaking sound, very much  like that which is  heard in many
cases of chorea.  It has always been accompanied by a sudden  move-
ment of the throat, neck, and head muscles,  as in a sudden throwing
out of a note in singing.   It  is almost impossible to describe the
sound in words; indeed, it has seemed to me  more like a sudden
spasmodic  expiration,  such as would  be heard if a  person were
suddenly struck  upon the  abdomen, than any  articulation such as 
432
NEBVOUS DISEASES.
" hem" and " ah," as La Tourette would  have it to be in his cases.
The movement in the legs is usually that of a sudden extension, and
in the arms the extensors also seem to be mainly affected.  In all of
these cases  that I have seen the intelligence is not only unimpaired
but it seems to be the rule,  as is the case in chorea, that the patients
are unusually intelligent; thus, one of my patients, a man thirty-six
years of age, who has found this malady a great barrier to his suc-
cess in life,  yet learned stenography in three months sufficiently well
to take the  prize in a competitive examination into which one hun-
dred and fifty individuals had  entered;  whilst another patient, the
young woman  thirty-one years of age, of whom  I have already
spoken, is  of an unusual order of mental capacity.   This type is
also of long duration, commencing in early childhood and running
uncured, so far as I can judge  from my limited cases, as far as forty
years of  age.  In one of  these cases of this type there were at times
exacerbations lasting a week or ten days, in which the patient became
exceedingly pale, cold,  with slight  shivers, and evidencing  a condi-
tion of widespread motor spasm, in  which even the fingers would
participate for  a few hours, so as to assume the similitude of Ray-
naud's disease.
   I have seen only one  case of acute palmus.  It was in a boy of
six, whose heredity, as  far as I could ascertain from the statements
of his  mother, was not  neurotic.  He  had had trouble some six
months before coming to  me.  He had been labelled with a number
of interesting diagnoses, such as chorea, epilepsy, myotonia, hysteria,
and neurasthenia.  His  palmodic movements were  very  curious.
When standing near a table,  looking at something, the chin would
suddenly come  down with  a thump that would  leave a black-and-
blue mark, or his head would  be thrown violently to one side, per-
haps  coming in  contact  with  some  adjacent hard object with equal
force, or, while standing quietly, his legs would give a sudden twitch,
and he would be thrown violently to  the ground, and this even  hap-
pened several times when he was seated on the edge of a stool.  The
child was  under my care for  two weeks, and, probably because of
an intercurrent attack of diarrhoea, grew steadily worse during that
time, in  spite of the full doses of arsenic which were administered
to  him.   He was literally covered  with bruises from the sudden
and violent  contacts with articles of furniture, the floor, and  the
walls.  At  last, in despair at his condition, I ordered him to be un-
dressed and put  to bed, and steadily pushed the Fowler's solution of
arsenic until he  was taking ten drops three times a day, when to my
great surprise he began  to improve rapidly, and at the end of six
weeks  was perfectly well.   Keeping him under observation  for two
weeks longer, I finally sent him to his home in the West, and am
informed that he has since remained  perfectly well.  It has seemed
to me  that  many of the cases  recorded  as paramyoclonus multiplex
have been really acute palmus.
   General palmus with pseudo-melancholia.  I  have seen two cases
of this variety.   The muscular movements are of the usual sudden,
shock-like type, and of the same extent as in what I have ventured 
THE NEUBOSES.
433
to call the general form.   With them, however, there is associated a
curious pseudo-melancholia, consisting of certain fixed melancholy
suspicious delusions, without, however, any of the suicidal tendencies
and abnormal sensations up and  down the back of  the head, neck,
or spine, or the  sleeplessness, which are characteristic of most cases
of true melancholia.  In both  of my cases  the palmus had existed
for a  long  period, the exact limits of which, however, I could  not
determine, because the patient scouted the idea that  he had had any
trouble of the kind, but which the testimony  of friends  and relatives
seemed to vouch for.  They were both men, one thirty-six and  one
thirty-eight years  of age.  The pseudo-melancholia, however, had
only existed in one case for about  a year, and in the other  for six
months.  One case passed away from my observation,  and I  know
nothing of its further course.   The other  case recovered in nine
months' treatment, aud during the three years that have since elapsed
he has been  an  active business man, although  I have  not seen him
myself during that period, as  he took a great dislike to me because
I  was forced  to take strong measures to keep him under treatment,
so  persistent were his suspicions.   One of these cases was mistaken
 for general paresis, with a melancholy onset, by a competent neurolo-
 gist of this city, and he persisted in his diagnosis until the course of
 events demonstrated his error ; indeed, it is not wonderful that this
 should have  been the case, because anyone who is not  familiar with
 this type of disease might readily  be thus misled.  There was, how-
 ever,  no element of dementia in the case; on the contrary, the man's
 mind, except so  far as his melancholy delusions and  suspicions were
 concerned, was keen and intelligent, as were also his perceptions.
   The diagnosis of these cases can readily be made.   The only dis-
 ease with which they are  likely to  be  confounded  is  chorea, from
 which they differ  radically.  In chorea the  movements are  of  two
 varieties, and  both usually involve  the fibrillse of muscles and  not
 muscular groups either acting  singly or in co-ordination with other
 muscular groups.   The  fibrillary movements of chorea, too,  consist
 either of a sudden contraction, quickly beginning and quickly ending,
 or the contraction  in the  athetoid form is more gradual.  Chorea,
 moreover, is always generalized, so that the movements are found in
 the upper  and  the lower  extremities, in the trunk and in the face,
 and occasionally also in the abdominal and laryngeal muscles.  But
 the movements of facial palmus are always limited to the face; even
 in general palmus the distinction from chorea is very marked, for in
 the latter disease the movements are always fibrillary, of the  sudden
 or gradual character  that has been described,  whereas in the latter
 they are sudden—shock-like—with  much longer intermissions than
 is the case in chorea.
    The prognosis of these cases  varies according  to the type.   I have
 never yet  seen  a case of the  facial or general  variety cured, but  I
 think this  statement  needs to  be taken with some qualification, be-
 cause  in no  one  of these cases have  I ever been able to carry out
 thoroughly the rigid  treatment which is  usually so very successful
 in cases of chorea, namely, prolonged rest, with increasing doses of
                                 28 
434
NEB VO US DISEASES.
arsenic.  Whether or  not it would be of use in the  facial variety
might be a matter of doubt;  but I believe that there is reason to
hope for success in a certain proportion of cases of the  generalized
type.   Then, too, if  we carefully study our cases of chorea, it will be
seen that there  are  few of them that  are really thoroughly cured,
even by any  treatment,  for the most that we can hope  to do is so to
diminish the number and  the frequency of the fibrillary movements
as to obtain a large degree of improvement;  but it has  been my cus-
tom for years  to exhibit  so-called cured  cases  of chorea in which
patient  watching would demonstrate the existence  of a few isolated
fibrillary twitches.   With the relatively weak movements of chorea
this is a sufficiently practical result to obtain, but  with the sudden,
shock-like movements of  palmus  this would not answer the ex-
pectations of patients.  The  acute palmus was readily  cured, as I
have  already stated.   One case of palmus with pseudo-melancholia
was cured, I  believe,  although, as I have already said, I  cannot speak
positively about this  ; and the other case I was not able to treat.
   There has  been nothing to  throw any light upon the  pathology of
this affection.  It  is  true that Gilbert Caddiot  and Roger claimed
that they stopped a so-called palmus of the ear in a dog  by removing
the nucleus  of the facial nerve  in  the pons, having without effect
previously destroyed the  cortical centre of the  facial,  the internal
capsule,  the  optic thalami, and  the  cerebellum.  But, whilst this
experiment is interesting,  any neurological experimenter knows that
it is impossible  to limit a destroying  instrument to  such a  minute
space as would be constituted by the facial nucleus.
   I am sorry that I cannot say much about the therapeutics of pal-
mus.   Arsenic certainly has a  beneficial effect upon it, but this is not
of so long duration as the same drug has in chorea.  My acute case,
however, was cured by the arsenic and the rest.  It may, of course,
be questioned as to howT much was done by the rest and how much by
the arsenic ;  but in regard to this I can only say that even before the
case was put to bed the  arsenic had effected some amelioration.  In
the facial and general varieties the arsenic alone will not answer, and
in the one case  of generalized palmus with  pseudo-melancholia I
could never perceive that arsenic had any effect whatever.   Hyoscya-
mine and hyoscine have a  beneficial  effect that has only seemed less
than that of arsenic.   I gave them in doses of  y^-j grain three or
four times a day.   Iron, which is so extremely  beneficial in chorea
in large doses, in  conjunction with  increasing quantities  of arsenic,
has been utterly without effect in this disease, as have also the bro-
mides.  Galvanic electricity is of distinct benefit, quite as much so
as the arsenic in the cases of facial palmus; but I have not had the
opportunity of using  it in the other varieties.   In facial  palmus, also,
as I have said, I have seen distinctly beneficial results  from the re-
moval of errors of refraction or irritative lesions of the naso-pharynx.
My impression is that the treatment of these  cases should be as fol-
lows : Arsenic  should be given in the form of Fowler's solution, at
first three drops three times a day, and gradually increased, so that
in the course of a week or  two eight or ten drops three times a day 
THE NEUBOSES.
435
are taken.   At the same time galvanism should be applied carefully
to the pes anserinus iu facial palmus and to the spinal column in the
general form, a current of three to five milliamperes being used every
day, from three to five minutes at a time.   Absolute rest of  the pa-
tient  iu bed, for a period of one to two weeks at the outset, should
always be used, even in the cases of facial palmus.   At the end of
this time the patient should be allowed to  sit up two or three hours
a day, and  this period of  sitting  up  should be very  gradually in-
creased, so that at the end of three or four weeks more the  patient
should be out of bed throughout the afternoon hours,  but should re-
main at rest during the morning aud evening for a period  extending
for at least eight to ten weeks from the onset of treatment;  and even
after this long walks and rides and strenuous occupations  should be
carefully avoided for several months.   All errors of refraction should
be corrected and all irritative lesions of the naso-pharynx should be,
if possible,  removed.   In conjunction with  these special  measures,
the patient's general health  should be brought to the  highest point
possible by careful and generous diet and proper tonics.

               PARAMYOCLONUS MULTIPLEX.

  Paramyoclonus Multiplex is a condition of clonic muscular spasm
affecting the limbs  and the  trunk, occasionally the neck or the face,
abdomen or diaphragm.   The  muscles affected  are  usually in the
trunk and the  limbs, and not in the toes  and hands; occasionally
the movements are tonic as well  as clonic ; the degree of spasm varies
greatly, aud may sometimes be  so violent  as to  throw the  patient
down or out of the chair, whilst in the slighter degrees it can  only be
observed when the patient is stripped.  The  muscular contractions
are sudden  and shot-like, and bilateral; the toes and  the fingers are
not affected. The symptoms generally yield quickly to treatment, and
especially to electricity, so that it is easily diagnosed from chorea, facial
spasm, torticollis,  palmus, Huntington's chorea, and myotonia con-
genita.
                     SALTATORIC SPASM.
   This condition was  first  described by Bamberger in 1859, and  is
extremely  rare.  It consists of springing  or jumping movements
which ensue when the patient attempts to stand, and is apparently
 due to clonic spasm of the calf-, hip-, and knee-muscles, and in some
 instances also in the muscles of the back.  Its cause is  unknown.
 It yields very readily to treatment, such as general tonics,  or  copious
 sweating, and, in  some cases, electricity.  It  is  easily differentiated
 from the jumping which is  seen  in palmus,  because it is a transient
 disease, and because there are none  of the widespread twitchings of
 palmus, or the imitative tendencies or the  mental symptoms of the
 latter disease.
                          WRY-NECK.

   Wry-neck is due to  a shortening of  some one  of the cervical
 muscles, generally the sterno-cleido-mastoid.   It may be fixed or 
436
NEBVOUS DISEASES.
spasmodic.  In the former variety it is met with chiefly in children,
and the causes  are obscure.   The  muscle is often atrophied. ^ In the
spasmodic form it  usually  occurs in adult life, between thirty and
fifty-five years  of age, and the exciting cause is generally an emotion,
or cold, or exposure.
   The symptoms are simply those of a malposition of the head from
action of some one of the  muscles, either  the sterno-mastoid,  the
splenius, or the trapezii.  It is usually unilateral.   The onset may be
sudden or gradual.  There  may be a certain amount of pain with it,

                              Fig. 161.
Case of spasm of the trapezius.
but this is seldom acute.  Fig. 161 represents a child with spasm of
the trapezius.
   The pathology7 is unknown.
   The diagnosis is very easy, and all  that is needed in order to make
it  is a sufficient knowledge of anatomy to recognize the position into
which the head can be thrown by spasm of the different muscles, as
well as sufficient information to be able to exclude any possible co-
existing organic disease—which scarcely ever, if ever, occurs.
   The prognosis of torticollis is usually good as regards life, but it
often is very obstinate, and, in some  cases, incurable.
   The treatment of spasmodic torticollis by means of belladonna is
sometimes beneficial.  Leszynsky advises such doses as will be suffi-
cient to  cause marked  dilatation  of the pupil and dryness  of the
mouth, and  I have no doubt that  the treatment should never be
regarded  as ineffectual until this point has been reached, and until
the patient has been thus kept under the influence of belladonna for
several days or weeks.   The cases, however, wThich I have treatedby
belladonna have  all of them been office patients, many of them hying
at too great a  distance in this city or  neighboring cities to permit of
my putting them  fully under the influence  of belladonna,  so that
my results have  been obtained with  far less doses.   If  the case is a 
THE NEUBOSES.
437
mild one, I usually begin with one drop of a  reliable fluid extract
of belladonna morning  and evening, and increase this  to  three or
four drops, unless the spasm is relieved.   Galvanism of  the affected
muscles  is sometimes of considerable  temporary  value.  One  pole
should be placed on the  cervical  spine, electrode No. 68  being used,
and  another  pole,  electrode  No.  71,  should be  placed  over the
affected muscles, and  a  current of three to  five milliamperes passed
from three to five minutes  every second day.  Faradization of the
affected muscle has never proved of any use in my hands.   Stretch-
ing the nerve-trunk from which  filaments come to the affected muscle
is often of considerable value.   Other  drugs, such  as morphine,
chloral, conium, and Indian hemp, I consider to be almost worthless.
If the case should prove to be incurable, and a great  deformity has
resulted, section of the tendon of the contracted muscles should be
resorted to for the relief of the  deformity; but it is useless except
for this purpose, as  it does not  check  the spasm, and the subjective
discomfort of the patient is apt to be greater because the shortened
muscle contracts more vigorously.   In  a  hopeless case a mechanical
support, so arranged as  to give rest to the head, will be palliative.

                          HYSTERIA.

   Definition.   Hysteria may be defined as a peculiar increased
reflex excitability of the cerebro-spinal nervous system, possibly also
of the sympathetic,  with decrease of cortical inhibitory power.
   Causes.   The causes of hysteria are—
       Heredity;
       Diseases of various kinds;
       Trauma ;
       Emotion;
       Mental and physical strain ;
       Imitation ;
       Mental contagion;
       Sex;
   Heredity is a frequent cause.  It is  not necessary that the direct
heredity should have been hysterical, for a general  neurotic heredity
or insanity will suffice.   The neuroses  and insanities are  intercon-
vertible in different generations of human beings,  so that it is quite
usual to find insanity in one individual or one generation and neurosis
in another individual or another generation, or vice versa.
   Diseases of various kinds  are very  common causes  of  hysteria,
even in those who are not predisposed, and  this fact should always
be borne in mind.
   Trauma occasionally causes hysteria, it is true;   but it has not, in
my experience, played the large part in  the causation which has been
attributed to it by the French school and also by many physicians
in this country.   (See Chapter on " Railway Injuries," etc.)
   The emotions, especially the passions, are frequent causes of hys-
teria, both in the predisposed and in the non-predisposed.
   Mental and physical strain may cause hysteria even in the non- 
438
NEB VO US DISEASES.
predisposed, and in the predisposed it plays a much larger part than
is recognized by physicians.
  Imitation and mental contagion are the causes of those hysterical
epidemics which we see occasionally in girls'  schools, and of those
curious outbreaks of the Middle Ages, of which a history is given in
another chapter. (See " Chorea.")  Besides this, susceptible children
and women, or even men,  will become hysterical at times upon wit-
nessing an hysterical outbreak.
  Sex.  Although females most frequently have hysteria, it yet fre-
quently occurs iu males.
  Clinical History.   The clinical phenomena of hysteria are as
various as are the phenomena of the cerebro-spinal and sympathetic
nervous systems, and of them may be said what Shakespeare said of
Cleopatra (who probably charmed Csesar by her very hysteria), that

                ''Age cannot wither her nor custom stale
                 Her infinite variety.''

  But, various as they are, these clinical phenomena can be classified
under the five heads of mental, motor, sensory, visceral, aud convul-
sive symptoms.
  The typical mental  symptoms of hysteria are  generally supposed
to  be an alternation of laughing  and crying, with an accompanying
globus hystericus—i. e., a feeling as if something were in the throat;
and it is generally supposed that the diagnosis must be based upon
them.  This is a very serious mistake, for, as a matter of experience,
it is only a very small  proportion of cases in which these symptoms
are observed.   In reality,  the  mental symptoms  of hysteria in the
slighter degrees are  practically undistinguishable from  those  of
caprice or lack of self-control, whilst in the graver forms they equal
in  severity the  mental  disturbances of such neuroses as epilepsy or
catalepsy, such cerebral alteration as is  indicated by the different
forms of coma, or such as is  present in  those forms of insanity to
which  has been given  the  name of the  " psycho-neuroses."   It is
the rule that the graver forms manifest an altered mental condition
only  at the time of the attacks, whilst  milder types manifest a far
more continuous abnormal  mental  condition.  When the  peculiar
mental condition is  observed in the milder  forms, it consists of a
tendency to an emotional condition that is not controlled by the usual
cortical inhibition ; or, to put it iu less technical language, the emo-
tions and the  passions aud the sensations have freer play than is
usual with an individual  of the same sex and  condition in whom
self-restraint, a proper sense of the fitting, aud good judgment act as
guides.   An  hysterical individual  can be made to laugh or cry, can
be  angry, or  depressed, or  elated,  or frightened,  without adequate
cause in the  environment, in the circumstances, or in the condition
 of  the health otherwise.  In the typical cases of hysteria of milder
degree this non-inhibited  condition of emotionalism is often pitiable;
as  I  have seen  it in a woman who, having passed through several
attacks  of insanity  caused by terrible  domestic  misfortunes  and
attempts at suicide, could not be spoken  to  upon any subject that 
THE NEUBOSES.
439
required ordinary thought, could not hear the noise of a door closing
or a door-bell ringing or a church-bell chiming, or could not discuss
some ordinary matter of domestic detail,  without having her eyes
fill with  tears and her face twitch convulsively.   In  the  severer
types of mental disturbance the mental symptoms approximate those
of insanity or coma.  An hysterical patient who is violently excited
is, for the time being, often as far beyond control as a case of acute
mania, and  the mental confusion is often quite as great.  In these
violent outbreaks  the  salient phenomena are  the violent emotion-
alism, the incoherence, the  impulsive acts, and  the entire  loss of
mental inhibition.   I have seen many curious and almost incredible
exhibitions of this  kind.   I  have seen  gentle women, ordinarily of
mild temper and perfect modesty, behave in a way that would have
shocked a female of the savage tribes of equatorial Africa, and that
did overwhelm them with mortification when the  attack had  passed.
I have seen ordinarily strong and self-controlled  men, holding posi-
tions of trust that called for  the constant exercise of great decision
and good judgment, lose such control of themselves as to behave like
panic-stricken boys.  The same mental characteristics obtain  in hys-
terical insanity.  (Vide "" Mania.")   After most  of the violent out-
breaks—indeed, during the  occurrence of them—there is a varying
degree of mental confusion that not infrequently passes into partial
or entire unconsciousness, so that the patient may not afterward re-
member what has taken place.
  The sensory symptoms of hysteria are characterized  by the same
capricious element  that is observed in the mental condition, so that
they are prone to come  suddenly, leave suddenly,  aud to persist for
most uncertain lengths  of time.  The sensory symptoms are infinite
in character  and variety, being sometimes  referable to  the motor
nerves, sometimes to the sensory nerves, sometimes to the sympathetic
nervous system, aud  ranging over all the tissues of the body.  An
attempt has been made by Charcot and his followers to  establish the
dictum that the sensory symptoms of hysteria are generally those to
which they have given  the name of hemiansesthesia, and in which, as
the name indicates, there is  an impairment of the different  sensory
nerves upon one side of the  body in varying degree, with the single
exception of  the optic nerve, which is usually affected bilaterally.
This optic nerve, it is claimed, shows its implication by a concentric
limitation of  the visual field aud by impairment  of the color-sense,
whilst the olfactory, the gustatory, and the cerebro-spinal  nerves of
tact, pain, temperature, and  the muscular sense are impaired in the
usual way.   It is not, however,  claimed that this hemiansesthesia is
usually a complete  one, inasmuch as the concentric limitation of the
field  of vision, with  some impairment of the color-sense, hyperses-
thesia, slight  analgesia, and  slight impairment of the tactile sense,
constitute the symptoms  of  most  cases.   Coincident  with these
symptoms, according to  the French school,  is a tenderness upon
pressure of  one or both ovaries.   But this Parisian dictum has not
been confirmed by other neurologists.   Thompson and  Oppenheim
have  shown  that hemiansesthesia, in the sense defined, is observed 
440
NEBVOUS DISEASES.
in very many other diseases than hysteria (vide " Railway Injuries,"
etc.), and, if I may trust my own experience, in this country it is an
infrequent symptom.   It is possible, however, that too little account
has been taken of the inherent differences that there are between the
Latin, the Anglo-Saxon,  and the race that is  growing up in this
country from  a larger fusion of different nationalities than has ever
taken place before in the recorded history of the world.
   The visceral sensations, which are only,  of course, a  subdivision
of the sensory, are as  infinite in variety as the latter.   The most
familiar one is the globus hystericus, that curious muscular sensation
of the larynx;  and, indeed, the hysterical  are exceedingly prone to
abnormal  laryngeal and tracheal sensations of various kinds, from
the typical aphonia to the obstinate  difficulties of deglutition which
so often  puzzle laryngologists.  The so-called ovarian tenderness is
probably merely a  muscular or visceral sensation, or hypersesthesia,
because  in  many cases it  extends over the whole flank, or, indeed,
the whole side, and its analogue in  the  male is found in a  similar
sensitiveness of the testicle.   Support is lent to this view by the grave
doubt that has been cast upon its being  possible to reach the ovary
in the precise locality which is indicated by Charcot.  Borborygmi
and  flatulence are  other very common forms of perverted visceral
sensations in the hysterical.   It is not  uncommon to witness as rigid
a distention of the anterior abdominal walls  as is seen in cases of
peritonitis, and, indeed, the differential diagnosis may sometimes  be
a matter of difficulty.   Hysterical dyspepsia is sometimes observed,
although it is rare.  The secretion of large quantities of limpid urine
in which the solid  materials are not notably increased belongs to the
same class of phenomena.
   The motor  disturbances of hysteria commonly accompany the sen-
sory ones; but the so-called hysterical joint is an example of motor
disturbance pure and simple.  Attention was  first called to it by
Sir Benjamin Brodie, and  it has been well studied by the Schleswig-
Holstein surgeon, Von Esmarch.   It  may be bilateral or unilateral,
and  is  not attended by any of the swelling, redness, or  great pain-
fulness of the joint seen in  organic joint  troubles.  The joint of the
knee is usually affected.   I have seen this, too, in some rare instances
after the cure of a melancholia.
   The  convulsions of hysteria can  be divided into two classes—the
purely hysterical aud the hystero-epileptic.  In the  former the loss
of consciousness is seldom complete, so that the patients never fall
in such a way as to injure themselves as they do iu epilepsy; whilst
the convulsive movements of the extremities, instead of being char-
acterized by the limited range and  automatic character of the tonic
and  convulsive movements of epilepsy, are of much wider range and
are much more  purposive.   In epilepsy, for instance, the muscular
movements usually consist  either  of muscular rigidity,  with  or
without slight tremor, or of shock-like alternate movements of flexion
and  extension.   In hysteria the patients throw the limbs  about, or
roll  over,  or strike out, or kick.    Charcot has made very precise
studies of  hvstero-epilepsy, which  he  also calls hysteria major, and 
THE NEUBOSES.
441
an attack of which  he divides into four periods, as well as a pro-
dromal stage.   The latter consists  of malaise, anorexia, occasional
vomiting, silence, and melancholy,  or excitement, increase of a  pre-
existing hemiansesthesia, visual hallucinations, globus, etc.  The first
period is the epileptoid, which is subdivided into the tonic  and the
clonic stages, and that of resolution.  The second  period is that  of
contortion, in which the patient has widespread  and half-purposive
movements, or a series of salaaming movements.  The third period
is that of hallucinatory  or melancholy attitudes which are evidently
the result of passing  mental changes.   In  the period of resolution
the patient  manifests either a  melancholy delirium with hallucina-
tions of animals,  or general or partial contractures, which are often
painful, or great exhaustion.   The attack  generally lasts  about a
quarter of an hour, and, according to Charcot, it can be stopped by
pressure upon  the ovarian region,  or by an electric current.   After
it has ceased the patient may remain in a similar condition to that  of
status epilepticus (i. e., comatose) for as long a period  as  twenty-four
hours.   But this  hysteria major is seldom seen either in  this country
or in England ; indeed, I have never myself seen more than a dozen
cases of it in an experience  of  twenty years.
   Prognosis.   The prognosis  of hysteria  varies  greatly.  The
hereditary forms  are seldom or never entirely cured, although careful
attention to the general  health and  to the removal of exciting causes
may effect  immense improvement.   The  attacks  occurring in the
non-predisposed,  or  the hysterical  status which  may be excited  by
various causes in such individuals, are always perfectly curable.
   Diagnosis.  At the outset of this aspect of the  subject, let me
seriously impress upon  every medical man the need of being very
cautious in making a diagnosis of hysteria.   For ages  it has been
too much the custom of the medical profession to ascribe unknown
diseases or the  effect of undiagnosed diseases to hysteria.  I  have
been present at a number of autopsies  of individuals supposed  to
have been hysterical, but in whom a gross organic lesion has  been
found: in several cases, an aneurism; in two, a  nephritis;  in one,
a myelitis; iu  one, a  pachymeniugitic hemorrhage.  It has  been
my fortune, too, to  be called  in  consultation a number of  times  to
so-called hysterical cases really suffering  from organic diseases,  such
as intracranial syphilis, myelitis of the  anterior spinal cornua, pro-
gressive muscular atrophy,  neuritis, diabetes, pelvic  abscess,  etc.
Even in those who  are  known to  be predisposed it should not be
forgotten that the immediate exciting cause of hysteria  may be an
orgauic lesion.  In  any doubtful case, therefore, the urine should be
carefully examined quantitatively, qualitatively, and microscopically ;
the heart aud lungs should  be carefully auscultated  and percussed ;
the ovaries, the  Fallopian tubes, and the uterus should  be carefully
examined, and all  possible diseases should be thought of.    In  fact, the
diagnosis of hysteria calls for the exercise of the broadest information
and the greatest skill.   The  history of the patient should be patiently
and carefully elicited.  Especially should the following nervous dis-
eases be excluded  : 
442
NEBVOUS DISEASES.
       Neurasthenia;
       Melancholia;
       The early stages of other insanities ;
       Progressive muscular atrophy;
       Lumbago, especially that following stricture ;
       Hydrophobia;
       Simulation.
  Do not forget that  neurasthenia may be an exciting cause of hys-
teria, so  that the  latter  may complicate  the  former and  sometimes
render it a difficult matter to know how much is due to the one disease
and  how much to the other.   In true neurasthenia, however (vide
section upon " Neurasthenia "), the emotional condition, the aberrant
and  capricious motor  and sensory phenomena, and the convulsive
symptoms of hysteria  are lacking.   The fades, too, is different; the
hysterical individual does not have the worn and anxious countenance
of the neurasthenic.   In  the latter, too, the narration of  the symp-
toms is made precisely, without exaggeration or emotion.  In lithae-
mic neurasthenia the feeling of  fulness and  tension about the head,
the irritability, the vertigo, the numbness aud tingling, and the other
parsesthesise are more constant in duration and location than similar
symptoms would be in hysteria.   In traumatic neurasthenia the his-
tory  of the trauma, the melancholy that is often in marked contrast
to the self-control of the patient in other particulars, the spinal ache,
the slight insomnia, the frequent neuralgia, persistent in one or more
nerve-trunks,  the  muscular  atrophy,  the occasional  paralysis  of a
group of muscles or a limb, the peculiar  muscular movements—all
constitute a symptom-group that is lacking in the excessive emotional
condition and the seeming caprice and variability of the phenomena
that  are  characteristic  of hysteria (vide "Railway Injuries," etc.).
  Melancholia  is  always attended, as  I have  pointed  out (vide
" Melancholia"), by two  or three of the three symptoms, viz., melan-
cholia, the post-cervical ache, and  the insomnia; and even if these
are not  sufficient, the  sad and  suspicious fades, the hallucinations,
illusions or delusions,  the suicidal  impulse, the dull cerebral  reflex,
or the melancholic agitation, are amply sufficient  signs for a  differ-
ential diagnosis.
  Commencing subacute mania (vide "Mauia"), or the early stage of
general paresis (vide  "Paretic Dementia"), is sometimes mistaken
for hysteria.   In  subacute mania, however, the  accelerated mental
state, the quickened cerebral reflexes, the mental and physical rest-
lessness,  the heavy countenance  that contrasts so sharply with  the
seeming  brightness of retort to an individual question, aud the slight
mental confusion,  are  symptoms that are not seen in any form of
hysteria  except hysterical mania.   General paresis in its early stages
is sometimes characterized by so much irrationality of conduct and
action as to cause the patient to  be suspected of caprice; but  the
tremor of the tongue and facial muscles, or even of the body, the ine-
quality of the pupils,  the paroxysms of facial flushing, unsteadiness
of gait, and irrational  conduct can  almost always  be elicited by care-
ful  examination or questioning;  whilst the diagnosis is easy in  the 
THE NEUBOSES.
443
more advanced stages when the dementia, stupid delusions—usually
of grandeur—general tremor, and shuffling gait have supervened.
  Progressive muscular atrophy may be overlooked in some instances
where weakness  has been complained of, or in the cases  that are
probably due to peripheral neuritis, wherein  complaint has  been
made  of the pains.   In any suspected cases the  patient should be
stripped, and a careful examination  made of the different muscular
groups (vide " Progressive Muscular Atrophy").
  Lumbago is not infrequently very persistent  and very intractable
to treatment, so that the failure to relieve the patient may be ascribed
to hysteria.  But the lumbago following stricture is such a curiously
intractable complaint that there is a special danger of confounding it
with hysteria (vide Chapter on " Neuralgia ").
   That  the symptoms  of hydrophobia may be purely hysterical is
undoubted.  In such cases, however, there is a lack of the prodromal
stage of hydrophobia; and strong assurances of safety, with isolation,
will speedily make the  matter plain.  In the interests of science, no
injection of the Pasteur virus should ever be made until hysteria has
been excluded, for in an hysterical  case the injection of cold water
would probably answer quite as well.   In doubtful  instances, how-
ever, where danger seems imminent, the patient should be given the
benefit of the doubt, and the proper injection of Pasteur's virus should
be made (vide u Hydrophobia").
   Treatment.  The treatment of hysteria will call for the exercise
of much intelligence, tact, and knowledge of human nature, as well
as of medicine.   Before entering upon the task the physician should
disabuse his mind entirely of the idea that  hysteria is a caprice, and
not a disease, and should thoroughly imbue himself with the further
 idea that although the hysterical individual is exceedingly impression-
able, he or she may yet have the other diseases to which the human
 body is subject.  The  brutal  and forcible methods of former days
should never be  thought of for a moment.  The patient should  be
thoroughly studied,  and all the circumstances of environment should
 be carefully inquired into.   For purposes of treatment  hysterical in-
 dividuals may be divided into  two  great classes:  those who are suf-
 fering from  hysteria alone,  and those who are afflicted with  hysteria
complicated by other diseases.   Those who are suffering from hys-
 teria alone should be treated somewhat differently accordingly as the
 hysteria is mild or severe.   In the mild cases  the confidence of the
 patient  should  be gained by the infinite devices that  will suggest
 themselves to  a physician  of experience and knowledge of human
 nature.   When  this has been done, the cure  is  often effected with
 surprising facility, and it is a matter of  little consequence what par-
 ticular remedial measures  are employed.   I have had many young
 men and girls brought to me who were suffering from slight symp-
toms that their hysterical nature caused them to  magnify into enor-
 mous ones, so as to produce exactly the same  psychical effect as if
they were weighted down  with organic disease.    The  boys  have
abandoned their careers perhaps, and, aided by the  anxiety  of well-
 meaning relatives who could not be  made to  understand  the true 
444
NEBVOUS DISEASES:
nature of their symptoms, they  have wearied  of physicians and
resigned themselves to what they supposed  was their destiny of a
lifelong valetudinarianism,  overshadowed by vague forebodings of
impending evil.   Girls are  more prone to  fall  into a similar hope-
less condition, not  only  because of the greater impressionability of
the female mind, but also because of their less tendency to struggle
against adverse circumstances.  Yet  I have  on  my case-book the
histories of many such patients whom I have succeeded in restoring
to energetic participation in  the struggles  of  life without the use of
other  measures  than gaining their confidence, gradually and firmly
leading them to exert their self-control, aiding them in this task, ac-
customing them to understand that their sensations, however alarming
they may  seem, are really of no importance, and without the use of
drugs further than as placebos.  The example of the quack through
all ages has been too much contemned, I think, by the regular prac-
titioners of medicine, and yet every physician of experience knows
of the startling successes that they occasionally  obtain.  Indeed, I
believe that  if hysteria were to die  out  from the  human race the
fraudulent practitioners of medicine would be more than half exter-
minated.  Nevertheless, impostors as  they are, these men  have  done
with fraudulent intent what the scientists  ought to do with an honest
purpose, namely, recognize that the  human  mind  is a much more
potent instrument  to play  upon  than the nervous system  of the
stomach and intestines.   I deal  very frankly with  this  class of
patients.  I  tell them that their  disease is a purely functional one,
and that it can  be  perfectly cured.   Then, bit by  bit, I teach them
that they  can do many  things that  they had thought impossible,
taking a special  care  never  to  have  them enter  upon a task that is
too great  for them to conduct to a successful issue, because a failure
with an hysteric is apt to be fatal.   By this means I gain the prestige
of success with  them, and each  succeeding task in entered upon  with
a feeling of greater  confidence.  Sometimes I talk kindly, sometimes
I speak very  sharply ; but through it all, whether I sympathize  with
them  or whether I reprove them, I maintain their  confidence.  For
example, a girl  is brought to me who cannot go among crowds.  I
gradually  get her accustomed to them.  A boy cannot take part in
athletic sports.   After having gained  his confidence, I put him in
charge of some one  versed in athletic sports who has good judgment,
and whom I  instruct to get him to enter into  them by degrees.   In
the severer cases of hysteria, however, the patient  must be removed
from an unfavorable environment, taken away from home and friends,
and put in charge of a trained  uurse who is possessed of good judg-
ment  and  tact.   The selection of this nurse is a matter of consider-
able importance.  It would  be a fatal mistake to  place an old  and
worn-out woman in charge of a young and active girl; or au ill-bred,
coarse, untidy woman in charge of one who is refined and particular
about her person and dress; or an unkempt, frowzy, ill-conducted,
ill-mannered  man in charge of an educated and well-bred gentleman.
If the patient  suffering  with hysteria is  one of  that unhappy  type 
THE NEUBOSES.
445
of bedridden  individuals of whom neurologists know so many, the
nurse  should  also be a woman  of firmness.  Even  in these severe
cases, however, the same method of psychical  treatment should  be
employed.  It is supremely ridiculous at times to witness the rudi-
mentary  education that must  be impressed,  detail by detail, upon
these hysterical  individuals, with an unflinching persistence of pur-
pose.  I  have put upon their feet and practically cured patients who
had been bedridden for thirty years by means  of rigid attention to
these minutiae.  Day by day theyr must  be  taught like a little child
to do some one  thing  that they had not done the day before, until,
as the weeks creep by, the accretion of these  little things have  put
them on their feet.  First, they are told to stand  for five  minutes
each day, then for ten minutes, then  for fifteen, and so  on.  Next,
they are told to take a walk around the  room.  Next, as mental con-
trol over them is gained, they are suddenly some fine day told to go
out-doors.  The heart must, of course, be carefully watched in these
patients who have been bedridden so long, and if it grows weak and
rapid after some exertion of this  kind,  it is often advisable to begin
the administration of  fa grain of the sulphate of strychnine three
times a day, either in the form of pill or tablet triturate.  If there
is ansemia conjoined with one of these severe cases  of hysteria, the
treatment by  rest, large quantities of food,  and iron  should be insti-
tuted, as I have advocated  it in the chapter  upon " Neurasthenia."
All other sources of bodily  discomfort should be sedulously attended
to.  True hysterical convulsions need no special treatment further
than the exhibition of some one  of the well-known  antispasmodics
and sedatives, such as  the nitrite of amyl in  the so-called "pearls"
containing three to five drops, one of which  should  be broken in a
handkerchief  and placed under  the nose of the patient; a dose of
bromide of potash, gr. 15 to 20 ; the inhalation of a small quantity
of ether  or chloroform; a teaspoonful of Hoffmann's anodyne in a
wineglass of water; or sometimes a simple hypodermic of cold water.
I have, however, again aud again seen these  convulsions brought to
an  end  by firm  and  judicious  psychical  treatment and  isolation.
Hystero-epilepsy  should be  treated  as indicated   in the chapter
upon  "Epilepsy."  Hemiansesthesia occurring in  hysterical indi-
viduals  should  be treated by  a  combination of psychical  measures
and  electricity, the galvanic current being  applied to  the spinal
column, and the faradic current brushed over the affected limbs with
two wire brushes, the  current being strong enough  to be distinctly
felt by the patient.  It should always  be remembered, however, that
hysterical individuals  are not  exempt from the ills that flesh is heir
to, and that they  may just as  likely  have  neuralgia, neuritis, neur-
asthenia, etc.,  as individuals who are  not hysterical, although they
are apt  to respond  much  more promptly to treatment than  the
latter.
  To sum up, therefore, the treatment of hysteria should be mainly
by means of  psychical measures.  If, however, other diseases com-
plicate the hysteria, these should also be carefully looked after. 
446
NEB VO US DISEASES.
                        HYPOCHONDRIA.

  Hypochondria is a pseudo-mental disease that can scarcely be called
an insanity, consisting of a tendency to morbidly exaggerate the vari-
ous sensations of the body and their importance. At times this exag-
geration is so great as to amount to actual delusion. Every physician
is familiar with  these cases,  for they are the bane of every medical
man.   They complain of all sorts of sensations and dwell upon and
recapitulate them ad nauseam.  One patient thinks that his hair is
falling out; another that he is growing weak in his muscles ; another
that he has this, that, or the other symptom.  They all take  medi-
cines as a steady diet, and they all  fall a ready prey to quacks and
every " ism " that the morbid ingenuity of man can  suggest. Hypo-
chondria is sometimes met with in conjunction with mental disease;
and in some cases of mental disease there may be a prodromal period
of hypochondria, aud a hypochondriacal insanity  has  even beeu de-
scribed, but this latter is certainly rare.  Sexual hypochondria—that
is, hypochondria about sexual matters—is a very frequent form, and
is often described under the name of sexual neurasthenia.
  The diagnosis of hypochondria is  usually very easy.  The  only
questions  that can arise are as to whether the patient is not suffering
from melancholia, or the prodromal stage of some insanity, or from
some actual coexisting  disease.  From the melancholiac the hypo-
chondriac can  be readily distinguished  from the fact that the melan-
choliac does not  seek relief, is not prone to believe that medicine can
afford him any aid ; and in  the  slighter forms he also suffers from
the symptoms to which  I have elsewhere called attention ("Melan-
cholia"),  namely, insomnia,  post-cervical ache,  and  the  suicidal
tendency;  besides which he has a  peculiar fades of his own that a
little experience  will soon make familiar; whereas  the hypochondriac
readily takes  medicine—even eagerly solicits it—has none of the
three cardinal  symptoms that have been mentioned above, and has no
peculiar fades.  The hypochondriac prodromal stage of an  insanity
is usually not  prolonged  over a few days  or a week, and this fact
alone would distinguish it from the chronic course of hypochondria,
which is often life-long, even if the succeeding mental  symptoms of
the insanity were not sufficient.   Any  disease that may coexist with
insanity must,  of course, be recognized by the general medical knowl-
edge of the physician, and it is useless to catalogue these diseases, as
they embrace almost the whole field of medicine, especially in the adult.
  The treatment of hypochondria is very difficult.   I  believe that
the most success is to be obtained from the principle of suggestion,
that can  only  be fully understood after  reading  the chapter upon
" Hypnotism ;"  and, as  I have cured  several  cases of my own by
this method, I can give full credence to  the  many cures that have been
reported by the  French  schools of hypnotism of Nancy and Paris.
It  is not always  necessary by any means to  induce  full hypnotism.
It  may be well sometimes in obstinate  cases to hypnotize the person
sufficiently to prevent him from opening the eyelids, but in very
many cases even this is not necessary, and  it will  suffice if the con- 
THE NEUBOSES.
447
fidence of the patient is gained by making quiet and dogmatic asser-
tions and  ordering  placebos.  Any  person,  however, who adopts
this method of suggestion must be fully acquainted with the hypnotic
methods, so as to be prepared to carry out the treatment thoroughly.
I do not mean to be understood as saying that full hypnotization of
the patient would not be the best, but I merely mean to advise that
it is not usually politic to use the word hypnotism to the patient, or
to let him suppose that hypnotic methods are  being used, as there is
a widespread  prejudice in the lay  mind against hypnotism, which is
generally thought to be synonymous with  quackery,  aud  anything
that disturbs the confidence  of the patient in  the medical attendant
will be fatal to the treatment.
   Occupation of any kind that will divert the patient's thoughts, or
travel, or change of  scene, or great emotions, will  often act as tem-
porary palliatives and sometimes as cures, and  therefore it may be
well to make use of these methods. Of course, it is not always easy
to evoke an emotion, but this can be sometimes done.  In one case of
mine,  for instance (the patient elsewhere  referred to as  coming to me
with a specimen of black semen), a cure was effected in this manner :
I requested him to look sharply at  the piece  of rag upon which he
claimed there was black semen. I then took a black-bound book and
laid it alongside of this piece of rag, and asked him if he  thought
the book was of the same color as the stained rag.   He said it was.
I then told him that if he thought the rag stained  a faint yellow was
of the same color  as the black book-binding he must be suffering
from  one  of two troubles.  In the  first place,  he might have a
delusion, but  that involved  insanity, and I had  treated him long
enough to  know that he was not insane.   The other  was that he was
a  fool, and I bluntly told  him that  that was my  diagnosis.   He,
naturally euough, started back in  anger, and after some angry re-
marks, left my office; but he came back  in the course  of a week or
two to tell  me that he believed I was  right—that  my  blunt remark
had made him realize how  foolish  he was ;  and since that  time—
eleven years having now elapsed—he  has manifested but very slight
symptoms  of hypochondria.   I do not tell this as a funny story, but
simply to show that emotions can be evoked at times by the ingenuity
of a physician.  Indeed, I believe that in the capacity to play  upou
the mind in  its various functions, especially those which  we  now
call emotions, the future  therapeutics  of hypnotism  will lie; for  at
present we are stupid enough to think that it is science to play  upon
the peripheral terminations of the  nerves or the structures  in which
they terminate, whilst we deem it quackery to make use of the  gray
matter and all its wondrous molecular  play.  So-called faith-cure,
" Christian science," the great emotions of wars and politics, and love
and anger, and ambition  and avarice,  and, finally, the wonderful
but only half  understood phenomena of hypnotism, are all neglected
clinical illustrations  of the  magnificent influence of the mind  over
the body;  and in the full day of medicine, into whose  dawn we are
now peering, we shall make  proper application, I have  no doubt, of
these therapeutic methods. 
448
NEBVOUS DISEASES.
                        NEURASTHENIA.

  Synonym:  Nervous prostration.
  History.  Functional diseases of the nervous system  have been
held largely in contempt unless they were fortunately accompanied
by such  startling  phenomena as loss  of consciousness, convulsions,
epilepsy, the pain  of neuralgia, or the often violent muscular contrac-
tions of chorea.   The medical world has no heredity of training in
nervous diseases.   For centuries medical writers and  teachers have
called attention to the phenomena that could be studied in the pulse,
in the heart,  in the tongue, in the  feces, in  the temperature  of the
body;  aud within a few generations these and a few kindred details
have been made the language of a more precise diagnosis of thoracic
and abdominal diseases.  But nervous diseases  constitute a modern
study.   We may date them back really to the fifties, when the great
French school began  its career; and it is  only within a very few
years  that the medical  schools  of  the  United States  have  even
thought  of  having a chair especially devoted  to  this  branch  of
medicine.   So it is that while tens of thousands will be prompt  in
detecting the first  signs of deviation from the normal  in  the pulse-
beat, in the respiration, in  the tongue, in the  fades, in the urine or
feces, there are scarcely ten—and these only  with some special edu-
cation—who will  recognize the primary symptoms of organic  or
functional  nervous disease, which they are only too ready to ascribe
to hysteria.   Yet  all attentive observers of  disease, more especially
those engaged in neurological  study, could not help  observing  many
phenomena that could not be classified;  and  this, I  think, is the ex-
planation of the  enormous success that the writings of Dr. George
M. Beard upon neurasthenia have had in Germany—indeed, it may
be affirmed  that he has  started  a literature in that country, the con-
tributors to  which are such well-known writers as Arndt, Krafft-
Ebing, Erb, Westphal, Moebius, Seeligmuller, Strumpell, and Lang-
stein.   As far back  as 1828  C. Brown, of Glasgow, had  described
what he called spinal  irritation, and in  1860  Bouchet had written
fully upon what he termed VStat nerveux; each  of these writers has
had his followers to some extent, but Beard,  it may  be said, was the
first to formulate boldly the proposition that there was a widespread
condition of  functional nervous disease, for which he  proposed the
name of " neurasthenia" and for whose maintenance and prevalence
and varied phenomena he battled with the most alluring and pic-
turesque of  pens.  It  is curious,  nevertheless, that  the  Germans
themselves do not seem to admit that the malady is frequent among
them, but always  fall back upon Beard's assertion that America is
its home.   In 1874 Murchison, in his brilliant course of Croonian
Lectures, delivered before the Royal College of Physicians, described,
under the heading of " Functional  Diseases  of the  Liver," a group
of symptoms for which he suggested the name of lithsemia. For the
same condition Austin Flint  had some six years before coined the
name  of uricsemia;  but Murchison's designation has  been the one
that has come into vogue in the  time which has since elapsed.   Since 
THE NEUBOSES.
449
then  contributions to the subject have  been  made by Da Costa,
McBride, Lyman, Hudson, Potter, and myself.  The general feeling,
in  this country at least, is, I think, that  the term neurasthenia, as
denned by the writers upou the subject, embraces entirely too much.
I share in that feeling myself.   The fact seems to have been forgotten
that there  are already a number of well-studied functional nervous
diseases, as well as that  each  one of these has symptoms correlated
with  it, and that no scientific advance is made by jumbling together
the symptoms of these various and differently acting diseases under
one wide name.   Then, too,  it should  not  be forgotten  that the
nervous system stands pre-eminently' alone among the tissues of the
body in the highly important fact that its ramifications carry its in-
fluences into every other tissue, and in turn-carry back to it the influ-
ences of every other tissue, so that, much more than is the case  with
any other organ, the  nervous system is peculiarly at the mercy of
reflex disturbances.   Excluding, then, vicious habits, reflexes from
non-nervous organs,  and well-recognized  functional diseases, the
question arises :  Is there such a thing as nervous weakness or neur-
asthenia?  I believe there is.   But I also  believe that it  is much
more  limited in  its relative prevalence than is maintained by the
eager followers of Beard.
   Clinical History.   There  are, in my  opinion, three forms of
neurasthenia :
       1. Reflex neurasthenia;
       2. So-called lithsemic neurasthenia;
       3. Simple neurasthenia.
   1.  The  neurasthenia  that  results by  reflex from non-nervous
organs and vicious habits is,  in  my experience, the second most fre-
quent form, and can often only  be recognized by a very careful ex-
amination of the different organs of the body.   The very essence of
a  reflex disturbance  is its caprice, so that no one set of symptoms
can be relied upon,  as  a rule, to be  indicative of  a pure  reflex.
There are, to be sure, some seeming exceptions to this statement, as
in the occipital pain  of nephritis, the uneasiness at the vertex  in
uterine diseases, etc.   But clinical experience has taught me that these
vaunted localizations  of pain  are  all of very little practical value.
I know of no shorter way of determining whether a reflex disturb-
ance  in a  non-nervous organ  is the cause of a given neurasthenia
than by an examination  of the different organs, especially the  kid-
neys, the eyes, the naso-pharynx, the lungs,  the heart, the liver, and
the genitalia, and in every case the habits should  also be carefully
inquired into.
   2.  Lithozmic neurasthenia.  This form is the most frequent of all,
I think, and its symptoms are vertigo, a sense of pressure about the
head, slight insomnia, nervousness, occasional susceptibility to odors,
occasional  tinnitus  aurium,  neuralgia,  parsesthesia,  rarely  slight
anaesthesia, muscular  cramp and  twitchings, and vasomotor disturb-
ances.  It has also been stated  by some of the authors  that in this
type  we may also have fever, a delusional  mental condition, even
myelitis of the anterior horns, epilepsy, and  disseminated  sclerosis;
                               29 
450
NEB VO US DISEASES.
and when I wrote my first  paper upon  the subject in 1886 I was
inclined to think that there was a grain of truth in these statements-
but an experience since of nine years, ranging over several hundred
patients, has failed to bring to  my observation a single undoubted
case with these symptoms, and I think the  mistake has lain in over-
looking the fact that the diseases with these symptoms may be asso-
ciated with lithsemic neurasthenia.
   The vertigo  is  both subjective aud objective, although  it is gen-
erally of the latter kind—that is, surrounding objects seem to be in
motion and not the patient; or the patient may reel suddenly when
walking or when  sitting;  or he may feel a sudden vertiginous sen-
sation, the latter often so  pronounced  as to simulate the  vertigo of
Meniere's disease.  The vertigo is usually of short duration, although
it  generally recurs frequently, and  in some exceptional cases, espe-
cially during the hotter months of the year in our climate, is so con-
tinuous as  absolutely  to incapacitate the person from an active life,
whilst the  moral effect is  occasionally incredibly depressing.   Thus
I  have  known  prosperous and  ambitious  careers to be absolutely
checked by it for the time being; and many a man have I seen go
forlornly from  clime to clime in search  of relative  safety, weighed
down by the calamity of a supposed incurable malady which a short
course of intelligent treatment would  have done more to ameliorate
than the soft airs of the  Hebrides or the mountain grandeurs of
Switzerland.   Indeed, I know at this present time of one gentleman
who has entirely abandoned an  excellent  business and hopelessly
buried himself on a small farm ;  of another well-known public man
whom an attack of this kind of dizziness caused to forsake abruptly
his official post and travel hundreds of miles home in a special train
with the idea that he was about to be seriously ill; and I know of still
another public man of national reputation whose political aspirations
have been held in check for a decade by a needless fear of this  symp-
tom.  This vertigo may come without the slightest apparent reason,
or it  may  have  many exciting  causes, such as fatigue, mental or
physical, special  articles of food, often varying  in each individual,
sometimes  a  few glasses of hock or a single glass of burgundy or
champagne;  tobacco,  especially  cigarettes;  or slight strain of the
ocular mechanism of accommodation.  Purgatives and salines, per-
haps  relieving  the other phenomena, may increase  the vertigo,
although this increase is  usually temporary unless the purgation is
extreme or is continued so long as to  depress  the general nervous
system.   It can usually be palliated by lying down.
   A sensation of fulness about the head is a very constant symptom,
but it is not a true headache, although at certain periods of exacer-
bation it may become such.
   According to Da Costa and Murchison, repeated vertigo may lead
to  a limitation of the visual field, amblyopia, and double vision.  I
used to think that this was true, but a further and more accurate
knowledge of the malady has  taught me that  ocular couditions of
this kind are due either to hysteria or to some organic disease  of the
nervous system. 
THE NEUBOSES.
451
  I have never seen the temporary blindness of one eye or part of
one eye or the  retinal congestion  described by Da Costa.  The last
condition is, as is well known to ophthalmologists, often difficult to
determine, aud it may well be that what one observer may regard as
hypersemia will seem dubious to another.
  Nervousness, next to  the  vertigo, is the most frequent of all  the
symptoms, and it may be accompanied by irritability of temper, and
both these symptoms will often be beyond the control of those who
have usually a strong will, so that they are more apt to be present in
those of normally feeble volition, when the effect is often  mistaken
for the cause and hysteria is  diagnosed.
  The tinnitus aurium is a simple roaring of varying degree, usually
without  any attendant aural or naso-pharyngeal  trouble, although
it may be somewhat aggravated by naso-pharyngitis obstructing the
orifice of the Eustachian tube, and in gouty subjects Sir James Paget
has described a peculiar reddish and glazed appearance of the fauces,
as if they were smeared over with glycerin.
  The insomnia is usually very slight, and must never be confounded
with the insomnia of simple  melancholia,  which, as I have elsewhere
shown, is accompanied by melancholia of a peculiar type and post-
cervical ache, and is often mistaken for neurasthenia.
  There is an occasional  morbid susceptibility to odors, and I have
known patients to grow pale and nauseated at odors, or indeed savors,
that would ordinarily be unnoticed by them.
  The most usual  forms of neuralgia  are sciatica, neuralgia of the
different nerves of the arm aud forearm, of the tongue, of the breast,
intercostal neuralgia, gastralgia, and enteralgia.  The  fifth  pair  is
seldom affected.  Da Costa  believes that a neuritis is  occasionally
seen, but I have never seen  one—indeed, I am of the opinion that
the absence of neuritis is a diagnostic sign of value in differentiating
lithaemic pains.  There are  certain  pseudo-neuralgias consisting of
vague  aching pains like the so-called "rheumatic" ones, viz., a sharp
pain in the eyeballs, dull pains in the ensiform cartilage, a dragging
sensation along the course of the ureters, slight  wandering pains
which  may be mistaken for the ill-defined ones of locomotor  ataxia,
vague  distress over the region of the liver, etc.
  Parsesthesias are  very frequent, and consist of numbness, tingling,
fuzziness of the body or extremities, aud a whirling sensation at the
crown  of the head.
  Slight anaesthesias are occasionally, but rarely, observed.
  Cramps generally affect the gastrocnemii, usually at night  and in
cold and damp weather.   Twitchings  of the face  aud eyelids are
occasionally observed, or even choreic movements in children, and,
most rarely of all,  fibrillary muscular contractions.
  Vasomotor disturbances are among the most frequent symptoms,
such as flushings and pallor  of the face and sensations  of heat and
cold, and  McBride  has described that  rare lithsemic form of vaso-
motor spasm  of the upper extremities known as "digiti mortui."
  The typical urine of lithsemics has the following  characteristics :
It is acid, highly colored.  It possesses a high specific gravity, which 
452
NEB VO US DISEASES.
is usually 1.028 to 1.034 in a morning specimen, and it may be 1.030
in the whole  amount passed in the twenty-four  hours.   As to the
quantity, McBride and  Da  Costa differ.   The former says that it
may be  normal, increased, or diminished, while  the  latter affirms
that it is usually very scanty.   My experience coincides with Mc-
Bride's.   Uric-acid crystals are often visible to the naked eye, in the
well-known "cayenne pepper" forms.   The  pigment  is  increased.
Microscopically, uric-acid  crystals are seen,  occasionally octahedral
crystals of oxalate of  lime, commonly the amorphous urates, globular
crystals  of urate of sodium with spicules.   The urea is not generally
increased when flesh  is being lost (Da Costa). ^ I have recently been
able to demonstrate that most of these cases will have small amounts
of albumin and  sugar in the urine, aud also  a few hyaline casts;
thus evidencing a marked tendency to increase of the nitrogenous
excretion.  It also is possible that the hydrocarbons passing off by
the lungs would also be greater than usual.  There is no convenient
method  of estimating the amount of uric acid that may be contained
in a given specimen.  Pavy's test,1 to which  Dr.  Da Costa alludes,
takes some half-hour of time ; so that, unless the urinary peculiarities
are visible to the naked eye or the microscope, few men have the time
to make the necessary examination.  Even if a handy method of quan-
titative analysis were known, no one has pointed out what amount is
necessary to constitute the morbid condition of so-called lithsemia—a
very fatal omission when it is remembered  that the uric acid secreted
daily  by healthy individuals varies very  greatly in amount.  Dr.
Roberts2 observed a  difference of nearly one-half on two  successive
days, on the first day 5.45 grains being separated, on the second 11.7
grains.   In three healthy students, living on  a similar diet and under
similar circumstances, he obtained these figures :
          No. 1 (mean of 47 days).......8.051 grains.
          No. 2 (mean of 5 days).......3.462  "
          No. 3 (mean of 3 days).......6.071

   Sir William Roberts maintains that uric acid in the urine is the
 result of the decomposition of the  quadri-urates, and that it does
 not exist in the blood in any other form.
   3. Simple  neurasthenia.   By this I mean  the set  of  symptoms
 which constitute  the symptom-group of a true neurasthenia.  In a
 general  way, it may  be said that the functions of the nervous system
 are below par.   The patient complains of  weakness, either mental or
 physical, or both, and  any exertion is apt to be  attended by symp-
 toms of irritability of the nervous system.  An overworked business
 man will come complaining of incapacity for his work, and that when
 he attempts to force  himself to  perform his professional duties he will
 have a sensation of  cerebral fulness, or sharp pain at  the vertex, or
 an inability to exert those finer mental qualities which he has possessed
 in the past.  The celebrated author, Washington Irving, who wrote
 one of his  later works against  time, used  to  complain that his head

               1 Lancet, 1875.
               2 Urinary and Renal Diseases, Philadelphia, 1872, p. 77. 
THE NEUBOSES.
453
felt like a sponge squeezed dry at the end of a particularly hard day's
labor.  Or a woman may be  exhausted by household cares, parturi-
tion,  or the anxieties of a family, and  complain of a continual weari-
ness, so that she is obliged to spend most of her time reclining upon
a couch.  The cerebral form  of exhaustion  is perhaps least familiar
to general practitioners, but those who deal with mental disorders are
perfectly acquainted with it, for the constant difficulty after recovery
from the curable insanities is that patients are apt to become so much
discouraged for a long time with their inability to perform any sus-
tained mental  labor,  and many ambitious students at our large colleges,
especially those who have stood high in their classes, at the same
time that they have  given much time  to  athletics, have a degree of
cerebral exhaustion which sometimes incapacitates them for years
after leaving  college, perhaps with  honor.   Auy person whose ner-
vous strength  is impaired from any cause whatsoever  is, of  course,
liable to erratic nervous manifestations, simply because  of weakness.
Every physician is familiar with this fact and has seen it exemplified
in the hysterical weeping of strong  men in hospital wards,  in  the
nervous tremblings, in the flushing of the face, and in a thousand
and one different ways ; so that one would expect to  find symptoms
of nervous irritability even iu these cases of pure neurasthenia; and
we do find them, but not  nearly so often as one would expect or as
in the reflex aud so-called lithsemic neurasthenias.   We should bear
in mind, however, that the  hysterical, hypochondriacal, or neurotic
individual may be afflicted with a genuine neurasthenia, when it will
be a very nice question to determine  the  relative proportion  causa-
tively of  the predisposing  neuroses  and the  true   neurasthenia.
Nevertheless, I wish to lay great stress upon the fact that most cases
of the true neurasthenia which I am  describing are not complicated
with true hysteria or hypochondria, although there may be occasioual
emotional disturbances and considerable anxiety about  the condition
of health, as  is very natural.
  Causation.  The causes  of reflex neurasthenia are to be found
in some one of the non-nervous organs, either the kidneys, the naso-
 pharynx, the eyes, the heart, the liver, the genitalia, and in such  vicious
 habits as masturbation, alcoholism, morphinism, and cocainism.   In
all cases of neurasthenia, therefore, these organs  should be carefully
examined.  Disease of the kidneys can easily be determined by  careful
quantitative, qualitative, and microscopic examinations of the urine.
 In the uaso-pharynx the most frequent causes are, in my experience,
diseases of the nostrils, such as hypertrophies of the turbinated bones,
 deflections of  the septum, aud pathological septa, which  interfere with
 proper respiration.   In the eyes errors of refraction and ocular in-
 sufficiencies causing exophoria undoubtedly do cause an occasional neur-
 asthenia.  Great stress has been laid of late years upon exophoria as an
etiological factor, and there has been fierce discussion among  oculists
about this question,  so that for some time I was  myself in considerable
doubt as to the exact truth of the  matter.  I have seen a number of
cases of neurasthenia which  obstinately resisted  all forms of treat-
 ment until the exophria was  removed.  Nevertheless, I believe  that 
454
NEBVOUS DISEASES.
the frequency of this form of neurasthenia is  much overestimated
and I also believe that even in this type it is very rarely that opera-
tion upon the ocular  muscles is called for, inasmuch as the use of
prisms is generally quite sufficient.   The form of neurasthenia caused
by ocular insufficiencies bears so close a resemblance to the symptoms
of the lithsemic type that  the differential  diagnosis is often difficult
to make.  The cardiac disturbances  that are most apt to cause neu-
rasthenia are a nervous heart, next valvular troubles, and then a fatty
heart.   Hepatic disorders  are not frequent causes, in my experience,
of neurasthenia, contrary to the general belief of the profession; and,
as I shall have occasion to explain in a few minutes, the functional
hepatic derangement of the so-called lithsemic form is only one of
several  symptoms, and it is a question as  to whether it is a cause or
an effect.  These same remarks  are  true  as to stomachic disorders.
As to the genitalia, derangement of the vagina and  uterus and the
uterine appendages frequently causes neurasthenia,  although, as in
the case of the eyes, I think the  frequency of this causative factor is
much exaggerated.   Alcoholism, morphinism, and cocainism are fre-
quent causes.
   Pathology.  The  pathology of  lithsemic  neurasthenia has been
involved in considerable doubt.  The theory that has been advanced
by Murchison  has  met with general  acceptance and was based upon
some undeniable clinical facts—as that in  gouty persons  uric acid
was to  be found  in the blood, as Garrod  had  shown, and that uric
acid and the  urates in seemingly large quantities were also to be
found in the urine of individuals of  gouty heredity or gouty tenden-
cies—and upon one  assumption,  which was that therefore these neu-
rasthenics were to be regarded as suffering in a less degree from the
same underlying hsemic troubles as were the gouty.   Thus supported,
the theory was elaborated with a wealth of learning aud a charm of
style that made it attractive, the more  especially as  it was so very
simple.   "When oxidation," says Murchison,  "is imperfectly per-
formed  in the liver,  there is a production of insoluble  lithic acids and
lithates instead of urea, which is the  soluble product  resulting from
the last stage of oxidation of nitrogenous matter.   .   .  .  When
more food is taken  into the blood than is  necessary for the nutrition
of the tissues the excess is thrown off in  the form of urea, carbonic
acid, and water, or in the  imperfectly oxidized forms of lithic acid
and oxalic acid.   Under these circumstances the excess of uric acid
is thrown upon the liver and other organs, and  one result is that a
quantity of albumin, instead of being converted  into urea, is dis-
charged by the kidneys in the less oxidized form of lithic acid and
its  salts.  But what in  most persons is an occasional result of an
extreme cause  is in some  almost a daily occurrence, either from  the
food being always excessive  in  amount,  or unduly stimulating, or
from some innate defect of power often hereditary in  the liver, in
virtue of which its healthy functions are liable to be deranged by the
most ordinary articles of diet.  Most persons appear to have more
liver, just as they have more lung, than is absolutely necessary for
the due performance of its  functious; but  in others of gouty appear- 
THE NEUBOSES.
455
ance the organ in its natural condition seems only just capable of
performing its  healthy  functions  under the most favorable circum-
stances, and functional derangement is at once induced by articles of
diet which most persons digest  with facility.   This functional de-
rangement may manifest itself by  various symptoms of indigestion,
by disturbances of circulation aud of other  physiological symptoms,
but especially  by deposits of lithic acid, lithates, and  pigments in
the urine."  I am by no means a votary of this belief in the dogmatic
and limited form in which Murchison  has  stated it, but I am  thor-
oughly convinced that lithsemic neurasthenia bears some relationship
to a  condition  of  mal-excretion, because  a large proportion of the
cases occur in individuals whose urine will be found to  contain undue
quantities of the amorphous urates and uric acids and whose stools
are defective in quantity and  proper bilious  coloring ;  because  many
of these individuals are  of  rheumatic diathesis, and the  English
writers state that  abroad these individuals are generally of gouty
predisposition,  which is by no means generally the case in this coun-
try ;  because many cases can  never be successfully treated  unless this
defect of excretion is  remedied partially or entirely; because  some
simple cases will end  in  perfect recovery  with  no  other treatment
than this;  and because the cases often follow an attack of malaria,
or occur in malarious individuals  at malarious seasons of the  year.
But Murchison's theory of lithsemia is too radically wanting in pos-
itive proof for  us to accept it  in its nakedness, or to do more than to
use the term as a convenient clinical designation  for a  certain group
of symptoms.   At the outset it should  be  understood that the name
lithsemia is a  misnomer,  because it is a pure assumption to say that
uric acid is to be found in the blood in this  condition, as it has never
been demonstrated, although  it is an undoubted fact that it is found
in the blood of gouty  people.   The older name of lithuria  was un-
doubtedly  a better one,  but a still  better  one would  be  lithoidosis,
meaning a lithic-acid-like  diathesis, as more comprehensive and less
dogmatic and more permissive of future developments.  The theory
that uric acid is a product  of sub-oxidation relatively to urea has been
met by  the fact that in birds and certain  reptiles,1  representing the
maximum  aud minimum of the  oxidative processes  in  the living
series, uric acid is to be constantly found in the urine, taking the place
of urea.   As a remarkable demonstration that oxidation can be no
great factor in  the production of the phenomena  with which uric acid
is associated is the further  fact that gout has been found in these two
oxidative extremes—birds and  reptiles.2  Megnin and  Bertin found
numerous urea crystals in the joints of parrots. Andriualdi saw chalky
deposits in the claws of hawks.  Pagenstecher, examining an alligator
sclerops five days after death, found deposits of urea and soda in all the
muscles, also free uric acid in  the hip-joint, the chemical analysis
being made by Prof. Carius.   Liebig saw uric-acid crystals in  great
number  in the muscles of another alligator.  Foster's conservative
  ictum upon  this  subject would seem  to  be the only one warrant-
1 Foster: Text-book of Phvsiologv, 1880, p. 452.
2 Ebstein : Die Natur und Behandlung derGicht.  Wiesbaden, 1882. S. 51. 
456
NEB VOUS DISEASES.
able:  "All the facts  known go  to show that  the  appearance of
uric acid is  the  metabolism slightly diverging from that leading to
urea;" nor does  the  assertion that the excessive formation of uric
acid is  due to functional disease of the liver rise above the dignity
of a pure assumption.  The source of uric  acid is not known. Von
Schroeder extirpated  the kidneys in  fowls  and reptiles aud  ligated
the aorta and  vena cava in  fowls, and still uric acid was found in
considerable  quantity, thus  demonstrating  that it was not produced
in the kidneys.  Meissner regarded the liver as the main  formative
organ, although he admits that the spleen and the nerve-centres take
part in the phenomena ;  but Meissner's experiments are lacking in
the crucial test of the elimination  of the liver, and simply demon-
strate the presence of large and constant quantities of uric acid in
the livers of  birds.   Ranke maintains that the  spleen  is the chief
producing organ.  Robin, Chrzonscensky, and Colasanti  believe that
uric acid originates  in  the  connective tissue.  Haig would have us
believe that uric acid  is constantly formed in the blood, to be excreted
when this becomes alkaline, and to be deposited in the joints and
tendons when this is acid, these alkaline and acid alternations occur-
ring daily.   But Sir William Roberts, as  has been said, seemingly
demonstrates that  uric  acid  is  due to  the decomposition  of  the
quadri-urates in  the  urine, and is  not found  in the blood.   If any
conclusion can be  drawn  from  these differing  experiments, it is
that the production  of  uric acid is  not monopolized  by  any  one
tissue, but that the  spleen, the nervous  system, the liver, and  the
connective tissues all  have their share in the formation of it.   Let
this aspect of  the matter, however, be decided as it  may—let uric
acid be  formed in one  organ or  in all organs—the  question still
confronts us :  Is it a cause or an effect ?   It is a familiar fact that
Claude  Bernard  produced  diabetes by irritating the diabetic centre
in the fourth ventricle.   Hence the possibility of diabetes  being of
nervous  origin is demonstrated, and the clinical features of many
cases are such  as to render  it extreemely probable that they are  due
to an affection  of the  nervous centres. Certain it is that  in the whole
vast range of  medicine there is nothing that has  been  more conclu-
sively demonstrated, clinically and post mortem, than  that  the ner-
vous system has a powerful  control of muscular action.  Atrophy of
muscle, conversion of muscular tissue  into fat, cutaneous eruptions,
sloughs,  ulcers, tumefactions of joints and serous  effusions into  and
around them, trophic changes in bones leading to  atrophy and frac-
tures—all these are phenomena that are now known beyond question
to arise from the diseases of the nervous system.   It seems absurd to
question that the agency which is capable of so radically perverting
cellular  action  is not also capable  of effecting so relatively slight a
cellular  change in some  tissue or tissues as  to lead to the production
of uric acid.   A priori, then, uric acid in so-called lithsemia  may be
a product as  well as it can be a cause, and it is a matter of great  im-
portance that this aspect of  the question should never  be  lost sight
of in the therapeutics of lithsemic neurasthenia.   Indeed, no one  has
yet pointed out what the normal amount of uric acid is in the urine, 
THE NEUBOSES.
457
and, therefore, no one  knows what an excess of it is;  and it is a
common observation to find the nervous symptoms altogether dispro-
portionate to the quautity of uric  acid discoverable in the urine, as
well  as to observe  these nervous  symptoms obstinately persisting
after the excretory  organs  are acting freely, or to have certain ner-
vous phenomena, notably the vertigo, increased by  the efforts made
to stimulate excretion.   If I may formulate conclusions based upon
many years of treatment, the most  frequent cause of lithsemic neur-
asthenia is functional derangement of the gastro-intestinal tracts—in
other  words, of  the  stomach and the  small  and large intestines—
and of the associated  glands,  the  liver, the pancreas,  the spleen,
and the gastro-intestinal glands, so  that measures  addressed to de-
fects of gastric or  intestinal digestion  or to increased  excretion of
the associated glands practically bring the  most success.  In some
rare  cases, too, sluggish  action  of  the large intestine  is alone at
fault.
  I have made  but two autopsies in cases of neurasthenia, and in
neither of these  cases was there anything discovered by microscopic
examination of the  brain, spinal cord, or peripheral nerves, and in
neither case was  the death due to the neurasthenia—resulting in one
from  an  intercurrent pneumonia, and in the other  from  trauma.  I
have, however, known of three cases of death from pure neurasthenia
in which  no autopsy was made.  I have myself made six autopsies
in cases that were improperly diagnosed as neurasthenia, and in which
the findings  were  respectively  aneurism  of the arch  of the aorta,
nephritis, cerebral hemorrhage in the early stage of general paresis,
enormous atrophy of the large intestine and of the spleen, Weil's dis-
ease, and fatty heart. I have also made autopsies in cases with hyster-
ical symptoms misinterpreted as neurasthenia, with different findings
that are detailed  under " Hysteria."   Neurasthenia of the simple, the
reflex, or the  lithsemic form is one of the so-called functional diseases ;
i. e., the pathological alterations are either  cellular or vascular in so
slight a degree that their exact nature has not yet been determined by
the aids to investigation  that are at our disposal  in  the present state
of knowledge.   It is idle to speculate as to whether they are  vaso-
motor or cellular, in the sympathetic uervous system or in the cerebro-
spinal, because we have  no data upon which  to  base any intelligent
conclusions.  The older writers of a  quarter of a century ago  wrote
very glibly about cerebral and spinal hypersemia and ausemia; but in
Chapter VIII., "Hypersemia and Ansemia of the Brain and Cord,"
I attempted to demonstrate that these supposititious vascular disturb-
ances  belong  to the  metaphysics of  medicine.   We should, however,
grasp clearly the fact that the nervous system can itself be in an as-
thenic condition, and that such an asthenic condition can also be pro-
duced by reflexes and by vascular disturbances.  Just as a nerve or
a spinal cord can be fatigued  by  repeated discharges of electricity
through either one of them, or just  as we constantly  see that  the
human cerebrum can be fatigued  by excessive functionation  of it,
so can we easily conceive  that  the whole  cerebro-spinal nervous
system or the whole sympathetic nervous system, or both, or either, 
458
NEB VO US DISEASES.
or parts of either, can become asthenic; but  precisely wherein  this
asthenia consists,  what cellular alterations compose it, whether  it is
the protoplasm of cells or the nucleus or nucleoli that become affected,
or whether, indeed, the cellular constituents of the peripheral nerves
may become altered—this is all an  undetermined field of investiga-
tion.   I see no  reason to doubt that the same cell that can become
organically altered can also become what we call functionally altered,
so that the  pathological alteration which we call general paresis or
poliomyelitis or peripheral neuritis may have its functional analogue
in cerebral, spinal, or peripheral  neurasthenia, with this difference:
that the  cell which is originally altered in its molecular constitution
cannot be made to return to the normal so readily by reflex influences
from other organs and from the surrounding outer environment as is
the case with the functionally impaired cell.   Extremely interesting
in this connection  is Hodge's demonstration of the difference between
the brain-cells of  a  homing pigeon that had  returned from a long
flight and those of another that had been kept in a coop.
   Causation.  Whatever may be the real pathologieal nature of
lithsemic neurasthenia acting as a predisposition, it  is often provoked
by extrinsic causes, such as—
       Changes of the weather;
       Fatigue, mental or physical;
       Special articles of diet;
       Certain wines;
       Improper clothing;
       Malaria.
   Iu my experience most of the relatively acute outbreaks are apt to
occur in  the spring or early summer, much  more frequently, singular
to say, than in the autumn.   In  some  there is especially apt  to be
trouble at the first onset of hot weather.  In our middle and northern
States  the  spring is a very uncertain seasou, the gradual rise of  the
thermometer  being  frequently interrupted by  quick and violent
changes  back to a wintry temperature  until the latter part of May
or early  in  June,  when the  heat may suddenly reach 85° to 90° or
even more, and then merge into moderate summer.  The changes  are
not apt to be so violent in the autumn, and when they are, the change
is from warm weather to cold,  which does not  have so great au effect
upou this form of neurasthenia.
   Fatigue,  mental or physical, is a very  frequent cause,  aud will
often bring back the nervous symptoms.
   Many patients  of  this  class have  an idiosyncrasy  about special
articles of diet or certain wines—far less, in my experience, about  the
former than about the latter.   Thus the fact to which  Dr. Wra.  H.
Draper has called  attention, that the gouty cannot digest starchy and
saccharine matters, is true to a certain extent.   Of  these individuals
some  cannot digest sugar, some cannot digest starch,  but the most
fail to digest more thau a moderate quantity of one or the other; and
I have never met  those deficient in the capacity to  digest both starch
and sugar.   Others again  cannot digest meat  during hot weather as
well as in other portions of the year.  Still others again cannot  digest 
THE NEUBOSES.
459
eggs.  The sweet wines, champagne, Rhine wine, burgundy, and the
malt liquors are generally borne badly.
  Improper clothing will, in some nervous systems that have become
susceptible, often bring about a return of the  nervous symptoms in
an incredibly prompt manner, and this applies not only to too much
clothing in warm  weather and  too  little  in  cold weather, but to
clothing that is not  made to follow the sudden changes  that  may
occur from day to  day in  our variable climate.   I have known an
alarming dizziness or a neuralgia to  disappear in a few  minutes by
the substitution of a thin for a thick coat on a hot day, or the reverse
on a cold day.  The curious thing is that this need for a  change of
clothing is often not  betokened  by a subjective sense of heat or  cold
or any alteration in  the bodily temperature, although in some cases
patients come to know by experience that the weather is  becoming
warmer by a feeling  of nervousness and chilliness.
   Malaria is often  ascertained to precede this affection, and the in-
efficacy of antiperiodics in some cases of so-called latent malaria is
often due to the non-recognition of  the presence of this  lithsemic
neurasthenia.
   Prognosis.   The prognosis of neurasthenia is  excellent,  with
proper treatment.   Indeed, the majority of cases themselves tend to
more or less imperfect recovery, although  there is a handsome  pro-
portion in which improvement does not take place without treatment;
but I have found that severe nervous disturbance beginning in the
late  spring  or  early summer,  especially of the  lithsemic variety,
cannot be overcome before the autumn, and  when the  tendency to
neurasthenia is once  established recurrences are frequent, especially
in the spring, and it often becomes hereditary.
   Diagnosis.  In every case of neurasthenia that is  brought to  us a
careful examination should be made of the urine, in order to deter-
mine whether there is present the so-called lithsemic uriue or whether
there are evidences of nephritis.  Careful search  should also be made
for possible reflex causes, such as lesions of the  naso-pharyux, marked
errors of refraction, exophoria, cardiac disease, hepatic disease, intes-
tinal disease, malaria, marked lesions of the uterus aud its appendages
in the female, of the bladder and the urethra in the male, or the pros-
tate in the elderly male, and for any peripheral nerve-lesions.   Care
should be taken, however, not to attach undue importance to any of
these causes unless  the onset of neurasthenia has  been coincident with
the beginning of one of these  lesions, or unless it has been shortly
subsequent to them.  In cases where the history  is defective as to this
chronological sequence, it should always be borue in mind that neur-
asthenia may coexist with these  affections and yet be capable of being
relieved without treatment of them—often aggravating them, indeed.
The diseases with which neurasthenia  may  be confounded are :
       Hysteria ;
       Migraine;
       Angina pectoris ;
       Chorea;
       General paresis; 
460
NERVOUS DISEASES.
       Nephritis;
       Brain-tumor;
       Certain non-insane delusional conditions often associated
         with  hysterical tendencies and morbid fears;
       Melancholia;
       Certain mild chronic insanities;
       Locomotor ataxia;
       Myotonia;
       Malaria;
       Progressive muscular atrophy, especially of the  neuritic
         form ;
       Traumatic neurasthenia;
       Meniere's disease.
  In severe cases of hysteria the characteristic limitations of the field
of vision, the ansesthesia or the hsemiansesthesia, the convulsions and
the emotional  conditions, are symptoms  of great  importance in the
diagnosis.   In the milder  forms of hysteria the  diagnosis is often
difficult, and it may be impossible to make it without careful observa-
tion for  a few days or more ; but the tendency to exaggeration, the
variability of the symptoms, the emotional  conditions  which have
dated back for years before the onset of the neurasthenia, and which
are not in proportion to the amount of neurasthenia, the caprice that
shows  itself in a myriad ways, are symptoms that are in sharp con-
trast with  the steadiness and persistency  and  unemotionability of
the neurasthenic phenomena.  As  has  already been said, however,
it should never be forgotten that the neurasthenic  may become emo-
tional ; but in such cases the emotion is temporary aud superadded to
the steady and  persistent substratum of continuing  neurasthenia.  In
some cases it may happen, too, that neurasthenia and hysteria may be
combined, and in such cases the characteristic symptoms of hysteria—
the limitation of the field  of vision, the  ansesthesia, and  the hemi-
ansesthesia—will be conjoined iu all their kaleidoscopic  variety with
the obstinate  and enduring neurasthenia.   The most brutal of all
mistakes, however, is the confounding of neurasthenia with hysteria.
This latter disease is too often thought to be what  any  other disease
is not—is too often the refuge of a moral cowardice that cannot look
a doubt squarely in  the face; and  how often is this so  in lithsemic
neurasthenia, with its vertigo, its sense of distention about the head,
its tinnitus aurium, its  undue susceptibility to odors, its  nervousness,
its slight insomnia, its peculiar neuralgia or perverted sensations, its
vasomotor disturbances, and often its outward  appearance of ruddy
health?  It provokes  a smile, too, to  see how  often  the sufferers
themselves are deceived,  even when  they are medical  men.  An
apologetic air  or a deprecating remark is the  common prelude to the
history of the  symptoms.
  There are certain  families iu which migraine or sick  headache  is
found in several successive generations, especially in the  female mem-
bers.   Not  infrequently in these individuals loss of consciousness
will take the place of the migraine, so that the two functional  affec-
tions may be interconvertible ; in others, associated with the migraine 
THE NEUROSES.
461
there may be symptoms simulating mild angina pectoris; still others
may  occasionally  have marked hysterical  symptoms;  and  in  still
others nervous  symptoms may run  the gamut of these and other
forms of functional disturbance.  All the individuals of this migraine
group are possessed of great nervous energy, and some of the finest
mental work of the world is done by them ; but it would be a great
mistake  to  confound  these symptoms with those of neurasthenia
although persons of this class may have the latter malady, notwith-
standing that they are no more subject to it than other people.
  It  is by no means so rare as one would expect that cases of general
paresis are  diagnosed as neurasthenia,  for the early symptoms of
this gradual, insidious, remittent, generalized interstitial encephalitis
are often so fugitive and changeable that it is scarcely to be wondered
at that their true significance should be occasionally overlooked.   In
general paresis, however, the dementia is a characteristic symptom
from the very beginning, coloring all the symptoms, however slight
they  may be, in a way that can  always  be detected by the  careful
examiner or observer; besides which, there are in the early stage,
the peculiar tremor of the face, tongue, and extremities,  the charac-
teristic difficulties  of pronunciation, the pupillary abnormalities,  and
the history of exacerbations, in which there are marked vasomotor
symptoms, and in  which the tremor, speech-defects, and the pupillary
abnormalities become temporarily increased.   In some few cases of
general paresis in  which the course of the disease is without exacerba-
tions and is persistent, the dementia is usually more marked ;  but the
symptoms we may lose for diagnostic purposes are more than atoned
for by the presence of this latter.  When general paresis has advanced
to the stage of delusions, they are always stupid  and illogical, so-
called unsystematized  delusions, aud  in some non-typical cases these
are present from the outset.
  If a case of nephritis be accompanied by oedema, either general or
limited to the eyelids and  ankles, the diagnosis can usually be made
without difficulty; but in certain cases of chronic nephritis, especially
of the cirrhotic form, repeated and careful chemical and  microscop-
ical examinations of the urine should be made.
  Certain non-insane delusional conditions, such as the morbid fears
of places and individuals, or the  semi-insanity which is known as
insanity of doubt,  have been classified  by certain authors under the
heading of neurasthenia, and this is where Beard catalogued  them ;
but if we are to accept the ordinary symptoms of neurasthenia as the
type of the disease as I have already given them, these semi-insanities
belong rather to the group of mental disease than  that of neuras-
thenia, and I have put them under the head of functional insanities.
  In  brain-tumor  the headache is  often violent and persistent, or is
at all events something more than a mere sense of fulness.   Neuro-
retinitis may be present, while I  have  never  seen  it in lithsemia,
although Da Costa claims that he has;  but I think he has mistaken
some  organic form of cerebral  disease for it.   Vertigo is seldom so
marked, and seldom occurs in such paroxysms; although in certain
cases  affecting the cerebellum or  its peduncles it  may  be equally 
462
NERVOUS DISEASES.
pronounced, but it is then that of a marked backward, or forward, or
rotary character.   When vomitiug is present it is of the sudden, ex-
plosive, seemingly causeless cerebral type; and in most cases there
will be some evidence of structural lesions of the intracranial con-
tents, such as paralysis of motion or sensation, aphasia, hemianopsia,
word-deafness,  or mental alterations.
  Many cases of simple melancholia are unaccompanied by illusions,
hallucinations,  or delusions, and simply manifest, especially in  the
early stage, the  melancholic tendencies—which are usually distin-
guished  from  hypochondria  with  ease,  because  in the latter  the
patient is querulous, seeking  new remedies and new physicians, the
disease lasting  usually many years;  whereas melancholia comes on
in a few  weeks, the simpler forms have an average duration of about
a year (unless treated properly, when they are usually much shorter),
and the patient is utterly indifferent about himself.  The melancholiac
has, moreover, a peculiar fades, which I have described  in the section
upon "Melancholia," of mixed suspicion and  suffering, to which may
be added, as the result of the impaired cerebral reflex, an expression
of bewilderment, which latter mental  condition,  if not evident at
first sight, may be elicited  by careful questioning, as the patient will
state  himself that he has been sometimes confused  in his thought, or
is unable to grasp quickly the meaning of remarks addressed to him,
or to respond to them  readily.  Besides this, there is in melancholia
the post-cervical ache, the obstinate insomnia, and the inherent ten-
dency to  suicidal impulses.   I have never seen delusions, illusions,
hallucinations,  dull  cerebral reflex, post-cervical ache, or  obstinate
insomnia in a case of neurasthenia.
   In some forms of insanity running a very mild and chronic course
it is possible to confound the symptoms with those of  neurasthenia,
especially when the hallucinations or delusions are concealed, and I
am always very suspicious of any patient  coming  to my office alone
and complaining of symptoms of cerebral exhaustion.  A  careful
history of the  patient from friends or relatives will, however, make
the diagnosis clear, and thus avoid the mistake of diagnosing a case
of acute or chronic paranoia or the early stage of a subacute mania as
one of neurasthenia.
   The early stage of locomotor ataxia is sometimes confounded with
neurasthenia.   Physicians are  not generally aware that the early
symptoms of this disease are  often of a purely sensory nature, and
that  the  ataxia may belong to the later stage.  The lightning- and
stabbing-pains, severe, sudden, seldom  fixed  in any one part of the
body; the peculiar pupil described by Argyll-Robertson—contracted,
irresponsive to light, only feebly responding to movements of accom-
modation ; the loss of the knee-jerk; the slight vesical troubles;  the
ataxia when present;  and the frequent atrophy of the  optic nerve:
these early symptoms  of locomotor  ataxia may be overlooked unless
they  are specially asked and looked for.
   It is  by no  means  unusual in my experience to see cases of pro-
gressive  muscular atrophy confounded with  neurasthenia.   Modern
observation, more particularly in the last ten  years, has done away 
THE NEUROSES.
463
with the old doctrine that progressive muscular atrophies commenced
in the thenar and hypothenar eminences (see section on " Progressive
Muscular Atrophy")   As  a matter of fact, most  of them begin in
the  muscles of the limbs, the shoulder-girdles, or  the  truuk, and it
is sometimes a very difficult matter to determine as to whether there
is an actual atrophy.  Thus, when the patient complains of a vague
loss of strength and vague  aching pains, such as are apt to occur in
the  neuritic forms of muscular atrophy, it may be very easy to over-
look the malady unless the patient were stripped and  the different
muscles and their outlines and the contours of the different muscular
groups were keenly observed.
  Iu traumatic  neurasthenia the history of the trauma will be of
crucial importance ; and then the tendency to emotionalism is greater
by  far than occurs iu ordinary or lithsemic neurasthenia.
  Meniere's disease has a predominance of aural symptoms of great
variety (see section on "Meniere's Disease"), to which may be added
a neurasthenic condition ;  whereas  iu  neurasthenia the most  pro-
nounced aural symptom, often absent, is a tinnitus aurium, which is
not explained  by any lesion of the external,  middle, or internal ear.
  Treatment.   The treatment should vary accordingly as the case
can be classified under reflex, lithsemic, or simple neurasthenia.
  In the reflex form careful attention should  be paid to the removal
of  the reflex irritant so far as that may be possible; but, as  I have
already said, one should  not be too hasty in  reaching the conclusion
that a coexisting minor trouble  of a  non-nervous organ is the sole
cause of neurasthenia, for it has been my experience that the  purely
reflex form—that is, neurasthenia entirely due to a reflex irritant—is
rare, whilst the majority of these reflex cases are caused  by a reflex
irritaut acting iu conjunction with other causes;  and it often hap-
pens that, on the one  haud, removal  of some reflex irritant has a
slight effect or none upon the neurasthenia, whilst in others the neur-
asthenia may be completely removed, although the supposed reflex
irritant remains.    Treatment should be  addressed,  then,  to any
marked lesion of the nasopharynx, of the heart,  of the kidneys, of
the stomach, of the male or female  genitalia, of the eyes, or of the
ears.  If then the neurasthenia  persists, or if the supposed reflex
irritants are really slight affections, the neurasthenia should itself be
treated.
   In the so-called  lithsemic variety the treatment has been for over
a decade a source of great  perplexity to me,  aud it has only been of
 late years that I have gradually settled down into a routine which
 has been  justified  by the  large percentage of success that  it has
 insured.  First of all, I divide  my cases of lithsemic  neurasthenia
into two classes: those that are sthenic, and those that are asthenic.
 In  the former I begin by giving them  a drachm of  Carlsbad salt
 in  a half-tumbler of tepid water every morning before  breakfast,
and I also  then  give  them a glass of Vichy, three or four times a
day, about two hours after  meals.  I pursue  this treatment for three
 or  four days aud watch the  results.  If the patient improves rapidly,
 I then continue  the Vichy, and also give a laxative in such doses 
464
NERVOUS DISEASES.
as to cause  at  least two easy,  feculent stools in the twenty-four
hours.  The best laxative for this  purpose is the cascara  sagrada
which I order to be taken  in sufficient doses to attain the effect  I
have spoken of, and this is  usually done  by either the solid extract
in 2-grain doses, one to three times daily, or  the fluid  extract in
drachm doses the same  number of  times.  My rule is to have the
patient determine whether one  or three doses a day  are necessary,
so that he  may commence  by taking  the first dose  at bedtime,
and,  if that does not give the desired  movement, take the second
one between breakfast and  the mid-day meal, the next between the
mid-day and the evening meal, and whatever dose they find neces-
sary they are directed to continue using.  Occasionally calomel, 3 to
5 grains at bedtime with 10 to 15 grains of bicarbonate of soda, will
assist materially; but I  never use calomel continuously, because, for
some reason that I  have never  understood, it is apt to increase the
vertigo, the nervousness, and sometimes even to weaken the patient,
this  latter result  being  often  observed  with small doses.  If this
treatment does not have a happy effect, I then discontinue the alkali
altogether, and use nitro-muriatic acid, 20 drops three times a day in
a wineglass  of water just after meals, taking care at the same time
to continue the laxative.   Sometimes the acid will do best, some-
times the alkali, although it is generally the latter, and I know of
no  means  of  determining  beforehand  which  will  be  best.   If
neither the acid nor  the alkali, with  the laxative, cause improvement,
or if they cause only a partial improvement, I then begin to probe
the intestinal tract, as it were, and this I do by the use of  the diges-
tive  substances or the intestinal antiseptics, such as salol and uaph-
thalin.   Salol should  be given in  the form of compressed  tablets,
tablet triturates, or  capsules, in  doses of gr.  ijss. three times daily,
although occasionally gr. v. may be needed  at the same  intervals. If
the patient has difficulty in the digestion of nitrogenous substances,
evidenced by flatulence or discomfort immediately after meals, I use
pepsin ; or pancreatin if the symptoms of indigestion appear an hour
or two after meals;  or salol or pancreatin if  the stools are lumpy,
or irregular, or sometimes hard and sometimes loose, or if there is great
flatulence.   If I can obtain no evidence from the patient's statements
or symptoms as to whether the stomach or  small or large intestine is
affected, I am not by any means debarred from the use of these sub-
stances, for experience has shown me in many cases that there may be
functional conditions of  these various portions of the intestinal tract
that are reflex irritants, although they may produce no localized symp-
toms, so  that in such cases I systematically use first pepsin;  then, if
that  does not effect any relief, pancreatin ; and then, if that in its turn
brings no amelioration of the  symptoms, salol or naphthalin.  The
pepsin should always be of an  indubitable make, and should never be
given with alcohol, except possibly in the form of some light wine, and
in many cases it cannot be given with an acid, contrary to what is often
advised by therapeutists.  If pancreatin is  used, it should also be of
an indubitable make,  because with both  pepsin  and  pancreatin I
have  found, as has been shown again and again by experiments, that 
THE NEUROSES.
465
many of the preparations on  the  market are absolutely inert.   If
neither the pepsin nor  the  pancreatin  have brought any relief, I
then use salol in 2J  to  5-grain doses in capsule, tablet triturate, or
compressed tablet, three times a  day for a few days.  If this also
proves useless,  I  use  naphthalin, which I administer in a carefully
made suppository of cocoa-butter with about three drops of castor oil,
having the patient insert one  of  these  morning  and evening, great
care being taken that the cocoa-butter is  fresh and soft, so that it will
melt readily at  the  temperature of the rectum.   By the use of the
alkali or acid with laxatives, or by the  use of one or more of these
digestives, I succeed in the majority of the sthenic cases.   In these
patients I also  regulate the diet, and in this I  am  guided by  the
patient's statements as to whether they  can  best digest the meats or
the farinaceous substances and the vegetables, so that if I find any
difficulty in the digestion of any one of these three classes, I restrict
the amount of the offending articles, or prohibit  them entirely for a
short time.  It is a curious fact, though, that most cases of lithsemia
in any form will not bear the reduction in diet well  except for a
short time, and in none of the forms have I ever seen any difficulty
of digestion of fatty substances of food, and in many cases not even
of fatty medicines, such as cod-liver oil.  In addition to these me-
dicinal and dietetic measures  I regulate the exercise, but  very cau-
tiously at first.   In some  I have the  patient take a walk  regularly
once or twice a  day within bounds far short of any fatigue, or I may
have him ride on horseback, or I may  send him  to the gymnasium
to have gentle  gymnastic exercise under the care of some  medical
superintendent, or, if he is not accustomed  to walking or  riding far
enough to  be a long time in the open air, I have him take  a drive
for an hour or more every day; or, if this last is  not within his
means, I have him wrap himself up as if for a drive, shut  the doors
of his room, open the windows top and bottom, and sit quietly in a
chair for an hour  or more.  Indeed, I may say that in all these cases
of neurasthenia I believe  that fresh  air is relatively of much more
importance than  exercise, and exercise  is always a failure  if it  be
followed by fatigue.   In the asthenic cases of lithsemic neurasthenia,
however, my treatment is  very different.  In them I  use the acid or
the alkali sparingly for a short time and with caution; I am very
careful not to weaken the patient in the slightest degree by a laxa-
tive, and I seldom use the pepsin, pancreatin, salol, or naphthalin—
for in these cases, plus the peculiar symptoms which have been called
lithsernic, and overshadowing them, are the signs of true neurasthenia,
and the treatment should always  be that of true  or  simple neuras-
thenia.
   In this latter form the restriction of the expenditure of energy, or,
in less scientific terms, rest, is  the keynote of my  treatment, and with
this I conjoin a superabundance  of nourishing food.  I restrict the
expenditure of energy according to my judgment of the needs of the
case.  This seems like a very simple statement,  but  the application
of it is often a very difficult matter, calling  for much experience aud
nice powers of  clinical  perception.  In all  cases, however, where I
                               30 
466
NER VO US DISEASES.
am in doubt  as to  the  amount of rest  that should be ordered, I err
on the safe side, and prefer to give the patient too much rest rather
than too little, inasmuch as hundreds of cases have reluctantly forced
upon me the conclusion, against all the prejudices of my earlier medi-
cal training,  that too much rest can never do harm, while too little is
frequently the cause of failure.   I cannot emphasize this point too
strongly to express my fixed convictions.  If the patient is utterly
worn out, nerveless, incapable  of  any usual  exertion, I put him or
her into bed, if I can.   I say, if L can, because there is a great differ-
ence in this respect  between the two sexes, for it may be said in gen-
eral terms that it is only too easy to get a woman into bed, and only
too hard to  get her out, whilst it is only too hard to get a man into
bed, and only too hard to keep him there ; so that it is often useless
to make the  attempt with a man,  whilst this may even be the case
with some women.   If I can keep a patient in bed for a few days or
a week, I then allow him  or  her to get up at noonday, and stay up
until an early hour in the evening, and, as  the case  progresses, I
allow them  gradually to  sit up to a later hour in the evening, and
then gradually to rise at an earlier  hour in the morning, although in
all these cases I endeavor to keep them in bed at least until noonday
for a period of ten  or twelve weeks, and, in some extreme cases, even
longer.   Many active business men in the  full  flood-tide of their
career  cannot go to bed,  however, and this is  sometimes  true of
women.   In such  a case I carefully inquire  into the necessities of
the patient's  life  and  his  habits, and exert my ingenuity to cut off
as much expenditure of energy as is possible.   There are a hundred
ways of doing this  in almost  everyone's life.   A man, for example,
may be able to cut  off just so much  expenditure of energy by riding
to his place of business and from it, going to  bed immediately after
his evening meal, and  rising late the next morning ; coming home
for an hour or so before his dinner, if  that be  in the  evening, and
lying down on a lounge ;  and staying in bed from Saturday evening
until Monday morning, and on holidays.  It  will be seen that in ail
this I have taken no account of exercise.  This  is another conclusion
to which  I have been  forced reluctantly by years of experience, in
the teeth of my earlier medical training.  I  have  seen again and
again that exercise  is not only not  needful in these cases of simple
neurasthenia, or in  the asthenic forms of lithsemic neurasthenia, but
that it is positively harmful, for the brisk walk or drive which may
exhilarate the robust individual will depress the neurasthenic and
increase his nervous symptoms.  Massage is a method of treatment
that has  come into vogue of late  years, with  more  credit than it
deserves in this form of disease, I think.  I have also almost entirely
discontinued  its use in neurasthenia for tw7o reasons : first, because in
the lithsemic patient it increases the nervousness and vertigo, and in
the cases of simple  neurasthenia it depresses whilst it is not at all
necessary.  In all these cases, however, as I have stated, I am a great
stickler for fresh air without fatigue, and this I obtain in the extreme
cases by having  the room in which the  patient lies flooded with air
without  a draught  whilst he is warmly covered; or, in  the cases 
THE NEUROSES.
467
 which can stand the fatigue of it, by a drive in the open air, but this
 should never exceed an hour or an hour and a half.   Unless the case
 of neurasthenia be extreme,  these  measures of rest will usually in-
 crease the appetite and the digestive powers so that excellent quanti-
 ties of food  will be taken without special direction from the physi-
 cian.  If this does not come about, however, I systematically feed the
 patient.  First, I take care  that  he has  three good meals a day  of
 well-cooked food  in great variety, not  permitting him to  limit him-
 self to any few special articles.   Good cooking is of quite as much
 importance for these people as is good food, although it is not neces-
 sary to have  all the arts of a chef or a cordon bleu, but simply that
 the food shall be  properly prepared and properly served.   I have
 again and again seen a patient whose nutrition had been a source of
 anxiety gradually take large quantities  of food that were prepared  in
 the proper manner.  After he has been taking the three meals for
 four or five days, I then order a  glass of milk every three or four
 hours, and this quantity  I rapidly increase, so  that  in  the course  of
 a week he shall be taking a quart  of  milk in the twenty-four  hours.
 At the end of a week or  ten days, to the milk and the three meals a
 day I add the equivalent of a  pound of beef in the form of beef-
 tea or beef-extract.  When  I  use the  former, I  prepare it  by the
 formula given below,1 or  I advise  one of the beef-extracts.   It must
 be borne in mind, however,  that  in  the  majority of cases beef-tea
 or a  beef-extract  can only  be  given for a  short time, as most
 stomachs revolt against its  prolonged use, and in most of  the cases,
 too, which are not extreme enough to  need rest in bed, beef-tea can
 be taken for only a few days.   Although  this is the rule, there are
 nevertheless  many exceptions to  it,  and  beef-tea or a  beef extract
 should always be  tried when needed.  Finally, at about  the tenth
 day I commence the  use  of a malt-extract, and for  this purpose  I
 prefer one of the alcoholic extracts, of which I give 2 ounces with
 each meal, or I use one of the freshly prepared non-alcoholic extracts.
 The treatment of  these  cases  of   simple neurasthenia, or  of  the
 asthenic forms of lithsemic neurasthenia,  should be continued for at
 least twelve weeks, and then the patient should keep up the dietetics and
 the medicines for such time longer  as the physician may deem neces-
 sary, but he well only need then the occasional supervision of the lat-
 ter.  The  tonics which I have found  most useful  in the simple and
 the asthenic forms and in the lithsemic variety are iron and the sul-
 phate of strychnine.   The iron should be  in the form of the dialysed
 iron, a drachm to 2 drachms  three times a day, or Dree's albumi-
 nate of iron,  a drachm to 2 drachms  three times a day, or the pep-
 tonate of iron, in compressed  tablet, 3  grains  three times daily, or

 reSiSi,!b!!mula J °Ye 1° Dr:Weir Mitchell's book On Fat and Blood-making, and if it serve my
 Donnd 15 rf g°£d ltead, as, U has myself for ten vears> both win be content.  Chop up one
 hvd?ophinrt „^ef'^ place lt; lna i)0ttle with one pint of water and five drops of strong
 in a can of w„tir at T^o £"xtUJ1 staD*ds onlce a11 niSht> and in the corning the bottle is set
 on to » 2f™»Iffu 11(£ ?- and kept two hours at about this temperature.  It is then thrown
 eivpn in lh  clotband strained until the mass which remains is nearly dry. The filtrate is
isTouintiJ ^tP°Atlons dail& If *,neL raw taste Prove verv objectionable, the beef to be used
scXa %h0asted.°,n one side, and then the process  is completed in the manner above de-
It shonirt vf    p th^s ma.de's for the most part raw. but has also the flavor of cooked meat.
«snould be seasoned to suit the palate of the patient. 
468
NERVOUS DISEASES.
ferratin, gr. iv.-viij., three times daily.  The dialysed and albuminate
of iron should be administered in a cup of water immediately after
meals.  The sulphate of strychnine  I  use in the  cases which I am
permitting to get up out of the bed, or in very asthenic ones in which
the rest can ouly be kept up for a limited time that is really insuffi-
cient, using  it in  these cases as an invaluable cerebro-spinal and
cardiac stimulant.  The dose should  be fa to fa grain three  times a
day, generally the  latter.   Occasionally cinchona  bark may  be em-
ployed, preferably in the form of the officinal elixir in half-ounce to
ounce doses three times a day, but  usually cinchona does  not agree
with  these cases.   Sulphate of quinine usually acts as an irritant  to
the nervous  system.  Electricity is a very valuable adjuvant in the
treatment of lithsemic neurasthenia in both its forms, and of the simple
neurasthenia—either by the faradic or galvanic currents.  The former
may be employed by a  modified  faradization, obtained by having the
patient place the bare  feet upon  a large electrode, and putting both
hands upon another large electrode, turning on a current just gentle
enough to be appreciated  by the  patient,  and continuing to increase
the amount gently as the patient  becomes less perceptible of its effect.
Where a patient is confined to the bed, a nurse or attendant may
gently pass two small electrodes (Fig. 71,  or the roller electrode, Fig.
80)  about three inches apart, with  a gentle current,  all  over the
body, taking fifteen  to thirty  minutes for the sitting.   This  is quite
as effective as stripping the patient,  putting  him or her on  a  lounge,
and going  through all the cumbrous procedure  of general faradi-
zation  that  is  generally  recommended   in  the  text-books,  besides
which  it is  a saving of  time of no mean  importance to  a  general
practitioner  who may  have to treat the patient in his office, or who
may  not  be  able to obtain a  proper attendant  to give electricity to
him at his house.  Galvanism should be  of the spinal cord  aud  of
the  brain.   In the former case, one large electrode (Fig. 68) should
be  placed at the nape of the  neck,  the other (same, Fig. 68) on the
dorsal spine, and a current of 3 to 5 milliamperes should be carefully
measured off by means of the  rheostat, and continued for from three
to five minutes.  Cerebral galvanization should be by means of  an
electrode (Fig. 67) at the nape of the neck, another one on the brow
(Fig. 69), and a  very moderate current of 1 or 2 milliamperes, rarely
3 milliamperes,  should be very gradually turned on and  passed  at
the  first  sittings for two minutes, then  for from three to five, takiug
the most extreme care not to move the electrodes or to jar the patient,
and then the current should be as carefully turned off.  Useful, how-
ever, as  faradism  and galvanism are,  there are  many  cases which
can be conducted to a successful issue without them.   The static cur-
rent  I  have never  found of much use except as a light aud pleasant
stimulant in the stage of convalescence, and then the electric air is
the most beneficial.
   It will  be seen  by all this that  I am no believer in  the heroic
methods  of treatment which  have  been so generally advocated  in
neurasthenia.   If I am  asked why I should  be  so dogmatic about
the matter, my answer  would be simply that my dogmatism has been 
THE NEUROSES.
469
forced upon me by a long series of mistakes in my earlier days, and
since I have reached my present conclusion I welcome cases of neur-
asthenia, whereas I formerly dreaded them.  Cutting down the diet,
violent exercise,  heroic doses of purgatives, especially calomel, re-
striction of food to one particular  article or articles, travel, diver-
sion of interest—have again  and again failed at  my hands.   I do
not mean, however, to  say that the  patient should be permanently
restricted from healthful outdoor exercise.  On the contrary, when
health is again established, I always  advise that exercise should be
systematically begun, taking care not to  have any fatigue attend it.
Observation has  convinced me that even this advice  must be cau-
tiously given, as  in these cases it  is  often years  before full exercise
can be taken  with  impunity.   Even  in cases which  have  been
brought to this successful point, and much more so in the ones which
have not been fairly restored, there are certain seasons of  the year in
which the patient should be very careful to avoid  any fatigue, and
these are usually the spring months in  the variable  climate of our
northern and middle States, and  the summer.  At these times the
patient, who has  thought that health had been restored, will be  often
completely discouraged  by a return  of the old symptoms, especially
in the lithsemic variety.  The best means of removing these will be
as much restriction of energy for a  few days as  is in  any way pos-
sible, with perhaps an easy laxative  and the use  of an acid or alkali
in the lithsemic forms.  In these slight relapses,  due to the weather,
it may often be advantageous  also to restrict the food for a day or
two, either by cutting off meat or by reducing the quantity of all the
food taken ; but this restriction should be only temporary, as continu-
ance of it may bring about, in its turn, a return of the old  symptoms.

                   OCCUPATION-NEUROSES.

  The term "occupation-neurosis" has been suggested by Gowers to
designate certain  curious muscular spasms of inco-ordination excited
by excessive use of certain groups of muscles in  certain occupations.
The German term is Beschdftigungs-Neurosen.  Hammond has coined
the phrase, anapeiratic,  from dvanecpdco, to do or attempt again; but
I think that  Gowers'  term is a simpler  one.  These occupation-
neuroses consist of writers' cramp, or scriveners' palsy;  pianoforte-
players'  cramp ;  violin-players' cramp;  seamstresses' cramp; teleg-
raphers' cramp; and smiths' cramp.   The  names indicate sufficiently
what they are.   In all  these the main symptom is muscular spasm,
although in certain cases there may  be neuralgic  symptoms and foci.
They are mainly  diseases of the active period of  adult life.  A neu-
rotic predisposition may be traced in some of them.  The predisposing
causes are  sometimes overwork and nervous depression,  but the
exciting  cause  is almost invariably actual or  relative overstrain of
the affected extremity.   In some cases the exciting cause may also be
a local disease or injury.
  The symptoms vary according to the muscles affected.  In writers'
cramp the muscles of the hand or the forearm are usually affected, 
470
NERVOUS DISEASES.
although the whole upper extremity may suffer.   According to some
authors,  this writers' cramp depends largely upon the way in which
the pen  is held, there being a greater predisposition to  it in those
who write crabbedly and  with  the  small muscles, using the little
finger or the wrist as a support.   I have, however, not been able to
find that this distinction is of  much etiological importance.  The
patient finds that his  hand  becomes  spastic and  tremulous after
writing for a time, so that  he  is unable  to  co-ordinate in the usual
free way.   This may  vary, of course,  iu  degree.    The followiug
specimens of handwriting will show the difference  between the first
writing and that which is done when the tired feeling come on.  In
other cases the  patient  may be absolutely unable to write.   The pen
cannot be properly held  or guided, slipping away with involuntary
rigid, tremulous movements that are very characteristic.   If the
patient is stripped and  the whole upper extremity is examined, it will
be found  that this is generally weak, and that when the physician's
hand is  grasped with the  utmost strength of which the  patient is

                             Fig. 162.
capable there is a  singular consentaneous movement of the muscles
of the upper arm aud shoulder that is relatively far too marked for
the amount of strength  that is manifested in the hand-grasp.  If
the sound arm is observed by grasping the hand iu a similar manner,
the difference  between the muscles of the affected and the unaffected
extremity can  be clearly seen.   The  muscular spasm and sensory
symptoms may extend to the muscles of the neck, and even to the
other extremity.   In some cases other co-ordinate acts than those of
writing can be done perfectly well; but in most there is some slight
awkwardness about any acts of  the  hand requiring continued co-
ordination.  In  pianoforte-players' cramp one finger or a thumb
may fail to  act in co-ordination with the rest of  the fingers, so that
it may remain  extended or not move in harmony.   In violin-players'
cramp the same affection may be met with  in the finger of either
hand, that which moves the strings or bows, and  sometimes in both. 
THE NEUROSES.
471
In seamstresses' cramp it is the thimble-finger of the right hand that
is most  often affected.   In telegraphers' cramp it  is the one finger
accustomed to tapping  the instrument that is most affected, and if
another finger is substituted for this, it may also become implicated.
In the cramp of blacksmiths or metal-workers various  muscles may
be affected, according to those  most used.   The  treatment of any
disease should be based  to some  extent, at least,  upon our knowledge
of the pathology ; and, as I have already said, we have no knowledge
of the modus operandi of the different forms of muscular cramp and
inco-ordination  constituting occupation-neuroses, except that  they
are caused in certain  individuals by actual or  relative overuse of the
affected muscles.  In writers' cramp Gowers states that the  majority
of cases occur in those who use the fingers alone iu writing,  and who
do not consentaneously  use the forearm and the upper arm, and he
therefore recommends that every patient afflicted with this malady

                             Fig. 163.
Specimen when the hand was tired.
should  lay the arm and forearm  upon  the table and write with the
wrist- and forearm-muscles  mainly, using the fingers only as  neces-
sary  guides.   My experience, however, has not  confirmed Gowers'
observations, for I  have not been able to ascertain that the malady
is prone to occur in those who  use the finger-muscles in writing,
nor have I found  that using the arm and forearm, as well as the
wrist and fingers, will be of more than temporary use in those who
already have the disease.   Indeed, I  have never been able to cure
a case,  although a  number have been reported  as  cured by other
observers.  I  have  in several cases made persistent use of galvanism,
faradism, and  the bromides, but have never observed more than tem-
porary  benefit.  A teacher of  caligraphy, named Wolfe, is said to
have cured a number of  cases, and  to have given  great relief to
several  others.  He entirely failed  in two cases of my  own.  His
method consisted of massage and gymnastic exercises of the finer
muscles affected.  In two cases I  have seen great  relief obtained
by entire disuse of the  affected  muscles so  far  as writing was
concerned, but in a number of other  cases abstention  for several
years has  proved  valueless.   I  do  not  believe, therefore,  that  a 
472
NERVOUS DISEASES.
patient  afflicted with  writers' cramp can  be treated  successfully.
This, of course, will often prove a great hardship to those who are
dependent for their living upon  the  use of the pen, and in a great
many instances the patient can do his writing quite as well with a
typewriter  or by  means  of  a phonograph, or can  learn to write
with the left hand, although  this  may also in course of time become
similarly affected.  The  sensory symptoms  which  are  sometimes
observed in writers' cramp can generally be greatly improved by
the use of galvanism, one electrode (Fig. 68) being applied to the
cervical spine, and another roller electrode (Fig. 80) being gently
passed over both surfaces  of the hand and forearm with a current of
5 to  10 milliamperes, in sittings of  five to fifteen  minutes every
second day for  a period of six to eight weeks.  Bernheim claims to
have cured several  cases by means of hypnotism, and suggests that
this is the modus operandi of the cures that  have  been effected by
Wolfe.   I have had no experience with hypnotism in treating these
affections, but I have seen one apprehensive girl cured of a piano-
player's cramp by placebos. 
CHAPTER   X.
   NERVOUS DISEASES OF PROBABLY MICROBIC ORIGIN.

                          TETANUS.

  Definition.   Persistent tonic spasm with violent exacerbations
of the muscles of the jaw  aud trunk, and secondarily those of the
limbs.
  Etiology.  The etiological factors of tetanus are—
      Sex;
      Age;
      Race;
      Locality;
      Injuries;
      Dampness and cold or extremes of temperature ;
      The puerperal condition.
  It occurs much more frequently in males than in females, the pro-
portion of the former being about six to one of the latter in the trau-
matic cases, somewhat less in the  idiopathic.
  Most cases  occur from ten to forty years of age, and it is seldom
seen  uuder five,  although  it is  occasionally met with in  old  age.
Tetanus  of  the  newborn is very common in  some tropical coun-
tries, especially among the  colored races, but it is rare in temperate
climates.
  The negro  and the East and West Indian races are more prone to
the disease than  the  Anglo-Saxon or  the  Latin  peoples, even where
both are exposed  to the same climate.
  Traumatism plays a considerable part in the causation of tetanus,
and it is said to be most  common after punctured, contused,  and
lacerated wounds  and  extensive  burns, whilst it  is uncommon after
incised wounds or surgical  operations.   Upon the southern shore of
Long Island, to which allusion is made in the following section of
this chapter, it is  supposed to be very common after gunshot-wounds
or mere  pricks, and especially after lacerations  inflicted by oyster-
shells.  The  interval between the injury and the first symptoms of
tetanus is usually from four to sixteen days, but  it may set in earlier
or later—in one case a negro cutting his hand with a piece of porce-
lain being dead  in  fifteen  minutes;  on the other hand, it  may not
commence till the fourth  or fifth week  afterward.   Injuries to small
nerves are  supposed to give  rise to it more frequently than injuries
to nerve-trunks, and it is said that it has sometimes followed such
traumatisms as flogging and falls.
  Beard called attention in 1877 to the frequency of tetanus upon
Long Island, which, as most Americans know, is an island about  120 
474
NER VO US DISEASES.
miles long, running southeastwardly along the shore of the Atlantic
Ocean, and forming by its western end a part of New York harbor.
He illustrates this frequency by showing  that whilst in New York
City tetanus  occurred once  in  about  30,000 wounds of all sorts, it
occurred  in this district of Long Island  once  in about every 200
wounds, or above  150 times as frequently.   The inhabitants were
prone  to attribute it to  the  use of fish  as manure.   Of late years,
however,  indeed for some time before Beard's paper, it would seem
to have been dying out.   Beard also states that tetanus is more fre-
quent  in Bombay, India, than  in any other part of the world, inas-
much  as  in  the Jejeebhoy Hospital during  seven years, from 1845
to 1851,  there were  195 cases of  tetanus admitted,  and 70 or 80
more were  attacked after admission, making 260 cases in all, this
being probably,  as the reporting surgeon remarks, the largest number
of cases treated in any hospital in the world.  The influence  of dif-
ferent  localities may be gathered from the following table taken from
Beard's article :
Locality and date.
Total deaths.
Bombay, India.......1851-1853
New Orleans, La. (whites and blacks) .    . 1847-1873
Charleston, S. O (blacks).....1846-1865
New Orleans, La.      .....1849-1850
Charleston, S. C. (whites and blacks) .    . 1846-1865
New Orleans, La. (whites)   .... 1849-1850
Nashville, Tenn. (whites, blacks and colored) 1838-1848
Charleston, S. C. (whites).....1846-1865
Augusta, Ga. (whites, blacks and colored)  . 1845-1866
Augusta. Ga. (blacks and colored) .   .    . 1845-1866
Savannah, Ga........1804-1853
Philadelphia, Pa.......1807-1827
Augusta, Ga. (whites).....1845-1866
Philadelphia, Pa.......1827-1830
New York........1819-1834
Philadelphia, Pa......1830-1840
Massachusetts.......5 years.
London, Eng........1850-3-4
Ireland........1831-1851
 42,651
165,435
 9,020
 3.336
 17,150
 14,306
Deaths
 from
tetanus.
 912
1727
 93
 34
 132
 96
8,880	39
10,884	34
4,240	19
14,332	58
53,004	125
6,645	15
16,579	29
83,783	112
49,686	51
104,823	75
224,515	73
,187.374	238
Proportion.
  46
  95.7
  97
  99.4
 130
 149
  80
 207.1
 320
 228
 2298
 424
 443
 573
 748
 974
1,907
3,075
4,987
   Exposure to  dampness  and  cold  may  be a  cause of  tetanus.
Napoleon's surgeon, Larrey, observed  both  iu Egypt and Germany
that tetanus did not often follow wounds unless there were extremes
of  temperature,  and  that  after the battle of Aboukir ten of the
wounded, on being transported  to  the hospital of  Alexandria, were
exposed to the cool night air and died of tetanus.   Francois relates
that on the frigate "Amazon," before Charleston during the American
war, most of those wounded by firearms were attacked by tetanus
when wet and stormy  weather had  succeeded a dry spell.  After the
battles of Bautzen  and  Dresden the wounded were exposed on very
cold nights,  and many cases  of tetanus  occurred.  Baudens relates
that while in Africa forty men  slightly wounded  were placed during
the prevalence of a  northeast wind in December on  the exposed north
side of  a gallery, and that out of these  forty fifteen quickly developed
tetanus and twelve died, while  the remainder were taken to a more 
   NERVOUS DISEASES OF PROBABLY MICROBIC ORIGIN.  475

sheltered position  and were  not attacked.   Kane  lost two men and
many dogs by tetanus in his North Pole expedition.
  The puerperal condition is a frequent cause of tetanus in hot coun-
tries, but  it is a rare one in temperate climates.  Of 50 cases col-
lected by  Gowers occurring in temperate climates, it occurred in 18
after abortion  and in 32 after labor at  or near full term—in most
of them there having been severe hemorrhage ; in 7 the vagina was
plugged, the interval between the abortion and the symptoms vary-
ing from  five to thirteen days.  Of the cases after labor, in all but 3
there was au  abnormal condition during  or after parturition, the
most frequent lesiou being  adhesion of  the placenta, which existed
in nearly  half the cases ; metritis  occurring  in 2, in association with
pharyngeal diphtheria  in  1, the forceps  having been used in only 1
case, in 1 there having been placenta  prsevia.
  Pathology.   Nicolaier has found that injection of the earth of
urban streets into  rabbits, mice, aud  guinea-pigs will often produce
symptoms resembling tetanus.   As Carle and Ratone have produced
a similar  malady in the rabbit by the inoculation of the products of
tetanus in the  human being, it has beeu deemed  probable  that the
same parasite is the cause in both  cases.   Rosenbach has been able,
he claims, to  isolate the same microbe  from individuals  dying of
traumatic tetanus.   In  inoculating the  powder of hay into guinea-
pigs, Rietsch  has  produced tetanus in animals; and the pus formed
at the point of inoculation has served to inoculate other guinea-pigs,
which died  with  the same symptoms as the first.  The pus  of the
second  series of guinea-pigs  has  been cultivated in serum, aud has
displayed the bacillus described by Nicolaier.  Oue of these cultures
was hypodermically injected into an ass, which presented, at the end
of fifteen days, all the typical symptoms  of tetanus in  animals,
namely :  trismus, opisthotonus, contracture of all the muscles  of the
face, of the dorsal and pectoral  muscles, and progressive rigidity of
the hind limbs, death supervening upon the twenty-fourth day.  The
pus and  the walls of the  abscess from  this ass were in their turn
injected into rabbits, causing the usual tetanus. Rosenbach has never
been able to obtain the pure  culture of Nicolaier's bacillus.  He
believes that  this  bacillus, which  is  localized in the wound, acts by
secreting a poison whose absorption produces tetanus.   From impure
cultures of this bacillus Brieger has  obtained tetanine, Cl3H30Az2O4,
producing tetanic  symptoms,  notably touic convulsions  and opis-
thotonus.   He has also obtained other products called tetauotoxine,
C5HuAz,  spasmotoxine, aud  diamine, which all produce cramps and
convulsions.  Beumer witnessed thedeath by tetanusof a man of thirty-
one, who  had wounded himself in the finger  with a splinter  of wood,
and also the death of au infant, who, walking barefooted, wounded
himself on the toe with a small  pebble;  and the  particles of earth
covering  these two objects produced tetanus and cultures of  Nico-
laier's bacillus. Beumer has  also seen  in  newborn children, who
died from trismus  at the time of cicatrization of the umbilicus, the
umbilical  wound  and the neighboring  tissue possessed  of tetanic
properties for animals, and giving virulent cultures.   Bonardi has 
476
NERVOUS DISEASES.
found  in  the  pus from a tetanic wound various microbes, such as
abundant cocci resembling the staphylococcus pyogenes aureus, bac-
terium termo, the bacillus pyogenes fcetidus, and  finally an unnamed
bacillus of some length, possessing a spore at one of its extremities.
He was not, however, able to obtain pure  cultures of these different
microbes.  Other  authors,  however, have obtained such pure cul-
tures of the long bacillus  with a spore,  and this  is regarded by
Nicolaier and Rosenbach  as  the true tetanic  bacillus.   Some doubt,
however, has been cast  upon the matter, especially by Kitasato. In
all cases of tetanus  observed by Cornil and Babes  the microbe of
Nicolaier was not found.  In another case of tetanus originating in
a double tuberculous otitis it was also absent.  In  the laboratory of
Fliigge, where  Nicolaier  did his work, it  was ascertained that, in'a
case of tetanus, caused  by  a wound with a splinter of wood, the
wood produced  tetanus in  animals,  but  neither the wood nor the
organs examined after  death, nor  the wound itself, contained Nico-
laier's  bacillus.   Fliigge  has  also reported two  observations of the
same kind.  Chantemesse and Vidal, working in the laboratory of
Cornil and Babes, have been able to isolate and to  cultivate in all
its purity the bacillus of Nicolaier from  the  wounds of tetanic men
and  animals.  These observers have  also ascertained that in a ward
where  tetanus  had often been small quantities of  dust taken  from
the  walls,  the  furniture, and  the iron  casing were all inert, except
one particular  dust containing  earth taken  from  the  grooves of a
window-grating.   The  inoculations  made  from the  organs  of a
woman dying with tetanus were  inert when injected into animals,
with the exception of that taken from the  mucous membrane of the
uterus, and this produced marked tetanic symptoms.  Chantemesse
and  Vidal have demonstrated  the marked diminution of virulence
in tetanic agents under  the influence  of air, light, and warmth; for
the earth which they took from the window-sill invariably produced
tetanus if inoculated immediately after  being found, but could be
rendered inert by being pulverized  on a sheet of paper and left for
twenty-four hours in the atmosphere of the laboratory.
  Clinical Symptoms.   There  are seldom prodromal symptoms,
and  when  they are present they  usually consist of vague pains in
the head.   The first real symptom that is noticed is generally a sense
of stiffness or rigidity in moving the head or neck or in swallowing.
This increases  until it  becomes difficult to  separate the jaws, and
there is what is known as trismus, due to rigidity of the masseters.
To  this  succeeds increasing  stiffness of the  neck, and  the head is
bent backward.   The  spinal  muscles  next  become  affected,  and
the vertebral column is bent backward, inducing the conditiou of
opisthotonus.  The extremities  are not affected  to the same extent,
although  the  legs may  become  stiff  and  extended.  The  facial
muscles are last  affected, and the angles  of the mouth  are  drawn
outward and downward,  and  the upper lip  is pressed against the
teeth, causing  the so-called risus  sardonicus.  The muscles are not
at first painful, but there soou supervene paroxysms of pain and
rigidity lasting several  seconds, during which  muscular spasm  may 
   NERVOUS DISEASES OF PROBABLY MICBOBIC OBIGIN.  477

be present to the most extreme degree of opisthotonus, whilst the
muscles of the face and abdomen are also  involved.  Exceptionally,
however,  the muscles of a limb  or of the throat may also become
involved.   In some cases the rigidity in the abdominal muscles and
the flexors  of the spine  may  bend  the  trunk forward  and cause
emprosthotonus,  or there may be  a  slight lateral  flexion, pleuro-
thotouous, or the trunk and neck become rigid, straight up and down,
producing orthotonus.  These  varieties  are,  however, exceptional.
Usually the  muscles  of respiration do not participate  in  the tonic
spasm, and when they do there is great danger of death.  The spasms
are usually  intermittent, and they  are absent in sleep.  Conscious-
ness is  never affected at  any time  throughout the course of the dis-
ease.  The pulse becomes more frequent and small.  The temperature
may be normal,  or may rise 2° to 5°,  and there may be an evening
rise or a continuous elevation, the latter without evening  remission,
although  there may be an increase of the bodily heat at each par-
oxysm and a moderate fall iu the intervals ; or there may be irregu-
larities of temperature that bear no relation to  the  symptoms.   In
some rare cases the temperature  may  rise  as  high as 108°, 110°, or
even 114°.   The urine is scanty  and high-colored,  although the
nitrogenous matter is not  increased  in quantity, contrary to what is
observed  in  the  urine of most  fevers.   Micturition is usually not
affected, except slightly during  the  paroxysms, but occasionally there
may be slight retention.   Moderate constipation generally prevails.
   When cases do not terminate fatally they gradually diminish  and
pass off in the course of a few  weeks.
   Prognosis.   The  prognosis  of tetanus is extremely  unfavorable,
the mortality varying from 70 to 95 per cent., and in the  mortality
of newborn  children it  is about 90  per  cent.  In  idiopathic cases
mortality is undoubtedly less than in the traumatic cases, but I have
found it impossible to make an average, because, in looking over the
literature ou the subject, in so many cases that have recovered the
diagnosis  has been a matter of doubt.   In 150 cases  that I have
seen myself death has occurred in 140.
   Diagnosis.   This can  be understood by reading the section upon
this branch of the subject in the following chapter upon " Tetany,"
which is the ouly disease that is likely to  be confounded with it.
   Treatment.  In  all the cases of tetanus  that I have seen com-
mon sense would dictate  that,  in view of the enormously increased
irritability of skin and muscle, the most sedulous attention should be
paid to keeping  the patient absolutely quiet and secluded.  The room
should be darkened, the attendants should move lightly and gently,
their dress should create no rustling noise, aud they should  wear soft
shoes or slippers, whilst all draughts  should be carefully excluded,
even to the motion of air that  may be created by the opening of a
door, at the same time that sounds should be deadened in every way
that human ingenuity can suggest.   Liquid nourishment alone should
be given, best by means of a tube  through the  mouth  or the nose  ;
but if this produces spasm, the nourishment should  be given by the
rectum.   Milk, preparations  of beef-tea, beef-peptonoids,  koumyss, 
478
NERVOUS DISEASES.
and alcoholic stimulants should  be used.   In  the  traumatic  cases
any irritable wound should be carefully attended to, and any irri-
table cicatrix  should be excised.  I can see no  use,  however, in ex-
cising a wound or a cicatrix unless  it is  irritable, because this  only
produces a fresh wound or a fresh cicatrix.  The drugs that should
be  used are chloroform, nitrite of amyl, bromide of potash, chloral
hydrate, belladonna, atropine, cannabis indica, aconite, Calabar bean
and curara.
  The most efficient treatment I believe to be that of a combination of
bromide of potash, chloral hydrate, and opium.   Of the former, the
commencing dose should be 3 drachms, and of the chloral  1 drachm;
and these should  be used every two or three hours,  and their effect
observed.   Should this not  be favorable, the dose of  bromide should
be  gradually increased  to  as much as an ounce, and the  chloral
hydrate to as much as 7 drachms,  but these  extreme  doses  should
never be given except with the utmost caution.   If moderate doses
of bromide and chloral do not control  the symptoms, it will  always
be well to try the effect of simultaneous employment  of opium in the
form of a hypodermic  injection  of J  grain  sulphate of  morphine,
and this must be  used  according to the judgment of the attending
physician.   Care  should always  be taken that the morphine has
been obtained from some perfectly reliable manufacturer, because the
morphine of the shops is too often entirely unreliable, either  for the
reason that it has been made from cheaper grades of opium or that it
has become stale.   If Calabar bean  is used, the dose  hypodermically
should be ^ to 1J grains, or by the mouth 1 grain  to 3,  and much
larger doses have been given, and in none of the cases does  it produce
the usual effect upon the pupil.   Atropine given at the same  time is
said to counteract the constitutional effects  of  the Calabar bean.
Curara  has been given in doses running from -j-j^- to f grain every
hour, but  it is a very dangerous drug to use.   Inhalation  of chloro-
form  is one of the most effective measures, but I have  usually pre-
ferred to use it only to control  the more violent  paroxysms, trusting
to the bromide, chloral, and morphine  for the continuous  treatment
of the disease.   Whatever drug be used should  be continuously ad-
ministered even after the patient greatly improves.
  Simmons suggests that the wound be  thoroughly  cleansed  with a
gold needle, that this be attached to a hypodermic syringe, a 4 per
cent, solution of cocaine sprayed over the wound, then a solution of
nitrate of silver (gr. v., aquas gss.), or an alcoholic solution of corro-
sive sublimate and carbolic acid (hydrarg. bichlor. gr. ij., acid, carbol.
gr.  xv., alcohol 5ss.).
  Artificial respiration  should  always be  employed when seeming
death has  occurred  during a paroxysm, because it is possible by this
means to  reanimate the patient again.  Such far-fetched  operations
as tying the vertebral arteries or stretching a nerve have not been
warranted by the results.  Much  can be done in the way  of tetanus
of newborn children, however,  iu the way of  antisepsis, and this
should also be rigidly insisted upon in the treatment of all wounds
in localities where  the disease is prevalent.  Assistants, nurses, and 
   NERVOUS DISEASES OF PROBABLY MICROBIC ORIGIN.  479

physicians should  be scrupulously clean, washing their  hands in a
solution of bichloride of mercury, 1  to 500; and the wound should
be antiseptically dressed.  The use of serum from immunized animals
seemed at first of  great  promise, but it has not proven successful;
and, moreover, there is great difficulty in  obtaining it promptly in
case of need.

                          TETANY.
  Synonym:  Tetanilla.
  Definition.   Tetany consists of tonic, bilateral, intercurrent,
usually painful spasms of certain muscular groups, without loss of
consciousness.
  History.  This  affection was first described by Sternheim, a
practising physician  of Altona, in 1830, under the heading of" Two
Rare Forms of Rheumatism."   In 1831  Dantz  described the same
affection  as tetanus intermittens,  having no  knowledge of the previous
article.  As usual,  the older authors seem to have had some glimmer-
ings of the malady,  from Hippocrates down to such writers in  the
seventeenth century as  Imbert-Gourbeyre, Delamotte, Delaroche,
Lenoble, Tissot, Ramel, Miiller, and Wolf.  Iu 1832 Tonnel6 made
publicly  known the results of the  first autopsy.   Courvisart first
suggested the name of tetany, and since then the literature upon the
subject has been abundant.  It is a very rare disease  in America,
and no death from it has ever been recorded by the Health Board of
the city of New York.
  Clinical History.  Tetany consists of tonic intermittent spasms
of the extremities  without loss  of consciousness.  These spasms  are
almost always symmetrical and  generally affect the hands first and
afterward the feet,  generally with  flexor spasms.  The hands  are
thrown into a position such as they assume in writing, or such  as
is taken by the hand of a midwife; but this attitude of the hands is
not constant, and they may sometimes be closed like a fist, and occa-
sionally only iudividual  fingers may be  affected.  In the  feet  the
toes are drawn downward and the instep up, as in equinus.  Flexions
of the elbow are not frequent, and only occasionally is there adduction
of the shoulder-joints.   In the  knee-joints  there may be a contracture
of the quadriceps and consequent extension, and very seldom, if ever,
flexion in the knee-joint.   The contracture may be slight, or so pro-
nounced  that the physician cannot overcome it, and  usually in these
eases of excessive contraction the muscles can neither be extended  nor
flexed.   The jaw-muscles are also generally affected, so that there is
trismus, or lock-jaw.   When the facial muscles are affected, the risus
sardonicus is present,  aud this  has been seen on one side alone.  In
the severe cases the muscles of the neck and chest and  even of the
trunk are affected, so that opisthotonus may supervene.   The tongue
is seldom affected,  or those of the pharynx and  larynx.   The eyelids
are  more often involved, and occasionally  the ocular muscles them-
selves, producing strabismus and  diplopia.  Whilst the rule is that
the  spasms  are bilateral, there are occasional exceptions,  and  in
several instances the hand alone has been affected, or the upper and 
480
NER VO US DISEASES.
lower extremity on one side.   The duration of the spasms varies from
a few minutes to a half-hour or two hours, rarely several hours, and
in some very rare cases  they have been known to last several days.
These spasms may be induced by mental excitement and nervousness.
In some rare instances so-called intentional spasms have been seen •
i. e., a voluntary movement  being performed, the muscles  entering
into this movement become affected by spasm.   With these spasms
goes usually a certain amount of paresis of the affected extremities,
which  may last for months after the attacks,  and in some instances,
when the lower extremities  are implicated, the gait is tottering and
uncertain.   The intervals between the  spasms vary in length from
hours to days, but the spasms themselves seem  to occur with a certain
periodicity, especially  in the afternoons and at night.
  Trousseau called attention to a phenomenon in tetany to which his
name has  been given, so that it is called by the European observers
the Trousseau  phenomenon.   It consists  of the fact  that  pressure
upon the affected extremities at certain points will produce the pecu-
liar spasm.  The best  place in which  to do this is the bicipital sulcus
or the crural sulcus, but this  pressure must be exerted from half a
minute to four or  five  minutes.  In certain exceptional  cases  pressure
upon the  bones of the  hand will suffice, or upon painful vertebral
prominences, or pricking with a pin, or sprinkling with cold water.
It is not, however, a constant phenomenon, but is of great diagnostic
importance when  present.  It is  evidently due  to irritation of the
nerve-trunks or of the muscular nerve-fibres, and not to any com-
pression  of the capillaries or arteries, as Trousseau at  first supposed,
because experiments have shown that pressure upon the arteries was
not sufficient.  Chvostek called attention to the fact that the mechan-
ical excitability of the nerves was greatly increased in tetany, espe-
cially in  the  face, and  this phenomenon has been called the Chvostek
symptom.  It is evoked  by stroking and  pinching the muscle with
the finger,  or in lesser cases percussing the muscle with a percussion-
hammer  of rubber, when instantaneous contraction of the neighbor-
ing muscles will be observed.   But this symptom has been observed
in other morbid conditions of the nervous system, such as hypnotism,
the later stages of facial paralysis, and certain  forms of pellagra, and
also  in healthy young adults, occasionally  in  healthy individuals of
more advanced age.   The electrical excitability is almost always in-
creased.
  As a  rule, the  sensorium is unaffected, but  it may happen that
there  is  some confusion, delirium,   melancholoid  states, or confu-
sional insanity.  The temperature is subnormal generally, but it may
be above the normal or even high.  Pulse and respiration are  affected,
usually in  proportion  to the severity of  the attack, somewhat quick-
ened in the lighter attacks, or very much increased in the severe ones.
In almost every case there are increased respiration, redness of  the skin
of the extremities, especially in the region of the joints, slight degrees
of oedema,  and  there sometimes is even a slightly bloated appearance
of the face, occasionally a herpes, urticaria, alterations of the hair,
nails, and even, but rarely, muscular atrophy.  The knee-jerks may 
   NERVOUS DISEASES OF PROBABLY MICROBIC ORIGIN.  481

be normal, subnormal, or exaggerated, and are of no diagnostic value
whatever.   Epileptic attacks frequently occur with tetany.
  Etiology.  The causes of tetany are—
      Certain seasons;
      Certain occupations;
      Certain stomachic and intestinal affections ;
      Certain acute infectious diseases ;
      Toxic agents;
      Parturition and its sequelae ;
      Extirpation of the thyroid gland.
  The disease is most  frequent  in  infaucy and the  secoud  decade of
life.  Heredity is  but very rarely an important etiological factor.
  The disease  is  very much more apt to occur in the months of
February, March, April, and May than in  the other months,  and
Frankl-Hochwart, analyzing cases occurring among  200,000 patients
admitted  to the  hospitals of Vienna  for nine  years, from 1880 to
1889, found that the increase iu cases generally occurred in  January,
rose  rapidly during February,  attained the  maximum in March,
decreased through April, and  in  May sank  below the point from
which it had started.
  It would seem  that certain occupations are particularly prone to
this disease.  Thus, shoemakers are the most prone to it; next in
frequency, tailors, and  then,  far  less  frequently,  joiners, turners,
locksmiths;  whilst  saddlers, hostlers, day laborers, wagoners, book-
binders, watchmakers,  butchers, coachmen, and masons are singularly
free from it.
   It may  occur  after  diarrhoea,  dyspepsia, worms, constipation,
typhus,  cholera,  measles, scarlatina, and many infectious diseases.
It has also been observed iu conjunction  with ergotism, alcoholism,
chloroform, and  ursernia,  and in pregnant, parturient, and nursing
women,  as well  as from extirpation of the thyroid  gland,  which
procedure probably  induces it, as it does myxcedema, by the poison-
ing of the mucin, since two German observers, Wagner and Hammer-
schlag, have induced tetany in cats by the injection of mucin.
   Pathology.   The pathology of tetany is  unknown, although it
is probably due to some  microbe.
   Duration and Prognosis.  Tetany may be chronic, the attacks
recurring at intervals for years, and Hoffman speaks of one such case
which had lasted over  twenty-one years; but this is rare, as is also a
fatal result iu the disease. The duration is usually a short oue, but the
tendency  to relapses is often considerable.   The duration of the first
attacks is usually  four to fourteen days.  The form which occurs with
dilatation of the stomach usually ends  fatally, but most of  the other
 cases recover, unless they are  mere  symptoms accompanying some
disease that is in itself fatal.  It may occur sporadically, iu epidemics,
 or isolatedly.
   Diagnosis.  The only disease with which there may be any danger
 of confusing tetany is tetanus, but  in the latter disease the muscular
 cramps begin in the neck and the muscles of mastication, whilst the
 hands are not usually affected at this time, and there is an  enormous
                                31 
482
NERVOUS DISEASES.
general reflex excitability; besides, there are none of the facial phe-
nomena or the increase of galvanic excitability, nor can the cramps be
evoked by pressure  upon certain points (Trousseau's symptom). It
is claimed that  tetany can exist without cramps, in which case the
diagnosis can be  made  by the  increased mechanical  irritability of
nerves and muscles, the  increased  electrical irritability,  and  the
presence of  the characteristic pains.  Hysterical  contracture  may
resemble tetauy, but it  is generally unilateral, and the differential
diagnosis can  be easily made by the symptoms.
   Treatment.   If a cause can be found, it should be removed, as
in the case of tetany occurring with dyspepsia or constipation.
   Bromide of potash is very useful  in overcoming the spasms; from
15 to 20 grains  should be administered three  times  a  day, or every
four  or  five  hours.  In  a less  degree chloral, morphine,  Indian
hemp, chloroform, cold to the extremities, and ice to the spine have
had an excellent effect.  Electrical  treatment is of doubtful value.
Gowers speaks of digitalis as  a  most  useful remedy for nocturnal
tetany, a dose being  given at bedtime.  In all cases tonics, nourish-
ment, and supporting  treatment should  be also made use of in
accordance with  the  need of the individual case.

                  HYDROPHOBIA, or RABIES.

   At the very outset of this  question  some details of nomenclature
should be  briefly  considered.   By usage the term rabies is given to
the disease in  the animal,  while the malady in man is termed hydro-
phobia.  This was  so stated  in  Fleming's book in 1872, and has
since  been adopted by the standard dictionaries  and writers.   I see
no reason,  however,  why it should not be called  rabies in the  human
subject.  The disease  was termed  lyssa by  the Greeks, meaning a
worm, a term given to the frtenum of a dog's tongue, which  was
supposed in the  early days to be a worm, and was extirpated as such.
This  superstition lingered until the early part of this century, when
a Russian physician  by the name of Marochetti claimed that in  all
cases  of hydrophobia pustules appeared under the tongue at a certain
time  of the incubation of the disease.   The German  writers still
retain this  name of lyssa.   The spread of an infectious disease among
animals is called an  epizooty (from ini, upon, and ^wov, an animal),
just as the spread  of an  infectious  disease in the  human being is
called an epidemic (from ixi, upon, and or^uo-, the people).
   At the very threshold of this  subject we  are confronted  by the
question as to whether  there is such a thing as rabies or  hydrophobia.
There has  been  much and bitter  discussion upon this  point  during
the last few years.   Those who would  answer this  question in the
affirmative allege as  proof the fixed  belief of ages and the many epi-
zooties of which we have historical record.  The very earliest writers
speak of rabid dogs, and they were known as far back as the  days
of the AsclepiadaB, the descendants of the god of medicine, iEscula-
pius; while there are  very few  parts of the world, whether in the
tropics or  the arctics,  in which au outbreak  of  it  has not  been 
   NERVOUS DISEASES OF PROBABLY MICROBIC ORIGIN.  483

described at some time or other.   At times it has raged with great
fury, as in  Northern  Germany  from 1851 to 1856, when at Ham-
burg alone 600 cases were observed among dogs, 267  occurring  in
the year 1851.  In England, in 1856, it  raged severely among dogs
and in a herd of deer, destroying  nearly  oue  hundred  of  the latter.
In Wiirtemberg, according to the veterinary professor,  Hering, from
January  1, 1840, until the  end of February, 1842, it affected  230
dogs aud 21  bitches.  Iu 1866  there were thirty-six deaths from
hydrophobia reported  by the Registrar  General  of Great Britain.
It has never been rife in this country, although local epizooties of it
have been reported from time to time.  It is stated that it  raged two
years in a herd of deer  belonging to the Marquis of Ipswich.   In
almost  all of  these epizooties human beings have been  bitten by the
rabid animal and have died,  although it has never spread  from one
human being  to another, as it has done iu animals.  It would seem,
therefore, to be conclusively  proven that there is a disease which can
rapidly  exterminate a kennel  of dogs, a flock of sheep, a drove  of
hogs, or a herd  of deer, and  which can render the timid  skunk,
badger,  and fox ferocious and dangerous and make the wolf a beast
of prey as fierce as a royal Bengal tiger.   It would also appear to  be
conclusively proven  that  many  people have died after being bitten
by these rabid animals.  But there has sprung up in this country, in
the last few years, a small number of very decided opponents of these
claims, such as Spitzka, Brill, Dulles, Stockwell, and  others; and,.
unless I am very much mistaken, they  have voiced to some  extent
the feeling of skepticism  that prevails among American physicians.
In the first  place, they say, many  mistakes are made in diagnosis,  so
that animals are said to have rabies when in reality  they have some
one of  mauy  disorders that  may cause similar symptoms, such  as
epilepsy, angina or  sore-throat, gastritis and enteritis, distemper,
foreign bodies in the mouth and throat, tetanus, worms in the frontal
sinuses or in the small intestine, and ulceration of the internal  ear.
In certain countries, extending  from the sources of the Vistula to the
Carpathian  Mountains,  there  is  endemic a  disease known as the
"plica  Polonica," attacking  mankind,  horses, cows, sheep, wolves,
foxes, and dogs, in the latter  closely resembling rabies,  although the
bite of these animals is not followed by hydrophobia.  Spitzka has
introduced into the skull-cavities of dogs  such non-rabic material  as
the spinal cord of a healthy calf, common yellow soap and stale horse-
urine, producing a purulent meningitis and meningo-encephalitis, and
the symptoms of dumb rabies.  Miller has reported three cases  of
seeming rabies in the cow, in which clusters of the  parasite  known
as strongylus  tetracanthus were found  in the intestines.   It  is not
unreasonable to suppose  that the bite of an excited  animal may be
very dangerous, as it is  an  elementary fact in physiology that the
secretions of the human female breast are at times fatal to  the child.
My friend, Dr. E. F. Brush,  informs  me that  oue of the earlier Bor-
gias obtained a subtle and most dangerous poison by dipping a ring
in the saliva of a hog which  had been hung up aud kept excited to a
blind fury for a long time. 
484
NER VO US DISEASES.
   The variations are almost incredible that are alleged to exist in the
period of incubation of hydrophobia.  Fleming states that the aver-
age in England has been from thirty to fifty-nine days.   According
to Tardieu, it may vary from one month to twelve.   Trousseau says
that it  may  run  from a fewT days to  a  year.   In Algiers it varies
from twenty  to two hundred days.  Sauvage speaks of a peasant who
was suffering from the most  pronounced  hydrophobic symptoms on
the third day after being bitten  by a mad wolf.  Chirac tells of  a
merchant who  was bitten by a mad dog at Montpellier, afterward
resided ten years in Holland, and was suddenly attacked  by hydro-
phobia on his return to France, on learning of the death of a brother
cadet who had  been  bitten by the same animal.   Finco, of Padua,
narrates the case of a young woman who became  hydrophobic four-
teen years after the bite of a rabid dog.  Even Gowers states that the
period of incubation is longer  and more  variable than that of any
other known acute specific disease, and  believes that many well-
authenticated cases have occurred  eighteen  months after the wound.
This extreme variableness in the period of incubation lends credence
to the belief firmly held by many competent observers that death
from fear can occur with symptoms closely resembling the true dis-
ease.  These are the cases of so-called lyssaphobia or hydrophobia.
Although a recent writer has characterized such a belief as childish,
it is yet a matter of clinical observation that great psychical shock
can produce mental disease and death.  I have a patient in whom an
attack of melancholia of eighteen months' duration was caused by her
lover being suddenly thrown from his horse and killed before her
eyes.   I know of another patient to whom her  husband, who had
been  supposed  lost  at  sea, suddenly appeared, when she became
speechless, mumbling, and, preserving only consciousness enough to
caress  his face gently for a few hours, sank into  a coma and died.
Another patient of mine with transverse myelitis, who had improved
greatly, was  much frightened by his room catching fire, and in a few
hours he became delirious, and within twenty-four he was dead.   I
have  had under my care a stalwart, resolute young  man, to whom
the Secretary of the Treasury  has just presented  one of those rare
medals of gold that are given  only to those who save  a life at immi-
nent danger  to their  own, and who, notwithstanding  he had nerve
enough  to plunge into the raging surf to  rescue a fellow-being, has
not been able to do a day's  work since, suffering from those well-
known symptoms which  Oppenheim describes as traumatic neurosis,
and which occur so frequently after railroad accidents.  (Sec " Rail-
way Injuries," etc.)  If these instances be not sufficient, a perusal of
Tuke's book on The Influence of the Mind on the Body ought cer-
tainly to convince  any impartial  person that such an  overwhelming
fear as is that of hydrophobia is quite sufficient to cause death, the
more especially as a number of suicides have been committed from
this very dread.
  Very few men in this city of New York, or, indeed, in this country,
have seen a case of hydrophobia.  Indeed, one of the great difficulties
that I encountered in arranging a recent debate upon  this subject in 
   NERVOUS DISEASES OF PROBABLY MICBOBIC OBIGIN. 485

the New York Academy of Medicine was that there was not a neur-
ologist in New York City who had seen  more than one case in his
own practice, although some few had observed two or three cases at
the great hospitals, while many men of great experience had never
come in  contact with  any.  For my part, in an  experience of over
twenty years as student and practitioner, I have never seen but one
one case, and, to be guilty of an  Hibernianism, I would not  swear
to  that   Iu the  city of New York, from 1855  up to  the present
time, the number of deaths from hydrophobia have been as follows,
according to the  figures very kindly furnished me by Dr. John  T.
Nagle, viz., 1855, 4;  1856,3; 1857, 2;  1858,0; 1859,  2;  1860,
0; 1861, 5; 1862, 1; 1868, 3; 1864, 1; 1865, 3; 1866,  2;  1867,
4, 1868, 1; 1869, 5; 1870, 3; 1871, 7; 1872,  6; 1873,  0;  1874,
5; 1875, 0; 1876, 5; 1877, 4; 1878, 2; 1879,  0; 1880,  0;  1881,
3; 1882, 1; 1883, 1; 1884, 1; 1885, 0; 1886, 0; 1887,  1;  1888,
0; 1889, 1.  Thus, in a period of time covered by thirty-five years
there have been seventy-six deaths, in nine of these years there have
been none, and it  has twice happened that for two years at  a time
there was not one.  One of the deaths in 1874 is that of a  man who
was bitten by a dog supposed to be rabid, and a coroner's inquest
was held, the cause of death being stated to have been  lyssaphobia.
I come in contact every year with  many physicians  from different
parts of the country,  and it is  very exceptional to  have one tell me
that he has ever seen a case of hydrophobia.
  From this necessarily cursory review of the pro and con of the
subject we may draw  the conclusion, I think, that frequent mistakes
are made in the diagnosis of rabies and hydrophobia; that death can
be caused by the fear  of the disease; that the symptoms of so-called
dumb  rabies may be caused  by  simple  purulent meningitis and
meningo-encephalitis; and that very few cases of either rabies or hy-
drophobia have been observed in  New York City or in the country
at large.  Admitting all this, however, the question still remains as
to whether there is a true rabies or a true hydrophobia.  It all de-
pends  upon whether  the virus obtained  by Pasteur is capable  of
causing, when inoculated into a given  animal, the same disease  as
was exhibited in  the animal from  which the virus was taken.   Pas-
teur maintains that the poison of rabies is to be found  chiefly in the
medulla, spinal cord, and brain ; that animals are made rabid gener-
ally by subcutaneous inoculation of this virulent nervous tissue, but
that they are always made rabid by subdural inoculations  after tre-
phiuing;  that rabbits when thus  inoculated will develop a paralytic
form of rabies, which  has a period of incubation lasting from fifteen
to twenty-one days, and  that this  paralytic  rabies in  rabbits is true
rabies, as dogs inoculated with its virus develop true rabies.   Pasteur
claims that nearly all animals can  be thus inoculated, although in
the different species there are differences in the virulence and periods
of incubation, the former being  shortest  and the latter longest  in
monkeys, and the  former longest and the latter shortest in rabbits.
  If the virus, however, is  passed successively through a  series  of
rabbits  first inoculating one and then waiting for the rabic symptoms 
486
NEB VO US DISEASES.
to appear, theu inoculating the second from the spinal cord or medulla
of the rabic animal, in each case making the inoculations beneath the
dura mater, the period  of incubation can be  lessened finally from
fifteen to eight days after passage through  a series of twenty-five rab-
bits, and by further transmission through  a  second series of twenty-
five  rabbits it can be still further reduced to seven days, which seems
to have been the limit of reduction.   The virus is prepared by ster-
ilizing in a sterilized bouillon or beef-tea portions of the medulla or
spinal cord from rabid animals.  The medulla or cord is removed with
all possible care to prevent contamination from foreign matters, aud is
suspended  in a jar, the air of which is artificially dried and subjected
to a  constant temperature of 20° centigrade.   At the end of fifteen
days this medulla or spinal cord will have entirely lost its virulence,
and  any degree of virulence may be  obtained, therefore, by using a
spinal cord upon any given oue of these fifteen days.  If the  infec-
tious cords, while in a moist condition, are submerged in carbonic acid
gas  and kept aloof from the air and  its  micro-organisms, they will
remain virulent for several months.
  In order to protect a dog from rabies, Pasteur inoculates in the fol-
lowing  way :  Ou  the  first day an inoculation is made with  virus
obtained from the cord of a rabbit in  whom the incubation has been
seven days, this cord having been rendered non-virulent by preser-
vation as above for about fourteen or fifteen days.  On the following
day a cord of twelve or thirteen days old  is employed; on the next
day, one eleven days old; then on the fourth day, one nine days old;
on the fifth day, one seven days old; on the sixth day, one six days
old ; on the seventh day, one five days old ;  on the eighth day, oue four
days old;  on the ninth day, one three days old; on  the tenth day,
one two days old ; and on the eleventh day, one one day old.  By
this  means, it is claimed, the dog is finally rendered non-susceptible,
so that no  symptoms follow the last inoculation.  These  tests have
been repeated  and verified by Dowdeswell and Horsley in England,
Shakespeare, Ernst, and  Biggs in America, Hogyes of Buda-Pesth,
Di Vertia  and Zagari in Italy.   Spitzka claims,  however, as has
already been  stated, that he has been able to produce paralytic rabies
in dogs by subdural inoculations of the spinal cord of a healthy calf,
common yellow soap, and stale  horse-urine, thereby producing a
purulent meningitis and meningo-encephalitis.   It does not seem to
me,  however, that these  latter experiments  should militate against
Pasteur's, inasmuch as in none  of the Pasteur cases was meningitis
or meningo-encephalitis  produced.  Indeed,  Pasteur and his  asso-
ciates do not claim any definite characteristic lesions for rabies.  They
simply maintain that iu  the  medulla  and the spinal  cord there are
found accumulations of round cells in the perivascular spaces, form-
ing a so-called miliary abscess, and even  these  may not be found at
all in the  early stage, although iu  paralytic rabies in man they are
more marked.   Golgi  states that the nuclei of the medullary nerve-
cells are altered.   Gibier describes a microbe in the brain of a rat,
but he has not been able to color  or cultivate it.   Fol has demon-
strated, in  spinal cords of rabic animals,  groups of small granules 
   NEBVOUS DISEASES OF PBOBABLY MICBOBIC OBIGIN.  487

resembling micrococci lodged in the  neuroglia, or between the axis-
cylinders and the sheath of Schwann.  Cornil and Babes, however,
have not been able to find  these microbes of Fol.  But Babes has
found in the spinal cord of  rabic animals round  microbes in groups,
which he has been able to cultivate, and the injection of which into
animals  produced rabies.  He  has also found another microbe in the
cerebellum and spinal cord.  This  is very brilliant, and ordinarily
forms dense and thick colonies resembling diplococci or ovoid bodies,
often with a transverse striation in the middle.  Rivalta and Dowdes-
well have found certain microbes, but their conclusions have not been
accepted by bacteriologists.
  If we may trust the present writers upon the subject, the symp-
toms of furious rabies in the dog are  as follows : Alteration in the
dog's demeanor, so that it becomes sullen, shy,  and restless; hallu-
cinations of  sight, so that imaginary objects will  be bitten or snapped
at;  strange and erratic movements,  indicative  of mental aberration ;
transition from  obedience and affection to semi-delirious outbursts, or
to frenzy or fury ;  au irresistible tendency to roam, so that great dis-
tances may be covered iu a surprisingly short time; great tendency
to bite; greatly increased salivary secretion, which becomes thicker
and more viscid ; a peculiar howl, which is described by Fleming as
being neither a  bark, howl, growl, nor snarl, but a curious jumble of
all, the  howl being predominant; finally, exhaustion, paralysis, and
death.   In dumb rabies there  is the characteristic paralysis of the
lower jaw. so that  the dog is incapable of either eating or drinking,
or of closing the mouth ; sometimes also a  certain amount  of tume-
faction of  the pharynx and tongue, and finally,  paralysis of the ex-
tremities aud death.   In so-called tranquil rabies the animal is in a
condition of coma.   None  of  these animals  show auy aversion to
water, contrary to the popular belief.
  The symptoms in  the human being consist  at first of  general
malaise, mental depression, slight insomnia, and  some vague distress
about the throat.   Attempts at drinking occasion pharyngeal spasm,
which spreads  to the muscles  of respiration,  causing a short, quick
inspiration, like that produced by a sudden  affusion of cold water,
this increasing in severity to a strong inspiratory effort, in which the
extraordinary muscles of respiration take part, so that the shoulders
are raised, and  even the facial muscles may draw the  angles of the
mouth  outward.   Reflex excitability  is enormously increased, the
slightest cutaneous impression  bringing on a spasm.  Salivary secre-
tion is much increased.  Vomiting is common.   The muscular spasm,
confined at first to the muscles of  deglutition and respiration, may
spread to the other  muscles of the body, and the convulsions may
become  general, causing continuous muscular rigidity, or opisthotonus,
or the convulsive movements may be co-ordinated and  closely resem-
ble the  hysteroid variety.  Delusions  may occur, or even  delirium.
There is no such dread of water as to warrant the term hydrophobia,
as many of even the recent writers  would have  us suppose; but the
spasm of the muscles of deglutition at the sight of water is only  a
part of  the general reflex excitability, as is  shown by the fact that 
488
NEBVOUS DISEASES.
glittering objects, loud  noises, draughts of  air, may cause the same
spasms, or kindred  ones, in  other  muscles.   In many cases there is
a curious alternation of consciousness with furious  action.  Thus, a
patient begs the bystanders to go away, as he fears he may do them
damage; or, as Dr. Ernst tells  me that a patient of his did, a man
may fly  at the throat of an attendant, saying, " I can't help it!"
The temperature ranges from 100°  to  104°  F., or, exceptionally,
106° F.   Remissions are frequent.  Death  is sudden, or by gradual
coma.  Paralysis does  not  generally occur, although  it  has  been
stated that paralytic symptoms  similar to those of acute ascending
or Landry's  paralysis may  supervene; but as there  are only two
cases to  support this claim, and as one—a man named Goffi—had
been inoculated by Pasteur's " intensive "  method, and died notwith-
standing, it needs no eminent logician to perceive that the probabil-
ity of the symptoms having been  caused  by Pasteur's intensive in-
oculation is much greater than  the probability of their having been
caused by rabies.
   The differential diagnosis  in the human being is from the follow-
ing diseases:
       Tetanus;
       Delirium grave;
       Acute mania;
       Epilepsy;
       Hysteria.
   Tetanus has none of the cerebral symptoms.
   Delirium grave is  a  disease of long duration, although in some
cases it may be very difficult to make the differential diagnosis.
   Acute  mania has  a more gradual onset on  the one hand, or a more
acute one upon the other, and  has not the remissions or the reflex
excitability of hydrophobia.
   There  should never  be  any  question  about the diagnosis from
epilepsy—in which  there is  none of the reflex  excitability, none of
the  remission,  and  in which there is,  on  the other hand, definite
tonic or clonic convulsions, and the history of many cases of epilepsy
(vide Chapter IX.,  "Epilepsy").
   In hysteria there  will be the history of  the hysterical diathesis, or
the peculiar emotional condition, or the hemiansesthesia; and sudden
recovery  from stout assertions of the absence of danger will confirm
the diagnosis.

                 DIPHTHERITIC PARALYSIS.
   History.   Diphtheritic  paralysis was  first  described by Lepois
in 1580,  again  by Heredia in 1690, by Ghisi in the Italian epidemic
of 1747  and  1748,  by Chomel  in France in 1748, and by Bard, of
New York, in America  in 1771.   Singularly enough, these observa-
tions attracted  but  little attention until  the early part of the nine-
teenth century, and  since theu it has been  observed by all the promi-
nent writers.
   Clinical  Symptoms.   The paralysis is usually not observed
until the first or second week after the convalescence from diphtheria, 
   NEBVOUS DISEASES OF PBOBABLY MICBOBIC OBIGIN.  489

although it may occur earlier or later.   It is generally preceded by
some of the usual buccal symptoms,  although they may  be very
slight, but  it has been claimed that it may occur without  them,
and Boissarie  has related  several  such seeming  cases, which are
certainly rare  enough  to  be worthy of note.   The most common
symptoms  are  loss  of the knee-jerk and palatal  paralysis.    The
latter  is evidenced by the nasal intonation, slow speech, snoring in
sleep,  impaired deglutition, and nasal regurgitation  of liquids.   In
such cases  there are usually a sensory paralysis of the fauces  and
uvula and   loss of the reflex.   Multiple paralysis is the next most
frequent form,  and this may  be  preceded or  not by  the  palatal
paralysis, although it  is usually preceded by the loss of the knee-
jerk.  Different muscles may  be affected.   The  limbs are  most
frequently  implicated,  the  paralysis is usually bilateral and  sym-
metrical, aud occasionally there is some impairment of sensation ;
the trunk-muscles may also be affected.  Cardiac  disturbances are
comparatively infrequent, but they are  of very grave import when
they do  occur.  Hemiplegia is very rare.  The bladder is affected
in  only very severe cases.   The  most common symptom due to
implication of the eye  is impairment of near vision, due to paresis of
accommodation, and with this is  sometimes associated a  paralysis of
the internal muscles of the eyeball or of the internal recti, and even
ptosis.  Almost  all the senses may be affected in different cases,
although impairment  of hearing  never occurs.   Convulsions occur
occasionally in  severe cases.   After the  paralysis has lasted for
several weeks  there is generally a  decreased faradic reaction,  and
this may proceed  to entire loss of  response to this current, although
the muscles ordinarily respond to  the galvanic current.   There may
even be a reaction of degeneration.
   Pathological Anatomy.  To  the  naked  eye there are seldom
any morbid appearances except some hypersemia or minute extrava-
sations.  Microscopically the muscles are sometimes normal, aud in
other  cases they present granular and fatty degeneration.   In the
nerves degeneration is found  in  all the severe cases, either in the
peripheral  portions or in the whole trunk, although the posterior
roots  are usually normal.   The  medullary sheath  breaks up, the
nuclei of the sheath of Schwann multiply, and occasionally the axis-
cylinders disappear.   The interstitial tissue is generally unaffected.
These changes  have been found both  in the palatal nerves and in
those  of the limbs.  The changes are usually limited to the peripheral
nerves, but occasionally the cells of the anterior cornua of the spinal
cord  undergo  granular and  fatty  degeneration,  or are  swollen,
atrophied,  with degenerated processes, or free nuclei are  found in the
gray substance.  Occasionally, though rarely, the walls of the vessels
are found thickened, or the vessels are dilated and congested.  There
is sometimes softening of the  substance of the cord, and in other
places a hypersemia without softening, in conjunction with the cellu-
lar chauges that have already been noted.   The pathological appear-
ances  differ very much in different cases, so that they may vary from
scarcely any change to the  most  marked  of those  which we have 
490
NEBVOUS DISEASES.
detailed.  The truth of the matter  seems to be that the disease is
dependent upon the capricious action of  a  micro-organism,  so that
sometimes one lesion  is found, sometimes another,  sometimes one
portion of the nervous system is affected and sometimes another, and
it has even been observed in certain  cases that a single branch of a
nerve may lose its function while the other branches are unaffected.
  The micro-organism, however, is still a matter of doubt.   Atone
time it was supposed that it was the micrococcus or spherical bacte-
rium ;  others have stated  that the diphtheritic  micrococci were the
same as the septic micrococci.   Curtis  and Satterthwaite, reporting
to the New York Board of Health in 1877, affirmed their belief that
the micro-organism could  not be distinguished from that  which oc-
curred in the ordinary septic material, as well as that it was the
chemical substance or ptomaines produced by the diphtheritic micro-
organisms that caused  the usual  symptoms.   Wood and Formad, in
1882, confirmed these statements.  In 1883 Klebs  found  a peculiar
bacillus  in the  pseudo-membrane and in the surrounding inflamed
tissue,  and this was afterward investigated by Loeffler, and has since
been known as the Klebs-Loeffler bacillus.  This bacillus is motion-
less, straight  or curved, about the size of the tubercle bacillus, but
doubly thick.   Whilst it is found in the membrane, it is  not  found
in the lymphatics, internal  organs, or bloodvessels.  Loeffler, how-
ever, was not able to find  this bacillus in  some typical cases of diph-
theria, although Wellenhof has it.  Oertel states that there are two
kinds of microbes, namely, chain-forming  cocci (streptococci) and rod-
shaped  bacteria with  rouuded extremities (bacilli), the former being
found in the pseudo membrane, the latter in the fibrinous networks.
Prudden goes  no further than  to say that there  is a streptococcus
almost constantly present in the pseudo-membrane.   M. W. Taylor,
of London, has seemingly adduced proof to show that common mould
may be a cause of diphtheria, as several cases occurred in a sleeping-
room  whose walls were wet, and from which were taken the asper-
gillus,  coprinus, and penicillium moulds.
  Prognosis.   The  prognosis  of diphtheritic  paralysis  is usually
good, although cardiac symptoms, weakness of respiration, or long-
continued difficulty of deglutition may  make it a serious matter.
  Diagnosis.  The diagnosis of diphtheritic paralysis must be made
upon the history of a paralysis having succeeded a throat trouble;  or
if this is not possible,  by  the ocular symptoms conjoined with the
absence of knee-jerk and inco-ordination that have come on within a
brief time.   Hysteria  is said sometimes to simulate diphtheritic
paralysis, and I can imagine that this might occur, but I have never
seen a case.   The diagnosis can easily be  made  by the fact that  in
hysteria there  is not the atrophy, the ocular symptoms, the loss  of
knee-jerk, or the partial paralysis and loss of reflex.
  Treatment.  The  treatment of diphtheritic paralysis  should  be
by rest, careful feeding, drugs, and electricity.  The patient should  be
put to bed if the paralysis involves any important nerves or muscles,
or if it is in the neighborhood of such.  Even if the muscles affected
are  not of great importance to life, it is certainly a good rule to keep 
   NEBVOUS DISEASES OF PBOBABLY MICBOBIC OBIGIN.  491

the patient  in bed until it is determined exactly how far the disease
is going to progress, for the  first symptoms are not necessarily the
severest ones.  The diet should be  of the  most nutritious character,
and suitable to  the age of the patient.   It  should always  be fluid
where there is  any difficulty in deglutition, and with little children
the best food is milk, with farinaceous substauces and nutritive jellies.
With children of more advanced age milk should always be  the basis
of the diet, and to  this should be added either a home-made beef-tea,
or some one of the beef-preparations, and the meat should be cut up
into minute particles or the juice squeezed from meat.   With adults,
milk, farinaceous substances, nutritive jellies, beef-tea or  beef-ex-
tracts, and  koumiss,  will form an  abundaut diet  so long as there is
danger of failure of deglutitiou.  As soon, however, as the difficulty
of deglutition recedes, the diet should be rapidly pushed to the highest
point of nutrition  that is  possible, and there is no danger whatever
of too  much food, provided that  the  skin and the bowels act fairly
well.  It is also generally advisable to employ alcoholic stimulation
in adults, and the amount used should  vary according to the age and
habits of the patient; but, as a rule, the quantities will range from 1
to 3 ounces in the twenty-four hours.   When there are cardiac symp-
toms the patient should be kept iu  a recumbent posture  and digitalis
should be administered, the dose varying in a child from 1 to 5 drops
of a good, freshly and reliably prepared tincture every  four or five
hours, or ^ to  2  drops of a trustworthy  fluid extract at  the same
intervals.   Alcohol is also of considerable value in doses of 5 to 10
drops in  a  child to a teaspoonful  for an adult, every two or three
hours.  Use should  always be made of the aromatic spirit of am-
monia when dangerous cardiac symptoms suddenly supervene, and
in diphtheritic  paralysis of gravity it is  my custom  to have this
aromatic spirit of ammonia  kept at hand in case of an  emergency
arising.  The sulphate of  strychnine is also a very useful drug  in
cases of cardiac paralysis.    These  four substances—digitalis, strych-
nine, alcohol, and spirit of ammonia—should be used with a method,
however, and not  indiscriminately.  The  ammonia has only a tem-
porary effect, aud should therefore  be employed until the other drugs
can begin to act.   The alcohol  will act  most quickly next to  the
ammonia.  The strychnine and digitalis  begin to act at about the
same period of  time.   For  these reasons the ammonia need only be
used at the onset of the symptoms, or in case of a  relapse, whilst the
others  should be  continuously used until danger is past.   The sul-
phate of strychnine is best administered hypodermically, and  the
physician, during  a case  of diphtheritic  paralysis, should have  a
solution at hand ;  T^-¥ grain in a  very young child, g1^ grain in one
older, or in an adult fa grain usually will be sufficient, injected ouce
a day.  When the immediate danger of any fatal  result has passed,
attention  may be directed to arresting  the degeneration of nerve and
muscle, and the best means of doing this are massage and electricity.
Massage  must  be  used very gently, only upou the affected muscles,
and never  prolonged over  ten  or fifteen minutes, and it should be
borne in mind in giving it that the object is to facilitate the passage 
492
NEBVOUS DISEASES.
of blood through the muscle with the least possible mechanical irrita-
tion.   Faradism  should  be applied gently to the muscles and nerves
affected, the current at first being used  only sufficiently to be just
felt by the patient, and  then gradually increased, but never made
painful, and the  sittings  at first  should  not  be  over three  to five
minutes, and  increased  by degrees to ten  or fifteen  minutes.  At
this stage, also, tonics should  be administered, and the best of these,
in my opinion, is a tonic of bark or  quinine, strychnine, and iron.
The ordinary citrate of iron and quinine of  the Pharmacopoeia is as
good as any, and the dose  should be 1 grain three times a day to
children, 3 grains  three  times  a  day in  adults;  and with this may
be combined sulphate of strychnine, y^-g- grain three times a day in
infants, fa in  children, and fa in  adults, also  three times a day.   If
children cannot take pills, or if there is difficulty in giving them any
medicine that has much taste, the  quinine  may be given in the form
of the tannate in chocolates,  1  or 2 grains each.   The iron may  be
given in the form of the subcarbonate of iron, 10 to 30 grains, accord-
ing to the age, and this may be put into some hot milk darkened with
tea, or into a cup of cocoa,  where  its taste will hardly be  perceived,
and the strychnine may be  given  in solution.   All these substances,
however, may be administered almost as well in the form of the tablet
triturates which  are made up nowadays so reliably by many manu-
facturing  houses.  As the  patient  progresses into  convalescence,
treatment should not  be abandoned, but tonics, in some cases small
quantities  of alcoholic stimulants, abundant  and varied diet, and
electricity,  should be continued, and  every effort  should  be made  to
avoid  fatigue.  These patients  often  remain weak for a long time
afterward,  and they must be subjected as little as possible to fatigue
and  depressing  influences.   Even after  a recovery has  been  made
there will often be left awkward postures from muscular paresis, and
sedulous efforts should be made to overcome  these by the use of mas-
sage and gymnastic exercises, the latter being directed  to exercise
and  strengthen the  affected muscle or muscles.   Braces or mechan-
ical supports, however, should not be used, because their tendency is
to cause the patient to rely upon the steel or iron of them rather than
to increase the strength of the paretic muscles. 
CHAPTER  XI.
 CERTAIN NERVOUS SYMPTOMS  COMMON TO DIFFERENT
                          DISEASES.

                          VERTIGO.

  Vertigo is a symptom of so frequent occurrence and its import is
apt to be so much exaggerated  that I  have thought it wise to devote
a special  section to the subject.  The meaning of the word should
be precisely understood.  By vertigo  is meant a subjective sensation
of loss of equilibrium without loss of consciousness.  It has been the
custom of late years to employ the term in certain losses of conscious-
ness, notably  in  the so-called laryngeal  vertigo,  which  is  really a
laryngeal epilepsy.   In true vertigo consciousness is very seldom lost,
although  there may  be a momentary obscuration of  consciousness.
The causes of vertigo are manifold, and they may be  catalogued as
follows:
      Lithsemia;
      Aural disease;
      Eye-strain;
      Anaemia;
      Alcoholism  ;
      Gout;
      Nephritis;
      Intracranial lesions;
      Spinal lesions.
  Of all these causes the most  frequent in my experience is lithsemia.
Gowers states  that aural lesion is the most common  cause, but his
experience has either been contrary to mine, or else the types seen in
England  are  different from  those observed in this country.   The
vertigo of lithsemia, as has been described in the section upon a Neur-
asthenia," may vary  from a slight  sensation of loss of  consciousness
to a dizziness  that  causes a  person to reel almost as if intoxicated.
The diagnosis of this form of vertigo can easily be  made by attention
to the symptoms that have been narrated when speaking of lithsemic
neurasthenia, as well as by an exclusion of other causes.
  Aural lesion I should classify as the most frequent cause of vertigo
next to lithsemia.  The lesion may be either in the external auditory
meatus, the middle ear,  or the internal ear, and  the  diagnosis be-
tween these different localities will  be  found stated in detail in Chap-
ter  XV., " Meniere's  Disease."   As has  been seen, the auditory
nerve terminates peripherally in the internal ear,  thence runs up
to the pons, to  the nuclei in  the  floor of the fourth  ventricle, and
thence to the cerebellum, whilst its  cortical termination  is  in the 
494
NEBVOUS DISEASES.
posterior portions of the first two temporal convolutions.  It is still
uncertain as to  whether  lesions along the trunk of the  nerve are
capable of causing vertigo.  Dana has  related a remarkable case of
lesion of the temporal lobe with great disturbance of equilibrium,
but he was himself uncertain as to whether there was not trouble in
the middle or internal ear.   It has not  yet  been proved that the
disturbance of equilibrium  of cerebellar  disease is due to the im-
plication of the auditory nerve, and there is very much to contradict
any  such view.   It is generally no difficult  matter to make the
diagnosis between a  lesion of the ear in its  external, middle, or
internal departments, and a lesion of the nerve-trunk or of the base
of the brain or  the  cerebellum  or the temporal convolutions.  (See
chapter on " Localization of Lesions," etc.)
  Nephritis is sometimes a cause of vertigo, but the diagnosis can
be readily made  by a qualitative,  quantitative, and microscopical
examination of the  urine, although it must  be remembered that a
small quantity  of albumin or a few casts may be found with various
dietetic and functional anomalies.
  Eye-strain has been  generally supposed in the profession to be a
very common  cause of vertigo, but this has not been  my experience.
It is  undoubtedly sometimes a  cause, but not nearly so often as is
supposed. This eye-strain may be due to strabismus, errors of accom-
modation, or exophoria.
  Ansemia is sometimes, though  rarely, a cause of vertigo, and in all
doubtful cases  not only should  the heart and  the great bloodvessels
coming off from the heart be carefully examined and auscultated, but
it may even be necessary to examine the blood.
  Alcoholism,  like ansemia, is sometimes, though rarely, a  cause of
vertigo, and the diagnosis can be made with ease.
  What has been said of ansemia and alcoholism is also true of
gout.
  Intracranial  lesions of various kinds may be the cause of vertigo,
but this is  seldom the  case unless the intracranial  lesion  is  pro-
nounced.  This fact should be impressed upon  patients, because it is
popularly supposed that vertigo means intracranial  lesion, and I
have again and again seen  lives blighted from a fear of this and  the
doubt of physicians.   It is easy enough to make the diagnosis by
the presence  of  the  classical  symptoms  of  intracranial  lesions,
namely, vomiting, pronounced headache, optic  neuritis,  optic-nerve
atrophy, paralysis, motor or sensory, such defects of vision as hemi-
anopsia or amaurosis,  word-deafness, aphasia,  and mental impair-
ment.
  Lesions  of the spinal cord  are infrequently the cause of vertigo,
except in the case of locomotor ataxia.   The diagnosis must be made
by the presence of the well-known symptoms of spinal lesions, such
as paralysis of motion and sensation, the bladder and rectum, atrophy,
loss of tendon-reflex, violent pains, etc.
  In the vast majority of cases, however, vertigo is due to lithsemia,
aural  disease, or  eye-strain ; indeed, so much  is this the case that
it is usually safe  to assume that one of these three causes is at play 
NERVOUS SYMPTOMS COMMON TO DIFFEBENT DISEASES.  495

when a patient comes complaining of vertigo,  for when  there are
graver lesions the vertigo becomes a minor symptom in the patient's
estimation.
  The prognosis of the vertigo will depend  upon the  lesion.   In
lithsemia it is very apt to be persistent, especially during the warmer
months of the year, and  it may continue for years or throughout a
lifetime, so that it is well to inform  the patient of this fact, and in-
duce  him to become accustomed  to the  symptom and to regard it
as  of no  importance.   In the section upon " Neurasthenia " I have
spoken more fully upon this subject.  When the vertigo is caused
by aural lesion the prognosis will depend upon whether  the cause
is removable, which is generally the case in  lesions  of the external
ear, often the  case  in  lesions of the middle ear,  and seldom the case
in lesions of the internal ear.   When the vertigo is due to eye-strain
the prognosis  varies.  If there is exophoria, or  strabismus, or error
of accommodation  that can  be  removed, the prognosis is good; but
when it  is due to  amaurosis or hemianopsia,  the causes are  usually
not removable, and the prognosis is grave.  The vertigo of ansemia
is of excellent prognosis.  When due to alcoholism  it is usually cura-
ble if the alcoholism can be cured and has left no structural lesions.
The vertigo of nephritis depends upon whether the nephritis  is cura-
able,  so that the prognosis is good iu the acute nephritis of children
after  the  exanthemata, and also often good in the acute nephritis of
adults, whilst it is grave in the chronic forms of nephritis.  In intra-
cranial and spinal  lesions the  prognosis of vertigo  depends upon
whether  the  spinal lesion is one  that can be cured.   Usually, with
the exception  of intracranial syphilis,  intracranial  lesions  are of
grave prognosis, so that the vertigo resulting from them is a serious
matter, and this is also true of  spinal  lesions  capable of causing
vertigo.
  For the vertigo  itself there is no treatment except the removal of
the cause.
                         HEADACHE.

  Like vertigo,  headache is so  general a  symptom that  I  have
thought it best to devote a short section  to it.  The causes of head-
ache are—
      Migraine ;
      Eye-strain ;
      Nephritis;
      Anaemia;
      Alcoholism ;
      Lithsemia;
      Reflex  headache;
      Melancholia;
      Acclimation;
      Indigestion;
      Intracranial lesion ;
      Locomotor ataxia.
  Migraine, when typical, is a quasi-periodical headache limited to 
496                   NEBVOUS DISEASES.
one side of the head or spreading over the whole head;  but when it
is non-typical it may be more or less localized.  The typical migraine
can be easily diagnosed, because it comes only at  intervals,  lasting
a day or a  few days, between which the patient is  entirely free
from  the attacks.   The non-typical or localized  migraine, however,
is often not  properly recognized, and more especially is this apt to
be the case when  the  typical  attacks of  migraine  have become less
in degree or have largely died out, and their  place has  been taken
by a constant localized headache or neuralgia.   Migraine, it  should
be remembered, is a very mobile disease, aud it is by no means infre-
quent, as I have pointed out in  the chapter upon it, to find its place
taken by epilepsy,  and it  may  also disappear aud lose its typical
periodicity and intensity.   The  diagnosis, however, can  be made by
any one who is  aware  of this  circumstance, for all that  is necessary
is to inquire  carefully  into the antecedent history,  when  the patient
will be found to have had previous attacks of migraine; and to some
extent the  diagnosis will  be confirmed  byr the  success of the proper
treatment.
  Eye-strain  is sometimes a cause of headache, but not nearly so
often  as  physicians  generally  suppose.   Errors of refraction, stra-
bismus, and exophoria may cause it.  The diagnosis can  be made by
exclusion  of other  causes  and by the determination of the  causes
capable of  causing eye-strain.
  Nephritis  is a frequent  cause of headache, and  in every  case of
headache occurring in  an adult that cannot be  properly  explained a
careful qualitative  aud quantitative chemical  analysis  should  be
made of  the  urine.
  Ansemia is also a frequent cause of headache, and the diagnosis
must  not be  made by  observation  of the color of  the lips and the
conjunctiva,  but the heart  and large vessels leading off from the
heart  should  be carefully auscultated, and, if necessary, a microscopi-
cal  examination should be made  of the blood.  The  diaguosis is
readily made.
  Alcoholism is not a  very frequent cause of headache, but it does
sometimes produce it.
  The headache of lithsemia is not mentioned here because  it is  a
true  headache, but rather  because I  desire to  call attention to the
fact that it  is more  often a  sense of pressure and fulness about the
head.
  Headache  may sometimes occur reflexly  from  disease of  non-
nervous organs,  such as the stomach and the pelvic viscera, the latter
especially in the female; but this cause is by no means  so frequent
as is generally supposd.
  The headache of  melancholia, like the headache of lithsemia, is
not mentioned here  because it is a true headache, but rather  to call
attention to its distinction from a true headache.   The melancholiac
suffers only from various  abnormal  sensations  about the head when
he is  afflicted with what I have called  simple melancholia,  and in
such a case the sensations arc mainly or  entirely in the  back of the
head and neck,  but  they will  sometimes  pass  up to the vertex and 
NEBVOUS SYMPTOMS COMMON TO DIFFEBENT DISEASES.  497

diffuse themselves over the head, and  they may even occasionally
be intense.   The accompanying melancholia, the peculiar fades, the
insomnia, and the suicidal impulse will, as has already been stated
(vide " Melancholia "), make the diagnosis easy7.
  The process of acclimation will often  produce vague, diffused
headache that may at times become quite severe, and this process of
acclimation, as  is often  overlooked, is  not only  observed in those
who take up a permanent residence in a place, but in those who go
to a different climate for a short time.   It is constantly seen in the
mountains  and at the seashore during the summer movement of our
American  population, and in a less degree  in  the  winter resorts.
Nor is it observed only in those  who have made a great  change of
climate, for even the dwellers  in our seaboard cities suffer from it in
first taking up their residence at the seashore.   It is generally, but
erroneously, ascribed to errors of digestion, although often no proof
whatever can be obtained of the  existence of these.
   Indigestion is sometimes a cause of headache, but not  nearly so
 often as is  generally supposed.
   Intracranial lesions causing headache can, of course, be  readily-
 diagnosed  by means of the characteristic symptoms, such as neuro-
 retinitis  or optic-nerve atrophy, paralysis of motion  and  sensation,
 word-deafuess, aphasia, blindness or partial defects of vision, vomit-
 ing and convulsions.  The headache of intracranial syphilis is, as I
 have already stated  (" Syphilis  of the Nervous System"), a quasi-
 periodical  headache occurring either toward night  or during the
 afternoon, sometimes in the  morning, and is accompanied  by obsti-
 nate insomnia,  and  the  headache and the insomnia  cease  upon the
 supervention of paralysis or convulsions, or dementia—i. e., upon the
 supervention of destructive lesions.
   Of all the spinal  lesions,  locomotor  ataxia is the only one that
 will give rise to headache, and this is only exceptionally.   When it
 does occur it is an  intense burning, stabbing, or  lightning-like pain
 that either comes and goes  with great violence and caprice, or iu
 some  exceptional cases is  localized.    The  diagnosis,  however,  is
 readily  made  by the coexistence of other symptoms of locomotor
 ataxia, such as  the characteristic ataxia, stabbing and lightnjng-like
 pains in the limbs and truuk, the loss of knee-jerk,  the optic-nerve
 atrophy, aud the bladder-symptoms.
   The prognosis of headache will depend, of course, upon the cause.
 That of lithsemia, eye-strain, alcoholism, ansemia, acclimation,  and
 reflex disorders is  good.  The  headache  of nephritis is  of serious
 omen, unless the nephritis is an acute and  transient one, such as
 occurs in children after the exanthemata, or in some cases  in adults.
 The headache of intracranial  lesion is usually a serious matter, except
 in the case of intracranial syphilis in  the early stages, before struc-
 tural lesion has taken place, as indicated by paralysis and convul-
 sions, when it  may be entirely  cured by vigorous and proper treat-
 ment.   The  headache of locomotor ataxia  is of grave  prognosis,
 although it may often be alleviated considerably.
    The treatment of headache depends upon the cause to a certaiu
                                 32 
498
NEBVOUS DISEASES.
extent, for if this  is  removable, such removal may be all the treat-
ment that is required.   For the relief of the pain itself the best drugs
are opium or morphine, antipyrin, phenacetine, the bromides, canna-
bis indica, menthol, and cerebral galvanization.   Opium, or, better
still, its alkaloid, morphine, is undoubtedly the best drug with which
to relieve violent and  acute  headache, and the physician should not
hesitate to employ  it in proper cases.   He should always administer
it himself hyrpodermically, however, and never trust the hypodermic
needle in the patient's  hands, nor should he give it by the mouth, not
only because it is far less efficacious  than when given hypodermically,
but also because there is great danger  of the patient forming the mor-
phine-habit.  It should be laid down as an axiom that a headache must
be controlled and that the headache-habit must be broken up, and, if
necessary, this must be done by means of morphine.  In most cases,
however,  it  will  not  be  necessary to  resort to this drug, which,
although it is undoubtedly the most efficacious, may  yet lead to the
formation of a dangerous habit.  It  is a  curious  clinical fact that
although morphine or opium may be  given with impunity in melan-
cholia, so far as  the formation  of the habit  is concerned, it is very
apt to lead to the  formation  of such  a habit when used in simple
headache unless there  is a grave necessity.  In other words, it would
seem as  if great pain or grave disease protected the human being
against the formation of the morphine-habit.  Antipyrin undoubtedly
stands next to opium in its effect upon the headache, but the objec-
tion to the drug is that it is apt to be depressing, aud it should there-
fore be employed with great caution.  It is best to give it in doses of
5 grains every hour or two until the headache has been controlled or
until 15 or 20 grains have been given,  watching the pulse carefully all
the time, and ascertaining  by the experience of one attack what the
patient can stand iu the next.  Phenacetine is not a reliable drug in
cases of headache,  as it has in my experience a more peculiarly bene-
ficial effect upon the nerves of the  trunk aud limbs  than  upou the
nerves of the head  and neck.   Nevertheless, in some exceptional cases
it will act very well, and it  is  always worth while to make a trial of it
if the headache is not  very acute, as it produces very little depression,
so that doses of 15 to 30 grains may be  given to a healthy individual
of average strength in the course of the twenty-four hours.  The bro-
mides are not of much use except in the headaches due to acclimation
and migraine, in which they sometimes act like a charm, and occasion-
ally they will do very well in the  headache  of eye-strain, lithsemia,
nephritis, and some headaches that are due to intracranial lesions.
Cannabis indica is seldom of any use except in the headache of intra-
cranial  lesions  and migraine, but iu  the latter it  must be given in
continued doses of J or | grain  between the attacks, and during the
attacks  opium or morphine, bromide,  antipyrin, or phenacetine must
be employed.  Peppermint in doses of 10 to 15 drops of spt. menth.
pip. (U. S. aud B. P.) every  hour or  two, in a wineglass of water, or
in the form  of  a  menthol-pencil  rubbed  over  the aching head or
brows, is sometimes of great  use in  the lighter  forms of headache,
but it  is absolutely worthless in severe cases.   Cerebral galvaniza- 
NERVOUS SYMPTOMS COMMON TO DIFFERENT DISEASES.  499

tion is only of use in the cases of slight continuous headaches, and it
is valueless in  the acute attacks.   A small current of two or three
milliamperes, with a sitting of three minutes, repeated every day or
several times  in the day, should be employed. Combinations of these
different  drugs may often be made with advantage.  Thus, in cases
of migraine a combination  of cannabis indica with bromide of potash
aud phenacetine will  often act like a charm, as in this prescription :

       R.—Potass, bromid........3j.
           Phenacetine.......^ss.
           Cannab. indicae .......  gr. jss.
   M. ft. in chart, no. vj.
   S.— Dose, one powder in a wineglass of water ;  to be repeated as needed.

Or in the headache of intracranial lesion a combination of cannabis
indica, bromide of potash, and sulphate  of morphine, will also act
beneficially, as thus :

       R.—Ext. cannab. ind.......gr. ij.
           Potass, bromid.    ......  Qiv.
           Morph. sulph........gr. j-
   M. ft. in chart, no. viij.
   S.—One powder once or twice daily, in a cup of milk, beef-tea, or cocoa.

  Sulphate of quinine may be combined  with some of these drugs
with great advantage in  certain  headaches, such as those of intra-
cranial lesion,  locomotor  ataxia,  acclimation, nephritis, and intra-
cranial syphilis.   It  is  a curious clinical fact, however, that the
headache of  intracranial  syphilis cannot  be  controlled by any of
these analgesics, and the best  remedy for it is the iodide of potash in
the large doses that have been recommended in the section on " Syphilis
of the Nervous  System."   When the headache is  acute, quiet, rest,
cold or warm  applications, as may be most agreeable, will be useful
adjuvants, and at such periods a brisk movement  of the bowels or
eveu an emetic will also aid greatly.   In  headache from  indigestion
a full dose of a reliable pepsin will often give remarkable relief when
the indigestion is stomachic, but when it is intestinal 5 grains of salol
will  act  much better  than pancreatin.  The salol may be repeated
three or  four times during the day if necessary.   The headache of
ansemia can  be overcome not  only by the administration of large
dose  of  iron (vide " Neurasthenia"),  but  it should  be  remem-
bered that this will often not be sufficient, and in such cases sulphate
of quinine, 2 grains three times a day, with g1^ grain of the bichloride
of mercury, should also be administered, and care should be taken
that the bowels are kept  in good order,  although there should be
no violent  purgation  or  excessive use of mercurials.  The general
health  in all  cases of headaches should be carefully attended  to.
The  diet should  be as  nourishing as possible, and great attention
should  be paid  to its variety.  Even in  cases of headache due to
indigestion  the patient  should not  be allowed to enter upon the
Sisyphus-like  task of eliminating  those  articles  of food which are
thought to cause indigestion, for experience has  shown me that 
500
NERVOUS DISEASES.
systematic elimination of this  kind very often leads to a downright
process of starvation.  The details of such a feeding process have been
fully  dwelt upon in the section upon " Neurasthenia."  Indeed the
treatment of  the different varieties  of headache should be  studied in
the different chapters in which I have discussed the various causative
lesions.
                           INSOMNIA.

  At the very outset  of this subject we  are met by the query as to
what  we know of the exact molecular alterations in the  brain that
constitute sleep, and to this our auswer must be absolutely negative.
There have been  all  sorts of theories, to be sure, as to the rationale
of sleep, but they  have been pure theories.  Durham,  Hammond,
Mosso, Veit, Pettenkoffer, and  others have thought that  sleep was
due to ansemia,  or, more properly speaking, to ischsemia of  the
cerebral substance, or to a diminished use of oxygen in the cortical
cells.   But no one has made  the  slightest effort to show whether
these  phenomena are cause or effect; nor is it possible in the exist-
ing state of our  scientific apparatus to know anything more, for the
molecular changes that  take place  in  purely functional  phenomena
can never be known until we have reached  such  a point in our
scientific development as  to be able to plunge some instrument into
the brain and study the  action of the living cell.   It must be re-
membered that the cortex of  the  brain, some alteration  in which
probably produces sleep, is a wonderfully complex structure.   Seven
or eight cortical layers have been described, each differing as much
from  each other  as do  the cells of different organs; and  we know
absolutely nothing of the function appertaining to each layer of cells,
except that there  is a probability that certain of the larger ones—
the so-called ganglion-cells—are possessed of nervous functions.
  At  the very beginning, therefore, we  must confront squarely the
unwelcome fact that sleep aud its derangements must be studied from
a purely clinical and therefore somewhat empirical point of view,
and that  in  order  to combat insomnia  intelligently we must study
the conditions of disease  in which it is  manifested.   Limiting our-
selves in this manner, we find that insomnia is caused by—
       The passions, especially worry, anxiety, and grief;
       Pain ;
       Febrile disorders;
       Neurasthenia;
       Certain insanities;
       Certain organic diseases of the cerebrum ;
       Certain drugs or food-substances.
  The treatment of insomnia will vary  very greatly according as it
is beiug produced by one or the other of these causes, with which it
will be best to deal separately.
  At  this point  it may be well to dwell  for a moment upou  the
means at  our  disposal  for inducing sleep,  aud especially  upon  the
different hypnotics now in vogue, namely: chloral, sulphonal, trional,
chloralamid, urethan,  and paraldehyde.    I  have  ranked these in the 
NERVOUS SYMPTOMS COMMON TO DIFFERENT DISEASES.  501

order  in which I consider them the most efficacious.   In my hands
chloral hydrate is the most effective  of them all; but it is a drug
which I rarely employ, because of the depressing effects it  is likely
to produce, especially if long continued.  Sulphonal  is the drug
which has acted best, by all odds, in my hands, although I seldom
give it alone, but usually in combination with  bromide,  or, as  I
shall have  occasion to indicate later on,  with opium.  Ten  grains
of sulphonal, with 10 or 20  grains  of the bromide of potassium,
are an effective sleep-producer in the majority  of cases, and  the dose
of sulphonal can be  increased, if necessary, to  20 or 30 grains,
although it is  seldom necessary  to  give  more  than 20 grains of
bromide.  Sulphonal  should always be  given  about an hour before
bedtime, best in a cup of bouillon, soup, milk, or chocolate, or in a
compressed tablet.   In my experience it is not absorbed for  an hour
or so, and its maximum  effects are  produced three or four hours after
it is taken ; so that it  is not a reliable drug to produce sleep  quickly,
for which purpose chloralamid is preferable.  The dose of chloralamid
should be much larger  than that of sulphonal, never less  than 30
drops at the outset, and  frequently 40 to 60.  The objection to it is
its taste, which can be disguised by giving it in  capsules or  tincture
made with  some bitter substance.   Lately, however, it is  made into
compressed tablets, which are the best means of administration.  In
many cases, when it  is necessary to  induce sleep  immediately, and
when  the sulphonal alone  or with the  bromide will  not  do this,  I
use chloralamid first, and theu instruct  the patient to take  the sul-
phonal when  drowsiness is  beginning.  Trional is fairly  reliable in
some cases, but it is capricious in its effects, and  much more apt to
produce unpleasant  results.   Urethan in  my  hands has not been a
reliable drug except in the very mildest forms of insomnia.   Paral-
dehyde is ranked  by some authors  as a very effective  hypnotic,
but I have not found it reliable, perhaps because my use of it has
been limited  on account of the very unpleasant,  mawkish  odor of
the breath  that  it is  apt to induce in  certain  patients when con-
tinued.  This odor  cannot be removed by any means that   I have
tried, although  the tincture of bitter orange-peel  has been  vaunted
against it—which, however, I have  found to be perfectly useless.
Aside from the use  of these hypnotics,  pure and simple,  we can in
some cases induce sleep by mental and physical repose, by hypnotism,
by cold  and warm effusions, by electricity, byr change of scene and
surroundings, by travel, by massage, and by stimulants.
  Probably the most  intractable  of all forms of insomnia is that
caused by the passions.   In such cases it becomes a matter of infinite
tact to know how far  it  is best to use a pure hypnotic and  to what
extent it is  wise to accustom the  patient to the use of such drugs.
Usually, however, sleep  can be at least temporarily induced by the
employment of the bromides in combination  with one  of the pure
hypnotics.   Isolation  that shall  conduce  to  mental and physical
repose will,  of course,  be of very great aid; but, after all, there is no
means, save time, of lessening the  perturbation of a great passion. _
  The insomnia produced by pain usually proceeds from  neuralgia, 
502
NERVOUS DISEASES.
neuritis, the  early  stage  of pleurisy,  pneumonia,  peritonitis, and
certain acute  pelvic affections in the female, articular and muscular
rheumatism, certain painful affections of the eye, certain infectious
disorders (especially influenza), intracranial tumor,  cerebral menin-
gitis, aud  intracranial syphilis.    In  all these conditions  the rule
should be to  ascertain first how far the pain can be controlled by
the proper treatment  of the disease, aud then how  much sleep will
come when the pain is relieved.   In no case, however, should anal-
gesics and hypnotics be used except as adjuvants to the proper  treat-
ment of the disease directly causing the  pain  and indirectly the in-
somnia.   Then the  next consideration should be as to whether the
pain is acute,  subacute, or chronic ; for while it may be permissible,
and often necessary, to use analgesics and hypnotics for the relief of
pain that is acute and  of short duration, it might be very inadvisable
to use them in chronic cases.   In  one disease, however, intracranial
syphilis, it is perfectly useless to attempt to overcome the pain or the
insomnia except by means of iodide,  with or without mercury, and
this should never be  forgotten.   In neuralgia the cause of the pain
producing insomnia should  always be carefully sought for, and it is
generally to be found in a condition of malnutrition or some direct or
indirect irritant.  In the case of malnutrition the pain and  the result-
ing insomnia should  first be treated by means of rest and abundance of
good  and varied food,  with milk and beef-tea (vide section on "Neu-
ralgia").  Every case of neuralgia that is not due  to a direct or reflex
irritant should be treated by means of such combination of rest and
dietetics, to which in many cases it may be useful to add iron, either
the dialysed or the  albuminate, in 2 or  3 drachm doses, three  times
a day, given in a cup of water after meals, or the peptonate of iron,
in compressed tablet, gr. iij three times daily, or ferratin, gr. iv-viij,
three times daily, in capsule.  But if  neuralgia is due to  a direct or
reflex irritant, it will have been caused by either a neuroma, a cica-
trix, a mass of callus, an inflamed joint, a pulmouary or  abdominal
adhesion, an inflamed viscus,  a lesion  of the  naso-pharynx, of the
ear, or of the eye (either error of  refraction  or muscular insuffi-
ciency or direct ocular lesion), nephritis, lithsemia,  gout, ansemia,
or  leucocythsemia; and all of these should be carefully sought for
and treated, if present, before the pain  and insomnia are directly
attended to.  Iu many of these cases, therefore, it will happen that
the pain and subsequent insomnia  will cease without the direct need
of any analgesics or hypnotics ; but if this should not be the case,
it  may become necessary  to relieve the  pain  absolutely, and  this
should be done by means of quinine in  2 or  3 grain doses, in com-
bination with  a reliable and fresh preparation of salicylate of sodium
in 2  or  3 grain doses, two or three times a  day;   or, if this will
not answer, phenacetine  may  be  added,  5  or 10 grains  at a dose;
or it  may even be advisable to try antipyriu, in doses of 10 to 15
grains, but I am very much  opposed to this drug because  of its
depressing effects, of which I have  seen some sad examples, so that I
should not advise its use even  in the most robust individuals, except
temporarily.  Blisters along the  course  of the  affected  nerve, or 
NERVOUS SYMPTOMS COMMON TO DIFFERENT DISEASES.  503

occasional cauterization with  the  Paquelin  cautery, will often be
found of great value.  Exalgine has not proved reliable in my hands.
If morphine is to be used, it should  only be for the control of acute
pain that cannot otherwise  be relieved, and then it should never be
given except by the physician himself.   I am not one of those  who
place much credence in the sensational stories about the formation of
opium-eaters by physicians, for I believe that when a man or womau
becomes an  opium-fiend, in the vast majority of cases  there is an
original defect  in that man or woman w hich would have led them
to form this or some  other habit  upon favorable opportunity.  I
kuow of no  reason why  all of us  cannot steal  or forge  or take
opium  or hasheesh  or  gamble or lie or do other things which the
moral sense of civilization condemns, unless it is that we have within
our brains and spinal cord that restraining force which physiologists
call inhibition  and  theologists call  conscience; and  the individual
who forms the opium or any other drug-habit is usually oue of those
afflicted with an hereditary or personal predisposition toward vicious
habits.  I should therefore not use opium in  one of this class, but I
should employ it freely for the relief of acute pain in one who is  not of
this type.  If hypuotics are needed, after all, sulphonal or  chloral-
amid  is usually the best.   Of neuritis  the same remarks  may be
made as of neuralgia.
  In the early stage of pneumonia and pleurisy the pain aud insomnia
may often be relieved  by hot  fomentations, an oil-skin jacket,  and
rest in bed,  without resort to analgesics or hypnotics;  and  either
analgesics or hypnotics should be administered with very great regard
to the condition of the heart and extent of implication of the lungs ;
indeed, in all cases it will be best, if possible, to rely upon the  effects
of stimulation  by means of eggnog,  milk-punch, and  some light
food-substance  at bedtime, rather than upon pain-relievers or sleep-
producers. If hypnotics have to be used, sulphonal and chloralamid
are again the best.
  In peritonitis opium can be  used with  a far freer hand than  in the
pulmonary affections, for the well-known reason that it restricts the
friction of the  peritoneum,  and it  may be quite sufficient to relieve
the  insomnia.  If not, hypnotics must be used, and I know of no
particular choice among them except for the general  reasons  that
have been stated iu  the introductory paragraph.
  These  same  considerations apply to the treatment of acute  pelvic
affections of the female.
  In acute articular rheumatism the salicylates, alkalies, lotions,  and
rest will usually be  found to be of more  value for the relief of pain
than morphine or the other analgesics; and therefore, if the iusomnia
is not relieved by the former means,  use should immediately be made
of the hypnotics proper, but these, of course, should only be employed
so long as the cases are acute, aud should be withdrawn as the dis-
ease becomes chronic, when the continuance of the  insomnia should
be met with some light food or stimulant; or with massage or  gentle
faradization  at bedtime.  The insomnia caused by the pain of articu-
lar rheumatism should  never be treated by morphine or opium  unless 
504
NER VO US DISEASES.
it is very acute, when it may have to be met temporarily in this way;
but in the vast proportion of cases  hot applications,  galvanization,
faradization,  massage,  salicylate of sodium, oil of gaultheria, and
rest, will suffice to overcome the insomnia if the causative disease is
properly treated.
  In some acute affections of the eye the pain may be so sharp as to
cause insomnia, and in  such conditions the relief of pain  by means
of cocaine will usually be all that is  needed, although it may happen
that morphine will have to be  used.   If we could employ cocaine
with such instantaneous effects about other parts of the body as we
can about the eye, we should have at our disposal for general anal-
gesic purposes a drug of far more potency than any of which we can
now boast.
  Certain acute affections of the ear causing sufficient  pain  to pro-
duce insomnia must, of course,  first be treated, so far as is possible,
by relief of the particular lesion  presented, but  if then  the insomnia
and pain continue, the former will generally disappear with the latter,
so that analgesics—best of all, morphine—will be all that is needed.
If the condition should,  however, become  chronic, then some less
dangerous pain-reliever should be used.  In  some irritable and hys-
terical  individuals, however, a very  slight irritation of the internal
auditory meatus in the form of some  little ulceration is often the cause
of considerable pain and insomnia, both of which maybe relieved by
treatment of the cause.
  When certain infectious diseases cause pain aud secondarily insom-
nia, it  may happen that analgesics alone may relieve, or, as is gen-
erally the case, both analgesics  and hypnotics will  have to be em-
ployed.
  Intracranial tumor seldom causes  insomnia, unless it is syphilitic;
indeed,  there  is often  a tendency to too much sleep, verging upon
coma rather  than insomnia.  If, however,  insomnia should result
in a case  presenting  symptoms of intracranial  lesions,  this fact
of itself should  render us suspicious  of intracranial syphilis, and
careful trial should therefore  be made at once of large doses of the
iodide,  commencing with thirty drops  of the saturated  solution
of the iodide of potassium, given  every four or five hours in a
full  tumbler  of water, Vichy,  or Giesshiibler, and increasing the
dose every day by three to five drops at  each dose, uutil  100 or
200 grains in the twenty-four hours  have been  reached  in cases
that have not been treated before for syphilis, and in cases that have
been so treated, until a dose shall be reached that is  fully double the
maximum of what they had ever  taken before.  I  have not  much
faith in the use of mercury in  intracranial tumors of syphilitic origin
or in intracranial syphilis.  Iu few of  these  syphilitic cases will
hypnotics or analgesics be found of any use.
  The pain of cerebro-meningitis can  usually be better treated  by
ergot, bromide of potassium, and iodide of potassium thau  by anal-
gesics, and these will often be  sufficient to relieve the insomnia if it
be dependent upon the pain.   Where  this is not the case, or where
the insomnia is a symptom per se of the meningitis, hypnotics must 
 NERVOUS SYMPTOMS COMMON TO DIFFERENT DISEASES.  505

be used; and of these I  think that chloral is usually by all  means
the best, if the cardiac condition of the patient will warrant it.
  The insomnia of  febrile  conditions will usually require the use
of hypnotics,  and those  used should be  governed by  the strength
of the patient.  I prefer sulphonal in these febrile conditions—10
grains of it with an equal quantity^ of bromide—and,  if necessary, a
small quantity' of opium or morphine, the latter hypodermically.
The sulphate of quinine or  strychnine  can be combined with them
with advantage in asthenic conditions.   Nevertheless, in none of the
febrile conditions should  the hypnotics  be used, in my opinion, un-
less the effect of alcoholic stimulants and the bromides has first been
tried.  Great care should  be taken not to  render the  patient depen-
dent upon any hypnotic.
  In  neurasthenia insomnia is not  apt to be a frequent condition,
for I think that most cases  of so-called neurasthenia with obstinate
insomnia are really simple  melancholia, with the diagnostic  symp-
toms to which I have already called attention, and to which I shall
again allude.   It may happen,  however, that neurasthenia will be
accompanied by a slight degree of insomnia, and  then  it should be
first determined as to whether the neurasthenia is reflex, lithsemic,
aural, or simple.  In many  of these cases the reflex irritant must be
removed, although  I  may  say,  in  passing, that too  much stress
should not be  laid upon slight  conditions of  non-nervous  organs
as possible reflex causes, and the connection between cause and effect
should be carefully demonstrated  before a positive conclusion is
reached.  In all these forms of neurasthenia the underlying  disease
must  be  treated, and most relief will be obtained from dietetics  and
rest rather than from hypnotics.   Neuralgia and neurasthenia of the
simple variety are best treated in the way that I  have indicated when
speaking of neuralgia.  If the insomnia  should not be relieved by
this general treatment, a glass of milk, a cup  of cocoa,  or  a half-
ounce of whiskey in  a milk-punch  or  eggnog,  or in water, as the
patient may desire,  should  be given at bedtime, with, possibly, in
those who can digest food at this time, a light supper.
  In certain exhaustive diseases, such as typhoid fever and ansemia,
hypnotics should  never be used until they become absolutely neces-
sary, as every purpose will be answered by continued  doses of heart-
stimulants through the day, with or without quinine, and proper sup-
port through the twenty-four hours with alcoholic stimulants, with
an extra dose just before  bedtime in the  shape  of a  milk-punch or
an eggnog;  and I have seen hypnotics produce very disastrous results
in such cases.   If it becomes necessary to use them,  a  second dose
should never be given uutil  the  effect of  the first  one has been ob-
served  by the attending physician, and  only very moderate quanti-
ties should be employed.
  I have had occasion to call attention to a certain group of symp-
toms as diagnostic of simple  melancholia, namely, melancholia,  ob-
stinate insomnia, and a peculiar sensation  to which I have given the
name of post-cervical ache, which is  located iu the head, occiput, or
upper cervical  spine, and which is  differently localized  by each 
506
NER VO US DISEASES.
patient.   (Vide section upon " Melancholia.")   By means of these
symptoms a positive diagnosis can  be  made between  a commencing
melancholia and a simple neurasthenia.  The insomnia of this form
of disease should never be mistaken for the insomnia from the other
causes I  have enumerated, and attention to the presence of the post-
cervical ache and the peculiar melancholia should prevent any con-
fusion iu diagnosis.   The treatment of this form of insomnia is the
treatment of melancholia.  In  geueral  paresis  hypnotics  may he
needed, but  usually the administration of hyoscine,  jfa grain, or
hyoscyamine, j^q- grain (far preferably the  former, because it is much
less  depressing), together with  10 to 15  grains of the bromide of
potassium, will often be sufficient, when given two or three times a
day, to quiet the patient and overcome  insomnia.  Should this not
be the case, it will usually be because  the  excitement  has not been
removed, and then it  will often be wise to make use  of sulphonal
in 5- to 10-graiu doses, two or three times  a day, the last dose being
given  at  bedtime, with or without the hyoscine or the bromide of
potassium; but this should only be done with robust individuals, or,
if temporarily  employed with others,  the  heart should be watched
carefully, and  in all cases  it is usually best to give  tonic doses of
quinine at the same time. -In the  acute forms of insanity, such as
hallucinatory insanity or acute  paranoia,  insomnia is not  usually
more than a temporary symptom,  and it  can be overcome  by any
one  of the hypnotics.  The insomnia of the chronic  insanities be-
comes  a feature at certain times  of  the  month or at certain  periods
of the year, but it is scarcely worth while  to interfere  with it unless
it becomes very marked and disturbs the patient's nutrition, in which
case it will be best treated  by hypnotics  given with a light supper
at bedtime, or eveu with some alcoholic stimulant in debilitated cases.
  Certain  organic diseases  of the  cerebrum may produce insomnia,
such as tumors, the different forms of meningitis, abscess, and chronic
arterial disease; but  in  these maladies  there is more  of a tendency
to too much sleep, frequently bordering upon  coma,  rather than to
insomnia.  In one organic disease of the brain, however—intracranial
syphilis—as I  have poiuted out (vide section upon " Syphilis of the
Nervous System "), the insomnia in the early stage is apt to be very
obstinate, and is accompanied by quasi-periodical headache, the quasi-
periodicity beiug generally nocturnal,  although it not infrequently
comes  in the afternoon or morning, and the headache and insomnia
cease abruptly upon the supervention of any hemiplegic or convulsive
symptoms.  In intracranial syphilis the insomnia is  never  affected
iu the least  by hypnotics,  whilst  administration of  the  iodide of
potassium in sufficiently large doses will  invariably relieve it; and
for  this purpose use  should be made of the saturated solution of the
iodide, beginning with 20 drops after meals in  a full tumbler of water
or Vichy or Giesshiibler, and increasing rapidly by the addition of 5
drops  each day to each  dose until the  insomnia and  the headache
yield, or iodism has been produced.  No arbitrary dose short of these
effects  should deter  one in  the administration  of the drug.   As a
matter of fact, it will usually require  from 100 to 200 grains daily 
 NERVOUS SYMPTOMS COMMON TO DIFFERENT DISEASES.  507

for a  person who has not  been accustomed to much iodide, whilst
in old syphilitic cases it will require much larger doses, one in my
experience having  needed 600  grains in the day.  When the iodide
is given  in these large doses, as I have directed, it is  very seldom
that  any unpleasant  symptoms arise  from the stomach or the  skiu.
In intracranial  syphilis I have little faith in mercury, and I never
use it in these  insomnic cases unless I am  unable to push the iodide
far  enough, when  I  endeavor  to increase its effect by means of the
mercury, although  I  firmly believe that  for some unknown reasou
iodide  alone  is much more effective in these cases than  mercury
alone.
  Excluding  the insomnia which is  caused by  the passions,  pain,
certain exhaustive diseases, simple melaucholia, certain chronic insan-
ities,  and intracranial syphilis, the  most common cause  is to be
found in the use of certain drugs, stimulant narcotics, or foods; and
insomnia from  these  three latter causes is  much more frequent than
is generally imagined.  We are all familiar with the effect of coffee
in producing sleeplessness, aud yet there  seems to be au idea that
coffee can be drunk  ad libitum in the morning if it be avoided at
night.   I have  found  that many individuals have sleeplessness which
 is produced by  this cause.  Tobacco  in some susceptible individuals
will produce  insomnia when used in any  form, aud the only safety
 for such persons is to eschew it altogether.  I am inclined  to think
that the number of such people is larger than is geuerally supposed.
 Tea is also a  substance that will produce insomnia, although not in
 many cases.   Some individuals have a susceptibility to certain kinds
 of wine, so  that one individual  cannot drink champagne  for this
reason, another cannot use burgundy,  a third cannot employ brandy,
 and a fourth  must abstain from pork.

                             COMA.

   Coma may result from—
       Trauma;
       Nephritis;
       Alcoholism ;
       Diabetes;
       Cerebral hemorrhage ;
       Epilepsy ;
       Migraine.
   In  every  case the  treatment of coma will materially  depend, of
course, upon  the cause, so that the diagnosis of the  latter should be
carefully made.
   In  trauma  the patient should be allowed to recover from the shock
of the injury, which  should be remedied as soon as possible, so that
fractures of the bones of the extremities,  trunk, skull, or cord may
be properly attended to or prevented from complicating matters by
pressing upon the viscera which they  should shelter.
  In  nephritis  the patient should be  purged  freely, best by l-grain
doses of a reliable preparation  of elaterium, or by croton oil, 1 or 2 
508
NERVOUS DISEASES.
drops at a dose, at the same  time that a profuse perspiration  is in-
duced either by a hyrpodermic injection of pilocarpine or a full dose
of jaborandi.
   In the coma of alcoholism there is, of course, nothing to be done
but to sustain the patient's strength,  if need be, and wait  until the
effect of the alcohol has passed away.
   In diabetic coma free purgation will be most effective.
   In the coma of cerebral hemorrhage a careful inquiry should at first
be made to ascertain whether it is the cerebral hemorrhage of nephritis
or chronic endarteritis, of  general  paresis or some other structural
disease,  such  as disseminated sclerosis,  tumor,  etc.   The diagnosis of
nephritis can always be made by examination  of the urine, and pos-
sibly by oedema  of the eyelids, feet, and  hands.   The diagnosis of
chronic  endarteritis can  be made by the  exclusion of nephritis, by
the presence of tortuous and rigid arteries, by a hypertrophied heart,
and  by the age of the patient.   The diagnosis of disseminated sclero-
sis may be much more  difficult unless a history of the  patient has
been obtained before the  coma  supervened, although  the  fact of the
patient being a youth or young adult with a tremor may lead to a
suspicion of the cause. 
CHAPTER  XII.
         SOMNAMBULISM AND ALLIED DISORDERS.

                      SOMNAMBULISM.

  Somnambulism is a curious phase of nocturnal cerebration that is
most aualogous to  the condition which is  produced by hypnotism,
whilst its next closest analogue is the double consciousness which is
occasionally observed in epileptics.  Although the  somnambulistic
mind  is usually much more automatic than the waking one and
capable of a far less degree of reasoning intelligence, there are yet
some remarkable instances upon record of the  intellectual vigor of
this semi-dreaming  state.   An  old  friend  of mine, a physician of
distinction, tells me that  when  he  was at college he had a  certain
essay to complete, and  that  he went to bed tired out, intending to
complete it the next morning; but when he awoke, he found the essay
completely written to the end in his own handwriting  with exactly the
same vein of logic and subtle thought in which  he had begun it, so
that he must have gotten  up in  the night and finished it in  a som-
nambulistic condition.  Tuke tells  of a schoolboy who had been set
to prove the 47th problem of Euclid,  Book I., but he was unable at
first to master it, and retired to bed still thinking of the subject.  He
was found by his teacher late at night kneeling on his bed with his
face to the wall, pointing  from spot to  spot as if following a proof in
a figure on a blackboard,  so absorbed in his occupation  that he paid
no attention to the light of the candle or when addressed.   The next
morning the teacher said  to  him :  " Well, John, have  you finished
your proof?"  To which he  replied :  "Yes, I have; I dreamed it,
remembered my dream this morning, got out of bed as soon as I
could see, and wrote it out at the window."   Another story is told of
several ambitious young ladies, who found in the morning that they
had learned their lessons without any  knowledge of having  studied
them.  This puzzled them all for some time, until late one night the
mother, returning home  from a visit when the  moon  was shining
brightly, found one of her daughters seated at the window in her
nightdress only, sound asleep, with her lesson-book in her hand.  In
1878 a man named Frazer killed his child in Glasgow.   When he
was put upon trial some most remarkable facts were  proved as to his
somnambulistic feats.   He had been accustomed when a boy to fetch-
ing milk from a farm near by, so he once got up in  the night while
asleep, dressed himself, got the pitcher, and went to the farm.   At
another time, when asleep, he went to a timber yard and moved logs
until the rain awoke him.   When a young man of tweuty-one he
was frequently found at the landing-place of a pond, asleep, walking 
510
NER VO US DISEASES.
into the water, loudly calling  his  sister by name, and reaching out
his arms as if to rescue her from drowning.   Although the contact
with the water sometimes roused him, it did not always do so.   He
had no recollection whatsoever  in  the  morning of these  escapades.
At other times he would wake up in the night with a feeling  of some
great impending evil,  such as that the  house was on fire, that its walls
were about to fall  upou him, that his child was falling down a pit,
or that a wild beast had got into the  room and was about to attack
him, so that he would  tear his wife aud child out of bed to save them,
all  the  time roaring  inarticulately; or  he would  pursue the beast
through the room, or  he would suddenly seize his companion by the
throat with the idea that he was engaged in a struggle with the beast.
His eyes would be wide open and staring, he would avoid the furni-
ture, would lift up chairs and throw them at the beast, and had often
injured  himself.   He  had frequently attacked his father, wife, half-
sister, fellow-lodgers, and a fellow-prisoner in the jail.  When he killed
his child he  had seen  " a large white  beast flying  up from the floor
and passing  through the back of the bed where the child lay; he
grasped at the beast, trying to  catch it;  succeeded  in  seizing it, and
springing out of the bed, he dashed it on the wall or floor to  destroy
it."  He manifested the greatest horror  upon coming  to and finding
what he had done.  A  pupil of the school of St. Pons, while somnam-
bulistic, attempted to stab his teacher in the night, was disarmed, and
taken to another room, where he slept till morning, when he had not
the faintest memory of what had taken  place.   A certain Madame
X., whose story is told by Mesnet, made  a  suicidal attempt in his
presence whilst she was somnambulistic.   She  made a noose of her
apron, fastening one end to a chair and the other to the top of the
window.  Then she kneeled down  in prayer, made the sign of the
cross, mounted the stool, put her  head  in the  noose, and tried to
hang herself.  Mesnet,  scientific to the core, very properly let her
hang as long as he dared to, and then stopped the performance.
At another time she attempted to kill  herself by violently throwing
herself on  the floor, after having failed to fling herself out of the
window.  At still another  time she tried poison, filling a glass with
water, putting several coins in it, and hiding it after bidding fare-
well to her  family in  writing; the  next night,  when  she was again
somnambulistic,  she took the  glass, but changed  her mind again,
writing to her family explaining  her change  of purpose.   Mesnet
relates some interesting experiments made upon a French sergeant in
a condition of somnambulism, demonstrating the excitation of ideas
in the mind through the  sense  of  touch  in the extremities.  This
soldier  touched a table, passed his  hands  over  it, and then,  finding
nothing, opened  a drawer, took  out a pen, found paper aud  an  ink-
stand, got a  chair and  wrote  a letter to  his   commanding officer,
speaking of  his own  bravery and asking for a medal.  A thick
metallic plate was then placed before his  eyes  so  as completely to
intercept vision.   After  a few moments, during which he wrote a few
words with a jumbled  stroke, he stopped, but without any petulance.
The plate was removed, and he went on writing.   Water was  sub- 
SOMNAMBULISM AND ALLIED DISORDERS.
511
 stituted for the ink, and when he perceived  this, which  he did
 quickly, he stopped, carefully examining the pen but not the inkpot.
   The prognosis of somnambulism  is usually good, as the phenom-
 ena can generally be made to cease by judicioustreatment.
   The diagnosis is a simple matter, and difficulty concerning it can
 only come up in a criminal case, when, of course, the previous history
 of the patient will be  of crucial importance.
   The physician should endeavor  to break up  the somnambulistic
 tendency as well as treat the immediate attack.  The general health
 of the patient should be carefully ascertained, any mental or physical
 overstrain  removed, and any tendency to ansemia  should  be reme-
 died.   The treatment of the immediate attacks should be by the
 use of belladonna, bromide of potash, circumcision, and removal of
 genital or rectal irritation, or by suggestion of some device for effec-
 ting a sharp tactile  impression just prior to the  onset of the attack.
 Belladonna should  be used in the  form of a  reliable fluid extract,
 one to two or  three drops just before going to  bed.  If this fails,
 bromide of potash, in water, 20 to 60 grains, according to the age and
 strength of the patient, should be administered at bedtime.  If neither
 the belladonna nor the bromide of potash acts beneficially, they should
 be tried in combination, always  at  bedtime.   In some cases sugges-
 tion has  been of considerable efficacy; thus an epidemic in a school
 was stopped by peremptory commands to the boys  before they went
 to bed not to have any attacks during the night.  In  two cases
 also I was  able  to bring about a cessation of the attacks by hypno-
 tizing the patient for several successive evenings, and in one case by
 hypnotizing the  patient during the daytime in  my office, and then
 peremptorily making the suggestion that he would  have no more at-
 tacks. Circumcision has sometimes been found to be of great use, even
 when there was  no  genital irritation ;  and I  have known a case in
 which treatment of a leucorrhcea in a young  girl  was  curative.
 Ascarides should also  be treated, if present.  Attacks can sometimes
 be cut short by a sharp tactile impression, as by placing a  tub of
 cold water in such a way that the patient must step into it in getting
 out of bed.
                     ECSTASY,  or TRANCE.

   Ecstasy is a rapt condition of mind in which ordinary impressions
 are not received in the ordinary way.
   This is a rare condition which generally occurs in hysterical indi-
 viduals.  Probably the most remarkable case on  record, and the one
 which has  been best  studied, is that of Louise  Lateau, of Bois
 d'Haine.   This  occurred  in  1869,  in  a village of Belgium,  in a
 girl of twenty-three, whose previous  life had offered nothing remark-
 able.  One Friday  Louise Lateau  noticed that blood was flowing
 from the left side of her chest, and this recurred every Friday.  On
 each Thursday morning  an oval  surface, about one inch in length,
 on the back of each hand, became pink in color and  smooth, whilst a
similar oval surface on the palm of each hand took on the same hue,
and on the  upper surface  of each foot a pinkish-white square ap- 
512
NERVOUS DISEASES.
peared.  Examined under a magnifying glass, the epidermis appeared
at first without solution of continuity, but delicate.  About noon on
Thursday a vesicle  formed on the pink surfaces, containing clear
serum.  In the night between Thursday and Friday, usually between
midnight and one o'clock, the flow of blood  began, the vesicle first
rupturing.   The amount of blood lost during the so-called stigmata
varied, aud some observers estimated it at about one and three-fourths
pints.   The blood itself was of a reddish color, inclining to violet,
therefore of about the hue of capillary7 blood, coagulating in the usual
way, and the  white and red blood-corpuscles being normal  both in
character and  relative proportion.  The  sanguineous flow ceased on
Saturdays.  During the flow of the blood the patient  was in a rapt,
ecstatic  condition.   The facial expression was one of absorption and
far-off contemplation, changing often to  melancholy, to terror, to an
attitude of prayer or deep contrition.   The patient herself stated that
at the beginning of the ecstasy she imagined herself surrounded by a
brilliant light, theu figures passed before her, and the successive scenes
of the crucifixion were panoramically progressive.  She saw Christ in
person, his clothing, his wounds, his crown of thorns,  his cross, as well
as the Apostles, the holy women, and  the assembled Jews.   During
the ecstasy the circulation of the skin and heart was regular, although
at times a sudden flush  or pallor overspread the face, according with
the play of expression.  From mid-day on  Thursdays, when she
took a frugal meal, until eight o'clock on Saturday mornings, Louise
Lateau took no nourishment, not even  water, because it was said that
she did not feel the want of it, and could not retain anything upon
her stomach.  During  this time the  ordinary  secretions were sus-
pended.  Tuke  has resurrected the remarkable  case of John Engle-
brecht, reported by Arnold, of Leicester, in  the early part  of the
century. This man passed  into a condition of catalepsy in which he
heard everything about him distinctly, but seemed in his imagination
to have passed away to another world, this coudition coming on with
a suddenness  which  he  describes as " far more swiftness than any
arrow can  fly when  discharged from  a crossbow."  He always lost
his sensation from the head downward, and recovered it in an inverse
direction.
  These conditions of ecstasy or trance  are  very rare, as  I have
already said.   Much  ado has been made about the danger of people
being buried  alive whilst in this condition, aud  an indictment was
brought  two  years  ago  in  the city of New York against two well-
known  physicians, who were alleged (without the slightest evidence)
to have made a  post-mortem upon a person  in this condition.  As a
matter of fact, there  are but  very few  so-called authentic cases of
premature  burial, if any.  A well-known editor in this city has for
many years had  the scientific fad of ascertaining the facts about every
such supposed case, and in  no single instance has he found sufficient
evidence to warrant him  in a belief  that a person  had been buried
alive.
  The prognosis of ecstasy is usually good.
  The diagnosis is easily made. 
SOMNAMBULISM AND ALLIED  DISORDERS.
  The pathology of the condition is totally unknown.
  The  treatment  should consist  of general hygiene,  dietetic  and
medicinal measures, and also of hypnotic suggestion.

                          CATALEPSY.

  Catalepsy is a condition in  which  there is a peculiar wax-like
muscular rigidity, loss of sensation, and complete suspension of nor-
mal mental action.  The  paroxysms last for minutes or hours,  and
in some cases they even continue for days.  The  limbs retain  any
position in  which they are placed.  There is often a neurotic heredity,
and frequently the immediate exciting cause is au emotional disturb-
ance.  The prognosis is  usually favorable.  The pathology is entirely
unknown, although in  a few cases some cerebral lesions  have been
reported which were  probably merely coincidental.   The condition
is undoubtedly similar  to  that which is known as cataplexy (vide
"Hypnotism") and is, therefore, akin to  the  hypnotic condition.
The diagnosis  is made with great  ease.   The treatment should be by
means  of general dietetic,  hygienic, and medicinal measures, as in
somnambulism and ecstasy, aud  in several instances suggestion has
been found to  be of great efficacy.

                        NIGHT-TERRORS.

  When a  child has night-terrors, as is well known, it  starts  up in
its sleep with  a cry, the eyes staring, the  face twitching, and seems
to be alarmed, whilst no persuasion or soothing has  anything more
than a slight  effect, the child  being really in a condition analogous
to that  of  the somnambulist, with the difference that  the attack is
temporary and does not lead to perambulation.  These troubles are
very apt to have  the same causes as somnambulism, namely, predis-
posing ones of heredity, bad health, indigestion, constipation, worry,
anxiety, and exciting ones of over-eating, intestinal parasites, mental
strain, etc.   But night-terrors  are much  more  manageable than is
somnambulism.  They  can best  be  treated by means of bromides,
belladonna, warm baths, electricity, removal of any indigestion,  and
circumcision.  When  the bromides  are given, they should  be used
in doses of 10 to 30 grains, according to the age of  the  child,  and
administered an hour or so before bedtime.  The dose of belladonna
should  be  sufficient to  cause moderate dilatation of the^ pupil  the
next morning and slight dryness of the throat, although it may not
be necessary to have these effects continued throughout the day.
Occasionally a tepid bath every second night at bedtime will answer
the purpose. Electricity is  not usually of great value in  this malady,
although it will occasionally do good.  I prefer general faradization,
which can best be employed in these cases by having the whole body
faradized, with a gentle  current just strong enough to  be perceptible,
by a nurse or  mother just before the  child goes to bed.  For  this
purpose any good electric battery  will answer.  It should have  two
electrodes (see  Fig. 71)  covered with absorbent cotton, which should
                               33 
514
NERVOUS DISEASES.
be well soaked in warm water before being  used ;  and these should
be kept about two inches  apart whilst about fifteen to twenty min-
utes is taken to go over the surface of the body.  Any causes of indi-
gestion in a child with night-terrors should  always be removed, and
in all cases it is well to have the evening meal a light one.  Circum-
cision is  generally of very great avail, for although its effect is only
temporary, yet in so functional a disease this is often  quite sufficient
to lead to a cure.  It may even be done with  benefit in cases in which
there is no phimosis or redundant prepuce.

                          HYPNOTISM.

   Although the phenomena which are now classified under the name
of Hypnotism have only been scientifically studied during the latter
half of this century, there  is yet excellent reason to believe  that they
were known to the ancient nations of the East of whom there is any
history, to the Greeks in their  palmy days, to the Romans, to the
Egyptians, and to the nations of Europe that slowly evolved into
civilization after the downfall of the Roman Empire.  The fakirs of
India, the magicians of Persia, the oracles of Greece, the seers  of
Rome, the priests and priestesses of Egypt, the monastic recluses  of
the Middle Ages, and the  ecstatics of the seventeenth and  the early
part of the eighteenth centuries exhibited many symptoms that were
and are still attributed by  religious enthusiasts to supernatural agen-
cies, but which are explicable by what we know of hypnotism.  The
Hesychasts of Mount Athos, who remained  motionless for days with
their  gaze  steadily directed to the  navel;  the Tasko-drugites, who
remained statuesque for long periods with their finger applied to the
nose; the Jogins, who could hibernate themselves at will;  the Dan-
dins of India, who became cataleptoid by twelve thousand  repeti-
tions of the sacred  word  "om;" St. Simeon  Stylites, who perched
on a  lofty pillar, preserved for days an attitude of saint-like with-
drawal from earthly things; and even Socrates, of whom  it is said
that he would stand  for  hours motionless  and wordless—all these
were probably instances of auto-hypnotism.   But when Mesmer began
his career  in Paris, in 1778, the  attention of scientists  was first
directed to  the subject, although he had written a paper  upon the
subject some eleven years  before aud had presented it to the medical
faculty of the University of Vienna.  Mesmer's career in Paris was
a singular one, and it is difficult to form an  opinion as to how much
he was actuated by true belief and how much by mere sensationalism
and cupidity.  Certain it  is that he was one of the leading figures  in
the great European capital  until the public mind was  diverted by
the terrible events  of the French  revolution.  His  waiting-rooms
came to hold such mobs of so-called patients that  he  finally devised
his celebrated baquet, which was nothing  more  than a  great tub
filled with  broken glass and odd  remnants of metal,  the sides pene-
trated by pieces  of  wire, so that the  patients could sit around this
queer receptacle, and, hypnotizing themselves  by  grasping hold  of
the wires,  thus  economize time!   Since the time of Mesmer the 
SOMNAMBULISM AND ALLIED DISORDERS.
515
subject has been studied with increasing interest, and the literature
of it has grown  to be so enormous that Dessoir has lately compiled
a bibliography covering some ninety pages of  quarto size.  Braid,
of Manchester, paid great attention  to the  matter  from  1840 to
1860.  Of late years Charcot and  his  scholars in Paris, Pitres in
Bordeaux,  Ladame in  Geneva, Binswauger  in Jena, the so-called
school of Nancy—consisting chiefly of Bernheim, Beaurnis, Liegeois
—Renterghem and Eedem in Holland, in England  the Society for
Psychical  Research and Hack Tuke, have attempted to  study the
matter in  the light of modern  methods  and  clinical knowledge;
whilst  in America,  Grimes, Dodds,  Stone,  Darling, Durand De-
Gros, and Beard, have contributed their quota, and even the quack
Perkins made for himself an unenviable  reputation with his cele-
brated metallic tractors.  Czermak (1873), Prior (1878), and  Hoe-
bel (1876) have demonstrated the existence  in animals of similar
phenomena, to which they have given the name of cataplexy.
   There are  many methods of hypnotizing the human being, and
those who can be  hypnotized, either  from natural predisposition or
from training, can be put into this  condition very readily in differ-
ent ways that have suggested themselves by  experience, either with
or without the  aid of other persons.   The methods are usually as
follows : Let the person to  be hypnotized take some object in one
hand and  regard it fixedly;  or let the hypnotizer take the hands of
the person to be hypnotized, lift them  up and move them slowly
from above downward, from the top of the head to the stomach,
parallel with the  front of the body, taking  care  not to touch the
body of the person to be hypnotized;  or let the hypnotizer place the
person to be hypnotized  upon a chair and  then  look  keenly and
sharply into his eyes;  or  let the  person to be hypnotized be seated
on a chair, then  let the hypnotizer say to him, " Think of nothing
else but that you will fall  asleep ;" then in a few minutes let the hyp-
notizer say, " Now your eyelids are falling; your eyes are becoming
 more weary ; the  lids  are  going nearer together;  now they are
trembling; now you are beginning to feel tired ; now your arms are
asleep; now your legs are asleep ; now your whole body is becoming
heavy aud sleepy ;" and so on in this vein.  Braid hypnotized all his
patients by having them look fixedly at an object held or fixed well
above the  level  of the eyes, so that the ocular  muscles would become
weary, which is the method I generally employ; and he narrates
many curious instances of how effectual this was, especially in the
case of his man-servant, whom he would  usually put into this con-
dition  by  telling him  to  watch closely the flame of a spirit-lamp
in his laboratory.  All these methods can usually be  assisted greatly
by gentle movements of the hypnotizer's hand  across the brow and
down the sides of the  face, taking care always to make the move-
ments in the  same direction, as well as by occasionally closing lightly
the eyes of the subject  and pressing gently through the eyelids upon
the eyeball.
   There is a variation  in the behavior of hypnotized  individuals.
Usually, however, the  first  signs are a closure of the eyes, with a 
516
NER VO US DISEASES.
slightly tremulous movement of the eyelids.'  Beyond this  there are
four great manifestations of abnormal nervous and psychical condi-
tions which are grouped under the names of lethargy, catalepsy, sug-
gestion, and somnambulism.  In my experience the condition of leth-
argy is by far the most common.   In it the person is like one asleep,
and the unconsciousness is so pronounced in some cases as almost to
merge into coma.  On one occasion, when lecturing upon the subject,
I suspected a certain person of malingering, and therefore placed him
against the wall when he had passed into a seeming condition of leth-
argy ; but  in a few moments, whilst I was proceeding in my lecture
with my back turned to him, I  heard  a thud, and lo  and behold!
my patient lay prone upon the floor in an alarmingly comatose con-
dition !   I have upon a number of occasions seen lethargy as profound
as this, although such a pronounced condition is exceptional.  In
some individuals who have been rendered lethargic there supervenes
a curious hyper-excitability of the muscles and the motor nerve-points,
so that the limbs can be made rigid by merely passing the hand over
them ; or the motor nerve-points can  be touched with a pencil, and
contractions of the corresponding muscles will ensue as if a faradic
current had been employed.  Iu others the lethargy can be made to pass
into catalepsy, and one of the best means recommended for this purpose
by the Parisian school is to open the patient's eyes before a strong
light.  In some susceptible individuals, so Charcot and his followers
claim, the catalepsy may be made to affect only one side of the body
by opening only the eye upon  that side, and it  may be very pro-
nounced. In most individuals who have been passed into the hypnotic
condition suggestions may  be made of the most curious character,
and they will  be carried out after the  patient is awakened; and at
this time also there is sometimes a curious automatism displayed, so
that the hypnotized will imitate the hypnotizer's movements or repeat
his words.  When somnambulism can be evoked, it is by gently rub-
bing the vertex of the skull of an individual who is already lethargic
or cataleptic.   Persons in  this  condition,  half  conscious,  will re-
spond automatically to questions and commands, and  they will some-
times display a most remarkable increase of all their mental  faculties
and  sensations.   They  may be awakened  from  the  lethargy by
pressure upon the ocular bulbs, by shaking or  by slapping;  from
somnambulism, by laying a hand upon the vertex ;  from catalepsy, by
putting  before them a dazzling light,  but not infrequently a stronger
peripheral excitation must be employed, such  as  dashing cold water
upon them, blowing  into the face, pressure upon  the  ovarian region,
etc.  The Nancy school, however,  have demonstrated that a simple
suggestion or command to the patient to wake up will answer better
than any of those means;  and this I  have verified  over and over
again.   Very many other curious phenomena can be  evoked besides
those which  have been detailed; indeed, it is difficult to say what
cannot be done by an individual susceptible to hypnotism.
   The so-called cataplexy in animals is a much less complicated phe-
nomenon, as is  to be expected from the inferior organization of the
nervous system in these subjects when compared with that of the human 
SOMNAMB ULISM AND ALLIED DISORDERS.
517
being.   A chicken, a rabbit, a frog, a crab, a lobster, almost all birds,
can be put into a cataplectic condition by simply seizing them firmly
and quickly in such away as to make struggling impossible, aud then
gently and imperceptibly removing the restraining  hand, when the
animal will remain motionless in the position in which it has been
placed.  A chicken can be seized, for instance,  put into any position
that is desired, held gently but firmly there for a few seconds, and
then,  if  the hands are very gently removed without any abrupt move-
ment that  shall constitute a distinct peripheral impression, the chicken
will remain motionless for some time, even for a half-hour, as I have
frequently demonstrated.   Even wild birds of  passage can be seized
in the same way, and will lie  motionless in the hand of the person
seizing them when the fingers have thus been  carefully withdrawn.
During  this period of cataplexy birds  and  chickens keep their eyes
wide open, glance around,  move their heads and necks in order to do
it, and yet remain in the same position.  The success of the so-called
horse-tamers is probably due to such a condition of cataplexy having
been induced.   The awakening is done by a slight  peripheral impres-
sion, such as blowing  or touching with  the fingers.   That the ner-
vous impression is a profound one, although it  seems to be so slight,
is evidenced by the fact that I have often found frogs, tadpoles, small
birds, and even crabs, dead a  few hours after they had seemingly
recovered  from the cataplexy.
   It  is  impossible to doubt that we  are dealing with great laws  of
nervous action in these hypnotic aud  cataplectic conditions, but it is
as yet entirely a matter of speculation as to what the cellular changes
are, just as much as it as  yet a matter of speculation as to what the
cellular changes are in thinking, in sleeping, in the emotions,  in
neuralgia,  in  catalepsy, in hysteria, or  in  most of the insanities.
There has been a great war of words waged over  the question  as  to
how much of  these phenomena are due to hysteria or to suggestion.
That  the hysterical are more easily hypnotized than others demon-
strates that the theory of suggestion cannot be regarded  as offering
a full explanation, although it probably contains a large portion  of
the truth.  Certainly the cures  effected  by  so-called "Christian
science" and "faith cures" are indubitable evidence of the potency
of suggestion.   The truth of the matter  is that the whole subject is
one which has as yet been imperfectly studied, and the truly scien-
tific attitude toward it should be  neither one of skepticism nor cre-
dulity,  but simply of expectancy.
   Imposture should be readily detected.   Almost all individuals who
can be  hypnotized  will pass into the  condition of lethargy, and  if
imposture is suspected, it will be simply necessary to let the lethargy
increase, when the facial expression of the patient, the slight pallor,
the insensibility to painful impressions,  and the appearauces of un-
consciousness which are  familiar to every physician, will  show that
there  is  no simulation.  The  hyper-excitability of the muscles and
motor nerve-points  in the lethargic condition  cannot be simulated,
because contracture  and muscular  movements  in  the limitation of a
given nerve-branch  are not within the control of any person's will. 
518
NERVOUS DISEASES.
 I know of no  means, however, of detecting simulation of hypnotic
 catalepsy or of somnambulism.
   The percentage of persons susceptible to hypnotism has never been
 determined, as so much depends upon the skill and quickness of ob-
 servation of the  hypnotizer, but it is probable that most adults can
 be hypnotized, although  it cannot always be  done the first  or even
 the  second time, and  in  some  instances it may require a half-hour.
 Usually the superinduction of this  state is not attended by any ill
 consequences, but some individuals  may be so profoundly disturbed
 by it as to  suffer for hours or even days afterward from malaise,
 insomnia, nervous vomiting, nervous  excitability, etc.
   From a medico-legal point of view hypnotism is a matter of some
 import, for it is a question as yet not determined  as to whether a
 person  cannot  be made  to  commit  a crime by suggestion,  as was
 alleged  in the trial of the  Parisian  strangler, Eyraud, when it
 was  claimed  that his accomplice  in  crime, Gabrielle Bompard, had
 been hypnotized.   There  can be  no  doubt  that  outrage  can  be
 effected in the hypnotic condition,  and there  was a  notable trial
 demonstrating  this  a  few years ago in the south of France, as nar-
 rated by Bernheim.   Public exhibitions of hypnotism should be for-
 bidden  by law, and even  private exhibitions should  not be held
 except by competent persons  who are acquainted with the proper
 methods and the dangers of them.  It is my rule in my clinic never
 to hypnotize persons  without their  full  consent,  after explaining
 to them the possible ill consequences.
   The therapeutic value of hypnotism is small, it must  be confessed.
 The  French authors have done some wonderful things by this method,
 but  it would seem that  the Latin race is more hysterical, and from
 this  cause or from some other is more susceptible to hypnotism than
 the Anglo-Saxon.   Moreover, the  experiments which have been per-
 formed  by Charcot  have been  to a  large extent upon individuals
 congregated  within the walls of La Salpetriere, that great hotbed of
 neurotics,  and some of them have been hysterics of over thirty years'
 residence  in the institution.   Certain it is that no such results have
 been  obtained  either in  England  or in this country, except in  very
 rare  instances.  Iu hysterical individuals I have sometimes been able
 by hypnotism to disperse slight functional disturbances, such as pain,
 mild  forms  of neuralgia, nervous  irritability, even  light grades of
 insomnia.   In some cases of dipsomania, or even of intemperance, I
 have been able to control  the  extremely nervous condition and the
 insomnia  which is so apt to  follow prolonged drinking; but in none
 of the organic diseases of the brain, or the spinal cord, or the  insani-
 ties have  I ever seen any effect from  hypnotism.   It is a somewhat
 dangerous thing,  too, for a physician of  standing  to employ it,
 for it is associated in the  lay  mind, and even  in the medical, with
quackery  and  sensationalism, and so greatly did it demoralize the
discipline of one of my hospital wards that  I was reluctantly obliged
to forbid it there. 
CHAPTEE  XIII.
            DISEASES OF UNKNOWN PATHOLOGY.

                   FACIAL HEMIATROPHY.

  Facial hemiatrophy is a wasting of the bones, subcutaneous tis-
sues  and muscles, the latter suffering but slightly.  It is a rare dis-
ease, and needs only to be distinguished from  one-sided muscular
atrophy, which can be readily done because in the former there is no
loss of electrical reaction  in the facial muscles, and because there is
no atrophy of the  other muscles of the body.  It is a chronic affec-
tion, usually beginning in  early life, increasing slowly for years, and
then becoming stationary.  It is incurable.   The pathology of this
disease is  not as yet clearly ascertained, but the few autopsies that
have been  made would seem to show that the lesion is either in the
sympathetic, implicating the trophic fibres that run in this nerve, or
else that it is a peculiar form of multiple neuritis.

                    PARALYSIS AGITANS.

  Synonyms:  Schiittellahmung.   Shaking palsy. Parkinson's dis-
ease.
  History.   Paralysis agitans was first described in 1817, by Park-
inson, of London.   It is  a singular tribute to intellectual capacity
that nothing essential has been added to his description of the disease,
although almost all the well-known writers have considered it.
  Clinical  History.  The onset of the affection may be gradual
or sudden, very generally  the former.  It usually commences in one
of the extremities, although occasionally it begins in the lips, as it did
in one case  of my own, which had a duration of fifty years.  The
tremor gradually extends  throughout the  extremities, the  muscles
of the  neck  and  head, and sometimes the facial muscles and the
tongue.  This extension is usually bilateral, exceptionally unilateral.
The  tremor  is usually coarse, and in pronounced cases or in mild
ones  suffering from  temporary exacerbation it  may consist  of a
coarse  tremor intermingled with  movements that almost  resemble
a mild localized  muscular convulsion.  The speech soon becomes
affected, and  grows  to be deliberate  and  solemn,  like  the  ideal
speech  of  a  wise man, or that of a slow, hesitating, and deliberate
individual.    The  attitude soon  becomes  peculiar.    The patient
holds  the  head and  shoulders stiffly, bending the head and  neck
slightly forward, and walks with a short, shuffling step.  The facies
is as peculiar as the attitude, and cousists of a blank immobility that
is very difficult  to describe, but  that is admirably  represented  in 
520
NERVOUS DISEASES.
Fig. 164.  At this stage of the disease the hands are apt to assume
the so-called bread-crumbling position ; i. e., the thumb and the fingers
approximate and  move restlessly over one another, as in the act
of crumbling bread.  There is  often  a tendency on  the patient's
part to go forward—so-called propulsion—and this is  sometimes so
marked that if the patient is once started in a walk forward, his gait
becomes more and more rapid, and  he cannot stop himself.  This is
Fig. 164.
  Case of paralysis agitans, showing the attitude, the position of the hands, and the facies.

common.   In other cases  there is a tendency to go backward—so-
called  retropulsion.   This is not often observed.  In other cases,
again,  there is a tendency to go to one side—so-called latero-pulsion—
and this is rare.  In all the marked cases of paralysis agitans there
is a slightly red hue of the face, seemingly indicative of  health, but
really  due to  vasomotor paresis.   The  tremor is generally present
only when a voluntary muscular movement is made, and great stress
is laid upon  this fact as  a means of  diagnosis by Charcot; but 
DISEASES OF UNKNOWN PATHOLOGY.
521
whilst generally  present, it  is often absent, especially in the cases
that have not arrived at  the typical stage, and  too  much diagnostic
importance should not be attached to its presence or absence.  In-
voluntary movements are sometimes present  in paralysis agitans.
Attempts have been made to derive some diagnostic data by study-
ing  the sphymographic tracings of  the tremor, more especially to
distinguish it  from  the  tremor of multiple  sclerosis.   Charcot has
found  that in  paralysis  agitans the line traced by  the tremulous
extremity is one of slight tremulous, continuous waves when no vol-
untary movements  are made, but during such these waves are some-
what longer and more irregular.   In multiple sclerosis, however,
the  line  is almost a straight one  when no voluntary movement is
made, whilst  in such voluntary movements the line is oue of large
curves, much larger than at any time in paralysis agitans.  Grashey
has found the rhythm of the tremor of paralysis  agitans in three
patients to  be 0241, 0190, and 0187.   A number of others, among
them Marie, Charcot, Gowers, and Peterson,  have found  the average
rate of vibration of the tremor to  be from 3.7 to 5  per second.
Rigidity of the  muscles  is almost always present, as is also con-
tracture.   The tendon-reflexes are  only exceptionally increased.
Other  symptoms that are occasionally found are: a feeling of ex-
cessive heat over the whole body  or in certain areas, a feeling of
cold or numbness and prickling, pain, increased perspiration, and
tachycardia.   Most case  of paralysis agitans are extremely restless,
so that they cannot long remain quiet, and  clamor at times, even
when almost helpless with the disease, to be put on their feet and
allowed to walk  about.   The  mental faculties are usually  not  at
all  affected, and  I  have  seen  cases of over fifty years' duration, in
which the mind, subjected to the most rigid  testing, showed no ab-
normalities in  any way.   This was notably exemplified a few years
ago in  the case of a public man of national  reputation, who to the
last remained the leader of a great party.  In  some cases, however,
there is slight  mental dulness or peevishness, and even marked stu-
pidity.  The duration of the disease is  indefinite, and as it is never
cured entirely,  it lasts throughout the rest of life, and  whether it
curtails life is a question that  has  never been  solved.   I have seen
several  cases  that  lasted  thirty years,  and two  that  lasted fifty
years, and  these  all brought  the  patient up  to  sixty,  sixty-five,
and  seventy years  of age, so it might  well  be a  question whether
they Avould have  lived any longer without the disease.   But there
are  exacerbations, followed by remissions, and these exacerbations
are often so pronounced as to lead the patient to believe that  death
is approaching, or the physician to  maintain that  the last remedy
used has caused the remission that  follows.   In these exacerbations
the  patient may become, for  the time being, perfectly helpless and
occasionally semi-comatose.
  Etiology.   Age is an etiological factor of considerable impor-
tance.  Most  cases occur between forty and sixty years of age, and
even up to seventy.   Sex  appears to be of but little account, although
men  are somewhat more  frequently affected than women. 
522
NERVOUS DISEASES.
   In some cases, however, the exciting cause may be—
       Emotions;
       Cold and damp;
       Heredity;
       Strong peripheral irritation;
       Trauma;
       Gout;
       Typhus;
       Hemiplegia.
   The emotions are sometimes  very distinct causes.  One patient
of mine was  on a ferry-boat crossing the East River, when a baby
sprang out of its mother's arms into the river, and, buoyed up by
its long clothes, was swept down the  strong current until rescued
by some 'longshoremen in a boat.  My patient, on returning to the
cabin after watching this scene, found, to her surprise, that her upper
lip was " going," as she expressed it, " like a rabbit's," and this was
the beginning of a typical  paralysis agitans  that culminated fifty
years afterward in death.  Worry and anxiety have also been noted
as causes.
   Cold and damp  are generally supposed  to be the  most promi-
nent  causes by  the  European writers,  but this has not been my
experience, although I have occasionally obtained a history to that
effect.
   Heredity is a frequent  cause,  in my experience, although  it will
often need some patient questioning to obtain a history of it.  It
may not have been in the immediate parents of the patient, although
it may have been running through a family irregularly in  different
generations.  In our New York  clinics I have observed an unusual
proportion of cases among emigrants  from the northern parts of Ire-
land, or among the immediate descendants within one or two genera-
tions of the north of Ireland population, and also to the same  extent
among the Scotch.
   Westphal has reported  cases  of  paralysis agitans following  a
wound or a laceration, or burns of an extremity.
  Trauma is also occasionally observed as a cause, and the same may
be said of gout and typhus.
  I have seen some five cases of paralysis agitans following a hemi-
plegia and affecting the hemiplegic limbs, although  such cases must
not be confounded with those in which the  malady affects one limb
or one side of the body.
  Prognosis.   The prognosis,  so far  as  affects life, is generally
good, for  patients seldom die suddenly of the disease, and, as has
been already stated, it is very much  a question whether it  shortens
life.   The  prognosis of improvement  under proper  treatment is
good  also,  although I am  aware that  this is not the opinion of
writers generally upon the subject.  Some  cases, however, will re-
sist all treatment, and these  are apt to be those in which the tremor
is localized in oue limb or  on one side of the body, and in such cases
the tremulous limbs are apt to  become paralyzed and rigidly con-
tractu red. 
             DISEASES OF UNKNOWN PATHOLOGY.         523

  Pathology.  Paralysis agitans  has until  within a very  short
time beeu supposed to be a functional disease of the nervous system,
as no pathological  lesions were demonstrable.   Joffroy claimed in
1872 that he had  found the central canal of the cord almost oblit-
erated  by pigmentation in three cases, but  this condition has been
observed in mauy cases in which paralysis agitans was not clinically
manifested ; and it was also shown that in the aged are  often found
such indurations of the membranes as had been claimed as pathog-
nomonic lesions.  But this question  has again been brought forward
by the observations of Redlich, Koller, Borgherini, Schultze, Ket-
scher, Dana, and Saas, and a new light has been thrown  upon it.
These  authors have shown  that there are  islets  of  sclerosis in
the medulla oblongata and spinal cord of these  cases,  evidently
having  their origin in the vessels.  This is a condition which will
be known as perivascular sclerosis.  Aressels of small calibre are
those affected.  The  intima is slightly proliferated, there is a  nar-
rowing of the lumen, and a thickening of the layers of the media,
which  are also somewhat nuclear, concentrically  layered, and hya-
line.   There  is a  region of thick, horny tissue outside of these,
usually closely approximating  it, sometimes  with  a small inter-
vening  space, coloring  readily  in ammoniacal carmine, and which
answers topographically  to the adventitial lymph-spaces  or to the
layers  of the adveutitia.   Hemorrhages or miliary aneurisms have
been observed  from  this  cause.   There is  a thickening of the neu-
roglia from this point which extends  into the surrounding nervous
parenchyma, in places surrounding groups of nerve-fibres, and indi-
vidual nerve-strands only in  others.  These  appearances  diminish
toward the periphery of the cord.  Small islets of sclerosis may be-
come confluent if there are many vessels close together, forming large
masses of sclerotic tissue.  Where  the  sclerosis is  of small degree
and  especial groups of nerves  are  surrounded the nerve-fibres are
not affected, but the compression  of  nerve-fibres  is shown where
there is a more marked degree of sclerosis, so that diminution in size
or entire disappearance of the axis-cylinder and the medullary layer
is observed.  Even the large vessels outside the spinal cord may also
be affected, especially the interfunicular artery  aud the  posterior
fissural artery, in the coats of the media.   The posterior columns of
the cord show these sclerotic changes most clearly, particularly in the
middle and ventral  portions, in proximity  to the posterior commis-
sure.  But although the lateral columns are also affected, the lesions
are  not limited to them, as the  Gowers column, the lateral tract
proper bordering upon the gray matter, and  the direct  cerebellar
column are implicated in a diffuse manner.  Affection of the anterior
columns  is but very slight, and quite often entirely absent.  Thick-
ening of the vessels  of the gray  matter  often  occurs, but without
any involvement of the surrounding tissue.  The cervical enlarge-
ment and the lumbar cord constitute the location  of greatest impli-
cation, the lesions being relatively far less marked in the upper cervi-
cal and lower dorsal region, and in the middle and upper dorsal still less
so. Implication of the cortical region has also been apparent in some 
524
NER VO US DISEASES.
cases.  In some instances streaks of tissue histologically similar to the
cortical layer of the cord in this region extended into the lateral col-
umns, particularly in the region of the posterior portions of the lateral
columns, disappearing around the nerve-fibres; and a diffuse sclerosis
of slight degree, with increase of the septa aud of the neuroglia, evi-
dently not  of vascular origin, appeared in other cases, and  Redlich
found in one case a diffuse sclerosis of the perivascular character which
has been described.   The  ganglion-cells of the auterior  horns were
markedly pigmented in  almost  all cases, the whole body of the cell
beiug sometimes filled with yellow granules concealing the  nucleus,
and leaving only a small portion of the protoplasm visible, this pro-
cess, however, being unusual, the form aud processes of the cell gen-
erally  remaining.  Clark's columns  also  present  a  high degree of
pigmeutation.   Proliferated  ependymal cells  usually obliterated the
central canal.   A large number of amyloid bodies are found. Slight
thickening  and great pigmentation of the pia of the cord were  also
usually present.  The anterior and  posterior roots were unchanged,
although the  vessels have  been  found  widened, but not thickened.
Lissauer's  and  Clark's  columns  are usually found  to  have pre-
served their  nerve-fibres.   The axis-cylinders had a varicose shape
in one of Dubeuf's cases, and the upper and cervical dorsal cord was
found  to be the main  site  of the lesions.  Aueurismal enlargements
were  observed in a case of Borgherini's, with a  slight affection of
the posterior columns,  whilst he  discovered marked alterations in the
gray  substance,  in  which  he differs  from most  authors.   In  the
medulla oblongata Ketscher and Dana have found similar alterations.
Similar lesions of the  vessels have  been found  in the cerebrum in
some  instauces, the sclerosis, however, being absent.  Alterations
have  also  been described  in the peripheral nerves and muscles by
Saas,  Redlich, Borgherini,  and Ketscher, these changes consisting of
proliferated connective tissue and atrophy of the muscular and nerve
tissue, with thickening of the vessels.
   It has been a  matter of  discussion  as  to whether senility brings
about naturally these  changes that  are claimed as characteristic of
paralysis agitaus.   The appearances are  fairly constant in about
twenty cases  which have been  examined  so far, and in  most of
them  the clinical  phenomena and the severity of the pathological
lesions bear a fair  ratio to each other.  But it is a well-known fact
that in aged  people who  have  presented no svmptoms of paralysis
agitans slight thickening of the membranes, obliteration of the cen-
tral canal  of the cord by proliferation of the ependymal cells, in-
crease  of amyloid  bodies, and  pigmentation  of  the  ganglion-cells
are frequently found.   The observations of Redlich,  Leyden,  aud
Demange have shown this.  Most authors are inclined to  regard the
alterations  in the vessels, the increase in connective tissue running iu
from the peripheral tissue of the cord, and the perivascular  sclerosis
as purely  senile, although  neurological pathologists  differ  in  this
opinion.  In a  large number of observations made upon old people
by Ketscher similar alterations of the  vessels to  those which have
been described  in  paralysis agitans were found, although in less 
DISEASES OF  UNKNOWN PATHOLOGY.
525
degree, and the outer horny layer, as well as the perivascular sclerosis,
is  usually wanting, and it is  also noted that paralysis agitans may
occur in young  adults, although it  generally occurs in individuals
toward fifty.   Demange has described a progressive tabetic sclerosis
of the lateral and posterior columns, of vascular origin, characterized
by marked contractures, first of the limbs and subsequently of the
arms, without sensory defect, sensory irritation, or decided paralysis,
with primary increase of the tendon-reflexes, followed by loss of them.
These cases, according  to this  author, are  those of chronic  myelitis,
caused by an endo- and periarteritis, of the general character of an
atheroma.  Similar alterations in the aged, attended with  muscular
enfeeblement,  have been described by  Copiu, although they lack the
contracture described by Demange.   The senile paraplegia of Gowers
will probably rank with this class of cases.  A case has been described
by Buzzard of a man of thirty-nine years of age having syphilis, then
symptoms of diplopia,  entire disuse of limbs in walking or standing,
although movements of the limbs while in bed were made freely, patel-
lar reflex wanting, one-sided atrophy of the optic nerve, immobility of
the pupils, and marked sensory disturbances in the lower extremities,
and in  whom was found endo- and  periarteritis  to a considerable
extent, with connected sclerosis in  the lumbar and cervical cord, in
the  posterior  columns especially, and  also  in the lateral  columns,
although in a much slighter degree.  Histories of several  cases are
given by Redlich in which aged people manifested an alteration of
the  vessels  with perivascular sclerosis, particularly in  the ventral
portions of the posterior columns, the cervical cord  being but slightly
affected, while the dorsal  and  lumbar cord were considerably altered,
and in the columns of Goll a slight alteration was observed, consist-
ing of a small degree of ascending degeneration, although but slight
involvement of the lateral  columns was discovered.  It is apparent
from all this that the localization of the lesion in paralysis agitans is
more pathognomonic than its character, for there is no reason why in
the cases of Gowers and Demange the symptoms of paralysis agitans
should not have been produced by the same lesions if they  had been
located differently.  Tremor and contracture constitute the two salient
symptoms in paralysis  agitans.  It is  suggested by Blocq that an affec-
tion of  the muscles may be the cause of the contracture, but this has
not been demonstrated, and we must therefore attribute to the spinal
lesion both the tremor and the contracture.  Were it not for the fact
that a large proportion of the autopsies have shown that the posterior
columns are mainly affected, it would be easy, with our existing knowl-
edge, to suppose that both the contracture and the tremor could be
accounted for by the anatomical location of the lesion in the lateral and
anterior pyramidal strands. It would therefore seem as if the impli-
cation of certain fibres  in  these posterior columns must, under certain
circumstances, be held accountable for the clinical manifestations.
The only explanation, however, for the fact that the implication of
these posterior columns did not produce the symptoms of  paralysis
agitans  in  the cases of Buzzard, Gowers,  and  Demange  is the sup-
position  that  a different set of fibres is affected  in each of the cases. 
526
NERVOUS DISEASES.
 In the cases of Redlich and Demange there was no tremor and only
 a  slight contracture, so  that  by exclusion it would seem probable
 that the tremor  was probably caused by affection of the lateral col-
 umns and was not due to implication of the posterior columns.  It
 seems  probable, however, that implication of the posterior columns
 may cause contracture by irritation  of the  anterior ganglion-cells
 through the sensory-motor tract of Cajal, described on p. 32.
   Diagnosis.  The diagnosis of paralysis agitans is easily made in
 the majority of cases.  The age between forty and sixty, the coarse
 tremor, the characteristic attitude, the  bread-crumbling position of
 the fingers; the slow, deliberate, high-pitched speech; the  peculiar
 facies, the tendency to ruddiness of the complexion—all are  symp-
 toms which  are  readily  recognized in patients,  and by which the
 diagnosis of the disease can often be made on a ferry-boat or in a car.
 Non-typical  cases are very difficult  to diagnose.  Thus, there are
 patients in whom the tremor is absent, and here  the diagnosis must
 be made by the other symptoms.  Again, there are patients in whom
 the tremor is present, but who do not present the characteristic speech,
 attitude, facies, or color,  and if this occurs in a patient near thirty, it
 may be absolutely impossible to make the diagnosis without the aid
 of sufficient time to observe the progress of the malady.  The char-
 acter of the  tremor is  no longer  thought to be of the importance
 which it was supposed to have.  In the main, I do  believe, the
 tremor of paralysis agitans is  present when the patient  is at rest or
 performing voluntary movements; but there are  many cases, espe-
 cially in the early stages of the disease, in which the tremor is only
 present upon voluntary movements, or is greatly exaggerated at such
 times.    The sphygmographic tracings, of which so much has been
 made,  are open  to exactly the  same objection, because, whilst the
 tremor  is generally  continuous and  fine,  there are many cases  in
 which  it is not continuous, and in  which it  is at times very coarse.
 The diseases  from which  paralysis agitans  should be differentiated
 are—
       Disseminated sclerosis;
       The tremor of lead, copper, and mercury ;
       Alcoholism;
       Chorea.
   The typical case of disseminated sclerosis has a tremor that is
 present only  upon voluntary movements—the so-called intention-
 tremor—and there are also nystagmus, an interrupted, scanning speech,
 the patient is a young adult or a child, there may be symptoms  of
 focal disease of the brain  superadded; and  the  characteristic atti-
 tude, facies, bread-crumbling position of the fingers, slow, deliberate
 speech, and ruddy color of paralysis agitans are all lacking.
   The tremor of  lead, copper, and mercury is usually a fine tremor,
 and in lead-poisoning other symptoms of the  disease will be present,
 such as the  " lead-line " and  the wrist-drop, whilst the history  of
 the use of lead may be obtained; and in tremor from  mercurial  or
copper-poisoning the history of the use of mercury may be obtained
iu  the one case, whilst there will usually have been some history of 
DISEASES OF UNKNOWN PATHOLOGY.          527
ptyalism or the mercurial cachexia, and, on the other hand, in copper-
poisoning the patient will have been engaged in using copper in some
toxsemic way.
  In alcoholism, especially in the acute form after a debauch, there
is often a fine tremor, and this  may sometimes be of the intention-
tremor type;  but the history of the patient and  his general aspect
will  easily  make the diagnosis clear.  In some  cases of chronic
alcoholism there  may also be a tremor, but this need only be referred
to in order to put the observer upon the alert, for the diagnosis
can readily be made by the history of the  case and the well-known
symptoms.
  In ordinary chorea of the Sydenham  type there should  never be
any mistake in making a diagnosis, because the muscular movements
are fibrillary in character, either quickly beginuing aud quickly end-
ing,  or more gradual in their beginning and ending  when  they are
of the athetoid variety, and  the patient is almost invariably a child.
In some cases of chorea, however, that have become  chronic, gener-
ally  from lack of proper treatment or of the original attack of the re-
lapses, the tremor may become  so marked aud so  intermingled with
muscular spasm as to lead the  inexperienced observer to  confound
the disease with paralysis agitans; but a history of the  case and the
fact  that the movements are of the type  that have already been
described will be sufficient to make the differential diaguosis.  It is
unfortunate that some writers have designated as  choreic tremor the
fine jerky fibrillary movements common to  chorea.
  Treatment.   The treatment of paralysis agitans should be defi-
nite and energetic.   All the drugs that have been vaunted as specifics
are wellnigh useless except for temporary effect.  The patient  should
be restricted in his expenditure of energy ; in other words, the tremu-
lous muscles should  be  put  in  a position of comparative rest; and
this  can best be done  by keeping the patient  in bed up  to noon-
day  for several weeks  at the outset of treatment, and  at the same
time prohibiting walking or fatiguing drives.  As the patient grows
better he may be allowed to  get up at the usual time, but he should
religiously avoid fatigue, and if any error  is made it should be on
the side of too much rest  rather than  too  little.   This part of the
treatment should be carefully studied, and the most minute directions
should be given about it by the physician.   It will not do to advance
the general principle, but  the patient must be told just how many
hours he should rest, just how much exercise he should  take, just
what time he should go to bed,  etc.  Without this restriction of the
expenditure of energy no results will ever be obtained except tempo-
rarily.  The  diet  of the  patient should be varied,  abundant, and
nourishing.   It  should at least consist of three good meals a day,
and  generally it will be advisable to have at least a quart of milk
taken in addition to this in the twenty-four hours, and in some cases
it may even be useful to advise that a pound of  beef made up into
beef-tea shall be taken in the twenty-four hours, either  in  the form
of home-made beef-tea or some one of the beef-extracts or peptonoids.
Alcoholic stimulation  should be  continuously  employed,  two or 
528
NERVOUS DISEASES.
three ounces of whiskey being given  in  the twenty-four hours, or a
bottle or two of a strong ale, or a fairly equivalent quantity of alco-
hol in the  shape of some  of the  wines.   Malt-extracts are also of
great value in aiding this process  of nutrition.  In prescribing them
it should be remembered  that  diastase is that portion  of the malt-
extract which is alone of value to  the patient, and it  is therefore of
no consequence what particular preparation of malt-extract we em-
ploy, provided only that it is fresh and reliable.   The  liquid malt-
extracts with alcohol had better not be employed unless they are more
pleasant to the patient than the solid malt-extracts, inasmuch as  the
alcohol can be  obtained in  a more  precise way  in the manner that has
just been indicated.   Tonics should always be prescribed, and  the
best of these is the sulphate of quinine, 2 or 3 grains three times a
day,  given  an hour or  two after meals to avoid any disturbance
iu digestion, best  in the form of  the  tablet triturate or in capsules,
and never in solution with an acid, which is  apt to upset the diges-
tion.   In addition to these  measures of rest, diet, alcoholic  stimu-
lants, and  diastase, remedies  should always be used directly to
control the tremor.  The best of these is hyoscyamine, the crystal-
lized  and never the uncrystallized form, as the latter is more prone to
produce unpleasant constitutional effects.   The dose  should be jfo
grain once or twice a day,  continuously used for weeks or months as
may be necessary.   If the hyoscyamine alone does not control the
tremor  sufficiently, 10 grains of the bromide of potash may be given
with  it once or twice a day, usually also  for months.   Hyoscine,
either the hydrochlorate or the hydrobromate, is also a very useful
drug, as it can be given much oftener and has  none of the unpleasant
effect of the hyoscyamine in dilatating the pupil and causing dryness
of the mouth.  This treatment by rest, alcoholic stimulation, diastase,
and muscular sedatives like hyoscyamine and bromide,  is the treat-
ment  of paralysis agitans—not one element of it alone, but all.   The
ruddy color of the face so often observed has, I  think, misled observers
into unconsciously believing that the disease was not in need of stim-
ulant treatment, and therefore has led to the exclusive use of the
sedatives, as the result of which patients have  been unduly depressed.
In reality, however, the  ruddy flush of the face is a vascular paresis,
and I  have  found that the stimulating and nourishing treatment
alone  will do more than the use of the sedatives alone.  Galvanism
is almost invariably of great value, and it  seemingly acts as a ner-
vous  stimulant of high  order.  It should  be administered at least
three  times a week, with one large electrode (Fig. 67) placed on the
nape  of the-neck, and another of  Fig. 68 opposite the lower dorsal
spine.  The  skin should be wet with hot  water, and the electrode
should  be thoroughly moistened with the same.   A current of 3 to
5 milliamperes should be  passed  for three to five minutes, and, as
the patient  becomes accustomed to the  current,  this may often be
advantageously increased to 10 to 15 milliamperes and to a sitting of
five to fifteen or even twenty minutes.  With this treatment I posi-
tively assert that most cases of paralysis agitans can  be controlled,
and the life of the patient made comparatively pleasant.   After 
DISEASES OF UNKNOWN PATHOLOGY.
529
successful treatment  by these means for a period of eight to twelve
weeks, the  galvanism  may  be discontinued,  the  hyoscyamine  and
the bromide gradually withdrawn, and the patient allowed  simply
to keep up the rest  that  has been  found advisable, as well as the
diet, the alcoholic stimulant, and the  diastase.  Usually months or
weeks  will  intervene before another  exacerbation occurs, and  this
can be controlled by the same means.   I am  accustomed to explain
all this to my patients, so  that they will expect another exacerbation
at some time, when they need  not feel discouraged and fear that the
disease is becoming  uncontrollable.   I tell them frankly that they
cannot be cured, but that they can be materially helped.   Unfor-
tunately, however, the cases of paralysis agitans which  occur after
hemiplegia, affecting only one limb or one side, cannot  be  treated
with much  hope of  relief;  but a sharp distinction should be made
between these cases of paralysis agitans occurring after  hemiplegia
aud the cases of sudden onset in  one  limb, for the latter are usually
only the localized onset of  a general paralysis agitans which is subject
to the therapeutic laws that  have just been detailed.

                       ASTASIA-ABASIA.

   Jaccoud  first described this disease,  in  1864, as  "ataxia  with
defect of automatic  co-ordination."   Weir Mitchell wrote of it, in
1881, as  "hysterical motor  ataxia."   In 1883 Charcot and  Richer
called  attention to it as "a  special  form of motor impotency of the
lower limbs, with defect  of co-ordination relative to  standing  and
walking."  Numerous other authors  reported cases, and, in 1888,
Blocq collected eleven, and  gave to the disease the name that it now
bears.  Since then there have been  numerous  articles.
   The disease  consists  of an  inability to stand erect  or walk nor-
mally, although there  is  no impairment of sensation, of muscular
strength, or of  the co-ordination  of other movements  than walking
or standing of the  lower extremities.  In attempting to walk, the
legs  become spasmodic.   There are rapid flexions and extensions of
the legs  on the thighs and of the thighs on  the pelvis.   The steps
are short and the feet drag; or the body may make great oscillations
if the  patient  stands,  walks, or  sits, and the head and arms make
rhythmical  movements; or  walking may become impossible, and the
patient leaps on to  one foot and then on to the other,  the body  and
head oscillating as he  advances; or he can walk cross-legged, or by
raising the legs high ;  or  he can  walk on his  hands and  feet; or he
can walk at  certain times and not at  others; or  he can hop  with
both feet together, or  walk with  great  strides with  the arms ex-
tended ; or he  may  be  able to use his legs perfectly,  if suspended.
If the attempt to walk is persisted in, all these phenomena  become
intensified, and the patient  may  fall.   The most common  form of
these  varieties  is the  paralytic,  wherein the  legs bend  under the
patient in the attempt to walk.   There is no rigidity, spasm, or inco-
ordination,  and the  muscular  strength  is good whilst  the  patient
is in  bed, is  sitting, or is  suspended.   Almost as frequent as the
                               34 
530
NER VO US DISEASES.
paralytic form is some variety of spasm or ataxia, the most common
being  that  wherein walking is embarrassed  by erratic movements
and stiffening of the legs, causing  a sort of tremor, like that  of
spastic paraplegia.  Less  frequently there are  sudden flexions  of
the legs, so that  the equilibrium of the body is  nearly overthrown,
at the  same time that there are exaggerated and sudden flexions  of
the arms.   Charcot has called this type the choreic variety ; and  in
some cases  it  has been associated  with  so-called  epidemic chorea,
although  it must  be  borne in  mind that this so-called epidemic
chorea  is  probably hysteria.  A rare form is a saltatory variety.
Any emotional  disturbance increases the  difficulty of walking.   A
tendency to go  backward, or retropulsion, has been observed, as has
also a tendency to go forward, or propulsion.  A curious phenom-
enon in this  case is that the patients can use the legs perfectly well
while they lie  in bed.
   Astasia-abasia has often a distinct  history of heredity.   It occurs
in about equal  proportions in  the two sexes.   Most of the cases are
associated with hysteria, but it  has also  been seen  in conjunction
with chorea, epilepsy, such  morbid  impulses as agoraphobia, etc.,
as well as with  dementia, confusional insanity, exophthalmic goitre,
and neurasthenia.  Whether or not it is always an  hysterical symp-
tom has not yet been determiued ; but Blocq has hypnotized a patient,
and made  her the suggestion that she no longer knew how to walk,
and thus  produced astasia-abasia; and when  he furthermore sug-
gested  to her that she could not walk, paralytic abasia ensued.  The
cases which  I  have seen have certainly impressed me as being hys-
terical, and  Blocq's experiment would seem to be conclusive.  But
this malady has been  associated with many diseases  which are cer-
tainly  not hysterical,  and the  question  has yet to  be determined
whether astasia-abasia can be a symptom of these diseases, or whether
it indicates the association of hysteria with them.
   The prognosis of astasia-abasia is  good.   Children recover, as  a
rule; but relapses occur in adults, and exceptionally these are frequent.
It is never fatal.
   The treatment is that  usual in cases of hysteria (see "Hysteria").
Knapp suggests that a distinctly volitional act be substituted for an
automatic act, and hence in  his case he suggested the balance-step
with remarkable success. 
CHAPTER   XIY.
               REFLEX NERVOUS DISORDERS.

  Time was, and not more than a decade ago, when it was very much
the fashion to ascribe almost all nervous disorders to reflex from non-
nervous viscera, and cases of what are now well recognized as  cere-
bral  palsies of  childhood, amyotrophic  lateral sclerosis, myelitis of
the auterior cornua, pseudo-muscular hypertrophy, myotonia,  epi-
lepsy, chorea, aud a host of other nervous affections were anxiously
examined for phimosis, strictures, dyspepsia,  swallowed pins, consti-
pation, uterine or ovarian symptoms, and so on aud so forth ; and if
any of these non-nervous causes were found, the mental  symptoms
were supposed to be thoroughly explained.  In  reality this belief is
a kind  of atavism, for Hippocrates, who lived 460 years  before
Christ, believed that the causes of insanity lay in the four cardinal
fluids: the blood, mucus, the black  and yellow gall; and  it was not
until 160 years after  Christ  that  Galen made the distinction that
many practitioners have not yet made, namely, that there were pri-
mary insauities due to disease of the cerebrum, and secondary or reflex
ones due to an affection  of non-nervous organs.   Within the  last
decade this doctrine of reflex nervous disease has  been carried to such
au extreme that there are medical men of standing  who would have
us believe that almost all  mental and  nervous maladies can be cured
by the relief of that form of ocular asthenopia which is due to insuf-
ficiencies of the ocular  muscles, and  not long ago I had a surgeon
tell me that he could abort a pneumonia  by cutting a deep stricture.
Neurologists, however, have grown  to be very skeptical in regard to
the frequency of reflex nervous disorders.  Every educated medical
man  knows perfectly well, of course, that a malady of the abdominal,
thoracic, and pelvic organs may produce  general symptoms of a ner-
vous character, as well as fever, insomnia, restlessness, jactitation, and
vomiting, and every practitioner of  experience knows also that slight
lesions of non-nervous organs may  reflexly produce nervous  symp-
toms ; but every neurologist of experience knows,  in addition, that
almost every nervous malady,  of which  I have just given a  partial
list, has at first been thought to be  a reflex disorder, aud  that  with
the advance of neurological knowledge disease after disease has been
removed from this category.  The questions,  therefore, that  neurol-
ogists have  asked themselves of late  have been, first, What  is the
frequency of reflex nervous disorders'? second, What are their char-
acteristic  symptoms'?  and third, With what  non-nervous maladies
are they most prone to occur ?
  First, as to the frequency of reflex  nervous disorders.   It may be
positively stated that they are extremely  rare, and I have  no doubt 
532
NERVOUS DISEASES.
whatever that every neurologist has had an experience identical with
my  own, namely, that  many and  many a case of so-called reflex
nervous  disorder will be resolved into a familiar  nervous disease
which has not  been recognized.   Statistics are perfectly valueless
upon this question, because  everything depends upon the experience
and  the knowledge of the person making the diagnosis, and it is a
significant fact that none of the well-known neurologists of the world
have reported cases of reflex nervous disorders within the last ten or
fifteen years.
   Second, as to the characteristic symptoms of reflex  nervous dis-
orders.   To this it may be answered that the very essence of a reflex
nervous symptom is its  caprice, so to speak, so that we cannot speak
of its characteristics.  Thus, it has been said  that uterine disorders
are prone to produce a peculiar, distressing, aching sensation at the
vertex or in the dorsal spine; that insufficiency of ocular muscles
causes a peculiar brow-ache  ; that indigestion  induces an aching sen-
sation over the frontal region, and that hepatic trouble causes vertigo.
But  these different sensations and symptoms are seen so  frequently
with other disorders than those with which they have been correlated
that  they are but a broken staff to lean  upon in diagnosis.  The truth
is that when  a man presents nervous symptoms, the  first question is
as to whether he has a nervous malady, the determination of which
question  involves an  accurate and  extensive knowledge of nervous
and  mental diseases; and it  is only when all these nervous aud men-
tal diseases have been positively excluded that a nervous reflex can
be suspected, and this can  only  be absolutely diagnosed when it is
positively found, and time or  medical  experience has shown that it
is the cause of the nervous symptoms.
   As to the question which  non-nervous maladies are most prone to
produce reflex nervous symptoms, it may  be  said that the  follow-
ing diseases should  be  considered in  a case of doubtful diagnosis,
namely—
       Nephritis;
       Pelvic disorder in the female;
       Disease of the male urethra or seminal vesicles;
       Intestinal disorders;
       Lithsemia;
       Errors of refraction;
       Insufficiency of  ocular muscles;
       Aural disease;
       Ansemia  and leucocythsemia.
   In some cases of nephritis the nervous symptoms may be the ones
mainly to attract attention,  and this is especially apt to be the case
when there is a cirrhotic kidney;  but a careful examination of the
urine, and sometimes an examination  with the ophthalmoscope  or
the sphygmograph, will make the diagnosis perfectly plain.   In  my
experience the general practitioner is  much more prone to make a
mistake in this matter than  the  specialist, contrary to the general
opinion, for scarcely a month of my life passes in  which a case does
not come to me  of this kind.   I  had not long ago under my care a 
REFLEN NERVOUS DISORDERS.
533
lady who had been treated for two years for supposed neurasthenia,
and yet who was found to have albumin in the uriue to the extent of
1 : 20; whilst a young man once came to me who had beeu under
treatment for over three years for supposed hysteria, in whom I found
a typical albuminuric retinitis, such as represented on page 158, and
whose urine showed a large amount of albumin, with numerous hya-
line and granular casts.   In all  suspected cases of this kind a most
careful examination should be made, not only by the ordinary test of
nitric acid and heat,  but  also by the more modern  tests, and  there
should be a microscopical search for casts.  Care should also be taken
to have a specimen of the urine for twenty-four hours, and the whole
quantity passed during that period of time should be carefully meas-
ured ; and, if necessary, repeated examinations, quantitative and quali-
tative and microscopical,  should  be made.   If these precautions are
taken, there should never be a mistake in diagnosis
  Pelvic disorder iu  the female is popularly supposed to  be the cause
of many reflex symptoms, but I  do not think that lesions  in this
locality are any more prone to act reflexly than lesions of other non-
nervous organs except  so far as they act psychically, because every
woman is only too prone to believe that every uneasy feeling is due
to a  uterine disorder, and when this opinion is confirmed by some
physician it adds a certain satisfaction to her mental torture.  Gyne-
cological surgery is so fascinating, the temptation to report  a  series
of 100 cases is so  great,  and women are such easy victims, that an
enormous affirmative literature has  grown  up  upon this subject, to
be met by an  equally enormous  negative literature on  the  part of
neurologists, as an outcome of which the brain and spinal cord have
been almost transferred from the skull  and the vertebral canal to the
pelvis, and anatomical teachings have  been wellnigh revolutionized
in the mind of the general practitioner.  Not long ago I showed to
my class a woman who had had for many yrears attacks  of obstinate
vomiting, which had resisted  every therapeutic device.   She came
under the care of a well-known gynecologist, who performed a double
ovariotomy. For several weeks after this she was regarded as cured,
but  gradually the old vomiting returned, when the gynecological
surgeon opened the wound, thinking that there might be some inflam-
matory adhesions,  but found nothing abnormal.  After this explora-
tory operation the patient was again relieved for several weeks, when
the vomiting again returned.  She was then seut to me by the gyne-
cologist with  the  frank  statement from him that he had  never
regarded  the ovariotomy as advisable, but had ouly done it at the
request of a well-known  teacher of general medicine.  Upon exami-
nation  I fouud that  the woman had been a  life-long  hysteric,  had
inherited hysteria, had had hysterical convulsions, and had the char-
acteristic hysterical concentration of the field of vision, with patches
of anaesthesia iu the  upper extremities.   She  stated that the vomit-
ing had been so violent for weeks past that she had been obliged to
live on a pint  of milk and a few pieces of bread in the  twenty-four
hours.  As  she was  fairly plump and well nourished, I doubted her
statement, and directed one of my assistants to follow her when she 
534
NERVOUS DISEASES.
left the clinic, in order to see where she went and what she did.  To
our great delight she at  once directed her steps to a peanut-stand,
bought a pint of the luscious fruit, and  meandered her way merrily
home, strewing her track as she went with peanut-shells.  So when
the fair patient again visited my clinic I told her what we had dis-
covered, at which she flew into  a  violent temper, anathematized us,
and has not  since done us the honor of seeking our  professional
advice.  I state this, contrary to the rule which I have followed in
this book  of interpolating no histories of patients, because  the im-
portance of  the subject  warrants me, I think, in illustrating by a
case what  I so  frequently observe,  namely, the overweening and
illogical anatomical and unphysiological tendency to regard as a pelvic
reflex in the female what  is really a familiar nervous malady.
   Until within a very short time it has been regarded as legitimate
surgery to perform an ovariotomy  upon an epileptic female, but there
is not a case upou record in which epilepsy has been cured  by such
an operation or  by any operation upon  the  female pelvic  organs,
although temporary effects may be obtained by such  operations, as
they  are  obtained by  many  others.   (See " Epilepsy.")  It may
be positively stated  that  no nervous  disease  is produced by pelvic
diseases in  the  female, although there  may be  general  nervous
symptoms caused in this  manner.  Nevertheless, I  believe  that an
operation upon the pelvic organs of the female is often a very useful
therapeutic measure  in certain cases of nervous disease.  This may
seem like a paradox, but it is very far from being such.  Opium will
relieve pain, yet a man  who would get up  and say7 that opium is the
cause of all pain would  simply excite the merriment of nations; and
in the same way the fact that all  the component factors that make
up a surgical  operation  upon  the female pelvic  organs act as a
curative or palliative measure  does not prove that it causes them.
Incidental to the operation is the mental expectancy aroused by the
universal  belief of women that pelvic disorders in them are  capable
of producing almost anything, the profound physical  shock  of the
etherization or chloroformization, the bloodletting, the low diet, the
rest after the operation, often for  months, and frequently the relief
of some pelvic source of discomfort;  and all these causes, as a whole,
produce an  effect that  may be very potent in certain nervous and
mental disorders.  I therefore frequently advise an operation, some-
times where there is  no  local disorder,  in cases of mental disease that
are very tardy iu their convalescence and in which I desire to produce
a profound mental and physical effect.   On the other  hand,  it must
be remembered that cases of mental  disease have  been reported as
immediately following operations upon the female pelvic organs, and
I have seen fifteen such cases myself;  so that  this is a danger not to
be disregarded, and is one which has caused me considerable perplex-
ity.   My experience, however, has led  me to believe that it is safe to
operate with  the end in  view that I  have stated when the pelvic
lesion is a slight one, or when the patient is robust in general health,
or when there has been some slight pelvic lesion that has caused the
patient  much anxiety,  or when there is  no  local  lesion and the 
REFLEX NERVOUS DISOBDEBS.
535
 patient's general health is robust; whilst it is dangerous to operate
 on  patients who are very nervous and  apprehensive, or when the
 pelvic  lesion is very serious, or when the  general health has  been
 greatly  depressed, or when the patient  is  averse to the  operation.
 In  accordance with these rules  of my own I have frequently had
 my gynecological  friends curette the uterus,  remove a  polypus,  treat
 an abrasion of the os, and do similar operations, and I have almost
 invariably had good results  follow.  Not long ago, for example, a
 patient  was under  my care  for hallucinatory insanity, which  had
 lasted upward of eighteen months, from which  she had  recovered
 so far  as to be  relieved of her hallucinations, and  to be compara-
 tively docile and  reasonable  in her behavior, although she was still
 moody, occasionally depressed, aud  at times eccentric  in action and
 thought.  Medicines had lost their power, and she drifted along week
 after week  in  this listless, discouraging  way.  I  advised  a gyneco-
 logical  friend whose patient  she  was to curette the uterus, although
 he was  exceedingly reluctant  to do it, and  dubious as to  its effect.
 The  patient, however, was not only willing, but very eager to have
 the  operation done.   The success was brilliant, and  in the course of
 six  weeks she went home, I am told, completely cured, and has had
 no return of her malady in  the five years that have since elapsed.
 I do not believe, however, that ovariotomy is ever warrantable in
 these cases.  It has also been my fortune to meet with a number of
 cases with ovarian tenderness, frequently bilateral, without  hysterical
 symptoms, occasionally occurring in paroxysms lasting for a few days,
 a week  or  more ; as well as  cases of ovarian disease, which is often
 suspected, not  because  there  are positive  evidences to warrant such
 a diagnosis, but rather because of the localization of the symptoms ;
 and in several of these cases I have seen cures effected by galvaniza-
 tion with large electrodes  (Fig. 68), one being  applied  over each
 ovarian  region and  a current of 10, 20, or 30  milliamperes  being
 passed for five or ten minutes every second day for a period of  two
 to three weeks.  The objection will be made by gynecologists, I am
 well aware, that I am not a gynecologist,  and  may therefore have
 overlooked some organic local disease.   It is therefore proper that I
 should state that  all of these cases of mine have been examined by
 distinguished gynecologists, and that my attention was first called to
 the matter by a case which I took to a gynecologist for him to ope-
 rate upon, when, very much to my surprise, he refused to operate,
 had nothing to advise, and left me to my own devices, so that, know-
 ing of nothing  else  to  do, I experimented with galvanism, and,
 greatly to my relief, cured the patient.   These cases have, therefore,
 seemed  to me to be local neuralgia of a  peculiar  type, often  made
 worse by the menstrual period, and frequently following some pre-
 disposing cause such as malaria, lithsemia, or depression of the general
 health.
  Diseases of the male  urethra have been supposed to play as large
a part in the causation of reflex disorders  as  the pelvic lesions of the
female.   I believe, however, that the one belief is as much due to
defective observation  as  the   other.  It  is  undoubtedly  true  that 
536
NEBVOUS DISEASES.
nocturnal enuresis in children  and childish  disorders akin to som-
nambulism  and night-terrors, as well as these  two latter affections
themselves,  can  sometimes  be relieved by circumcision.   It is also
true that strictures of the male urethra and affections  of the seminal
vesicles may cause reflex pain  and uneasiness in the nerves coming
off from the lumbar  and dorsal cord.   But nocturnal enuresis, som-
nambulism,  and  night-terrors  can  be relieved often much more
effectively by other measures than circumcision, and  the reflex pain
and disorder due to  stricture and to disease of the seminal vesicles
are generally made worse in my experience by any treatment addressed
to  the urethra and the seminal vesicles that does more than relieve
the  stricture causing obstruction to  the  passage of urine,  or the
inflammation and occlusion  of  the  seminal ducts that prevent the
passage of semen.  In the chapter upon " Somnambulism," " Night-
terrors," etc., many remedies are spoken of that are quite as effective
as  circumcision, and much  less unpleasant.  In the adult  male
afflicted with disease of the seminal  vesicles, or a stricture, and who
has reflex nervous symptoms, there will often be found a large degree
of hypochondria which cannot be relieved  by any treatment addressed
locally to the urethra  or the vesicles.   That circumcision will relieve
all  the varied organic  nervous diseases which it was claimed to relieve,
and that it will  cure  epilepsy and chorea, have been disproved time
and time again.
  Intestinal  disorders will sometimes cause vertigo, slight insomnia,
and general  nervousness, but this very rarely ; indeed, the rule is that
intestinal disorders do  not produce general  symptoms,  and  wrhen
they do, they are  so  pronounced  as  to make the diagnosis an easy
one.  In the section  upon "Neurasthenia" I have stated  ray doubt
as  to whether the cause of the malady  might  not  be some error
of digestion  in  the stomach or the intestine, but this is so largely a
matter of uncertainty as yet that  it is impossible to speak positively
either one way or  the other.  Epilepsy' has seemed to me in some rare
cases, as  stated elsewhere (vide " Epilepsy "), to be excited  in a pre-
disposed  individual by intestinal disorder, and Herter has  described
some experiments to  show that toxic substances  capable of causing
epilepsy may be  generated in the intestines.   Nevertheless, this cause
of epilepsy is infrequent and not general, as has been  popularly sup-
posed, and even  in these rare cases it must be carefully borne in mind
that it is an exciting  cause and not a predisposing one.
  The relation of lithsemia to reflex nervous disorder has beeu thor-
oughly described in " Neurasthenia."
  Errors of refraction  are sometimes a cause of vague nervous dis-
orders, such as slight  dizziness, general nervousness, inability to con-
centrate the mind, etc.   But this is a rare cause,  and  even  Mitchell,
who has called attention to the subject, has recently so stated.
  What has been said  of errors of  refraction is also true of insuffi-
ciencies of ocular  muscles  causing so-called ocular asthenopia.  In
cases of  migraine  in  which  the attacks  have become frequent and
violent, a relief of muscular insufficiencies will often act remarkably
well as a palliative; and this is also the case in certain vague ner- 
BEFLEX NEBVOUS DISOBDEBS.
537
vous symptoms in neurotic individuals.  There has never been the
slightest proof adduced, however, that relief of muscular insufficiency
will  cure chorea, epilepsy, auy of the  insanities, or neurasthenia, or
even that it will act as a palliative in these cases, and I have derived
the materials for this statement from many cases under my own ob-
servation.
  Aural disease as a cause of reflex nervous disorder is thoroughly
discussed in  the next chapter, upou " Meniere's Disease," aud I can
add nothing to that.
  Ansemia and leucocythsemia  will  sometimes cause  pronounced
headache and  neurasthenia;  seldom,  however,  vertigo,  and  never
convulsions.   In  certain cases of insanity it has been  demonstrated
that ansemia is marked, but it is extremely probable that the ansemia
is much more  frequently an effect than a cause iu such cases.
  The diagnosis of a reflex nervous  disorder, therefore, will  be by
exclusion of all non-nervous  and  mental diseases capable of pro-
ducing similar symptoms, and then by the examination of the differ-
ent organs which we have been discussing.  The treatment will vary
with the cause. 
CHAPTER   XY.
                     MENIERE'S  DISEASE.

   In 1861 Meniere observed a case with intense vertigo which died,
and in which he found certain hypersemic and  hemorrhagic appear-
ances in the labyrinthine structure of the internal ear, and  since then
the name of Meniere's disease  has  been given to vertigo occurring
with lesion of the internal ear.   As a matter of fact, however, it has
been found that vertigo can occur with disease of the external and the
middle, as well as the internal ear.   An undoubted case of idiopathic
or primary labyrinthine disease has  not been observed, and most of
the cases which have occurred have been found  to be due to extension
inward from the brain or  from the middle ear.   Thus, meningitis
either  of  the epidemic or sporadic  cerebro-spinal type,  purulent
meningitis, and fracture of the base, particularly  that involving the
petrous portion  of the temporal bone, have  set  up labyrinthine
trouble.  From the middle ear the labyrinth can be  affected either by
direct  extension of disease into it, by pressure inward  upon  the
labyrinth through the apertures between the middle and the internal
ear, by products of inflammation within the middle  ear, or by a
closure of the Eustachian tube which admits air  into the ear-drum
and the membrana tympani, thus causing collapse of this membrane,
and thereby slight pressure upon the labyrinth.   Even disease of the
external ear, if it be sufficient  to exert pressure inward through  the
middle ear upon the fenestra ovalis  and  rotunda, may cause the pe-
culiar  symptoms.   Meniere's disease, therefore, as it is now under-
stood,  is really a complex of symptoms due to disease of the external,
middle, or internal ear.  The salient symptom is vertigo, and this
varies  somewhat in  degree and  kind according  to which portions of
the ear are affected.   In labyrinthine disease the  patient staggers to
one side, the vertigo is apt to come on in paroxysms, and these vary
in intensity, so that the patient may simply reel like a drunken man,
or may fall suddenly as if shot.  Incredible as the history may seem,
I once had  a patient under my care with  this sensational record:
He had been a peasant in Ireland, and  one day crossing one of  the
wide moors in a  dogcart, he was suddenly,  as  he thought, struck a
violent blow from  behind,  so that he believes he lost  consciousness
for some time.  At  all events,  when he was  able to  get up, he found
his horse and wagon some  distance  off, and, of course, not a soul in
sight.  Under the belief that he had been struck by some  enemy, he
went quietly home and said nothing about it.  Some time afterward,
however, in crossing another lonely place he had a  similar experience,
and as he came to the conclusion that nobody could have been near
him, he made up his mind that it was some  malevolent stroke of the 
MENIEBE'S DISEASE.
539
devil, and he consulted a priest, who agreed with him in his belief and
gave him an amulet to wear.  A series of similar attacks occurred,
and, puzzled as  to  whether there was some diabolical agency at
work, or whether he was the victim  of a  conspiracy, he emigrated
to America, and had no attacks for several months.   When a  new
paroxysm occurred he came to me, and I found indubitable evidence
of labyrinthine disease.   These paroxysms are usually accompanied
by nausea or vomiting.   The face grows pale  and the body is often
covered with a  cold sweat, so that the attacks are frequently mistaken
for apoplexy.  In disease of the middle ear the vertigo  does  not
occur in paroxysms,  but  is apt to be continuous.   In disease both of
the middle and internal  ear loud  noises  are generally heard,  and
sometimes  these  sound  like bells  or pistol-shots,  or  loud hissing
sounds like steam-whistles.  In  disease of the external  ear the  ver-
tigo is less in degree and continuous, and  the loud sounds are not
usually heard.
   The pathology of  Meniere's  disease, as  would  be  expected from
the foregoing remarks, is a complex one, involving lesions of the
internal, middle, and external ear, and possibly sometimes, of  the
temporal  lobe  of the brain.  In  labyrinthine  disease there   may
have been found an extension inward of a  meningitis or a necrosis
of bone.   In middle-ear disease there will often  be found to be old
lesions dating back to scarlatina,  measles, variola, and other childish
diseases, or there may be a purulent inflammation, or  a closure of
the fenestra ovalis or rotunda, or the Eustachian  tube may be found
to be impervious.   In disease of the external  ear  there may be a
simple otitis externa  or an accumulation of wax  or  a  furuncle.
Flourens, in 1828,  demonstrated that section  of the semicircular
canals  of the  labyrinth in pigeons caused peculiar pendulum-like
movements of  the head, which ceased a short time after one-sided
section, but  which   in bilateral section  were always in the direc-
tion of the injured   canal, so that after section of  both horizontal
canals  the pendulum-like  movement of  the head  was in a hori-
zontal direction from one side to the other, and after section of both
vertical canals in a vertical direction from above downward.  Answer-
ing to the movements of the head, the pigeons, after section of the
horizontal canals, moved  to the right or to  the left in  a circle, whilst
after section of the vertical canals they frequently stumbled forward
or backward.   The  ability to fly was seriously  disturbed in all
instances after bilateral section, and even on a level surface the birds
moved with difficulty.   The hearing of birds  so  operated upon  was
preserved.  These experiments were confirmed by Harless, Czermak,
Brown-Sequard, and Vulpian.  Goltz added some further important
facts.  He observed in pigeons, in which the semicircular canals were
destroyed, a rotation of the  head to 180°, so  that the hinder part of
the head was twisted around to the floor and  the  beak pointed  up-
ward ; at the same time there were pendulum-like movements of the
body, often movements backward or retropulsion, and loss of ability
to fly.  Goltz believed that disturbances of movement  of the body
were due to the defective position  of the head alone, for when  the 
540
NEBVOUS DISEASES.
head was fixed in an abnormal position in pigeons that had not been
operated upon similar disturbances of the body were seeu.   He also
affirmed that this abnormal position of the head was due to the loss
of the semicircular canals, and  he therefore regarded  these latter
structures as sensory organs necessary to the equilibrium of the body,
especially  of the head.  Bottcher advanced the idea that the disturb-
ances of equilibrium were due to a cerebral lesion, complicating and
following  the operation upon the semicircular canals, and that this
lesion was induced by the operative procedure injuring the cerebrum
or the cerebellar peduncles.   Baginsky claims to have confirmed  this
view, although he details no experiments.  A number  of very inter-
esting researches  were published  a few  years ago by Ewald upon
pigeons, daws, cockatoos, salamanders, frogs,  rabbits, and dogs;  as a
result of which he arrives at the conclusion that the  labyrinth con-
sists of  two functionally distinct apparatuses, namely : the auditory
labyrinth  and the tonus labyrinth.  The auditory labyrinth  is the
true auditory organ,  and is that  which is  irritated by waves of
sound,  and its excitation  passes to   the  sound-receiving portions
through the trunk of the auditory nerve. The tonus labyrinth is the
organ which exercises influence   upon the muscular  movements, so
that its  excitation is made evident by muscular disturbances  which
are not  as yet thoroughly understood.  Heretofore it has been assumed
that the auditory labyrinth necessarily converted sound  into nerve-
irritation,  but Ewald's experiments seem  to show that this auditory
labyrinth  simply  serves the purpose of directing the sound according
to its quality to  different  fibres  of the auditory nerve.  Ewald en-
deavors to make this plain by comparing the  labyrinth to the retina,
which only responds to light in certain locations ; with this difference,
however, that whilst the optic fibres  are not directly responsive to
light impinging  upon  them,  the auditory fibres respond directly to
sound.  In the higher vertebrates the auditory labyrinth is found in
that portion which is  known  as  the cochlea,  so that widespread dis-
turbance of the other portions of the labyrinth would not prevent
the animal from hearing perfectly, although it might  present  symp-
toms of muscular disturbance ; and conversely, a lesion of the cochlea
might impair or destroy the hearing-power, yet there be no muscular
disturbance present.  In one pigeon, for example, the whole labyrinth
on the left was removed, and on the right only the cochlea, in both
operations the naked  stump  of  the cochlear  nerve being seen in the
amputated.cochlear excavation.   When  this pigeon was suspended
the right wing hung motionless, whilst the left was drawn up to the
body.   If a noise was made, as by clapping the  hands or tapping
with a hammer upon an adjacent table, the right wing  was drawn up
more and  more until it hugged  the body as  closely as the left  one.
As the  pigeon did not possess a  cochlea  upon  either side, aud as it
remained  as irresponsive  to sounds as  a  pigeon  without  either
labyrinth, the conclusion is  a fair one  that the  movement  of the
wing that has been described was not in conscious response  to the
sound, but rather in response to the  excitation  set up in the tonus
labyrinth  by the sound.  As Ewald  states,  this would  explain the 
MENIERE'S DISEASE.
541
well-known fact that certain  rhythmical sounds have a tendency to
excite to rhythmical muscular movements, exemplified  in  the desire
to dance that is aroused  by the hearing of dancing music, or the
freshening of the step of tired troops by marching airs.  Indeed
Ewald shows that there need  not  be a rhythm iu  the sound in order
to excite muscular movements.   He cites a curious observation of
his own, which was accidentally made during some observations in the
registration of the normal  respiratory curve.   In a room in which
sat persons to be observed, breathing quietly, there happened to hang
a pendulum that ticked off every secoud with a short simple stroke,
and quite unconsciously most of  the individuals in this room  began
to breathe after a little while in  exact accordance with the rhythm
of the pendulum, twenty times  in every minute.   Similar are the
movements with which an equestrian  accommodates himself to the
gait  of his horse.  When both  labyrinths  are  removed from the
animal,  certain  peculiar disturbances become evident  in the use
of the  striated muscles, cousisting chiefly  of  the lack  of  pre-
cision, which may  be due to the fact that the  contraction of the
muscles begins too late, or proceeds too tardily, or is due to  lack of
strength, etc.   Which of these factors  it is that  causes the lack of
precision Ewald has not been able  to determine, although  he has
ofteu fouud the muscular strength diminished.  Those muscles which
require the most precision in  the performance  of  their  normal func-
tion  suffer the greatest from the removal of the labyrinth, and there-
fore  the ocular muscles are apt to be most affected, next the muscles
of the neck and head, which are especially used in many birds in
directing the beak to pick up the food; whilst the wings  in birds
suffer less  and the limbs still less, although in the  cockatoo, which
uses  its leg- and foot-muscles in  grasping its prey, the muscles of the
lower extremities become very greatly  disturbed in their precision of
movement.  Although Ewald is  of  the  opinion  that the  labyrinth
innervates all the muscles of the  body, he has found that  iu pigeons
lesion of it is more apt to impair certain muscular groups, so that he
believes that  in these birds it is the muscles moving the vertebral
column and the head which are most affected, alwayTs of the opposite
side; yet,  curiously  enough, he finds  that  it  is different  with
regard to the extensors and abductors of the extremities, on the one
hand, and the flexors  and  adductors on  the  other, as the laby-
rinth is  in  closer relation with the  former  upon  the same  side,
and with  the  latter upon the opposite.   The ocular muscles,  too,
seemingly with the exception of the  rectus externus, are mainly in-
nervated from the labyrinth  upon the  same side.  Removal of the
labyrinth in  these birds causes,  therefore, a spiral deviation of the
entire vertebral column toward the side  operated upon, and of the
head and the  neck to  the  same  side, whilst the extremities of the
same side are flexed and adducted, and those of the opposite side ex-
tended and abducted.  The muscles  of the eyes, especially those
upon the same side, deviate toward the side operated upon.  Ewald
regards these  muscular disturbances,  however, as  of indirect origin,
because  they  vary qualitatively and  quantitatively from moment to 
542                   NERVOUS DISEASES.
moment uutil death occurs, and also because excitation of the audi-
tory nerve causes them to disappear.  He therefore believes that
from the labyrinth flows out a continuous innervation  to  the mus-
cles, a sort of nerve-tonus, and hence he  calls  this  portion of the
labyrinth the tonus-labyrinth, locating it in the crista  ampullarum
and the macula acousticse.
  Diagnosis.  The  diagnosis  of Meniere's disease  must  be made
with the object of first distinguishing it from other forms of vertigo,
determining whether it is the external, middle, or internal ear that is
affected,  or whether there is a lesion  of the  temporal lobe of the
cerebrum  or of the cerebellum and its peduncles.  The differentiation
of Meniere's disease from  other forms of vertigo has been gone over
in considerable detail in the section  upon  " Vertigo," and it is not
necessary  to repeat here what has there been said.
  Disease of the external ear can be readily ascertained  by the ordi-
nary examination, as well as by the fact that the vertigo is  apt to be
slight in degree aud not continuous, and loud sounds  are not gener-
ally heard.   When there  is disease  of the middle ear the vertigo
does not occur in paroxysms, but is  apt to be continuous, and  the
diagnosis  can be made  by exclusion of internal and external  ear
disease, lesion of the cerebrum, or of the cerebellum and its peduncles.
Lesions of the middle ear  are especially apt to occur  in conjunction
with a naso-pharyngeal catarrh extending up the Eustachian tube or
occluding it, and in all these  cases a careful examination should be
made of the  rhino-pharynx.   In disease of both the  middle and in-
ternal ear loud noises are  generally  heard,  frequently sounding like
bells  or pistol-shots,  or loud whistling sounds  resembling steam-
whistles.   Again, in disease of the middle  aud internal ear there is
a tendency to much more marked disturbance of equilibrium than in
case of external-ear disease, and these are such that the patient stag-
gers to one side or the other,  or has a sensation  as if he had been
struck a severe  blow, as in the case I have narrated, or is at times
moved in a semicircle, as in disease of the  cerebellar  peduncles.   It
should, however, always be borne in  mind that disease of the middle
ear by pressure upon the fenestra ovalis or rotunda  may cause  the
same symptoms as disease of the internal ear  does.   Disease of the
mastoid cells,  especially abscess,  may also cause the symptoms of
lesion of the internal  ear.  Reference is  also  made upon p. 160 to
other means of diagnosis  of disease of  the external, middle, and
internal ear.  Moreover, according to Ewald, as we have seen,  a
muscular  inco-ordination  may be present in disease of the internal
ear, quite distinct from the disturbance of hearing.
  Prognosis. The prognosis of Meniere's disease will depend upon
whether it is due to lesion  of the external, the middle, or the internal
ear.  Labyrinthine disease is a grave matter, and although there are
cases  which can be relieved, there are very  few of them.  Disease of
the middle ear due to chronic lesions  of long date are incurable, but
some  cases of recent lesions can be treated very successfully.  Disease
of the external ear can usually be treated successfully, and is there-
fore of good  prognosis. 
MENIERE'S DISEASE.
543
   Tteatment.  The treatment of Meniere's disease will vary ac-
 cording to the cause.   Disease of the  external ear can  usually be
 treated with success by the ordinary means.  Disease of the middle
 ear can be treated, if  I may judge by the experience which I have
 had in a  number of cases, with much greater success than aurists gen-
 erally suppose.  I am firmly convinced that much more can be done
 in many  of these cases by treatment through the rhino-pharynx than
 by treatment through the external ear.   I have again and again seen
 cases of middle-ear disease to which no relief had been given  by the
 aurists through the ordinary methods, and which have been entirely
 or  largely relieved by removal of a naso-pharyngeal catarrh, and in
 several of these cases  the catarrh has been so  slight that the  laryn-
 gologist  himself was  in doubt as to  whether it could possibly affect
 the middle ear.  Dilatation of the  Eustachian tube by the ordi-
 nary  catheter is, I am quite  persuaded,  not  only useless in such
 cases, but it is positively harmful, inasmuch  as it will increase the
 vertigo and other nervous  symptoms.  The  best treatment will  be
 by means of suitable  sprays projected by the modern compressed-air
 apparatus of the laryngologist, and not by the ineffective hand-bulbs
 which are in frequent use, never by means of the antiquated insuffla-
 tion of powders, or salt and water, which are, I am sorry to say, too
 often recommended.   I am fully persuaded that  the aurists have
 neglected the naso-pharyngeal treatment of middle-ear disease induc-
 ing the Meniere symptoms,  aud I am never satisfied with  the prog-
 nosis of the aurist  in a case of this kind unless I know  that he is
 moderately skilful in  the treatment of naso-pharyngeal  disease.  In
 cases of disease of the middle ear it is often very difficult to do much,
 but that a great deal more can be done than has been generally sup-
 posed has been demonstrated  by the two remarkable cases  which
 Burnett  has  reported, in which he removed the membrana tympani
 and the  malleus, and completely relieved the nervous symptoms.
 Charcot has recommended the use of large doses of sulphate of quinine
 in Meniere's  disease, but this  was done  at a  period when we were
 scarcely acquainted at all  with the different forms of this complex
 symptom-group, and it is certain that it more frequently does harm
 than good ; indeed, I consider quinine in large doses in any of these
 cases a very dangerous  remedy, and  I have  in two  instances seen
 permanent deafness produced by it.   The bromide of potash in mod-
 erate doses will be serviceable  in  combating the nervous  erythism
 which often accompanies the local  aural symptoms, but it should be
 used with great caution, and the patient should not be allowed  to
 form the  bromide-habit. Tonics should  be given whenever they are
 needed,  but they  should be in the  form of ordinary bark, iron,
 arsenic, or the simple  bitter  tonics, and never in the form of quinine.
 When there is a purulent disease  of  the  mastoid trephining  should
 be done promptly, as the operation is  a perfectly harmless one in this
day of antiseptic surgery, whilst the results of purulent extension to
the middle ear cannot be foreseen  except by omniscience.   A  lesion
of the temporal lobe should be  operated upon if it can be  localized,
and the same is true of a lesion of the cerebellum.  Indeed, in any 
544
NER VO US DISEASES.
case where there is grave doubt as to whether a suppurative  menin-
gitis or a cerebral abscess has been set up, trephining should be done,
because such an  operation  is not a dangerous one in these days of
antiseptic  surgery, being of much less risk to life than pus pent up
in the cranial cavity.   But instead of mere peep-holes being bored in
the skull,  as it is the custom to do, a large flap of bone should be re-
moved  as advised in the section on " Intracranial Growths," so that
a goodly surface may  be exposed.  Moreover, careful but extensive
probing with a small ball-headed probe should be done, if the abscess
is not readily found.  It must, however, be borne in mind that puru-
lent extension inward from the ear may cause venous thrombosis and
lymphangitis, so that  in the former case  it  would be impossible to
afford  relief by any  operative  procedure,  whilst  in  the  latter an
abscess might form in some region far away from the  ear—indeed,
often in the posterior fossa of the skull, or in the cerebellum, or there
micrht be  multiple abscesses.  (See Chapter, " Thrombosis of Intra-
cranial Sinuses.")  Trephining, therefore, should always be regarded
as an exploratory measure, and this should be  made known to the
patient's friends or relatives. 
CHAPTER  XVI.
                   FRIEDREICH'S DISEASE.

   Synonyms:   Hereditary  ataxia.  Hereditary ataxic  paraplegia
 (Gowers).
   This malady was first described by Friedreich in 1861.
   The symptoms begin in early  life, and consist of ataxia, nystag-
 mus, defective speech, loss of knee-jerk, and curvature of the spinal
 column.  Ataxia of the lower limbs is  almost invariably the first
 symptom; then of the  trunk and the  arms.   The nystagmus is bi-
 lateral, usually transverse, and is generally observed only when the
 patient fixes or follows  an object; but it  should be borne in mind
 that it is not one  of the early symptoms.  The defect  of speech is
 due to a defect of articulation which causes the patient  to stammer,
 run the letters together, or make sounds that are not precise and that
 are evidently due to ataxia of the muscles of articulation ; and speech
 may finally become utterly unintelligible.  The knee-jerk is always
 absent.  The spinal curvature is usually a  combination of  lateral
 and angular curvature, but either one of these varieties may be pres-
 ent alone.   It is probably due to  ataxic implication of the vertebral
 muscles.  In addition to the cardinal symptoms that have been enum-
 erated there is one mentioned by Rutimeyer that may prove to be of
 some importance,  namely, a turning up of the great toes toward  the
 dorsum of the foot, although Orraerod has seen the same symptom
 in a case of long-standing multiple neuritis.   The gait  is a stamp-
 ing, stumbling, tottering one, and  when standing with the  eyes
 closed  and feet approximated (so-called Romberg symptom)  the
 patient sways.  There is often  inco-ordination in the upper extrem-
 ities, as has already  been said, although it is most marked  in  the
 lower extremities.  There is frequently a jerky  shaking of the head
 and quivering of the trunk-muscles, even when the body is at rest,
 and jerky  tremors of the fingers or of the whole body.  Sensory
 symptoms are  usually  absent, although  in  some  cases, after  the
 disease has been  well  developed, severe  pains  have been observed
 and diminution of sensibility.   There is never any mental disturb-
 ance.   The progress of the malady is exceedingly slow.   Some cases
 have lasted thirty-three  years, although others  have  terminated
 fatally  in eight.
  The disease is an eminently hereditary one in the sense that  the
 families in which  it occurs are almost invariably prone  to neuroses.
 It has  been a  question whether  the ataxia itself is ever directly
 hereditary, but Vizioli .has been able to decide this most  positively in
the affirmative,  for he tells of a family in which an ancestor begat
eight ataxic children, one of which cases this  author diagnosed  as
                               35 
546
NERVOUS DISEASES.
 Friedreich's disease, and  this patient in his turn begat two children,
 both of whom were, under Vizioli's observation, afflicted with Fried-
 reich's disease.  Nevertheless it does sometimes occur without hered-
 ity, and  Ormerod alone records three such cases, and I have myself
 seen two.  A very important characteristic of the hereditary tendency
 is that many members are generally attacked in one generation, and
 Buryr, writing in 1886, goes so  far as to say that there are only four
 instances where one member alone has been affected in a generation.
 It is essentially a  disease  of early life, usually beginning between the
 fifth and fifteenth years,  somewhat earlier in boys than in girls, and
 in some  cases so early that the patients have never learned  to  walk.
 The exciting causes have been numerous ; thus it has occurred during
 convalescence from scarlet fever and typhus, after  chorea, smallpox,
 migraine, gastric disturbance, and several acute diseases, although it
 is possible that in a number of these the febrile symptoms have really
 been due to the disease itself.
   In all but one of the cases that have been examined pathologically,
 some nine  in all, the principal lesion has been a sclerosis of the pos-
 terior columns of the cord, most marked in the lumbar region and
 least so in  the cervical, in the former affecting both the columns of
 Goll and of Burdach, in the latter chiefly the columns of Goll.  In
 Friedreich's cases the peripheral portion of these  posterior columns
 was most affected, while in  Brousse's the neighborhood of the central
 canal and  the  edge of the posterior cornua  were most implicated.
 The pia over the posterior  columns is usually thickened and  pig-
 mented,  and there are  fine adhesions between it and the dura mater.
 In  one  of Friedreich's  cases  the posterior  columns  alone  were
 affected,  but this isolation to one system of fibres  is unique, and in
 most the lateral and the anterior columns are affected as well as the
 posterior. The gray matter of the cord is almost invariably implicated.
 In one case there were two canals symmetrically placed on each side
 of the junction  of the posterior and anterior cornua; in another there
 was atrophy of some of the  cells of the anterior cornua ; in three the
 cells of Clark's column were degenerated aud signs of inflammation
 were present about the central canal.   The posterior roots of the
 cord are generally atrophied and  sclerosed.   Slight changes  have
 been observed in  the  medulla, mainly in the posterior pyramids as
 high as  the nucleus  of  the hypoglossal.  In  one  case of Fried-
 reich's there was atrophy  of the sciatic and  hypoglossal nerves, and
 to a less degree of the anterior crural and  median  nerves.  Until
 within a  very recent date  the pathological changes have been thought
 to be entirely spinal,  but a remarkable autopsy has recently been
 published by Menzel.   The patient was  undoubtedly a case of heredi-
 tary ataxia, and one of his children was  afflicted with the same dis-
 ease.  Macroscopically  a  high degree of atrophy of the cerebellum
 and  pons was observed.   In the lumbar cord there was degeneration
 of the posterior columns of the  lateral  pyramidal  columns and  the
 place of  the lost  nerve-fibres was taken by connective-tissue septa.
 The number of the nerve fibres in the posterior roots was  consid-
erably diminished.  The  rim-zone of  Lissauer  was  normal, but in 
FRIEDREICH'S DISEASE.
547
the spongy portion of the substantia gelatinosa almost all  the nerve-
fibres had disappeared, only a few being visible, coming directly from
the posterior roots, and certain others on the edge of the lateral col-
umns.   In the substantia gelatinosa itself the fine nerve-fibres had
almost entirely disappeared, and none were visible coming from the
posterior column, although a few were still present of the coarser fibres
from  the posterior roots.  Clark's columns were intact.   The fibres
passing from the posterior columns into the auterior cornua and tra-
versing the spongy substance were normal.   The posterior gray com-
missure showed very few medullated nerve-fibres, although the an-
terior gray commissure was normal.   In the auterior cornua the gray
cells were somewhat  diminished in number and size, and the anterior
roots were partly atrophic.  The posterior  root-ganglia were macro-
scopically diminished  in size,  and  microscopically showed  great
diminution of medullated nerve-fibre.   In the  lower dorsal  cord
there was degeneration of the  columns  of Goll  and Burdach, the
lateral pyramidal columns, and the direct cerebellar columns.   In
this  region the fibres  passing  from the root-zone of  the posterior
columns into the anterior cornua had  almost entirely disappeared,
and the cells of Clark's columns  had undergone  fatty and pigmen-
tary degeneration, whilst the fibres from the posterior columns into
Clark's columns and from  the direct cerebellar columns into them
had disappeared, as  well as those  fibres coming  from the anterior
cornua  and the  region of the  anterior commissure to Clark's col-
umns.  In the anterior horns the ganglion-cells were  atrophic, and
the anterior roots were also atrophic.  The upper dorsal cord dis-
played the same changes.  In the cervical  cord there was degenera-
tion of Goll's  columns, the columns of Burdach, the lateral pyram-
idal  column,  and  the  direct cerebellar column, although both of
these latter were but slightly affected.  There was no degeneration
of the anterior columns in this region.   In other respects the cervi-
cal cord was as the lumbar and dorsal.   The  medulla oblongata
was  macroscopically much  reduced in size.  The nuclei of the col-
umns of Goll  and of the columns of Burdach, especially the outer
nucleus of the latter, were greatly atrophied and diminished in the
number of their cells,  and  were  half of the normal size.  On one
side the territory which Darkschewitz has regarded as the origin of
the spinal  accessory was much  atrophied, aud atrophic fibres were
found in the trunk of the spinal accessory of this side.   The nucleus
of the lateral  columns was also markedly atrophied, and also the
larger olives.   The inter-olivary  layer aud the fibrse acutse internse
were normal or almost normal.   The pyramids were normal.   The
direct  cerebellar  columns were  so degenerated  that  scarcely  any
medullated fibres were to be seen.  In  the nucleus of the hypoglos-
sal was observed great  atrophy  of the cells, and the hypoglossal
root was markedly  degenerated.   The restiform body, or inferior
cerebellar peduncle,  was diminished in size to oue-fourth.   The
facial,  auditory, abducens,  and sensory trigeminal  nuclei were all
normal.  At the level  of the superficial origin of the fourth through
the pons the latter was so much diminished in size as to be only two- 
548
NERVOUS DISEASES.
 thirds of its normal volume, and this diminution of size was due to
 atrophy of the medullated  fibres in the cerebellar peduncles and to
 entire loss of the large nucleus of the pons.   In the middle of the
 pons the lemniscus was fairly normal, but the lateral lemniscus pre-
 sented  a slight atrophy.  The central  field  of the  tegmentum was
 normal, but the region behind it was so atrophic that the pyramids at
 this level were surrounded by but few medullated nerve-fibres.  The
 superior cerebellar peduncles were normal.   In the anterior and pos-
 terior quadrigeminal region there was nothing abnormal.  The pes
 of the crura cerebri was diminished one-third.  The  fourth ventricle
 and the aqueduct of Sylvius were found to be considerably enlarged.
 The cerebellum was markedly atrophied. The fleece surrounding the
 corpus  dentatum was somewhat diminished  in the number of its
 medullated fibres, the  nucleus of the corpus dentatum was also some-
 what degenerated, and still  more marked  was the  atrophy  of the
 nerve-fibres of the individual lobules, aud  in these  atrophic places
 connective-tissue septa had  taken the place of the nerve-fibres.   In
 the cerebellar cortex there was  a diminution in the  number  of the
 large cells of Purkinje,  and, rather curiously, where the cells  had
 disappeared they had  disappeared entirely and no degenerated ones
 were found.  The  upper portions  of  the  cerebellum  were more
 atrophied than the lower portion.  The medullated nerve-fibres from
 the direct cerebellar column could be followed in places directly into
 the medullary portion  of the cerebellum.  The atrophy of the resti-
 form body and direct  cerebellar column in this case of Menzel's  is
 confirmatory of Von Gudden's experiments that Morchi had already
 corroborated; and  a number of cases of atrophy of  the cerebellum
 have been reported (Huppert, Schulze,  Frazer, Seppilli, Kirchhoff,
 Claus, Ferrier);  but this case of Menzel's is  the first instance of a
 clinical history  having  been carefully studied in the cerebellar
 atrophy of children and the first case in which its relations to Fried-
 reich's disease have been shown.  The truth of the matter probably
 is that Friedreich's disease  is closely akin to locomotor ataxia.  In
 all departments of medicine  we have the same tissues afflicted by
 similar  diseases with different clinical  symptoms, aud this is proba-
 bly the case with  locomotor ataxia and Friedreich's disease.  In-
 deed, as Erb says, borrowing botanical languagp, the natural order
 of tabes contains two species  to which most individuals  may be re-
 ferred ;  and there are transitional forms,  as in Corre's case, in  which
 there was well-marked heredity and affection  of speech, yet the dis-
 ease  began with pain and numbness in the feet aud legs, and diplopia
 was observed; and Dreshfeld has reported three cases which would
 be indistinguishable from locomotor ataxia were it not for the fact
 that  two other members of the same family were affected.
 ^ The diagnosis  of Friedreich's disease is from locomotor ataxia,
disseminated sclerosis,  and ataxic paraplegia.   In locomotor  ataxia
the disease  usually commences later in life; there is  much more apt
to be a history of syphilis than a  marked heredity ; there are fre-
quently early bladder-symptoms, peculiar  stabbing  and  lightning
pains, and other  impairment  of sensation, such as ansesthesia, anal- 
                    FRIEDREICHS DISEASE.                 549

gesia, etc., and the ataxia is often  in the lower extremities and of a
peculiar stamping kind. Moreover, in many cases of locomotor ataxia
there are the pupillary symptoms,  the transient paralyses of the ocu-
lar  muscles, and the optic-nerve atrophy.  In disseminated sclerosis
there is almost invariably a tremor, and this tremor is fine  and does
not consist  of  large jerky, shaking movements,  which  are some-
times seen in Friedreich's disease.  It must be admitted, however,
that when disseminated sclerosis occurs in children it may be very
difficult to  make the  diagnosis, inasmuch as disseminated sclerosis
may be attended by a loss of the knee-jerk, and  among its usual
symptoms is a nystagmus; but  in such cases as these the history of
ataxia in  the family, or of some disease resembling it, may prove to
be of great  diagnostic value.   From ataxic paraplegia the  disease
can generally be distinguished, because in the former there is increase
of knee-jerk and ankle-clonus, and  because the nystagmus and articu-
lation of the latter do not occur.  In some cases of ataxic paraplegia,
however, when the knee-jerk is lost, the diagnosis may become very
difficult.
  The prognosis  of Friedreich's  disease  is  very  serious  so far as
regards arresting  the malady, but, as  has  already been said, it may
last over thirty years before proving fatal.
  Nothing  is known about the treatment.   I  have never been able
to treat a case myself for any length of time,  aud therefore cannot
speak of it; but  if  I  were to treat one, I should  treat  it upon the
same principle as  I would a case of locomotor ataxia. 
CHAPTER  XVII.
                          MYXCEDEMA.

   History.  In  1873  Sir  William  Gull read a paper upon "A
Cretinoid State Supervening in Adult Life  in Women," describing
very fully the disease  now generally recognized as myxcedema, not,
however, dealing with the pathology.   In  1877 Dr. Ord presented a
communication to the Royal Medical and  Chirurgical  Society of
London  on " Myxcedema, a Term  Proposed  to  be  Applied to an
Essential Condition in the Cretinoid  Affection Occasionally Found
in Middle-aged Women," containing observations that went back as
far as 1861, and  dealing quite fully with  the  pathology.   Many
papers have since been published upon this subject, notably that by
Charcot,  and by  Reverdin,  Kocher,  Semon,  Burns, Horsley, and
Virchow.  But by all odds the most exhaustive communication upon
the subject  is the report of a committee  of the Clinical Society of
London that was nomiuated in 1883 and reported  in 1888.
   Clinical History.   In this  disease the whole body is swollen,
this  swelling  usually  appearing first  in the head and face,  whilst
the lower extremities  are apt to  be swollen before the upper ones.
The features become coarse and puffy,  the eyelids  are always  trans-
parently swollen, the eyebrows generally raised to help in sustaining
the upper lid, the nostrils are swollen and broadened, the lower lip
thickened, everted and livid, and the mouth widened transversely.
Over the cheeks aud nose there is a reddish patch in the midst of the
pallid skin,  which is dry, scaly, and without perspiration or  seba-
ceous secretions.    The  hands are generally affected, the fingers being
swollen and moved with  difficulty.  The hair is dry and brittle, and
baldness generally supervenes, whilst  the eyebrows and  lashes may
also be lost.  The feet  are affected in the same way as are the hands.
The temperature is usually subnormal.   CEdema of slight degree is
occasionally observed, especially  about the ankles,  but persistent
dropsy is seldom seen.   There is no impairment of sensation, except
in the way of retardation, which has been observed in about half the
cases, possibly due to the  hebetude.  Dyssesthesia and  parsesthesia are
not infrequent, such  as a  feeling of coldness,  trickling of water upon
the skin, disagreeable smells and  taste, partial  numbness, noises in
the ears,  vertigo,  tinnitus, and  pains  and heat at top of the head.
In a  certain proportion of cases there is considerable occipital  head-
ache.  Paresis of the muscles of the head, neck, and limbs is frequent,
so that the head falls forward, the chin resting  on the sternum as in
the attitude of the cretin, and slowness of movement is character-
istic, being rarely absent from the gait.  Inco-ordination is also occa- 
MYXCEDEMA.
551
sionally observed.   The  mental  changes  consist of  sluggishness,
dulness, and abnormal persistence of thought and action, with marked
irritability.  Memory is also impaired at an early period of the dis-
ease.   Speech  becomes difficult  and deliberate.   Sleep is usually
good, but  occasionally  there are horrible dreams and odd sensations
at night.   Hearing  is  usually impaired.  The sense of smell is not
infrequently defective, but taste  is still  more  often affected.   The
heart is usually  normal, the pulse soft and  slow, whilst the capil-
laries of the face  are nearly always dilated.   In 59 cases out of 109
analyzed by the committee of the London Clinical Society, the  thy-
roid gland was not altered  in  size  in 23, but it must be borne  in
mind that the swelling of the neck makes it very difficult to examine
this gland.  In 22 of these cases  the gland was  atrophied or reduced
in  size, aud in 3 of  them  previous enlargement was  mentioned.
Respiratory troubles are infrequent.   The  urine  is usually lessened
iu  quantity ; albumin  is  preseut in  the later stages, and the excre-
tion of urine is  decreased,  whilst frequency of raicturitiou and incon-
tinence  have been described.  The progress of  the disease is usually
very slow, aud  some  cases have remained for ten years under observa-
tion.
   Etiology.  Most  cases occur between the ages of thirty and sixty-
five, but the disease may begin at almost any age.   Women are prin-
cipally affected  in the proportion of six females to one male.   The
disease has also been hereditary iu some females.  As myxcedema  is
so  pre-eminently a  disease of women, it has  been  supposed that it
would bear some relation  to the catamenia;  but  this belief has not
beeu confirmed, aud  it  has even been  found  that myxcedema does not
prevent pregnancy ;  so that this may even occur and go on to the full
period in the advanced stage of the disease.   In a few of such cases
the children died of phthisis, and in oue child there was a suspicion
of  myxcedema.  Prolonged lactation,  excessive  hemorrhage,  and
acute rheumatism have been supposed to be exciting causes.   It was
at first believed that myxcedema  was  a variety of sporadic cretinism,
and as such it was first described  by Curling and Fagg, of England,
and eleven cases  are reported from Lower Brittany by  Morvan, but
not a single record has  come from Derbyshire, in which sporadic
cretinism has been observed.
   Pathology.  The pathological alterations which appeared to the
naked eye are abundance of subcutaneous fat, occasional emaciation,
very slight anasarca, passive effusions into  the  serous cavities, occa-
sional interstitial changes  iu the kidneys, occasional hypertrophy of
the left ventricle of the heart (in which cases the kidneys are granular),
usually atheroma of the large arteries, without any marked  degree of
endarteritis, in  a few  instances tubercular disease of orgaus, and  in
still fewer instances cirrhosis  of the liver.  But in every case the
thyroid gland  was markedly atrophied,  usually  bilaterally, but  in
some few cases more  markedly  so in oue lobe thau  in the other.
Microscopically,  a series of alterations have been  observed.  In the
skin the coiled  tubes of the sweat-glands have swollen epithelium  in
which nuclear  proliferation has occurred,  obstructing  the lumen, 
552
NERVOUS DISEASES.
while in the later stages the nucleated fibrous growth is found  in the
peri-tubular tissue.  Similar, possibly identical, changes occur in the
sebaceous glands.  Around the hair-follicles there is a nuclear growth,
and around this occasionally a nucleated fibrous tissue.  In one case
there was a peri-neuritis  of the nerve-tubules  in  the subcutaneous
tissue.  There is often an interstitial nephritis and occasionally tuber-
cular deposit in  the kidneys.   Occasionally thick fibrous tracts have
been found iu the liver, or a thickening around the portal vessels, or
an excess of pigment in  the hepatic  walls, with  atrophy of them,
although the latter are generally unaffected.  Early cirrhosis has also
been observed.  It is seldom that the heart is affected, but when it is
the muscle-nuclei are abundant, and between the fibres are numerous
free nuclei, and  in one case there was a simple excess of pigment in
the fibres.   Infrequently, also, slight changes have been observed in
the lungs, such as early catarrhal pneumonia, emphysema, thickening
of the bronchial septa, or  miliary  tubercular anthracosis.  In only
one  case  was there a cellular accumulation, probably  tubercular,
observed  around  the vessels of the brain, the patient dying  from
general tuberculosis.   The cerebellum has always been found to  be
normal.  In  one case  the spinal  cord  showed  nothing more than
some thickening of the septa, especially of the posterior columns, and
in another case  there was some increase of the pia mater.  Fibrosis
was  found in several cases in the superior cervical ganglia of the
sympathetic ganglia, and  in three  others  interstitial changes.  The
lymphatic glands, spleen, pancreas, uterus, intestines, and aorta have
been examined,  but the only change that has been  found  was  early
tubercular infiltration  in  the small and large intestines in one case,
and  some atheroma of the aorta in another.  In every case,  as has
been stated, the  thyroid gland  has been affected.   Nearly  the  whole
gland is converted iuto delicate  fibrous  tissue, infiltrated with cells,
replacing the gland-vesicles.   The arterial adventitia is swollen.
In a more advanced stage  the  gland becomes  converted into a deli-
cate fibrous tissue, in which groups of small round cells are scattered,
evidently the  remains of the vesicles, aud  the gland-structure is re-
placed  with sparse collections  of round  cells.  It is evident,  there-
fore, that myxcedema is due to a destructive affection of the thyroid
gland;  that changes occur in the skin, mainly in the sebaceous and
sweat-glands; that this latter change is of an irritative  character;
and  that  interstitial change does not occur iu the organs as a gener-
alized condition, although it is occasionally present in the kidneys,
liver, heart, and submaxillary  glands.   In the case in which a chem-
ical analysis was made of the tissues by Ord there was a large excess
of mucin in the skin, and  from this, as well as from previous  obser-
vations of less  precision, it had  been supposed  that  one of the con-
stant factors of the disease was such an excess of mucin, but in none
of the succeeding cases has any such relative excess been found. As
Ord's case presented at the time of death  the full swelling of myx-
cedema, it is believed that the subsequent patients had died at a later
stage, when there was a trophic process  going on, and that in other
cases the subcutaneous tissue had become replaced  by  fat, whilst in
4 
MYXCEDEMA.
553
 still others the analysis had been vitiated by the keeping of the speci-
 mens for a loug time in alcohol.  The source of mucin in the body
 is twofold.   It  results from the degeneration of the protoplasm of
 epithelial cells, as in the goblet-cells of mucous membrane and in the
 cells of the glands, such as the submaxillary.  In  Horsley's  experi-
 ments on  monkeys from  which the  thyroid had been removed and
 myxcedema artificially induced, the cells of the parotid secreted a
 viscid saliva; these were swollen by mucinogen, and a chemical anal-
 ysis showed  that  mucin  was greatly increased in amount.   Mucin
 also forms a constituent part of the stroma of connective tissue.   It
 is chemically a muco-albuminous material, one of its constituents
 being mucin, the other a proteid of the globulin class, which resembles
 a serum-globulin or periglobulin of the blood in  its reactions: but in
 the chemical  analysis of myxcedema the  mucin only has been  esti-
 mated, so  that, as  the committee of  the London  Society suggests,
 future analyses should also estimate the globulin.  A number of ex-
 periments  were made at  the instance of the committee by Horsley.
 He extirpated the  thyroid gland in a number of animals.  Rats and
 rabbits showed no effect, but carnivora invariably died, death beinc
 preceded by myxcedema.   In dogs, 95 per cent, so succumbed within
 a period varying from a few  days to rarely as long  as two or three
 months.   The symptoms following the removal of the gland are at
 first dulness and apathy,  next fibrillary  twitchings in the muscles,
 then violent convulsions in the extremities and the trunk, with violent
 dyspnoea,  and often semi-coma or coma.  Paresis is always found,
 especially in  the voluntary  muscles of the limbs, and various dis-
 turbances of nutrition.  At first the temperature rises, then falls ; but
 it becomes subnormal before  death.  In the blood the red corpuscles
 diminish, whilst the leucocytes increase.  In one  sheep so  experi-
 mented on by Horsley no marked change was observed for a year
 and a half; but in May, as the weather was supposed to be becoming
 milder, the animal  was  shorn of its thick fleece, and shortly after-
 ward the weather became very  cold, when acute myxoedema  super-
 vened, and death occurred within a  fortnight, whilst post mortem
 the usual changes were found.  This observation is justly considered
 to be of considerable importance, as showing the effect of changes of
 temperature.   Horsley observed acute and chronic myxcedema  in
 monkeys after complete extirpation of the thyroid; but the acute con-
 dition may be averted by keeping the  animals iu a temperature aver-
 aging 90° F., and the average duration of life was thus extended to
 125 days instead of 25 days.   In such animals the mucin was found
 to be greatly increased  in  the skin, in the  tendons, the salivary
 glands, and in the blood.   The committee sent out a number of cir-
 culars to different surgeons in  order to obtain the results of partial
 or complete extirpation of the thyroid gland, but the answers  do not
 seem  to have been satisfactory.  Thus Kocher  and  Reverdin, the
 former operating on 32 and the latter  on  18, have found myxcedema
 appearing  afterward in a large proportion of the individuals; Bill-
 roth and Bardeleben, the former operating on  146 individuals and
the  latter  on 15, have found respectively myxoedema in only two 
554
NERVOUS DISEASES.
cases.  But, as the report shows, many patients died shortly after
the operation, others passed away from  observation, or were not
under observation for a sufficient  length of time, whilst it does not
appear that  accessory thyroid glands might  not have  remained.
These  accessory thyroid glands,  by the by, are very frequent, and
they are found in the neighborhood of the thyroid  body.   The com-
mittee  reached the conclusion that there is strong evidence that
myxcedema, sporadic cretinism, endemic cretinism, cachexia strumi-
priva, and  the operative myxoedema of animals, are species of one
genus,  and that the one pathological fact common to all these con-
ditions is the occurrence of morbid processes involving  destruction
of the  thyroid gland.
  Diagnosis.   The diagnosis will be gone into in detail under
" Acromegaly."
  Prognosis.   The prognosis of myxcedema is unfavorable, as death
results chiefly from  pulmonary intercurrent  maladies, although the
patients may die from the exhaustion of the disease itself.
  Treatment.  The thyroid extracts have effected improvement
that has sometimes  been  marvellous, often  lastiug for years;  and
although it as yet a question whether a  relapse does not  ultimately
occur in all cases, they should always be given a fair trial, as no other
treatment is of much avail.   Thyroid tablets  are  made  by several
manufacturing-houses, and if these are of a  reliable make they are
most convenient.  The thyroid gland can, however, be obtained by
any butcher, and an alcoholic  extract of it is easily made.  It is not
at all necessary to keep the  extract any longer  than is necessary for
its making, any more than in the case of any other extract, contrary
to what certain  interested persons would have us  believe.   Its use
must be continued for months.   The dose should be the  equivalent
of one  grain of the thyroid gland  to begin with in children and three
grains  in adults, given twice daily.   This should be slowly increased
until ten grains are reached with a child and twenty with an adult,
and even more may be given in some cases;  but muscular pain, car-
diac attacks, and emaciation must be carefully avoided.  If the thy-
roid extract does not do well, other means must be essayed.   In all
cases the patient should live in a warm and equable temperature, and
it has been found that the regular removal in the winter to southern
climates  has caused amelioration  in the symptoms.   This was espe-
cially evident in the case of Horsley's sheep and monkeys.  Jabo-
randi and pilocarpine are  exceedingly beneficial in myxcedema, from
their action  upon the skin.  Nitroglycerin has  also been  a useful
drug.  Tonics, especially  iron, quinine, and  the hypophosphites, are
also valuable. 
CHAPTER  XVIII.
                        ACROMEGALY.

  Synonym:  Marie's malady.
  History.  This disease was first described by Marie, and for it
he suggested the name that heads this  chapter, although he points
out that similar cases had been observed as far back as  the time of
Saucerotte-Noel in 1872.   Since that time there have been a number
of contributions upon the subject.
  Etiology.  Very  little is known  of the  causation.  Women
appear to be somewhat more  prone to the disease than men ; it has
in several instances appeared  coincidently in attacks of depression ;
rheumatisra, gout, and syphilis have been observed in several  of
the  cases ; and this insufficient  knowledge is about all we possess of
the etiology.
  Clinical History.  The onset of acromegaly is usually in the
hands, although the head may be the part first affected.   The hands
become of  an unusual size,  contrasting strongly with  the  almost
normal shape of the other parts of the upper limbs.  This exces-
sive development of  the hands is of all  the tissues—bones, muscles,
connective  tissue,  and skin.    The length of  the hand, measured
from the wrist to the middle finger, is about normal, but the width
and thickness are usually enormous, so that for them Marie has sug-
gested  the name of battledore hands, and the English  have called
them spade-like.  The consistence of  these hypertrophied hands  is
hard, and there is no pitting, as in oedema.   The inter-phalangeal
folds and the thenar aud hypothenar eminences are increased in size ;
but the fingers remain straight, and are  as large  at their tips as  at
their base.   The nails are small in comparison with the  size of the
corresponding fingers.   Although the  hypertrophy usually does not
involve the arm or forearm, as  has been  said,  these portions may, in
certain cases, be affected.   In  the course of time  the  head also in-
creases in size in a way that is pathognomonic.   The face is chiefly
involved, being enlarged especially in the vertical diameter, aud be-
coming elongated and oval, the forehead  is low, the orbits  are greatly
thickened, the borders of the  orbit  are  also increased in size  from
dilatation of the frontal sinuses surrounding the orbital cavity.  The
conjunctiva, fat, and  muscles  of the eye may  be also hypertrophied,
and exophthalmus  may be  present.  The lids  are long, thick, and
brown, and  in cases of exophthalmus  they may not cover the eyes.
The nose is generally greatly  enlarged in all its dimensions, the alse
being thickened, and the septum may be double its usual thickness.
The lips are especially swollen, the  lower  one most so,  so that the
latter may even turn downward.  The hypertrophy also  affects the 
556
NERVOUS DISEASES.
tongue; but this usually preserves its normal shape, although it may
be so large as to project from the mouth and interfere with the pro-
nunciation of words.   The palatine arch, the soft palate, the tonsils,
and the fauces are also increased in size, so that the voice becomes
guttural and metallic.   The uvula is  occasionally elongated and en-
larged, exciting cough.   The chin is an especially prominent feature,
being massive, projecting downward  and  forward, and all the soft
structures of the face are thickened.   The upper jaw is not nearly so
much affected as the lower, which often becomes prognathous, as the
result of which the teeth are separated more or less from one another,
and the upper dental arch tends to fit inside the lower.  The ears
are sometimes increased in size.  The cranium itself is somewhat
increased in its antero-posterior diameter, chiefly owing to dilatation
of the frontal sinuses.   Usually there is a curvature of the spine in
the cervico-dorsal region, the back being slightly humped, the patient
not being  able to  hold  the  head up, but bending it forward.  A
slight lordosis may also be present, usually in the lower part of the
dorsal and lumbar regions.  The vertebral spines have  been  found
hypertrophied in some cases.   Almost all the bones of the thorax
are also hypertrophied, so that the thorax projects in front, the antero-
posterior diameter being increased to a certain extent, apparently at
the expense of its transverse diameter, whilst the lower part of the
thorax also projects so as to cause a marked  prominence upon deep
inspiration.   The sternum is most affected by the hypertrophy.  The
xiphoid cartilage becomes less flexible; the clavicles, the ribs, and the
costal cartilages become larger.   The upper part of the thorax moves
slightly in the movements of respiration, which is mainly done by the
lower part of the thorax and the abdomen.  Hypertrophic changes
may also be found in the neck,  the cricoid and  arytenoid cartilages,
the pelvis, the penis, the scrotum, the testes, and the joints, especially
those of the  knee, wrist, and ankle.   The thyroid body is usually
diminished in size, although it has  never been seen to disappear
totally.  The mammary glands  may be atrophied and  soft, whilst the
nipple, on the contrary, is apt to be large, and the abdomen is  more
or less enlarged.  There is usually an area of dulness over the upper
sternal region, supposed to be due to persistence of the thymus gland  ;
but there is no real foundation for this  explanation of the phenomena.
The  muscles of the limbs are  sometimes atrophied and sometimes
hypertrophied.  In the vascular system important changes have been
induced.   The heart is enlarged ; the  arteries are usually rigid, as in
the early stages of atheroma ; and varicose dilatations of the veins are
often  observed.  Increase of perspiration is usually a symptom pro-
voked by the least exercise, and the  sweat may sometimes be dis-
agreeable in odor.   Occasionally there is a marked polyuria, with or
without glycosuria, and albumin has been occasionally observed.  In
several cases  peptones have been found in the urine.   Ansesthesia is
very  rare.  Little  cutaneous tumors, pedunculated, the  size of a
millet- or hemp-seed, reddish or violet-colored, and  numerous, are
sometimes observed.  There may be an intense and persistent head-
ache, and this is usually one of the first symptoms for which  the phy- 
ACROMEGALY.
557
sician is consulted.   This is usually in the occiput, and may be most
severe at night.   Pains in the bones and in the joints  may also be
complained of.   Disturbances of menstruation are exceedingly fre-
quent, and are early symptoms, being sometimes amenorrhcea at an
early age, or suppression of menstruation.  Vision is usually affected
in a greater  or less  degree, varying from amblyopia to amaurosis,
and definite changes can usually be detected ophthalmoscopically iu
the retina, or there may be narrowing of the field  of vision, or hemi-
anopsia.   Occasionally appetite is  markedly increased, as may  also
be thirst.   Deafness is also sometimes preseut, or impairment of the
sense of smell or taste.   The mental symptoms are variable, consist-
ing of a tendency to melancholia, with suicide, delirium, coma, som-
nolency, or sleep disturbed by nightmare.
   Duration.   The disease lasts from ten to thirty years or even
more, and is very slowly progressive.  Death usually occurs  from
syncope, probably induced by cerebral compression, but occasionally
some intercurrent malady closes the sceue.
   Pathology.  In  many cases of acromegaly there has been found
a considerable increase of the pituitary body,1 which is hypertrophied
to the size of a pigeon's or hen's egg, or even  that of an  apple.  This
hypertrophied mass exerts pressure upon the surrounding organs, such
as the olfactory and optic nerves and the crura cerebri, so that in this
way are explained the impairment of smell which occasionally results
and the frequent neuro-retinitis.   It  may also exert pressure back-
ward upon the  pons and the nerves arising therefrom.   The sella
Turcica and the pituitary fossa are deformed and enlarged in all their
measuremeuts, and the surrounding sinuses are also involved in these
pathological alterations, such as the sphenoidal, frontal, thymoid,
mastoid,  and  maxillary.  Microscopically the  gland-tissue of the
pituitary body has been found to be simply hypertrophied.  Andrie-
zen's recent researches upon the pituitary gland have seemed to show
that it is of great importance in  the human  economy.   The sym-
pathetic ganglia and nerves have  also been  found  to  be  hypertro-
phied, and this hypertrophic process affects the bones as well, such
as the vertebrse, the clavicles, the iliac bones, and the long bones of
the limbs, although  in the latter  there is neither lengthening nor
enlargement, but only increase in  size of the ridges, lines, aud pro-
jections  for the insertion of muscles  and  ligaments; whilst the
short bones of the hand and foot are much  increased  in  size.   In
what way these  hypertrophic growths are caused we do  not know.
The  thymus gland is usually lacking.
   Diagnosis.   The diaguosis of acromegaly must be from—
       Myxcedema;
       Chronic rheumatism;
       Gigantism;
       Partial acromegaly;
       Hypertrophic pulmonary osteo-arthropathy;
       Vasomotor paralysis of the extremities.
 i This connects the infundibulum with the cerebrum. (See Fig. 40.)  It consists of two lobes,
the posterior one being really a part of the cerebrum, and known as the lobus mfundibuli. 
558
NERVOUS DISEASES.
  In myxcedema the increase in size is due to a swelling limited to
the soft tissues, the skin is of a  yellow or waxy color, desquamates,
and becomes adherent to the subcutaneous tissue; the face  is puffed
out like a full moon ;  aud there is no prognathism.   In acromegaly,
however, the skin retains its mobility almost  unimpaired,  or even
has  a  greater  mobility than usual,  whilst there is  prognathism,
lengthening of the  face, and  the  hypertrophy involves not only the
soft structures but the bones.  In myxcedema  there is no curvature
or double hump, and the thyroid  body is generally atrophied.
  In some cases of  chronic rheumatism  there may be  some marked
deformities of the  fingers and joints resembling acromegaly;  but
the pain is much more marked; there are the distinct crackling
sounds  of chronic arthritis, with  some  functional  disturbances,
and  the  progress of  the  disease is  entirely different.   Marie  has
seen certain  individuals  in  whom  there was  a combination of
rickets  and rheumatic  disease,  which might  be  confounded with
acromegaly, inasmuch as there was an increase in the size of the hands
and  feet,  a thickening  and eversion of  the lower  lip, occasionally
swelling of the face, and a certain amount of palpebral oedema;  but
the fingers are distinctly  nodular, the  hand  is bony and deformed,
the soft parts do not present the greatly rounded prominences, there
is no cervico-dorsal curvature, and  no prognathism, and the evolu-
tion of the disease is entirely different.
  Gigantism  has been  often confounded with  acromegaly, but a
careful measurement will  show that there is a  marked lack of pro-
portion  between the size  of the extremities and  the length of  the
limb in acromegaly, whilst in  gigantism the  extremities and  the
length  of  the limb are in proportion.  Moreover, cases  of acro-
megaly are rather undersized, seldom over six feet, and  usually being
less  than  five feet nine inches in height.  Frequently, too,  in acro-
megaly the height and the weight, increasing greatly at first, subse-
quently diminish  to an  equally marked  degree.  In gigantism  the
relative proportions of  the face  and  limbs are preserved.  Acro-
megaly and gigantism may be combined, however, in the same person.
  Hypertrophic pulmonary  osteo-arthropathy was so  called  by
Marie  because almost all the cases  had pulmonary lesions, either
empyema, neoplastic formations, or bronchitis.  In this  disease  the
hands  are very  greatly  enlarged,  often more so  even  than  in
cases of acromegaly; but they are also deformed.  In  the fingers
it  is the  last phalanx that  is  especially  affected,  and they  are
of the  shape  of the legs of a  stool,  whilst in  acromegaly  the
natural form of the different segments is well  preserved.  The  nail
at  the  end of the deformed finger is also deformed, being greatly
widened, lengthened, and  especially curved, so  that  Marie says  the
thumb observed sideways has a resemblance to the head of a parrot
with its  curved  beak, whilst in  acromegaly  the  nails appear  too
small for  the  large phalanges which  they cover.   The hand, how-
ever, is but very slightly  altered, and  forms a marked contrast to
the fingers; whilst  in acromegaly the  metacarpo-phalangeal region
is enormously increased in size.  In  the wrist there  is very great
A 
ACROMEGALY.
559
enlargement, the lower ends of the two bones of the forearms being
enlarged in an abrupt manner,  the thickening taking place both in
the antero posterior  and lateral diameters, and the  lower portion
of the forearm  being  as  large  as  at the  middle  or  below  the
elbow, whilst the wrists are also deformed.   In  acromegaly there is
nothing of this kind; for if the wrist should be  larger than normal,
its size is still  proportionate to the rest of the upper limb, and there
is no projection, abrupt enlargement, or deformity.   In the feet there
is an analogous condition.   The toes,  especially the last phalanges,
are affected as the  fingers are, the tarso-metatarsal region showing
relatively  as  little change  as  in  the metacarpo-phalangeal region  ;
whilst the ankle is,  like the wrist, enormously, increased and the lower
part of the leg is found as large as the  middle portion—bearing com-
parison, as Marie says, with the foot of an elephant.  In this form of
arthropathy the hypertrophy is mainly in the bones,  and not, as in
acromegaly, both in  the bones and the soft tissues.   The joints are
also  limited in  their active and  passive  movements, the  patients
being clumsy  with their hands, aud  their elbows  presenting a more
or less prominent degree of flexion, so  that complete extension is
impossible.  There is a somewhat  analogous  condition in the knees,
hip-joints, and shoulders.
   There is a disease  known as  partial acromegaly, in  which there is
a considerable hypertrophy of one-half of the body, or  of a  lower
limb on one side and the upper limb  and side of the face on the other.
It may involve the hand and foot, the  fingers or toes, and sometimes
one finger aud one toe;  but there  is always  true deformity, and the
disease is usually congenital, remaining stationary  and being gener-
ally unilateral.  I have, however, seen one case  occurring in middle
life, and affecting one lower limb.
   In vasomotor  paralysis of the  extremities there is a marked in-
crease in the size of the hands and fingers, a  reddish tint with some
livid spots on  their dorsal  surface, occasional pain in these parts, a
certain degree of duskiness  extending  up the arm to the shoulder,
and occasionally there is a  slight  kyphosis of the  upper part of the
spine; but the hands are not of the shape of those in acromegaly,
the fingers being larger at  their bases  than at their extremities, and
there  is no oval face, prognathism, hypertrophy of the lips, enlarge-
ment of the tongue, hypertrophy  of the bones of the face, or altera-
tion in the speech.
  Prognosis.   The prognosis of acromegaly is  always unfavorable,
as treatment has never been able to affect  the course of the disease.
  Treatment.   Treatment can only be symptomatic to a triflingly
slight degree.  Antipyrin and  caffeine seem to  have been of some
use in relieving the  headache.  The glycosuria may be remedied by
treatment by  arsenic, alkalies, and dieting. 
CHAPTER  XIX.
                   EXOPHTHALMIC GOITRE.

  Synonyms :   Basedow's disease.   Graves's disease.
  This disease was first described  by Graves, of Dublin, in 1835,
and shortly afterward, in 1840, by Basedow, of Germany.
  The three cardinal symptoms are:  cardiac palpitation with rapid
pulse; enlargement of the thyroid  gland ;  and prominence of the
eyes,  or exophthalmus.   The disease may commence  with either
one of these three symptoms, most  frequently with cardiac  palpita-
tion and  rapid pulse.  The pulse generally rises to about  120, but
may even mount to 200 beats in a  minute.   The pulsations are apt
to be most marked in the carotids, whilst the radial pulse is usually
less affected, presenting a notable contrast to the other vessels.   The
enlargement of the thyroid gland generally begins after the arterial
alterations have been in  existence for some time.  This enlargement
is not usually very great,  and may be  temporarily increased by
exacerbation of the cardiac palpitation and by emotions.   The exoph-
thalmus varies very greatly in degree, being sometimes  so  slight as
to be scarcely perceptible, at others so pronounced that the eye is
protruded sufficiently to lay  bare the attachments of the  ocular mus-
cles, or there may even  be  absolute luxation of the  eye.   This ex-
ophthalmus is bilateral, but not always to the same extent upon both
sides. It  may cause trophic  alterations of the eye, from the lack of
the  usual protection of the  lids.  In  many cases a symptom is ob-
served that was first described by  Von  Graefe:  If the patient is
made to fix the eye upon an  object held before him, and attempts to
follow this object  as it is  moved downward, the upper eyelid will not
follow the movement of the  bulb of the eye, nor will it  do so when
the  object is moved up again;  in other words, there is a lack of as-
sociation  in  the movements of the bulb  and the lid.   With these
three  cardinal symptoms are occasionally shown  some  minor ones,
such as a sense of heat without actual fever, profuse sweating, and
sense of throbbing in the head, pulsating  noise in the ears, headache,
insomnia,  and vertigo.   Mental depression and muscular tremor are
frequent accessory symptoms.  Glycosuria  has been often observed,
sometimes early and sometimes late  in  the course of  the  disease.
Enlargement of the lymphatic glands or of the tracheal and bronchial
glands is occasionally observed.  Mental symptoms are  occasionally
present, such as melancholia, mania, or general paralysis.
  Charcot has also seeu some cases accompanied by mild paraplegia,
without spastic phenomena  or lancinating  pains.  Wolfenden  has
shown that the resistance of the body to  the electric  current is  low-
ered in a remarkable manner, as Charcot has poiuted out.   Thus, in 
EXOPHTHALMIC GOITRE.
561
some fifty healthy persons, he found that the resistance would register
in a moderate and  fixed current from 4000 to 5000 ohms; whilst in
two cases of this disease the resistance was as low as 200 and 300
ohms, and  in eight others it varied  from  500 to 700 ohms.   The
author ascribes this diminished  resistance  to  the  dilatation of the
skin capillaries, which saturate the skin writh fluid.   Shaw has  ex-
amined 46  cases with the same  results.  A.  bronzing of  the skin is
occasionally observed.   A  limitation  of the field of vision has been
seen in 20 cases by Caste and Wilbrand.  Louise Fiske-Bryson has
observed diminished chest-expansion in this malady, in a severe case
this being  one-half inch,  sometimes  less;  and this has been con-
firmed by Hammond.   The onset is generally gradual, and the dis-
ease is a chronic one.  Remissions and  intermissions occasionally
occur, and even recoveries, although the latter are rare.  When death
supervenes, it is usually the result of the cardiac svmptoms.
   The pathology of this disease  is unknown.   It would seem prob-
able that the lesion is  in  the  sympathetic  nervous system.  White
found a  hemorrhage in the floor of* the fourth ventricle in one case
which followed pneumonia.    Filehne caused increased  pulse-rate,
often accompanied  by exophthalmus and  once by struma, in guinea-
pigs by  destroying  the anterior  covering  of the  restiform  body.
Durdufi  has localized the point  of lesion in  the tuberculum acusti-
cum.  Bienfait  has, to  a certain  extent, confirmed Filehne's experi-
ments.  Ham mar  found no pathological  change in the cervical  por-
tions of the sympathetic nerve, but the spinal cord was not examined.
Roosevelt found the medulla, the  sympathetic, and the vagus normal.
Yet these  different findings  do not preclude the idea of the sympa-
thetic being the portion of the  nervous system that is at fault, both
because  our present  knowledge will not permit more than very  lim-
ited localization in any one  part of the sympathetic, aud it is a tenable
supposition that a central lesion could indirectly affect a large tract
of sympathetic  fibres.   Moreover, of late years many diseases  that
were formerly supposed to be  entirely due  to lesions of the sympa-
thetic have been shown to  be really caused by myelitis of the syringo-
myelic type of neuritis, especially of the multiple variety.  In the
heart, dilatation and hypertrophy  are   usually found  in a  slight
degree, and even  mild endocarditis or valvular lesions are occasion-
ally met with.  The arteries are dilated and occasionally aneurismal.
In the thyroid gland the vessels  are enlarged, and the connective
tissue  is increased in  quantity,  with occasional  cystic or colloid
degeneration.  In  the orbit there is generally a moderate increase in
the amount of fat, although this is occasionally normal; and upon
rare occasions there are dilatation of the veins, atheroma of the oph-
thalmic artery, and a fatty condition of the arterial muscles.
  The diagnosis of this disease is usually very easy when  the three
cardinal symptoms are present; but in the early stage, when only one
of the symptoms  is to be observed, the real  nature of the malady
may be overlooked.  Generally, however, the excessive pulse is  the
first symptom, and should arouse  suspicion.  In ordinary goitre there
are no cardiac symptoms or exophthalmus, although large goitre of
                               36 
562
NERVOUS DISEASES.
endemic  origin  may be associated  with rapid pulsation and exoph-
thalmus ;  in  such a case, however, the exophthalmus is generally
unilateral.
  The prognosis is generally grave,  although  relief is  frequentlv
obtained,  especially when  treatment is begun early, and sometimes a
cure is effected.
  The treatment should  consist of rest,  belladonna, hemp, iodine,
carbazotate of  ammonium, hydrotherapy,  electricity, and surgical
operation.  The rest should consist of keeping the patient as quiet
as possible, both physically  aud mentally, and, if necessary, by re-
striction  of the expenditure  of energy to the degree  that may be
needed by keeping the patient in  bed, by limiting the amount  of
exercise taken,  or by the abolition of all exercise except such as may
be necessary for the pursuit of a business or occupation.   In admin-
istering belladonna, either the fluid extract  or atropine  should be
employed—the former in  doses of 1 or 2 minims three or four  times
daily ; the latter in  doses of gr. -^fa as often.  The dose of carb-
azotate of ammonium  should be 1 grain  in  pill three times  daily
for the first week; for the second week 2 grains at the same interval,
and  for the third week, if it can be borne, 3 grains; but the  drug
can rarely be taken more than three weeks.   Iodine can be admin-
istered in the  form of tincture of iodine, 30 drops to 2 drachms
three times  daily, or  the iodide of potash, 10  to 30  grains  three
times daily.  Electricity,  in the form of galvanization of the cervical
sympathetic and of the cardiac region,  has  seemed to be of consider-
able  use in certain cases. Excision of the thyroid gland has been
of use in some cases when the disease  has not been too fully devel-
oped.  Digitalis has not  beeu  of  much value in this affection, and
has often been injurious,  except sometimes in the paroxysms of pal-
pitation and dyspnoea. 
CHAPTER  XX.
    DISEASES OF THE SYMPATHETIC NERVOUS SYSTEM.

  In former years  and until the last  ten  or fifteen, the  sympa-
thetic nervous system was held accountable  for a great  many dis-
eases whose pathology was shrouded in mystery; but, as year after
year has gone by, one disease after another has been found to be due
to lesion of the peripheral or  central nervous  system, and thus ex-
ophthalmic goitre, facial hemiatrophy, muscular atrophy, and pseudo-
muscular hypertrophy have been  shown  to belong only partially to
the domain of the sympathetic, or have been entirely wrested from it.
At the present day, therefore,  the main diseases of the sympathetic
are considered to be—
       Certain vasomotor aud trophic symptoms of  the head
         and chest;
       Diffuse vasomotor symptoms;
       Herpes zoster;
       Tachycardia;
       Vasomotor joint-neuroses;
       Angina pectoris;
  Angina pectoris and tachycardia  belong  to  general medicine, and
the joint-neurosis to surgery, so that they are not pertinent to a text-
book of this kind.
  The cervical sympathetic can  present symptoms of paralysis or
irritation,  cither  from direct  or indirect injuries.   In paralysis the
most constant symptom is contraction of the pupil, and less constanly
are observed approximation of the eyelids and retraction of the bulb
of the  eye.  Irritation  of the cervical sympathetic,  which is  rare,
causes dilatation of the pupil, expansion of the  eyelids, and propul-
sion of the bulb  of the eye.   Vasomotor symptoms  are seldom seen
with lesion of the cervical sympathetic, but  the ear and cheek of
the affected side  are  sometimes red aud  warm in cases of paralysis
and white and cooler iu cases of irritation.  Trophic disturbances are
occasionally observed, and consist of a slight flattening of the cheek.
These sympathetic symptoms, indicating lesion  of the cervical sym-
pathetic, have been observed in cases of tumor of the cervical sym-
pathetic itself, or of its rami communicantes  between the brachial
plexus, and even from affections of the apices  of the lungs (which,
by the by, are probably the cause  of the flush of the cheek in tuber-
culous subjects), or from fractures, dislocation, or caries of the lower
cervical or upper dorsal vertebrse.
  The diffuse vasomotor affections are those known  as digiti  mortui,
erythromelalgia,   Raynaud's   disease,  and  augio-neurotic  oedema.
Digiti mortui is  an  affection  consisting of a diffused pallor of the 
564
NERVOUS DISEASES.
upper extremities, occasionally of the lower extremities.  The fingers
become white in extreme cases, like those of a corpse, and  the  sur-
face-temperature is  diminished.    The pallor is remittent or inter-
mittent, the remissions or intermissions lasting for days or  hours.
Erythromelalgia, described by Weir Mitchell, is a curious  affection
of the soles of the feet in which circular redness and pallor are ob-
served, with some hot, burning pain in the part affected.  Raynaud's
disease consists  of paroxysmal  attacks  of  pain,  pallor,  coldness,
numbness, and ansesthesia of the lower extremities, and a gangrenous
condition  of the toes.   Angio-neurotic  oedema is generally inter-
mittent, and affects the skin or the mucous membranes of the larynx
and pharynx.  When  the skin is implicated, the swelling is localized,
and is about the size of a plate,  the skin being sometimes white,
sometimes slightly reddened, and generally in proportion to the oedema
are sensations of burning, prickling, and  stiffness.   The extremities
are most frequently affected,  especially near the joints, but  the eye-
lids,  cheeks, and lips, sometimes even the trunk, are occasionally the
site.    Vomiting, pain, and constipation  are  frequently attendant
symptoms,  and  occasionally  hemorrhages from the gums  and  the
vesical and bronchial mucous  membranes, sometimes even haemo-
globin uria.
  As has already been said, the tendency is nowadays to regard these
so-called sympathetic nervous affections as  really due  to  multiple
neuritis, although it is as yet a  question whether  they do not begin
in the sympathetic nerve-fibres running in the peripheral nerves, and
secondarily affect the  voluntary nerve-fibres ; whilst in  some other
case  actual disease of  the spinal  cord has been found.   Thus, some
cases of tingling and numbness in the finger-tips, which were formerly
regarded as due  to lesion  of  the sympathetic nervous system, have
been shown to be due to multiple neuritis ; whilst Morvan's disease,
an affection akin to  Raynaud's disease, which was at first regarded as
a malady of the sympathetic, then as a  multiple  neuritis, has been
shown to be due to  syringomyelitis.
   The prognosis of the diffuse vasomotor affections is  generally grave,
so far as  regards a cure, and that of Raynaud's disease and ery-
thromelalgia is unmitigatedly bad.
   The diagnosis of  these affections is generally easy, except that in
Raynaud's disease a distinction must be made from  syringomyelitis,
the details of which are given in the chapter upon this subject. The
treatment of Raynaud's disease  must be amputation, as speedily as
possible, before the strength  of the patient is exhausted, and before
sepsis sets in.  Of the other affections treatment should be by means
of electricity, ergot, and tonics.   The electricity applied should be
galvanism, faradism, and the static current.   Galvanism should be
applied to the spinal  cord  and to the peripheral  nerves.   For the
former purpose an electrode (Fig. 67) should be applied in  the nape
of the neck, another (Fig. 68) to  the lower dorsal spine, aud a current
of three to  ten  milliamperes, in  sittings of three to five  minutes
every day or every other day. To  the peripheral nerves an electrode
(Fig. 76), placed upon the spine about at the point where the affected 
     DISEASES OF THE SYMPATHETIC NERVOUS SYSTEM.   565

nerves have their origin, and another electrode (Fig. 68 or 69) applied
over the affected limb, and a  current  of three to ten milliamperes
used.   The faradic current should be applied by means of  the wire
brush, and a  sufficiently strong current should be passed over the
affected limbs for ten to fifteen minutes every day or every other day.
If the static current be applied,  the sparks  should be made use of,
and should be vigorously applied to the affected parts. 
CHAPTER  XXI.
             ALCOHOLISM AND MORPHIOMANIA.

   The prolonged effects of alcoholism upon the nervous system may
be manifested  both by mental symptoms and by paralysis.   The
chief mental symptoms are:  delirium, in the form that is technically
known as delirium tremens, occasionally a  variety of paranoia, some-
times  symptoms almost identical  with those  of general  paresis,  a
chronic meningitis, acute mania or melancholia, acute  hallucinatory
insanity, or a recurrent insanity known as oinomania. The paralysis
that is generally associated with alcoholism is that which is due to a
multiple neuritis, differing somewhat in its character from the other
forms of neuritis of this type.
   Delirium tremens is so familiar a disease in every community that
it needs only a brief description. It usually follows alcoholic excess,
or a  short  period  of abstinence  after such, and the exciting cause
may be some slight injury or illness.  The onset is usually gradual,
extending  over a few days, and the prodromata consist of insomnia,
anorexia, restlessness, and a semi-hallucinatory condition ; and these
gradually pass  into loquacity and  persistent delusions and hallucina-
tions,  often maniacal or violent outbreaks.  Hallucinations of hear-
ing are the most frequent, are generally very vivid, and are frequently
accompanied by hallucinations of sight.   The patient  becomes very
suspicious, and has sometimes marked delusions,  often of marital
infidelity, which are, however, much more frequent in the chronic
or subacute forms of insanity.   Occasionally there is an olfactory
hallucination.  Not only do these hallucinations excite suspicion, but
often  dread  and terror.  There is a characteristic tremor, generally
observed only  upon voluntary motion of  the muscles,  but occasion-
ally at all times, and it affects the tongue,  face, and extremities.  In
many  cases, also, there  is that peculiar picking at the bedclothes or
clothing, which is termed carphologia.   With the tremor there are
often  observed muscular twitching  or  shock-like contractions  of
muscles.  The  face  may be  flushed or pale, and  this condition  of
flushing or pallor may alternate.  The  pulse is  usually  frequent,
soft, and large at first; but it becomes smaller as the disease progresses,
and in severe cases it may mount up to 140 to 200.   There is usually
free perspiration.  The temperature is usually 100° to 101°, but it
may run up to  103° and 105°, and in fatal cases even higher.   The
tongue is coated, thirst is present,  and the  urine is scanty if the per-
spiration is great.  There may also be albuminuria.  Slight neuro-
retinitis has been observed. These symptoms will increase in gravity
in the fatal cases, aud may be accompanied by complications due  to
alcoholic disease of other organs,  as of the liver, kidneys, or lungs, 
ALCOHOLISM AND MORPHIOMANIA.
567
so that there may be cirrhosis and  fatty degeneration of the liver,
nephritis, and pneumonia.   Ursemic coma occasionally occurs also,
and sometimes,  though rarely, meningeal hemorrhage.  The delirium
lasts for a variable period extending from two to ten days.
  In some cases of alcoholic insanity a  variety of paranoia is ob-
served, in which there is a delusion of persecution  that  will fre-
quently, in the course of time, be combined with a delusion of self-
exaltation, although  the delusion  of persecution is  much longer in
its duration  than in ordinary cases of paranoia; and  in  these cases
there is the  same logicality or systematization of the delusions,  the
same keenness of reasoning power, the same preservation of memory
and  perception that  is seen  in the ordinary types of this mental dis-
ease.   It differs from the ordinary cases of non-alcoholic  paranoia
chiefly in the fact of the delusions having a tendency to weave them-
selves around some  belief of marital infidelity.   In  none of these
cases have I ever seen any hallucinations of  hearing or sight.
  In many cases of alcoholism there  is a fine tremor of the facial
muscles, the tongue,  and sometimes of the extremities, a thickness of
articulation, and a gradually supervening mental dulness or dementia,
which are all very similar to those observed in ordinary cases of gen-
eral  paresis; but ordinarily the former  disease is somewhat  more
rapid in  its  onset, and the pupillary symptoms are more generally
lacking.   It  is  of great importance to make  a distinction between
this  form of alcoholic  pseudo-general  paresis  and the true general
paresis, because the former is frequently of good  prognosis.
  A chronic cerebral meningitis is sometimes observed also in alco-
holism, and this is prone to affect the dura  mater, causing so-called
chronic internal  pachymeningitis, although it may  also affect  the
pia.   The symptoms are those of ordinary meningitis in a chronic
form.
  Acute alcoholic mania or melancholia does not differ much from the
ordinary forms of these mental maladies, aud the so-called recurrent
insanity known  as oinomania is characterized  by mental and moral
deficiency, various excesses, and indecent, absurd, and  silly demeanor.
  Acute hallucinatory insanity is more frequently observed than any
other form  of  mental trouble except delirium tremens, and has the
same characteristics  as ordinary hallucinatory insanity, with the ex-
ception that there are apt to be vivid hallucinations of hearing, per-
sistent aud logical or systematized, and the patient is more apt  to
pass into  a chronic  condition, in which  the confusion of the hal-
lucinatory  insanity  passes away or  merges  into a state  resembling
chronic paranoia.
  The multiple neuritis  of alcoholism has been already spoken of.
(Vide section upon " Multiple Neuritis.")
  The prognosis of delirium tremens will  depend upon the age of
the  patient,  the amount  of previous alcoholic excess, the  way  in
which  the patient has borne it, and  the complications due to disease
of other  organs.  As  with  all  the  narcotics,  the effect of alcohol
varies greatly in different individuals, so that what may be excess to
one   individual or a member of one race may be a matter of slight 
568
NERVOUS DISEASES.
account  to  another individual  or a member of another race.   Usu-
ally, the prognosis of the non-complicated cases is good, with proper
treatment.  The prognosis of alcoholic paranoia is grave, although a
certain proportion of cases recover in a period of two or three years.
The proguosis of the pseudo-general  paresis of alcoholism is also
grave; but many cases recover with proper treatment, and therefore
the prognosis is by no means the hopeless one that attaches to ordi-
nary general paresis.  The progress of alcoholic mania and melan-
cholia is that of ordinary mania and melancholia.  The prognosis of
the recurrent form of alcoholic insanity known as oinomania is grave,
although a certain proportion of cases recover with proper treatment.
The prognosis of the hallucinatory insanity of alcoholism  is grave,
because there is a great tendency to pass into  a chronic condition of
paranoia, in which the  hallucinations  of hearing  persist for many
years; but  some  few cases do recover.   The  prognosis of alcoholic
multiple neuritis has been already spoken  of.
   Pathology.   In chronic alcoholism the cortical vessels are en-
larged, tortuous,  atheromatous, and  fatty.  The nuclei of the  adven-
titia are numerous, or proliferate, or are  fattily degenerated, whilst
there is an abundance of  Deiters's or scavenger cells to be  found in
the upper region of the cortex, just beneath the pia. Around the pro-
liferated Deiters's cells is a dense connective tissue,  formed  by the
meshing of the processes of the Deiters's cells.  All these changes are
most marked immediately beneath the pia.  In the epi-cerebral space
there are often large quantities  of amyloid bodies, which  are found
in fresh sections from frozen brain, so that they canuot be due to the
action  of reagents.  The fifth  layer of  motor  cells undergo  fatty
change, extensive degeneration, or  absorption, according to  Bevan
Lewis.  The explanation of the selection  by alcohol of this site, and
of the outermost rim of the cortex simultaneously with  the  fifth
layer,  is supposed by Lewis to be  that this outermost layer really
represents the distribution of the apex processes  of the cells  in the
fifth layer.  The long, straight vessels  of  the cortex  are often enor-
mously distended, even showing minute aneurisms.  In the lowermost
layer of the cortex, the spindle-cell formation, great uumbers of the
Dieters's or scavenger cells are met with. In the spinal cord of chronic
alcoholism there is an increased vascularity,  the vessels of the posterior
and  lateral  columns being most affected,  and those  of the anterior
columns the least.  These vessels increase  greatly in  thickness,  from
hypertrophy of the muscular coat,  and the lumen  becomes  greatly
diminished—so that  a  vessel which measures eighteen millimetres
across, and which would  normally have a lumen of thirteen milli-
metres, may have its lumen diminished to five; or one of twenty-seven
millimetres  across, instead  of an approximately normal lumen of
twenty-three may have a lumen of only  nine.  This change in the
muscular coat seems to be identical with that of chronic Bright's dis-
ease, and is in the nature of a compensatory hypertrophy.  Besides
these changes of  brain and cord in chronic alcoholism, there may be
a simple fatty degeneration of the tissues and their nutritive vessels,
and this may be associated with interstitial sclerosis. 
ALCOHOLISM AND MORPHIOMANIA.
569
   Diagnosis.   The diagnosis of most forms of alcoholic mental dis-
 ease is generally easy.  The history of the case is the most important
 factor, and there is usually no difficulty in obtaining this.   The deli-
 rium tremens is readily recognized by the history of the  case, con-
 joined with the symptoms that have been detailed, and this is also true
 of the other forms that have  been mentioned.   In the pseudo-general
 paresis of the alcoholic it is sometimes impossible to make the diagnosis
 at the outset; but the alcoholic form may be suspected when the onset
 has  been relatively acute, when  the pupillary changes are absent  or
 slight, and when there has been  a  previous attack of the same kiud.
 Of some value  in this diagnosis  is also the fact that the case of alco-
 holic pseudo-general paresis does not usually have the characteristic
 delusions of grandeur; but this must be considered with considerable
 caution, since many cases of general paresis, as I have already said,
 are lacking  in this symptom.  A week or two of treatment, however,
 will make the diagnosis clear.
   Treatment.   The treatment of alcoholism should consist, in the
 first place, of treatment of the disease from which the patient is suffer-
 ing, and, in the second  place, of treatment of the habit itself.   The
 treatment of most forms of alcoholic insanity will not differ from that
 of the non-alcoholic types of the same kind, with  the exception of the
 cases of delirium tremens, oinomania, and pseudo-general paresis. De-
 lirium tremens should be treated  by the bromides, hyoscine, opium,
 stimulants, and isolation. The bromide should be given in doses vary-
 ing from 10 grains to 30 grains every three or four hours, with -^fa  to
 TUT gra'n °f hyoscine, either the hydrobromate or the hydrochlorate
 (it makes no difference which), and sulphate of morphine or bimeco-
 nate of morphine should be administered hypodermically in doses  of
 \ grain once or twice a day, or even ofteuer in severe cases.   Opium
 or morphine by the mouth is usually ineffective.  The question  of
 alcoholic stimulation is a very important one in these cases. Usually
 it may be regarded as unsafe to  make  any  rapid reduction of the
 whole amount to which the patient has been  accustomed whilst the
 patient  is suffering from  any mental disease, although generally  it
 will  be perfectly proper to reduce this quantity by one-half.  By this
 I do not mean to say that the quantity which  the patient  has been
 taking in some  excess immediately preceding  the  outbreak should be
 taken as the standard, but the quantity to which he has been habitu-
 ally accustomed for months or years past.  The sulphate of quinine,
 in doses of 3 to 15 grains in the twenty-four hours, will be found an
 exceedingly  useful adjuvant,  and it should be  given  in the form  of
 the tablet triturate freshly prepared or in capsules, and seldom or
 never in solution with a mineral  acid,  as this is prone to upset the
 digestion when long continued. The question of nourishmeut in these
 cases often becomes a very serious one, and in many instances it will
 be impossible to make use of other than such easily digested food as
milk, beef-tea, eggs, and koumiss,  whilst as the symptoms grow less
severe solid  food may be gradually added.  An excellent method of
giving a raw egg in this condition  is to get the patient to swallow  it
whole after the  shell has been removed, and  it is surprising to see 
570
NERVOUS DISEASES.
 with what facility patients can be taught to do this.  The most rigid
 isolation of the patient should be practised, so as to insure the most
 perfect quietude,  and the room should be  darkened and  all  noises
 carefully excluded. As the symptoms disappear and the patient con-
 valesces, the morphine may be reduced first, and often with compar-
 ative rapidity, but the bromides  and hyoscine should  be  continued
 longer and reduced more  gradually, whilst  the  nourishment should
 be pushed and the stimulation with quinine continued.   During this
 period of convalescence, too,  the alcoholic  stimulant should  be  re-
 duced, and  in its place should be given an  alcoholic malt-extract,
 frequently repeated, so that the patient may get it three or four  hours
 apart, with some slight nourishing food.
  The cases of oinomania, the recurrent insanity that has been de-
 scribed, should be treated iu the same  way  as  a  case  of delirium
 tremens, with  the exception that it will not be necessary to give such
 quautities of the  bromides, opium, or hyoscine.
  The  cases  of  alcoholic pseudo-general  paresis  must be treated
 differently from the two forms that we have been describing.  In the
 first place, the patient should be put upon a mineral acid, the best of
 which  is the  nitromuriatic acid, of which twenty  drops in a  wine-
 glass of water, three times a day, should be given after meals.  Then
 with this an aloetic should be  combined at bedtime, and I have for
 years been in the habit of using the time-worn prescription of—

      R.—Ext. aloes     \                                 ~.
          Ext. hyoscyami j......aa   db
          Ext. nucis vomicae    ......     gr-  v.
  M. ft. in pil. no. xv.  S.—One every day, two hours after the evening meal.

 Or  a dose of  a mineral water, such as Hunyadi or Rubinat, may be
 given every morning  before  breakfast.   The patient's diet should
 also consist largely of fish, soups, eggs, fresh fruits, fresh vegetables,
 farinacea, and custards; and all meat, either of chicken or the red
 meats,  should  be absolutely excluded for an iuitial  period of four or
 five days. At  the end of  this time chicken or turkey may be allowed
 ouce or twice a day, or if  the patient craves red meat very much, he
 may be allowed to eat this once a day.  After having treated the
 patient for four or five days, 10 or 15 grains of the iodide of potash
 should be given an hour after  meals, well diluted iu a  full tumbler
 of water or Vichy or Giesshiibler.   If the  patient is seen to be im-
 proving markedly at the end of a week, touic doses of quinine should
 be administered, two hours after meals, three times a day (the sulphate
 being used), or a half-ounce of elixir of  calisaya.   From the begiu-
niug of treatment cerebral galvanization will be found to be exceed-
ingly useful, and this should be administered every second  day, with
a current of two or three milliamperes,  in  sittings  of three to five
minutes.
  The  treatmeut of alcoholic multiple neuritis is that of an ordinary
multiple  neuritis  plus the necessity  of breaking  up the alcoholic
habit.
  The  question of the alcoholic habit  is,  as we  all know, a very 
ALCOHOLISM AND MORPHIOMANIA.
571
vexed one.   On the one hand, it has been considered as a vice, and,
on the other, it has been regarded as a disease.   The truth lies, as it
generally does, between the extremes.  A human being  who indulges
in alcohol to excess, knowing that it is certain to ruin his health, his
prospects iu life, and the  happiness of  those most dear to  him, is
certainly responsible, and alcoholism in his case is, therefore,  a vice;
but if he persists  in  becoming  a chronic inebriate, and  induces
structural changes or forms incurable habits that may be transmitted
to his children, the strain in these children is a disease as much as is
any other hereditary trait, although even  in them it differs from most
diseases in the fact that it is within the control of the will to  a large
extent.   There is not one of  us who could not drink, use  opium  or
cocaine, commit burglary, forge, steal, or do other vicious  acts, if it
were not that we were restrained by that force within us which theol-
ogists call conscience, which metaphysicians call will-power, and which
physiologists call  inhibition ; and  although this conscience,  inhibi-
tion, or  will-power, whichever we  may choose  to term  it, may  be
weakened by hereditary faults, it  is seldom entirely lost, and can  be
exerted  in  the majority  of cases if the individual will  make the
attempt.   Of late years the question of alcoholism has  been fashion-
ably and charitably regarded as a disease in all  cases;  but although
I do  full honor  to the  kindliness  of the  sentiment that is at the
bottom  of this mode of thinking, I do  yet firmly believe that  its
effect has been to create much maudlin sentimentality upon  the sub-
ject. Leaving, however, these primary considerations which are neces-
sarily intermingled with the more purely medical  ones, I would say
that I regard the cure of most cases of  chronic alcoholism  as likely
to be ineffective unless the patient is put under such care as to make
it impossible for him to drink, either in  a sanitarium or an inebriate
asylum.  In the last few years a great ado has been made  about the
alleged cures of alcoholism by the secret methods of certain quacks.
The statistics of the results  attained by these  methods have never
been published in  such a way as to be verified or as would  be done
if the possessors of the  secret method were strong enough to stand
such a  crucial test.   Nor have the ill results  that  many  practi-
tioners could  cite ever  been  published, nor are  they ever likely to
be  published,  because the seal  of professional  confidence closes
the  lips  of those  most  competent to  speak,  whilst the  patient
himself and his family are silent for obvious reasous.  The spread
of the metallic tractors of Perkins throughout America and Europe;
the grant of a large sum of  money by  the  English Parliament  to
Joanna Stevens for her wonderful remedy for the cure  of stone, that
turned out to be a simple alkali of  oyster-shells and utterly  worth-
less ; the wonderful stories told of the  Grotto  of Lourdes and the
various  sacred relics  that from time  to  time attract swarms  of
devotees;  the startling results that were at first claimed  but a few
years since for Koch's tuberculin, in spite even of that honest scientist,
whose words were given a meaning that he had never put into them ;
the fortunes made by quacks in every community, serving  to bribe
legislatures,  as well  as  scores  and  scores of journals  that  publish 
572
NERVOUS DISEASES
dishonest and lying advertisements on their back pages, at the same
time that they prate in their editorial columns  about the benefits of
civilization—all these have  made  a history that should teach man-
kind  to  place no faith  in secret remedies that dare  not come into
the light of day.  It has  been alleged  that  one of these  secret
remedies, known as the  Keeley cure, consists  of strychnine,  bella-
donna or atropine, ipecac, caffeine, cocaine, and codeine;  but I have
no means of knowing  whether these statements are  correct.   It is
true that as far back as 1880 Dr. Dobvonravoff claimed to  have met
with considerable success in  curing drunkenness in  the Russian army
by the injection of  the nitrate of strychnine, of which he  used gr.
^5-, once or twice a day.   He alleged that in this way he could induce
a distaste for alcohol in  two or three weeks.  In  certain cases this
would appear to be a fact; but  the remedy  has never met with
much  success in the  hands of competent men.   The  bichloride
of gold has certainly been  entirely unsuccessful with most  physi-
cians.  If a  case of alcoholic  habit  is to be  treated, the alcohol
should be  gradually reduced, and this can be done at first  with
considerable  ease, and  it  is generally only when  the dose  is be-
coming very small that  the  patient begins to  manifest  great
nervousness, jactitation, sleeplessness, and sometimes symptoms  of
one of the  alcoholic disorders  that  have been  meutioned.  At this
period bromide, quinine, strychnine, and hyoscine should  be  given
in the way that has been  mentioned in  describing  the treatment
of delirium  tremens, grading the dose  according to  the  symp-
toms.   In  most of the cases  of alcoholism the patient is usually
also addicted to the use of cocaine  aud morphine, and these  drugs
must  also be diminished  gradually in  the same manner.   I  have
no faith  whatever in the sudden  reduction of alcohol, cocaine,  or
morphine,  much as it  has been  vaunted of  late  years,  aud my
lack of faith comes from the fact that I have seen a number of cases
in which the sudden reduction has seemed to meet with charming
success for a short period,  to be followed by very serious  symptoms,
such as some form of alcoholic insanity, or even a convulsion. 
CHAPTER XXII.
   RAILWAY INJURIES AND OTHER  TRAUMATIC DISEASES
                 OF MEDICO-LEGAL INTEREST.

   Traumatic diseases are of such vast  pecuniary importance in
 this modern age of great railway and steamship companies and other
 wealthy corporations that they have been  studied with more assiduity
 than scientific exactitude.  Although  the older  works upou surgery
 discussed the question of cerebral and spinal  concussion, they did so
 much more from a traditional standpoint than as a result of the per-
 sonal observation of the authors.   Erichsen's first lectures in 1866, on
 Certain Obscure Injuries of the Nervous System commonly met with as
 the Results of Shocks of the Body received in  Collisions on Railways,
 marked a new era in the treatment of this  subject.   This was followed
 by his treatise on Concussion of the Spine, in  1875.  Page's book on
 Injuries of the  Spine and Spinal Cord,  published in  1883, was in
 the same vein ; and these three publications, together with the rapidly
 growing interest of the subject, have given rise to a  great literature,
 of which the most salient articles have  been those of Knapp, Put-
 nam, Walton, Oppenheim, Charcot, Clevenger, and Judge Bartlett.
 During the twenty-five years  that have elapsed  since Erichsen first
 made known his views, the study of the phenomena following trau-
 matism has gradually passed from the surgeon to the neurologist
 and very  properly,  too, as the nervous phenomena constitute  the
 most important part of the subject.  During this lapse of a quarter
 of a century neuro-pathology may almost be said  to  have been dis-
 covered.   Too much importance,  therefore, should not be attached to
 the older opinions which were formulated by  men who, however well
 informed they may have been in  their day, were  mere tyros to  the
 specialists of the  present time.  Physicians will scarcely need this
 reminder;  but  it should  be  timely to lawyers, whose professional
 reverence  for authority and precedent  is apt to render them inap-
 preciative of the difference in this respect between science and  law.
   Existing medical knowledge will  not permit us to say that there is
 any one disease of the human body that cannot possibly be caused by
 injury, except, possibly, one of an infectious nature.  It is quite pos-
 sible, to be sure, to compile from the medical journals and from one's
 own personal records a list of the diseases which  have been  so  far
caused  by injuries, but each new day may add to  this list.  When-
ever an injury has been received, and a disease has followed it after
such a length of time as to render it  probable  that  the latter has
been the effect and the former the cause, a new observation will have
been made.  Predisposition—whether  hereditary, or from previous 
574                   NERVOUS DISEASES.
disease, or  from coexisting diseases—may render the human being
more liable to the excitation of disease by an injury, and it may then
become a question  as  to  the  respective responsibility of the  injury
and  the predisposition in the production of the  disease.  Observa-
tion, however, has shown that injuries are peculiarly liable to pro-
duce certain diseases that have  been well studied,  and when  the
symptoms of these are  described by some individual whose means of
information have not  been  such  as  to have made him  acquainted
with medical writings,  their medico-legal value may become so great
as peremptorily to  exclude  simulation.    The diseases  that can be
caused by traumatism are—
       Injuries of the bones, ligaments, muscles, and peripheral nerves;
       Ordinary myelitis, with secondary degeneration of the motor
         and sensory tracts;
       Locomotor ataxia;
       Myelitis of the  anterior cornua of the spinal cord ;
       Progressive muscular atrophy;
       Tumors of the  spinal cord ;
        Insanity;
        Encephalitis;
        Tumors of the  brain ;
        Intracranial hemorrhage;
        Chorea;
        Epilepsy;
        Neuralgia;
        Hysteria;
        Neurasthenia.
   Injuries of the bones are not usually difficult to detect.  Erichsen
has stated that the brain and cord are not usually injured when  the
skull or the vertebrse are  fractured,  because the force of the blow is
spent  upon the bones  and does  not reach the underlying nervous
tissues.  This is a very  erroneous  statement, both  as a matter of
physics  and clinical observation, and  I  have beeu  surprised  that
so many writers should have thought it worthy of refutation  by the
recital of individual cases.  Every hospital interne has seen fracture
of the skull associated with serious injury to the  intracranial contents,
and the frequency with which fracture of the  vertebrse is conjoined
with injury of the cord is well known to every surgeon of experience,
and is proven by the cases  collected by Thorburn,  whilst I  can
myself cite many  from  my  case-book  in refutation of Erichsens
dictum.  We should be careful, therefore, not  to overlook a nervous
injury when we have discovered a bony one.  Injuries to  the liga-
 ments are usually easy of diagnosis, too, although time and observa-
tion  may  sometimes  be  needed to  exclude an implication  of the
peripheral nerves.   In examining injured muscles myositis and be-
ginning progressive muscular atrophy should be carefully sought  for;
but it should be remembered that in the latter widespread atrophy
 of bilateral muscular groups is something entirely different from the
 wasting of a single injured muscle or sets of muscles.  When the
 peripheral nerves are injured, neuralgia  or neuritis will be produced, 
RAILWAY INJURIES, ETC
575
for the diagnostic symptoms of which  reference must be had  to  the
chapters on these subjects.
  Injury of the spinal  cord may cause that  form of myelitis which
is known as ordinary, transverse, or central myelitis (vide section on
" Myelitis ") to distinguish it from the other forms to which special
names have been given ; aud secondary degenerations of the motor
and   sensory tracts  may  follow.   We  know  very little at  the
present time,  as has been stated  elsewhere,  of the symptoms of
the secondary degenerations of the sensory columns of the  spinal
cord; but the symptoms of a secondary motor  degeneration are con-
tracture and exaggerated reflexes of the different tendons, such as the
patellar reflex, the foot-clonus, hasty micturition, the commingled
contracture and exaggerated tendon-reflexes producing the spastic
gait.   ( Vide pages 166  and 169.)
  It  is a certain that  locomotor ataxia  can  be caused  by injury,
especially by one of a general nature.   One  of the most marked
cases  of this disease that I have ever seen quickly followed the cele-
brated Ashtabula railroad  accident, when a train was precipitated
from  a bridge at a height of three hundred feet.
  Myelitis of the anterior horns of the spinal cord, the poliomyelitis
of the Germans, or  the so-called essential infantile paralysis of  the
old writers, can be caused by injury.
  Progressive muscular atrophy is frequently caused by injury.
  Tumors of the spinal cord are also caused by injury,  although
rarely ; aud Leyden narrates a case of large  tumor of the cord, of
traumatic origin, the sufferer from which had been thought to be  a
malingerer.
  There is abundant evidence to prove that  injury may cause insan-
ity.   The symptoms of mental disease thus produced are not usually
well  marked, although there is a strong tendency toward dementia.
Mania, melancholia, primary demeutia, transitory mania,  delirium
grave, and katatonia cannot be classed among the traumatic insanities,
so far as we yet know,  but post epileptic insanity can.  The different
forms of encephalitis that  are classed under the generic head of gen-
eral paresis (see  under " Paralytic Dementia ") may also be of trau-
matic origin.
   Tumors of the brain, intracranial hemorrhage, and chorea can be
caused by injury.
   As we  have seen (vide "Epilepsy"),  epilepsy is a symptom of
various diseases  of the central and peripheral nervous structures,
and may also  be idiopathic—i. e., caused by  cerebral disease of a
functional nature; and all these varieties, except the idiopathic, may
be caused  by  injury.   Careful  regard  should  be had in this connec-
tion,  however, to the factors of diagnosis  thas have been  detailed on
page  406.
   The relation of hysteria and neurasthenia  to injury is the vexed
question of medico-legal medicine, and has given rise to most of the
modern  literature upon the subject,   luasmuch as vast interests of
money, life, and happiness  are at stake iu this query, it  is best that
we should enter into its merits at some length.   Hysteria is a  (lis- 
576
NERVOUS DISEASES.
ease (page 437) that is characterized by certain emotional conditions,
peculiar  convulsions  and paralyses,  and  by hemiansesthesia.   It
occurs in males as well as iu females, although  more frequently in
the latter, and also  in children.  The emotional condition does not
necessarily precede or accompany the graver convulsive, paralytic, or
hemiansesthetic phenomena.   The convulsions  are  readily  distin-
guishable from those of epilepsy, and even when conjoined with the
latter disease, as  iu  hystero-epilepsy, they have  marked features of
their  own,  and are  of much  more favorable prognosis.  Charcot
teaches that the sole diagnostic symptom of hysteria may be hemi-
ansesthesia,  consisting  of one-sided  impairment of  the  senses  of
touch, temperature, pain,  and heat, with  impairment of the color-
sense  and  concentric limitation  of the field of vision ;  and around
this dictum of Charcot's  has beeu waged a furious war.   The great
French  teacher has shown to his classes cases of  paralysis involving
the arm or leg, with a peculiar limitation of the anaesthetic area, and
has claimed  that  they were  hysterical in their  nature  because  the
patients also had  hemiansesthesia.   Oppenheim  and Thomsen have
found, however, that hemiansesthesia may exist in epilepsy, alcohol-
ism, nervousness, neurasthenia, chorea, conditions of fright, multiple
sclerosis, Westphal's  neurosis, organic brain  disease, and  after cer-
tain insanities, and  that  it  is  not characteristic of  hysteria, even
in which  disease it  is  very variable,  bearing no  certain  relation-
ship to the  bilateral  concentric limitation  of the  field of vision,
the most constant  symptom of hysteria.   Charcot's claim  that  the
functional  nervous symptoms of all cases from railway injury are
due to hysteria has not therefore been proven.   This much may be
regarded as settled.   Charcot has furthermore been able to produce
a paralysis by hypnotism  in these so-called hysterical patients,  and
also to relieve in them an existing paralysis, although the  relief  has
beeu only of short duration, and he would have us call this paralysis
a paralysis  of idea, at  the same time that he lays great stress upon
the distinction between it and an imaginary or simulated paralysis;
in other words, as  hysteria is a genuine disease of the nervous  sys-
tem, an hysterical paralysis should not be mistaken for one of sham-
ming, although it may closely resemble the latter; but as he does
not claim that the same phenomena cannot be produced in non-hys-
terical individuals, rather relying upon the hemiansesthesia  as  the
basic criterion, it is evident that this point is also not  proven.  His
cases  were taken from that great hotbed of nervous  disease, the im-
mense hospital of La Salpetriere, and two of the most remarkable in-
dividuals had been respectively thirty  aud forty years in the institu-
tion.  Putnam and  Walton have reported cases of hemiansesthesia
following railroad injuries, and  Oppeuheim's  latest monograph  con-
tains a history of traumatic nervous symptoms in 33 cases observed in
the nervous clinic of the Charite  Hospital of Berlin in a period of five
years.  That injuries, especially those received in railway accidents,
can produce a certain set of symptoms worthy of  being considered as
a distinct symptom-group was first  recognized by Erichsen, and this
fact has since been confirmed by many observers. To this symptom- 
RAILWAY INJURIES, ETC.
577
group Erichsen  gave the name of spinal concussion; then it was
designated  railway  brain, and finally Oppenheim suggested for it
the cognomen of traumatic neurosis, whilst Charcot, as we have seen
would call  it hysteria.   The symptoms  consist of disturbance in
varying degree of the various functions of the body, mainly of the
nervous system, and the latter are largely sensory and but slightly
motor.   The sensory symptoms are disturbance of  the different
senses, such as touch, the muscular sense, heat, pain, sight, hearing,
seldom taste or smell; whilst  the  motor  disturbances  are expressed
by exaggerated  tendon  and  sensory reflexes,  aud paralysis varying
from  slight to  severe;  and there  are almost  invariably superadded
such geueral nervous disturbances as vertigo, insomnia, a depressed
mental condition, irritability of temper, impotence, and loss of appe-
tite.   Hemiansesthesia  is occasionally associated  with these symp-
toms, as we have already seen. To go more into detail, the course of
the symptoms is generally as follows :  A man is injured in a  railway
accident, rendered unconscious perhaps, or perhaps only made dazed
and tremulous.  He goes home and returns to his work.  In the course
of a few days or a week he finds that he is not regaining his  normal
condition of health, that he  is nervous, cannot sleep, is not capable of
doing his usual mental  or physical work, is irritable and generally
unstrung.   As time goes on, his condition grows worse  and he  be-
comes depressed and emotional, easily excited to laughter or to tears,
moody,  brooding, and showing less and less capacity to apply himself
to his usual pursuits and more and more  inclined to isolation. If he
is examined several weeks or months after the accident, it will usually
be found that his tendon-reflexes  are  exaggerated, perhaps  also  his
sensory reflexes ; that there is some impairment of the various senses,
or even hemiansesthesia;  that bis  muscles are abnormally weak;
that he complains  of vague pains, especially about the back, hips,
and  groins; that his countenance is  pale, anxious, and  careworn ;
that he presents the picture, in a word, of a worried and anxious in-
dividual ; that he has also occasional vertigo, and a sense of distention
and fulness about the head, especially at the vertex. This is, I think,
a fair general picture of the  symptoms in this class of cases—in other
words, of the type; but there are many variations from this  type,
so that in one case  one set  of symptoms  may predominate, and in
another case a somewhat different set may be presented.  It has been
claimed that neuro-retinitis has  been occasionally observed, but I
have  never seen  this myself, although it has been my habit to ex-
amine carefully every case with the ophthalmoscope.  The attitude,
the movements in sitting down and rising, the peculiar efforts to
effect a voluntary movement, and  the  gait, are all characteristic, as
Oppenheim first had the acumen to observe, although I have myself
noted the same  thing in many cases without  having it occur to me
that there was anything distinctive about them.  The body is held
anxiously fixed,  the spine  bent stiffly forward, in sitting down or
rising the patient seeks  support with the  hands, and he  changes his
attitude carefully and slowly.  Oppenheim attributes this mainly to
the rigidity of the dorsal muscles,  and  only in  less  degree to  in- 
578
NERVOUS DISEASES.
stinctive avoidance  of movements of the vertebral column, and  I
think his explanation is thoroughly accurate.   In making a  volun-
tary movement the patient  seemingly makes  a great  effort, and yet
the resulting muscular movement is  relatively feeble, so that the im-
pression upon the observer is  that of simulatiou on the part of the
patient.  I must confess that such was my belief in my days of less
experience, although further  observation has firmly  convinced me
that such a conviction does grave injustice.   Oppenheim attributes
this muscular weakness to the fact  that  the motor impulses coming
from the brain are not so  precisely directed as in health, so that they
do not pass in full volume to the muscles for which they are intended,
but  are erratically  diverted  to other muscular groups  subserving
other but allied  movements.  Thus, if the patient  is told to press
the  observer's hand with his full  strength, the shoulder-muscles,
the flexors of the elbow, and the extensors  of the  hand  are  simul-
taneously thrown into powerful action.  When muscular paralysis
occurs, it is noteworthy that it is seldom or never confined to mus-
cular groups supplied by one nerve-trunk.   The motor paralysis is
generally a flaccid one, although it may be conjoined with contrac-
ture, which  may be due  to the pain that  is experienced in certain
muscular movements, or which may be truly  hysterical.   The gait
is peculiar. The patient walks with legs wide apart, with short steps,
and slowly ;  the movements at the joints are limited,  the foot being
drawn along with the whole  plantar  surface, or the  heel shuffling
on  the floor,  whilst the body is held in the position just described.
Usually one hand is placed  on the back or  on the side.   Although
this gait is like that which is usually known as spastic, it yet differs
from it in that the toes do not cling to the floor, and in that there is
not  the  springiness as of  a  stiff bedspring  (page  276).   Various
modifications of this gait  may be observed, but they can  always be
traced, in my experience, to  the same causes at play in different
muscles, viz., pain, giving rise reflexly to pseudo-contracture.  If all
these symptoms are analyzed, no other  conclusion  can be reached
than that they are the effect of exaggerated reflex action.
  We  do not  know what  is  the molecular coudition of the  great
nervous  centres causing this exaggerated reflex action.  Westphal has
advanced the theory that the cause is to be found  in small foci of
myelitis or encephalitis, analogous in their action to multiple sclerosis.
Bramwell suggests that there may be multiple capillary hemorrhages
in the brain  and cord, giving rise  to inflammatory  processes, and
eventually to sclerosis; and Vibert found in those killed at the great
railway accident at Charenton in 1881 very abundant  punctate hemor-
rhages in the upper part of  the body. Willigk has detected dilatation
of the finest vessels, with  infiltration into the perivascular spaces and
degeneration of the vascular coats.  Mendel fastened dogs on a table
revolving 125 to 130 times  a minute, the  revolutions continuing for
half an  hour, the heads of the animals being toward  the periphery,
and thus produced punctate hemorrhages in the brain and cord.  One
hundred and ten revolutions for six  minutes  a  day,  continued for
several weeks,  caused  adhesions between the  skull and  the brain 
RAILWAY INJURIES, ETC.
579
aud its membraues, an increase in the nuclei iu the cells of the con-
nective  tissue, as well as in the number of vessels, and changes in
the nerve-cells.   Furstner,  repeating Mendel's  experiments, with
sixty to eighty revolutions for one or two minutes, found double pri-
mary degeneration of the lateral columns aud of part of the posterior
columns, alteration  of the optic  nerves, and cerebral  change similar
to that described by Mendel.   Dumesnil, Petel, and  Edes have re-
ported degeneration of the lateral columns in the  human being.  But
it should be observed that AVestphal and Bramwell only theorize, that
Vibert speaks aloue of individuals who were  killed by an  accident
severe enough to cause quick  death, that Willigk simply mentions
one individual, that Dumesnil, Petel, and Edes report  no more than a
few cases, and that Mendel and Furstner obtained their results by a
method  which, however ingenious, is not at all analogous to ordinary
injuries  or those produced by railway accidents.   I may, therefore,
repeat my assertion that we do not know the molecular cause in the
central  nervous  system  that produces these  exaggerated  reflexes.
Clevenger enters into an ingenious argument to demonstrate that they
are due  to injury of the sympathetic nervous system ;  but, even if we
admit that this is correct, it only transfers the mystery from one ner-
vous system to another, whilst I do not think that  the marked sensory
and motor symptoms cau be at  all explained by any perverted action
of the sympathetic.  It has been suggested that spinal concussion is
the cause, but this suggestion can only be due to confusion of thought,
because  a concussion is simply another name for an injury, and it is
the molecular effect of the concussion  or injury that can alone give
rise to the clinical phenomena. Arguments about the question whether
spinal concussion can exist  are as idle as the endless discussions of
the schoolmen.  In the present state of our knowledge we cannot do
better than to say that these symptoms are functional—i. e., due to
molecular alterations in the brain and cord that have not been detected
by our  present methods of preparation and staining of nervous tis-
sue, even if it is possible that such methods can detect them.
   Belonging  to  the functional  nervous affections, therefore, as this
particular group of symptoms  undoubtedly does, I  think  that we
should  classify it with those other groups of symptoms which are
known  by the name of neurasthenia; aud, instead of adding to the
confusion already existing in our  medical nomenclature by coining
such new names as spinal concussion,  railway  brain  or spine, or
traumatic neurosis, I think  that  we shall greatly simplify matters
by simply designating  it as  traumatic neurasthenia.^  We  have
already  seen that there is no warrant for regarding  this traumatic
neurasthenia  as  hysterical.   It undoubtedly possesses a certain like-
ness to  other forms of neurasthenia  so  far  as  regards the pares-
thesia and the general nervous  and mental symptoms ; but it differs
from  them  in the  painful  sensations,  the  muscular rigidity, the
peculiar  attitude, the  gait,  the  disturbed  muscular  innervation,
and, finally, in the prognosis.   There has been  much difference of
opinion  in regard to this very question  of prognosis,  but  I think
that this has arisen mainly from the  fact  that  sufficient regard 
580
NERVOUS DISEASES.
has not been paid to the peculiar circumstances in which patients of
this class are usually  placed.   Few observers will  deny, I think,
that  the symptoms  of traumatic neurasthenia, especially  those due
to railway accidents, almost  invariably  continue  for  a long time,
disabling  the patients  for many  years,  aud in some cases even
terminating fatally;  but some of these veryr observers  contend that
the maintenance of  the symptoms is due to the psychical condition
of the patient, whilst others insist that it is inherent to the disease.
Certain it is that the psychical couditiou of these patients is a very
unfortunate one.  However uneducated they  may  be, newspapers
and  the  talk of every-day  life has  filled their mind with  dread
of the mysterious and  baleful  consequences  that  may  happen  to
those who receive injuries, particularly in railway accidents.   They
have  also heard for years of the damages, often  enormous, which
corporations  have been obliged to pay.   When  the accident occurs,
the nervous system undoubtedly receives a shock, perhaps intensified
by the sight of the killed and  wounded, writh  all the attendant hor-
rors, and  this shock should receive immediate and judicious treat-
ment by  rest,  isolation, aud  medicaments;  but instead of this, a
lawyer or his agent—the so-called  "runner"  of this country—
quickly appears upon  the scene, and  spurs  the  patient ou to a suit
for damages by exaggerating the injury and its  consequences,  so
as to  make  the too-willing sufferer  believe that the company can
be readily forced to pay damages.   Then  come the long years  of
weary suffering, anxiety,  waiting, and  disappointment, unrelieved
by  proper treatment, for although the patient and the lawyer may
not consciously discourage treatmeut,  yet too many hopes and inter-
ests  would  be blasted by a cure  to permit of treatment ever being
properly  carried  on, even  if any self-respecting  physician  could  be
found to  undertake it.  Months, perhaps a year  or more, are passed
in waiting  for  the  suit to be tried.  I have known of three years
having elapsed  before this was done, because of delay7 in obtaining
the evidence, then in  fixing the responsibility upon the right cor-
poration,  then by alleged corruption  of the attorneys, and, finally, by
the long  waiting before the case could be reached upon the calendar
of the  court.  When  the suit  has  been brought and  pushed to a
successful termination, an appeal to a higher court will usually  be
taken, perhaps to a second higher court, and  thus  months or years
more pass by.  In  some cases it may even happen that a successful
issue iu the court of the highest resort is contested upon a charge of
conspiracy or some matter of legal technicality that is  concocted  in
order to gain time.  Finally, the case being at last successfully ended,
it may turn out, much  more frequently than is dreamed of by those
who have not had a long  experience, that the costs of the action and
the lawyer's fee will leave but a pitiable sum of money at the dis-
posal  of  the patient.  This is  not  an exaggerated  picture by any
means.   It is a composite portrait of dozens of cases whose details
can be taken from my case-books.   All this disturbance that follows
the accident is oftentimes, I am firmly convinced, a  more potent
cause  of  the neurasthenia than the accident  itself, and I  feel sure 
RAILWAY INJURIES, ETC.
581
 that it is this  secondary psychical disturbance that makes this form
 of neurasthenia more intractable than other forms of neurasthenia
 although I cannot quite agree with the statement which I have often
 heard made on the witness-stand by very competent colleagues  that
 traumatic neurasthenia does not differ from other forms of neuras-
 thenia except in the psychical element. Notwithstanding that Charcot
 does not exactly say this, it is yet evident  that he takes very much
 the same view  in regard to the hysterical origin of these cases.   Not
 only, however, are their symptoms to a certain extent pathognomonic
 but there never yet has  been any clinical proof adduced to demon-
 strate that the  difference between them and other neurasthenic types
 is due alone to the mental element.  Nevertheless, I firmly believe
 that it is  the  psychical element, together with  the resulting lack of
 proper treatment, that makes the usual unfavorable prognosis of this
 class of cases.   In several  instances I have persuaded patients to
 place themselves promptly under treatment, and at the same time
 either to abandon or compromise the legal proceedings, and in every
 instance a cure has  been effected.   In  other words, in order to
 make my meaning perfectly plain  in a  matter of this importance,
 let  me  repeat  by stating that while I  do  believe  that traumatic
 neurasthenia is a  species of disease that  has distinctive features of
 its own, I do  not  believe that it is of unfavorable  prognosis, pro-
 vided that the psychical  element  can be excluded aud that prompt
 and proper  treatment can be undertaken.   It must be clearly borne
 in mind,  however, that this  statement applies only to this  group
 of functional  symptoms, and  that it does not apply to the organic
 diseases caused by injury;  but  moral  responsibility cannot  be
 hereby avoided by  the persons or corporations by whom  the injury
 has been  caused, for whether the neurasthenia is  rendered more
 intractable or  not by the accompanying psychical  element,  the
 injury itself has been  the cause of all  the  symptoms.   Whether the
 legal responsibility of these individuals or corporations is lessened
 on this account is a question of law for the courts to determine, and
 we physicians  have nothing whatever to do with that aspect of the
 question.
  The element of simulation iu all these diseases produced by injury
 should always  be carefully considered whenever there is a question
 of a suit for damages.   Physicians  make  a great mistake, however,
 in entering upon the examination in a mental state of bias against
 the alleged sufferer, and justice will be much more equally done if
 all the symptoms are carefully and impartially gathered before any
 conclusion  is  reached;  but a sharp  distinction should always be
 made between  the  symptoms that  are objective and  those that are
 subjective—i. e., between those for which we must entirely or mainly
 rely upon  the patient's statement, attitude,  or facial expression, and
 those which  we can entirely or absolutely determine  for  ourselves.
 Nevertheless,  the  value  is very  great  of a  group of symptoms
that are usual  to a disease, even  if  many of these are so  purely
subjective  as to make  us dependent in  a large degree upon  the
patient's statements.   For instance, the  stabbing and lancinating 
582
NERVOUS DISEASES.
pains of  locomotor ataxia  cannot  be seen  or tested  by the ex-
amining physician, and  yet  an accurate  description of them  by a
patient should carry convictiou, unless there is reason to believe, as
will  very rarely happen,  that the patient  has  special sources of in-
formation ; and this is also true, in varying degree, of the cincture
feeling and  bladder and rectal symptoms of  myelitis, the slighter
losses of  consciousness  of epilepsy,  and the parsesthesia, vertigo,
nervousness, insomnia, and peculiar emotional condition of traumatic
neurasthenia.   Nor should a purely subjective symptom  lose one
iota of the value that it ought to  have when it is conjoined  with
demonstrable objective symptoms in  such a way as to picture properly
a well-known disease.   Thus, when we can see  with our own eyes
that a patient has the glossy skin, the tapering and slightly swollen
fingers,  the muscular wasting, and the altered  electrical  reactions of
an ulnar neuritis, we should not reject the statement of pain, numb-
ness, and tingling which  maybe described.  The courts have a very
vicious  habit of ruling out the statement of a physician  that the
symptoms, when taken  together, indicate a certain disease, aud of
forcing the medical witness to confine himself to an enumeration of
the individual symptoms, leaving the jury to be  the diagnosticians.
  Subjective symptoms are—
       The senses of touch, pain, temperature, and the muscular sense;
       Parsesthesia ;
       Hearing ;
       Sight;
       Smell;
       Taste;
       Urination and defecation ;
       Sexual sense;
       Vertigo;
       Losses of consciousness, with or without convulsions ;
       Insomnia;
       Nervousness;
       The mental condition.
  Whilst objective symptoms are—
       Paralysis;
       Exaggerated tendon and sensory reflexes  ;
       Contracture;
       Ataxia;
       Muscular atrophy and hypertrophy ;
       The attitude and  gait;
       The ocular and retinal condition ;
       (Edeina and swelling;
       Fractures aud dislocations;
       The facial expression.
  Whilst many of these  symptoms  have been considered in Chapter
II. (pages 154-174), also in  connection with  the diseases in which
they have been found, and whilst others are so  very familiar to the
physician as to need no more than a bare mention, it is necessary to
go into special detail about the medico-legal bearings of most of them. 
RAILWAY INJURIES, ETC.
583
  In testing  the  sense of touch the ordinary method of employing
rough and smooth objects  and an  sesthesiometer  will  not exclude
simulation.   The test by means of a pin or other penetrating object
is not a test of the sense of touch,  as it has been assumed to be in so
many trials, but really of the sense of pain; and  this  is also  true
of the test by  raeaus  of the powerful  faradic current.  The  best
medico-legal  test of the sense of touch  known to me  is  to touch
lightly the patient upon the alleged  ansesthetic area when his atten-
tion  is diverted or when his  back is  turned, due attention being
paid to  differences in  tactile sensibility normally existing in  the
different  areas of the skin,  and to  any possible  marked degree of
mental dulness.   This  simple test is extremely effective, and I have
never known it to fail, even with  the  best informed malingerers,
and it is  especially useful in alleged hypersesthesia.   The best test
for the  sense of pain  is  a powerful  faradic  current.  A  very
gentle current should  first be applied, and should be  gradually aud
carefully increased to  a  moderate degree, so  as  not to alarm  the
patient, and then, the physician's hand having been all the time kept
on  the current-regulator, a powerful current should be suddenly
turned on.   Some means of measuring  the strength of this current
should be employed, so as to be able to reproduce it  and allow the
jury,  if  necessary, to test it for themselves.   The strength of the
current that is  to be  used should always  be determined before the
examiuation, so that care  may  be exercised to employ no more than
will be necessary  to cause a  distinct aud not extremely painful sensa-
tion.  The test by means of a  needle is  extremely unreliable, even
though that needle be concealed in the so-called aigue cachS, or hidden
needle, for we must remember that hypodermic needles can often be
thrust for inches into the tissues without exciting pain, so that it is a
very easy matter  for any determined person to accustom himself to
bury a pin in his flesh, as is often done in jest by boys.   The exact
position of the alleged pain and the attitude aud  gait  are frequently
of great importance.   If the patient marks out the pain  in the dis-
tribution of a nerve, this is strong  confirmation of the  truth of his
statement, although the converse of this proposition does not follow,
for pain is often vaguely distributed in indubitable disease ; so that
the positive  value of such  a statement is great, whilst it has no
negative  worth.  The presence of  the characteristic attitude and
gait  of  sciatica  and of  traumatic neurasthenia would  be  of great
value.   A very  efficient method of testing  the  temperature-sense
is  as follows : The patient should be blindfolded;  a tumbler or test-
tube should be filled with cold water, a second with  moderately warm
water, and a third with water  so warm as to be slightly painful but
not to scald.  The glasses  containing  the cold and  the lukewarm
water should then be applied  in succession to  the portion of the
skiu to  be tested, and  the  patient be asked  to  state which  is the
cold and which  is the lukewarm.  This should be repeated several
times, when, if the patient has failed to distinguish the  temperature
of the water in the two glasses, some of the  very hot water should
be suddenly  spilled over the  alleged thermo-ansesthetic area, care 
584
NERVOUS DISEASES.
being taken not to spill any water upou any portion of the skin that
has not been alleged to be affected.  I know of no  test of the mus-
cular sense that will positively exclude simulatiou.   When a patient
alleges that the sense of pain, the muscular sense, or the temperature-
sense is alone affected,  whilst no claim is made as to any implication
of the sense of touch, this would  argue strongly against simulation;
for any malingerer,  except one versed in nervous disease, would  be
most likely to  insist upon  impairment  of the  sense  of touch.   It
should also be borne  in  mind that these four different senses  may
be affected in different  diseases, either singly or in conjunction with
one, two, or all of the others. 
                      PART  III.


            MENTAL  DISEASES.




                     CHAPTER  I.

               CLASSIFICATION OF INSANITY.

  It may be justly regarded as an axiom that whenever great stress is
laid upon the classification of diseases the knowledge of those diseases
is as yet in its infancy.  In the older text-books upon insanity, there-
fore, much more attention was paid to the classification than to the
pathology and the clinical symptoms, and in  many of the  recent
ones this ill-omened  heirloom  of earlier times has been  thought to
be a matter of great importance.   In reality the classification of the
insanities is best made when the different types are simply catalogued.
Of what earthly consequence is the classification of the different forms
of disease that we have enumerated in the earlier portions of this
book,  such as locomotor ataxia, Huntington's chorea, acromegaly,
myxcedema, etc. ? and who would  think of troubling himself as to
whether locomotor ataxia should be classified among the spinal dis-
eases, or the cerebro-spinal, or the peripheral, when in reality it may
be any one of the  three ?   In the same way, what possible difference
does it make under what heading we put paranoia,  melancholia,
mania, delirium grave, or general paresis ?  The classification of in-
sanity, therefore, that I should adopt, would be the simple enumera-
tion of the different types, and the subtypes of each one of these.   My
classification, for the purposes at  least of the practising physician,  is
therefore contained in the table of contents.  I would like to impress
upou the readers of this book the folly of  attempting a classification
by mere symptoms, inasmuch  as the same symptom  may obtain in
different  types of insanity just  as the same symptom may be ob-
served in different types of all other diseases. 
CHAPTER  II.
      DELUSIONS, HALLUCINATIONS, AND ILLUSIONS.1

  There  are  three symptoms of the insane with which the general
practitioner should be familiar, namely, delusions, hallucinations, and
illusions.
  A delusion is a false belief.   It has sometimes been said that the
delusion or false belief of the insane differs from  the  false belief of
the sane in the fact  that the  former is  fixed  and not amenable to
reason.   This is a mistake.  The delusions of the insane are  often
not at all  fixed, but  fleeting,  and in a certain degree amenable  to
reason,  whilst the false beliefs of the sane are often fixed and not at
all  amenable to reason.  Indeed, what can be more fixed and less
amenable to reasou  than the beliefs  of sane  people about creeds,
politics, religion, matters of science, theology,  etc. ?  The only defi-
nition of an insane delusion is that it is a false  belief occurring in an
insane person.  Whether or not a  person is insane is a question of
diagnosis.
  An hallucination is an imperfect perception through  any one of
the different senses, and therefore hallucinations may be as various as
are the senses; so that, as there are the different senses of smell,  sight,
taste, hearing, touch,  pain, temperature,  muscular sense, the sexual
sensations, and the visceral  sensations, we may have  hallucinations
of all these.   Thus, a person  who imagines that he sees something,
or hears something, or tastes something, or feels something that he is
not seeing, hearing, tasting, or feeliug, has an hallucination.
  An  illusion is  a conversion  of  something  really perceived into
something  that is not perceived.  For instance, if one sees a table
before him and imagines it  to be an elephant, or hears a street-car
and imagines it to  be a cannon, he converts something real, the table
or street-car, into  something unreal, the  elephant or cannon, and he
has an illusion.
  If these hallucinations  or  illusions are believed  in, they are delu-
sive ; if not believed in,  they are non-delusive; so that we can have
delusive and non-delusive hallucinations aud illusions.
  It has been shown that many forms of insanity have  always the
same kind of delusion, so that it becomes one of the diagnostic  symp-
toms, and these  have been called  by Griesinger primordial  delu-
sions.   It is extremely  probable  that  the future will show that
each form  of insanity has its  primordial delusion, if it  has any at
all.   Thus, it is known at the present day that the primordial delu-

  i Delusion is derived from deludere, to cheat; hallucination, from alucinari, to wander in
mind ; and illusion, from illudere, to play with  anything; so it is very evident that the mod-
em technical meaning attached to these terms is not explained by their etymology. 
DELUSIONS, HALLUCINATIONS, AND ILLUSIONS.
sion  of paretic dementia is one of grandeur;  of paranoia, a com-
mingled delusion  of persecution aud self-exaltation ;  and of alcoholic
insanity, marital  infidelity.  Many forms of insanity have  also a
characteristic or primordial hallucination, so  that in mania the hal-
lucinations are genial  and exhilarating;  in  melancholia, terrifying
and  depressing; whilst iu  alcoholic insauity the hallucinations are
mainly auditory,  often startlingly so.
  Illusions  have not been so well studied as hallucinations, because
they are much more difficult of detection clinically.   If, for example,
a patient  speaks of having heard a cannon,  it  may  be very difficult
to ascertain that he has simply heard a street-car and supposed it to
be a  cannon; or if he complains of having seen an elephant, it may
be difficult to know that  he has merely seen a  table and imagined it
to be an elephant.  Several years ago I was  concerned in a will case
in which several days were wasted trying  to prove  that the testator
had  had illusions of smell.   He had  imagined that a certain closet
in his house had an offensive odor.   None of  the family or ser-
vants could  detect it.  A  plumber was sent for, but he  could  per-
ceive none.   The Board of Health was notified, sent two inspectors,
and  they could smell  nothing.  It was also  shown  that  there were
no pipes in  the closet or anywhere  in the adjoining wall or floors.
The  floor, however, was  taken up, and the  lath  and plaster of the
walls were removed,  and  nobody but the testator  during all  this
period could detect any odor.  Yet the  counsel upon the opposite
side  laughed the whole matter to  scorn, and contended simply that
the old man was  nervous.   The testimony of a rhinologist was in-
troduced to show that the testator had had no nasal disease capable of
causing the odor.  Aud yet the will of this old lunatic was admitted
to probate !
  The question whether  delusions and hallucinations are by them-
selves  evidence of insanity has been  much  discussed.   There is no
doubt, however, that they can both occur in persons who are sane.
Hallucinations especially are common  with those whose imagination
is artifically cultivated, as in poets and  novelists.  Dickens is said to
have wept over the death of Little Nell, aud was able to conjure up the
different characters in his novels to  his  mind's  eye as vividly as
if they had been existant.   Burns could never have written that vivid
account of the witches' orgie, in " Tam o'Shanter," without a mental
process that is identical with  what we call  an hallucination.   When
Shakespeare  causes Macbeth to fall  back  affrighted at the vision of
the  murdered Banquo, an hallucination of sight was pictured such
as might readily have  occurred in that age to an overwrought mind.
No great work of art, no great poem, no great drama, no great work
of fiction, can be written without an hallucinatory process going on
in the mind of  the writer  throughout  the work  of composition.
Milton's Paradise Lost and  Dante's Divina  Commedia are simply a
series of magnificent hallucinations of a healthy, great miud. A most
remarkable instance  of a  similar kind is  contained in the story of
Goethe encountering a vision of himself as  he rode to Rosenheim.
Because Constantine the Great saw the vision  of the Cross, because 
588                   MENTAL DISEASES.
Mahomet saw the heavens of the future Koran opening before him,
and because  other  enthusiasts have had hallucinations of sight and
hearing, it does not follow that they were insane.  Indeed, halluci-
nations can occur in  some conditions of simple overstrain, neuras-
thenia, and hysteria, although it must be admitted that they are rare,
and  that their  continuance would  be very ominous.   It is equally
certain  that  delusion,  accompanied  or  not  by  hallucinations, may
occur in  the  sane,  and of this we have confident proof in the belief
of the Highlanders of Scotland  in  the  so-called second  sight; i. e.,
the faculty of seeing upou the deathbed people who are destined to
die ; as well  as  in  the widespread belief in this country in the so-
called Spiritualism.  Every reader of this book is probably acquainted
with  perfectly sane people who are firm believers in the hallucina-
tions of hearing and sight of Spiritualism.   Hallucinations  and de-
lusions, therefore, are like other signs of disease—their  value must be
determined by accompanying symptoms.  An  hallucination or delu-
sion in a person who otherwise presents no evidence of lack of mental
health would be of  no importance unless there was a continuance of
it.  Medico-legally, delusions and hallucinations often become diffi-
cult to prove because of the  ignorance of juries and lawyers regard-
ing medical science.   In one case of mine, for example, it was shown
that a certain individual, wrho was on board a steamer plying between
New York and Cuba, came up to the captain when they were upward of
three hundred miles out in the Atlantic Ocean, and called his attention
to something that he thought he saw afar on the water.  The captain
could see nothing, but  my patient was so persistent that the captain
got his glass  and scanned the horizon carefully. Still he could see
nothing.  Then my patient broke out in a tone of anger :  " Don't
you see  those horses, aud that  brougham, and John," who was his
coachman, "sinkiug there into  the water?"   Although all  this oc-
curred, as I have said, three hundred miles out on the Atlantic Ocean,
an expert was found who was willing to testify that this was not an
hallucination,  notwithstanding  that  there were many other symp-
toms of mental impairment.   Certainly, it is not possible for human
testimony to produce any more conclusive evidence of an hallucina-
tion than was here afforded. 
CHAPTER   III.
                MORBID FEARS AND IMPULSES.

   There are certain morbid fears or conceptions, what the Germans
 call Zwangsvorstellungen, and  certain morbid impulses, which they
 call Zwangshandlungen, or imperative acts, that are  sometimes  classi-
 fied as neurasthenia, as has been done by the late George M. Beard,
 as well as  by his disciples in the  posthumous  literature  which he
 originated in foreign countries.  These are in exceptional cases con-
 joined with  insanity, but they are better considered, I think,  under
 the simple  heading of morbid  fears and impulses.   True neuras-
 thenia should be limited to the forms which  I have referred to  before
 (vide section on " Neurasthenia");  aud as most of these cases of mor-
 bid fears and impulses present no other mental symptoms, it  is  not
 warrantable to  class them as mental diseases.   The most common
 morbid fears are:  fear of places or  localities, and fear of pollution.
 Fear of places was first described  by Westphal under the name of
 agoraphobia.  G^lineau calls it kenophobia.   The name of claustro-
 phobia has been given by Arerger, of Milan, to a morbid fear of closed
 places.   These  individuals  have a great dread of  certain places,
 sometimes of a  large  place or hall, sometimes of  a bridge,  some-
 times of a ferryboat, etc.   A patient of mine came to me  one day,
 with horror depicted upon his  face, to state that  he  could uot go
 over the Brooklyn Bridge, or, indeed, over  any bridge at  all, or in
 any of the ferryboats.  After talking with him in  vain, and  ascer-
 taining in a quiet way that he was utterly unable  to control his
 morbid fear, I  simply told him to come to me on the following
 Sunday, only two days off, and I would treat him.   When he came
 I  had my carriage ready, got into  it with  him, and drove to  the
 Brooklyn Bridge.   There  I got out, took his arm, and told him  I
 proposed to walk across  with him.  I do  not think I have ever
 seen  a more marked picture of mental agony than was presented by
 this man, who almost sobbed as he begged me to desist.  I persisted,
 however, and walked across with him.   Then I turned around  and
 walked back with him with much  more ease.  I then drove to  one
 of the ferries, got  out, took my patient again  by the  arm, and crossed
 with him, having a milder repetition of the same mental agony ;  and
 after reaching the other side came back  on the same  boat.  I then
 said to  him that  he could now see  how groundless his fears were,
and that he ought to cross alone, which  he did.  I also advised him
 to  make it  his business to cross the  bridge and ferries two or  three
times every day, and to go out of his way to cross  any bridge that
he knew of,  and by this and other means (of which  I  shall  speak
when I come to the treatment) he was cured completely.  These cases 
590
MENTAL DISEASES.
must  be distinguished from the vertiginous sensations which some
people afflicted with  lithsemia or aural disease or refractive errors
experience  in  similar places.   The  fear of pollution was first de-
scribed  by LeGrande du Saulle, under  the  name of folly of doubt,
and later by William M. Hammond under the name of mysophobia.
Some authors  have  made a distinction between  Du  Saulle's cases
and those  of Hammond ; but I think they are both pseudo-insani-
ties of  doubt,  varying  simply- in the  clinical manifestations, and
I therefore believe that the name  given  by LeGrande du Saulle
is the best one—insanity of doubt, or folie de d.oute.  These patieuts
have a morbid doubt  about  everything  that they do.  One case  of
mine  would go out of a  door, close it, and then come back, uncertain
as to whether he had closed  it, close it again, go off a little way,
again feel uncertain as to whether he had closed it properly, go back
again, and  so on for many times.  Another patient washed her hands
innumerable times iu  the day, uncertain  as to whether she had really
got them clean, and it was a  case of this kind which caused Ham-
mond to coin the name  of mysophobia,  or  fear of pollution, as  his
patient claimed that she had such a fear.
  Morbid impulses are mainly acts which grow out of morbid fears,
and it is not necessary to go into them at length, as they  are largely
treated of in the chapters  upon sexual perversion and  the  different
insanities.  There are many which are scarcely worthy of classifica-
tion.  Thus there is an  impulse  to  set  fire  to things (pyromania);
an impulse to  collect pins ; an impulse to collect figures (arithmo-
mania); au impulse that Magnan has observed in certain old maids
who have a characteristic love for cats,  and to which he gives the
magnificent name of folie des  anti-vivisectionistes;  whilst  morbid
impulses to jump from great heights are very common, those of preg-
nant women are innumerable, and the ones which may come to different
persons at various times  are almost uncountable.  Most of these indi-
viduals have a neurotic predisposition, either personal or hereditary,
but it is exceptional to find in them any evidences of mental disease.
The medico-legal responsibility of these  individuals is a vexed ques-
tion.  Of course, it is possible, as we have  seen, that these morbid
fears  may  be so far beyond volitional control as to  render the
person irresponsible ;  but of this clear legal proof should be adduced,
because it is too often that a morbid  impulse of this kind is feigned
to cloak an  understood motive.    Thus, in  one case in which  I
acted  as expert on  behalf of a  county  not  far from New York, a
young girl  had set fire to her dwelling-house  in  such  a daugerous
manner that if the flame had not been  quickly discovered it would
probably have burned the building to the ground, together with sev-
eral  adjoining ones.   It was alleged that  she was suffering from
menstrual insanity, and that her prominent symptom was  pyromania.
There was not a single symptom of insanity adduced, however, either
before or  after the  act.   On  the  other hand, it was clearly shown
that this girl, who was extremely pretty, had  fallen  in  love with a
certain young man in the city of New" York; that  she  was in the
habit  of meeting and going to houses of assignation  with him; that 
MORBID FEARS AND IMPULSES.
591
 she had her goods insured for a sum which, though small, was large
 to her; and finally she confessed that she had set fire to her building
 in order to obtain enough money to  go  to New York and live with
 this young man.   The jury, sapient as  American  juries are and  as
 juries probably are all over  the  world, found  that she was'insane •
 but I was told that their real  reason in bringing in this verdict was
 that they thought the girl had already been punished enough •  that
 the confession had been wormed out of her by the arts of a profes-
 sional detective ;  and that the judge who was trying  the case was  so
 famous for his severe sentences that it was very probable he would
 sentence her to a year or more of imprisonment.  So they took the
 matter into their own hands.   This  was all very fine, of course, from
 an emotional standpoint, but it was nevertheless a travesty on science.
   The prognosis of these  cases of morbid  fears and  impulses  is
 usually excellent, with proper treatment.
   The treatment requires  considerable tact and judgment.  If the
 patient's general  health is in any  way depressed, this should be care-
 fully attended  to.  If the  morbid fears and  impulses occur at any
 time of functional disturbance, the disappearance of this  will prob-
 ably be sufficient to relieve  them.  Thus, cases that occur during
 menstruation  or  pregnancy need  no special treatment.  The young
 man  whose case I have detailed, and who had such a  morbid fear  of
 the bridges and ferries, was completely cured by placebos, suggestions,
 and being made to cross the bridges and ferries.  Curiously enough,
 several years after the time of which I  have spoken,  he came to me
 again with a return of his fears;  but as these were evidently caused
 by the impending death of his mother, I talked to him gently and
 kindly, gave him a placebo,  and after his  mother had died and he
 had returned to his normal condition, he had no further trouble.   I
 know of no medication by drugs that is of  the least value.  In  my
 opinion, suggestion is  the best method.   If any one  of my readers
 will carefully peruse  the section upon "Hypnotism," he will obtain
 some idea of the vast  power of hypnotism,  which is probably, as
 Bernheim claims, mainly psychical suggestion; and this principle of
 suggestion applied to these  morbid fears will often  work wonders.
 In  some  cases it will be well actually to hypnotize the person.  In
 many, however, it will not be necessary to do this.  Let  the  physi-
 cian  gain  the confidence  of the patient, talk to him gently and
 sympathizingly, use a placebo  in the way of a drug or some applica-
 tion  of electricity or the passage of a uterine or urethral  sound, and
 speak  very  confidently of the results  that will come.   Whatever
 suggestion  is made, either  with or without hypnotism, it  should be
 offered quietly and  unostentatiously.   It will sometimes be neces-
 sary  to take  women,  especially  young women, with or  without  a
 tendency to hysteria, away from  the environment  of well-disposed,
 sympathizing friends, whose judgment  cannot be trusted and who
 have  no  conception  of the  disease,  and place  them  in charge of  a
 trained nurse of tact and judgment.   Care must be taken, however,
that the nurse should be of kindred tastes and social  habits to that
of the patient, and the great mistake should never be made of placing 
592                   MENTAL DISEASES.
a coarse, illiterate nurse with a  refined and educated  woman, or
one who is a fool  with a  woman  whose  intellectual  capacity' is
high.   With men, however, aid can scarcely ever be obtained from
a nurse, partly because male nurses are not so well adapted  for the
treatment of nervous diseases as female nurses, and partly because
men are not so docile as women.  No case of this kind should ever
be sent to an  asylum unless  there are marked evidences of  mental
disease.  Even where there is a  tendency to suicide, this  can  be
guarded against quite as well  outside of an asylum as  in it, because
these  cases w7ould after a while be allowed almost as  much  liberty
in an  asylum as they would have at home.   Psychical  therapeutics,
in a  word, is of more value iu these cases  than visceral or vascular
therapeutics. 
CHAPTER  IV.
                     SEXUAL PERVERSION.

   To enumerate all the varieties  of sexual  perversion would  be to
 catalogue the  depths of intelligent human depravity ;  but there are
 certain well-marked types that are so frequently conjoined with mental
 disease or that are observed so often as to warrant a classification.
   Although these sexual perversions may be associated with insanity,
 their presence is not of itself evidence of the latter; indeed, it  may
 be said that there is no oue single symptom that is evidence of mental
 disease, any more than there is any one single symptom  that is evi-
 dence of other visceral disease.
   The main forms of sexual perversion may be thus enumerated :
       Masturbation;
       Sodomy;
       Anthropophagy;
       Necrophilism ;
       Homosexuality;
       Sexual hermaphrodism ;
       Masochism us;
       Sadismus;
       Erotic fetichism;
       Sexual metamorphosis.
   Masturbation is a very common  disease with boys, less common
 with girls.  Every large school, especially if it be a boarding-school,
 is apt to be a  hotbed of this sort  of thing  unless  the  discipline  is
 very thorough, and children teach  one another to indulge in it with-
 out the slightest inkling of the baneful effects.  The habit, however, is
 generally discontinued, I think, after adult age, and I should, therefore,
 be inclined to look upon its persistence then as a sign of true sexual
 perversion, whereas it  might have  been formed in  a child just as it
 would learn to walk in a peculiar way, or learn to talk in a peculiar
 way, or learn to do other things as it sees other people doing them at
 that imitative age.   That the habit is a baneful one there can be no
 question, but there may well be a  doubt whether  we know exactly
 the extent of its banefulness. It is one of the traditions of medicine
 hauded down for hundreds of years that a masturbator can be recog-
 nized by his furtive countenance,  by his tendency to introspection,
 and by his facies, which, like almost every other facies, is indescrib-
 able, but is soon recognized with a little experience.   I  believe that
 this description is often a good one of the manner of an  individual
 who thinks  that  his masturbation is a sin, and who therefore feels
ashamed  of it; but I do not think that the masturbator who is not
ashamed  of his habit  has  any such  hangdog look.  Any human
                               38 
594
MENTAL DISEASES.
being who does something that he knows  to  be wrong, or that he
thinks is wrong—whether it is really wrong or not makes very little
difference in its effect upon the mind so long as it is thought to be
wrong—wjH have a furtive countenance ; but I have very great doubt
whether there is anything  more peculiar about the countenance of a
masturbator than there is about the countenance of a burglar or a
smuggler or a counterfeiter or a confidence man.  The physical effects
of  masturbation are not  the  cause of the manner  of the facies.
There has been so much confusion of thought in this matter that very
vague assertions have been made which will not bear analysis.  Epi-
lepsy,  insanity, neurasthenia,  and a  host  of  other ills have  been
attributed to masturbation.  It is possible that the habit may some-
times act as a  predisposing or exciting cause of disease by an exces-
sive loss  of the seminal  fluid  if the masturbation be frequently
repeated ; but  I have seen  very few instances in which this causal re-
lationship was indicated, and I  have never yet seen  a case  of any
disease that has been directly caused in this manner.  I do not wish
to be understood, however, as saying that it is  not a habit extremely
deleterious to the general health ; but I wish to make it plain that its
effects are  more largely psychical than physical.  The insane are
very prone  to  masturbate.  In men this can, of course, be readily
detected.  In  women,  however, some skilful  observation may be
needed to ascertain  the fact, and in some cases  it will only be indi-
cated by a peculiar swaying of the body,  sometimes continued for
hours, an  adduction of  the thighs, and  an absent,  semi-ecstatic look
at times.
   Sodomy1 is a very common form of sexual perversion in our civil-
ized communities, much more so than is dreamed of by the general
public.   Every hotel superintendent and  every  police captain or
detective can verify this fact, and the individuals suffering from this
sexual perversion are a  source of great annoyance to the former.  I
am told by  those who are addicted to  this vice that they can go at
any time into one of the main thoroughfares of a city like New York
aud be certain of finding one or two fellow-spirits  in a distance of a
few blocks.  They recognize one another by peculiar and indescribable
signs and  gestures, and wThen I have  endeavored  to find out what
these were I have  been simply told that they cannot be  put into
words, but  that they are  such ordinary subtle signs as those by
which  it  is recognized that  a  woman is inclined  to flirt,  that
she is a street-walker, or that there is something suspicious about
her.  I have in my possession the diary of  a  male  patient who has
now reached middle age, aud who has been a sodomist since boyhood.
The autobiography is an  interesting one, and would read quite as
well as the autobiography of that other sexual  pervert, Jean Jacques
Rousseau. It tells, in words made vivid with delicate shades of emotion,
how one spring day he and a congenial companion wandered off to

 1 By sodomy I mean unnatural sexual intercourse between persons of the same sex.  Besti-
ality is t;,e intercourse of human beings with animals. Pederasty is sodomy with boys.
There has been  so much confusion in the use of these terms, especially in medical and law
works, that these distinctions should be made. 
SEN UAL PERVERSION.
595
the glades of the Park, how they mutually expressed their love, how
from time to time they penetrated deeper into the thickets away from
the gaze of man, and how finally, as the stars came out, they loitered
home in the twilight, hand-in-hand like Paul and Virginia, exchang-
ing gentle confidences.   This individual  came to me with the idea
that he might get rid of his sexual perversion.  He bowed sufficiently
to the conventionalities of the world to recognize that it was wise for
him to give up the habit, the more especially as an enemy had gotten
au inkling of the fact and forced him to  abandon a  certain  scheme.
But all the same he derived no pleasure from sexual intercourse in the
ordinary way.   The paederasty that is punished iu the State of New
York was praised  in  beautiful  sonnets by Hafiz, the Persian poet,
who  sings thrillingly  of  the charms of young boys, and, indeed,
more  than one revolution  occurred in  classic Athens from  sexual
passions of this kind.  These sodomists are divided into female aud
male, and  the one who acts as female always acts as female, while the
one who acts as male always acts as male too, for the reason, as they
tell me, that the one who  has become accustomed to the receptive
posture of the female  can  never derive any pleasure except in this
position, aud the same is true of the  one who takes the aggressive
attitude of the male.  It has seemed to me, too, that there is a differ-
ence  mentally between the males and the females of this sodomist
world, the males having  the virile  characteristics of males, whilst
the females are more effeminate and gentle.  I persuaded one of  my
sodomistic patients to  bring five or six of his  fellow-sodomists with
him to my office, aud  I was perfectly  amazed to  witness the shame-
lessness with which they answered questions  and went into details.
I firmly believe that iu every large city there is  a  large uumber of
individuals addicted to sodomy, and  who form, as  it were, a com-
munity apart.  I know of  no signs by which they can be recognized,
and  if I  were at liberty  to-morrow  to  tell the names of the life-
long sodomists that I  know iu and around New York, it would con-
stitute a chronique scandaleuse of the  most sensational kind.
   Anthropophagy is that variety of  sexual perversion which  is  ac-
companied by mutilation and cannabalism.  It is probable that  the
murders of  " Jack  the Ripper," which have excited  so much atten-
tion of late years in the Whitechapel  district of  London, have been
done by a  sexual pervert of this class, and that the mutilation of the
bodies was the regular gratification of a perverted sexual desire.   It
is  said that several of the Csesars took great pleasure in seeing virgins
slaughtered.  Some of these individuals will cut out certain organs,
as the genitalia  or the breasts, and  eat them, or drink the blood.
Sergeant  Bertrand  was a  celebrated  instance of  this form of sexual
perversion.  He would dig  up the bodies of young girls, cut them
open with  a sabre  or  pocket-knife, tear out the entrails, and theu
masturbate.  After a  while he  became indifferent to the sex of the
corpses, and he next  grew  accustomed to actual coitus with female
bodies.                                            .      .       ,
   Necrophilism is  that form of sexual perversion  in which dead
bodies are  dug up and violated. 
596
MENTAL DISEASES.
  Homosexuality is that form of sexual perversion iu which the in-
dividual conceives  a violent sexual passion for one of the same sex,
and  gratifies it either by sodomy, by titillation, or platonically.   A
curious book was written on this subject by a German officer of high
judicial standing named Ullrich,  in which this form of sexual love
was warmly defended, it being claimed that it was justified by natu-
ral laws, and he instances its occurrence in certain insects and among
certain  of the  ancient  nations.   These  individuals  were called
 Urninge.   Cases  of homosexuality are by no means infrequent.
Only a few years ago an instance of this  kind occurred in  Memphis,
Tennessee.  A young girl, Freda Ward,  had a  female friend  to
whom  she became very much attached.   They  had first met  at
school, and after leaving embraced every  opportunity  of meeting,
until attention was attracted to  the matter, and they were forbidden
to associate with each other. Upon this the sexual pervert murdered
her girl friend.  The murderess  gave as a reason that she had killed
her friend because she loved her and could not live without her; that
they were engaged to be  married, but that her wife to be had broken
the engagement, etc.  Her trial was  probably the  most remarkable
one  of the kind on record.  She bore herself calmly  throughout,
manifesting no realization of her crime.  When asked why  she had
killed her friend, she looked  hurt and surprised, and cried : " Be-
cause I loved her, of course !"  and burst into a flood of tears.  She
was  found to be insane.   On her way to the asylum she  was taken
to the grave of her friend, and displayed the extreme of grief.  I
have in my  case-book the history of a young girl  who  conceived a
violent affection for a nurse in a Pennsylvania so-called sanitarium.
This  nurse gave her massage,  and thus they  became acquainted.
Their intercourse  was by titillation of the vagina,  or rubbing their
naked bodies together.  Curiously enough, on the same day on which
the tragedy occurred in Memphis,  Tennessee, other murders occured
iu St. Louis and Mobile, respectively, from the same perverted sexual
passion.  In the former city a Dr. C. T.  Breedlove shot himself be-
cause his affection for Prof. Judson, one of  the teachers of the High
School, was not requited; whilst  in the latter city a negress named
Eleanor Richardson  slashed  her sweetheart,  Emmie Wilkinson,
another negress, because  the course of true  love had not  run smooth.
Adolphe Belot has lately written a curious novel upou this subject,
entitled Mademoiselle Girau—My  Wife.
  Sexual hermaphroditism is a  very rare condition, in which an in-
dividual at one period of life has the feelings and  sexual  desires  of
one sex and at another period of life has the sexual desires of the
other sex.   This may be conjoined with hermaphroditic  defects  or
not.
  By the term masochismus Krafft-Ebing designates a condition  of
sexual perversion iu which a member of one sex takes great  pleasure
in being dominated by  the other, so  that the male has a sensuous
feeling akin or almost akin to an orgasm in submitting to mortifying,
humiliating, and degrading acts from the female.   The  name comes
from  that  of the  writer, Sacher-Masoch, who  wrote a number  of 
SEXUAL PERVERSION.
597
 novels  upon this subject.  The well-known French author, Baude-
 laire, was  a sexual  pervert  of this class.  Zola has depicted some
 masochistic scenes in  his novels,  Nana and Eugene Rougon; and
 many of the newer Russian novels deal with similar matters. Krafft-
 Ebing  cites a  number of remarkable cases of this kind, and shows
 how Jean Jacques Rousseau  derived  voluptuous pleasure in receiv-
 ing blows  from  the hand of a certain  Mademoiselle  L. ; and so
 pleasant were they to him that his ingenuity was continually exerted
 in  provoking new punishment, aud this when  he was only a boy of
 eight years.  He says that to be at the knees of a mistress, to obey
 her orders, to ask  her pardon, was to him exceedingly sweet enjoy-
 ment.   Masochismus in the female is either a very rare affection, as
 Krafft-Ebing knew only  one case of it, or else the habitual  domination
 of  the female by the male would make it  difficult to observe.  And
 this difficulty would  be enhanced by the innate reticence of the female
 about sexual matters, at least to male physicians.
   Sadismus is the very opposite of masochismus, so that the member
 of  one sex  endeavors  to give pain and exercise force upon the other
 sex.^  The  term  comes from  the  Marquis de  Sade, whose obscene
 writings are well  known to those acquainted with French literature.
   Erotic fetichism  is  a  form  of sexual perversion in which sexual
 feelings are excited by  a species of fetich being made of some article
 of wearing apparel, a lock of  hair,  etc., belonging to one of the oppo-
 site sex.   Some obtain an orgasm by touching a piece of  a garment,
 or  a piece of silk or  velvet,  or stealing handkerchiefs, or shoes, or
 even  by cutting  off beads,  or by  throwing  vitriol  on  women's
 dresses, etc.
  Sexual  metamorphosis  consists  of having  the tastes and feelings
 and assuming the dress and habits of the opposite sex.  Spitzka cites
 the instance of Lord  Cornbury, a cousin of Queen Aune, son of
 Lord  Clarendon,  a  member of the House of Lords, one  time Gov-
 ernor of the colony of  New York, who used to dress himself up in
 feminine attire and promenade upon the Bowling Green,  as Spitzka
 graphically describes it, " with all the coquetry of a woman and the
 gestures of a courtesan."
  The treatment of these cases of sexual perversion is very difficult.
 Hypnotism has seemed to be sometimes of  value.  Eastman  has per-
 formed neurectomy of the pudic nerve  in a female with masturbation
aud effected  a cure.   If the individuals  afflicted are  young, proper
training and removal from vicious  companionship will be  sufficient;
but perverted adults  are difficult to deal with, unless some  effective
appeal can be made  to  their  common sense, or  unless their sexual
perversion is conjoined  with insanity. 
CHAPTER  V.
SIMULATION  OF INSANITY
  Many  words have been  wasted  upon the question as to how to
detect simulation of  insanity.   The  truth of the matter is  that such
Fig. 165.
Fig. 166.
Stupid melancholia.

    Fig. 167.
General paresis (maniacal stage).

        Fig. 168.
Simple melancholia.

     Fig. 169.
Melancholia attonita.

        Fig. 170.
General paresis (terminal stage).
Terminal dementia.
simulation  can only be detected by one who is acquainted, and thor-
oughly acquainted, with the different types of insanity, so that it can be 
SIMULATION OF INSANITY.
599
seen that the simulator is not giving an accurate picture of the form
that he is attempting to portray.  In many chronic cases of insanity,
and in  some of great intensity, the facial expression or facies is a
matter of great moment.  But this facies cannot  be represented  by
photographs.   Figs.  165-170 are portraits of different well-marked
cases  of insanity about which there has  never been a question, and
yet in some of them,  especially in Figs. 165, 166, and 167, it would
be difficult to detect that there was any mental aberratiou whatever. 
CHAPTER  VI.
               THE PATHOLOGY OF INSANITY.

  Unfortunately, at the present day our knowledge of the patho-
logical alterations in insanity is  in an embryonic state.  Of certain
of the insanities we  have excellent information, whilst of others we
have some glimmering of the facts, although of others still we must
be said to know nothing at all.  We  know moderately well, for in-
stance, the changes which take place in general paresis of the insane
in alcoholic insanity, in senile dementia, and in some of the terminal
dementias.  We are beginning  to know  something of the facts in
some cases of  epileptic  insanity, aud in most cases of syphilitic in-
sanity.   Finally, we know  nothing  at  all of  the textural  changes
which  are at  the bottom  of  most forms of mania, melancholia,
periodic insanity, paranoia, primary dementia, hallucinatory insanity,
or the insanities of pubescence or of  the puerperal condition.  It
will be my task to present in this chapter the general changes com-
mon to many  of the chronic forms, and then  describe those found in
the various  types in  the chapters dealing with the latter.
  The boues  of the skull  frequently present  no abnormality, but
when such are present  they generally consist of thickening or in-
creased density, or thinning.  When they are thickened, this may
be real or apparent,  in the former instance being due to  an increase
of rarefied diploe, in the latter case from increased thickness through-
out, as well as from subperiostitis.  When there is  increased den-
sity, this  may occur with or without thickening, and the  surfaces
may be eburnated.   In some exceptional cases the thinning may be
so extreme as  to render the  bone almost transparent.   In judging of
these conditions of the skull, however, one needs an accurate anatom-
ical knowledge, so as not to mistake normal conditions for abnormal
ones.   It is a  curious fact that different portions of the skull will be
found  to share alike  in these abnormal conditions;  thus, the left
frontal bone is often found to be thickened at the same time that the
right  occipital region is in the same condition.  Very  frequently
there is  found to  be some hyperostosis.   The subacute and inflam-
matory conditions are usually found in connection with increase in
thickness of the cranial bones, and senile atrophy is frequently asso-
ciated  with decrease  in thickness and density of the bones.
  In chronic  insanity the dura mater is frequently found to  be ad-
herent to the cranial bones,  and, exceptionally, bouy plates are found
in its folds.
  Thickening and opacities  of the pia and arachnoid are frequent in
the chronic insanities.  Care must be taken, however, not to confound 
THE PATHOLOGY OF INSANITY.
601
 this with the milkiness of the pia which is frequently found in the
 middle-aged and the aged.
   The normal cerebro-spinal fluid varies between two drachms and
 two ounces; but in the chronic insane it may be increased to eight or
 ten ounces, buoying up the soft membranes and soaking them. This
 abnormal cerebro-spinal fluid is acid in reaction, whilst normally it
 is alkaline.
   A frequent formation in insanities, especially of the chronic type, is
 the so-called arachnoid cyst.  There has been considerable difference
 of opinion in regard to the exact genesis of  these bodies.   Calmeil,
 Boyle, and Virchow have regarded them as  being due to an inflam-
 mation of the inner layer of the dura mater  and to pachymeningitis
 interna.   Bevan Lewis, on the other hand, maintains that they are
 of hemorrhagic  origin, stating as his reasons that these cysts  are
 readily removable, being but slightly adherent to the dura mater;  that
 in the majority of cases there is  no sign of  pachymeningitis, as the
 dura is not thickened, softened, or vascular, and there is no organic
 connection between  the cyst and the dura; that in the early stages
 they  seem to be  simple extravasations of  blood into the arachnoid
 cavity ; and, finally, that they coexist with  recognized vasomotor dis-
 turbances, as the othsematoma or insane ear.   Bevan Lewis believes
 that they are due to an extravasation from the vessels of the pia mater.
   The pia mater is frequently thickened, opaque, effused with lymph,
 and occasionally with pus, and frequently  there is a meningo-cere-
 britis, so that the pia is  adhereut and tears  away a  portion of the
 underlying cerebrum when it is  stripped off,  leaving an eroded  sur-
 face.   In the more recent adhesions the cortex is apt to be pinkish
 in color, either generally  or in limited areas,  whilst the pia is thick-
 ened,  its cells  proliferated,  its vessels tumid,  and  the overlying
 arachnoid  also  sharing  in the molecular  disturbance.   Numerous
 spider like cells are  found in the cortex immediately beneath the pia,
 in direct connection with its  cerebral surface and  with the vessels
 passing from it into the  cerebral  substance; and these spider-like
 cells  are  also found around the walls of  the bloodvessels.  When
 the adhesions are old there is a coarse fibrillar  connection between the
 pia and the cortex, and this takes the place of the normally delicate
 neuroglia.   That the spider-like cells are not found so frequently in
 advanced cases of insanity, such  as  senile  atrophy, is  supposed by
 Bevan Lewis to be due to the fact that they are comparatively early
 formations, having functions to perform, which, as we shall soon see,
 are not necessary in  advanced cerebral disease; whilst  in some cases
 they have succumbed to a fatty liquefaction.
   The vascularity of the cerebral substance, both gray aud white,
 varies very considerably in different forms of insanity, these variations
 probably being due not only to the particular form aud its mode of
 onset, but to  variable external factors.  In  some cases there is great
congestion, in others none at all.  In making  the post-mortem it should
 be remembered  that much will  depend upon whether  the  chest is
opened first or last, as in  the former case the blood draining off from
the thoracic vessels may very quickly make a great difference in the 
602
MENTAL DISEASES.
 vascularity of the cerebrum.  The increased vascularity is sometimes
 limited to certain areas mapped out by the nutrient arteries, and these
 are usually found either at the junction of the white and gray matter or
 also at the region of the fourth iayer of the pyramidal cells, this peculiar
 distribution  being probably' explained  by what  has been observed
 in  injections of  the cortex, viz, that the  long, straight vessels and
 their horizontal end-works at the border of the gray matter are most
 readilyr filled, next the  vascular  end-work around  the fourth  and
 fifth layers, and  lastly  the  vascular end-work  in the third and the
 first layers respectively7.  These limited mottlings  are  found in the
 more acute forms of insanity  or  where the patient has died in an
 epileptic status.  The mottlings are not necessarily pathological con-
 ditions, however, and in order that they should be so regarded there
 should be found with  them  minute extravasations of the small ves-
 sels, oedema of the tissues,  aud altered consistence of specific gravity,
 all of which should be evident  to  careful search with the naked eye,
 although, of course, microscopical  examination may disclose  disease
 which would not be otherwise visible.  An  ansemic conditiou of the
 cerebral substance is, however, most frequently found.  Thus, uniform
 pallor cases prevailed in 841 out of 1565, or in  53.7 per cent.   In
 melancholia, areas of pallor or diffused  pallor  are  not  infrequently
 found in  the cortex supplied by the carotid system, whilst there may-
 be  hypersemia in the area  of distribution  of the vertebral arteries.
 The most extreme forms of ansemia  are  found in  chronic phthisis,
 or as the  result of severe hemorrhage, as iu the post-partum  hemor-
 rhage ushering in puerperal insanity.
   Focal cerebritis, usually as the result of embolus  or thrombosis,  is
 commonly found in the insane, as is also chronic  meningo-cerebritis,
 but diffused cerebritis is very rare.  The tissue of cerebritis is  usually
 not discolored, but inflammatory exudates will be found, and granule-
 cells, nuclei, leucocytes, and  pigment, whilst the specific gravity will
 be increased.   Close to  such cerebritic  patches there is  frequently
 a white or yellow  softening of a  non-inflammatory nature,  due to
 plugging  of the  minute vessels or  to  the pressure of the oedematous
 tissue.  Iu most cases of insauity this cerebritis  is  due, as has been
 stated, to  vascular changes.   In general paralysis, however, the cere-
 britis spreads throughout the brain in areas that are not explained
 by any capillary distribution, in such a way as  to indicate that the
 lesion is due to cellular change, more  especially as the occipital con-
 volutions  are almost invariably spared, the changes being usually
 most marked iu the frontal  and parietal lobes.
  Softening frequently occurs ; thus, of 853 fatal  cases of insanity
 examined  by Bevan  Lewis, 45.7 per cent, presented brains that were
 of normal consistence or above  the usual  degree  of firmuess, whilst
 54.2  per  cent, were softeued, either as the result of disease or post-
 mortem change.  Aside, however, from any putrefactive alteration, a
 lessened consistence  of the  brain  is frequently found, although  it
 must  be  noted  that the cases  examined  have been  mainly those
of  senile  atrophy,  general paralysis, and organic  brain disease,
such as block the large asylums.  This lessened consistence is due  to 
                THE PATHOLOGY OF INSANITY.             603

oedema, structural  alterations  from senile fatty degeneratiou, wide-
spread  arterial disease, or inflammation.  At all events,  the  vas-
cular system  is almost invariably involved  in these cases.   Before,
however,  it  is determiued  that  the  brain   is lessened in consist-
ence,  great consideration  should be paid to  the following factors :
(1)  the length  of time after  death at  which  the post-mortem has
been made;  (2) the condition  of the temperature of the air; (3) the
general condition  of the  subject.  It is a  very difficult matter to
obtain firm brains iu our large cities  from the eleemosynary institu-
tions  filled with the  half-starved and  luckless outcasts of modern
civilization, and it is  especially difficult  to  obtain  them  in  warm
weather.  Thus,  the  brain  of the bomb-thrower who recently at-
tempted to kill Russell Sage with dynamite was in a firm state fifty-
three  hours  after  death, whilst  shortly afterward, in  the month of
April, when  the temperature for two or three  days had risen to 80°
and 85° in the shade, I examined a brain from one of the institutions
upon  Blackwell's Island, of a  man who had been apparently healthy
until  shortly7 before  his death, and found it so  soft as to make  it
useless for purposes of section.   In another  patient of mine consid-
erable medico-legal interest hinged upon the question as to whether
the brain  was pathologically softened, as I  thought it was, for the
patient was a young man of thirty who died suddenly from cerebral
syphilis in  very  cold weather,  in the month of January, and yet
only twenty-three  hours after death  the cerebrum was found to be
so  soft that  neither hemisphere could be  lifted by any large part
of it without the  dependent portions  slipping away.   When  there
are extreme degrees of softening, this  can  be  readily enough  deter-
mined, and oue of the best tests of this condition is to see whether
the brain-substance can be washed away by a gentle stream of water.
The localized softenings which are found in  insanity are very similar
to those which are found in  general  softening of the brain  (pages
306 and 307).
  Atrophy of the cerebral  gray and white  matter frequently occurs
after  the  acute insauities, and also in the chronic forms, and it  may-
be  either  general  or localized.   It may be  the result of an inflam-
matory process, from disease of the nutrient arteries, or it may be
due to non-inflammatory cellular alterations, as in epilepsy.
  Miliary sclerosis is a certain  change in the cerebrum about which
there  has been  great difference of opinion.   Many very competent
observers  believe that these  changes are artificial products, so-called
artefacts, whilst others  maintain that they  are genuine pathological
lesions, and among this latter number are Batty Tuke and Ruther-
ford, who first described it in  1868 ; Kesteveu, who wrote upon  it in
1869 ; and Bevan Lewis, who has given an  exceedingly minute and
elaborate account of it in his recent work. Lewis states that  this  con-
dition is found in perfectly fresh brains before any reagent has  been
applied.  I can confirm Lewis iu this latter observation, although I
am  not prepared to say that similar conditions may not be found in
brains that have been  preserved in alcohol.   The best description is
that of Bevan Lewis, just alluded to.   Miliary sclerosis is usually 
604
MENTAL DISEASES.
found in the white matter of the cerebrum, pons, and  medulla, and
the lateral columns of the spinal cord, and it  is best studied in the
latter site, although it is more often met with in the cerebral medulla.
On holding up a staiued  section to the light, little bright pellucid
points are seen scattered throughout it, just perceptible.to the naked
eye, aud they are also seen by reflected light, but not by direct trans-
mitted light.  A low power shows that each  of these consists of a
tabulated patch, some twenty to fifty millimetres in diameter.  In the
brain they are limited to  the white  medullated structure, abruptly
terminating as they approach the cortex, or, rarely, extending into
the lower zone of the gray matter.  The perivascular nuclei are
often  very7 greatly  proliferated, many granular  hsematoidin  masses
cover the sheath of the vessel, and at a certain stage there is  always
an increase  of the  spider-cells.  When present in the spinal  cord
miliary sclerosis becomes still more evident, and  in many cases  both
lateral columns are  filled with these minute bodies.  The latter con-
sist of colorless, translucent  patches  of molecular material,  with  a
stroma  of exceedingly delicate fibrils, and in  them  are  frequently
seen varicose medullated fibres, whilst they are  surrounded by scle-
rosed  tissue.   All the  medullated  fibres iu a line with the lesion are
markedly diseased, end directly in the lesion, and are often  regularly
moniliform, the medullary matter being  broken up into beads, or ir-
regularly varicose, or  it may lie  in  large pyriform masses, whilst
beyond the fibres often lie naked and swollen axis-cylinders.   Imme-
diately surrounding  these nerve-fibres are usually a large number of
spider-cells.  Tuke aud Rutherford had regarded these changes as
due to sclerosis, but the latter of these writers, after viewing Bevan
Lewis's sections in 1889, agreed with him  that  these changes were
due to a subacute inflammatory or degenerative change in the  medul-
lary nerve-tracts, at least in most cases.
  There are genuine forms of sclerosis  found in certain cases of in-
sanity, however, besides  the lesion which  is designated  as miliary
sclerosis.   Pozzi has  described a  form that  he calls  disseminated
atrophic granular sclerosis, in which he found symmetrical lesions in
the two hemispheres, particularly implicating the frontal and parietal
lobes  and the  paracentral lobule, and isolatedly in other parts of the
brain.  The convolutions were atrophied  and as if wormeaten and
granular.
  So-called colloid degeneration of the brain consists of certain round
or oval  bodies  from six  to twelve or  even forty millimetres in
diameter, often found in  the brain and spinal cord of the  insane in
great  numbers.  Like  miliary sclerosis, there is  a great difference of
opinion  as to whether these are artificial productions or genuine
lesions.   They are homogeneous, devoid of concentric  markings,
colorless and pellucid, slightly tinged by hsematoxylin, but unaffected
by carmine or aniline dyes,  and exhibiting no reaction to  iodine or
sulphuric acid.  They are seldom found in the  gray matter, and when
they are, it is only in the large medullated tracts, or, more rarely,
in the intracortical  arciform fibres.   They follow  the  course of the
medullated fibre, and the axis-cylinder  can often  be traced through 
THE PATHOLOGY OF INSANITY.
605
the centre of the swelling, or in other cases a pyriform body is pene-
trated by a swollen axis-cylinder, or, again, the medullated fibre may
seem to terminate within the swelling.  These bodies often have free
nuclei attached to them, which  seemingly come  from the spider-cell.
This colloid body  is attached to the medullated fibre, and  is not re-
movable like the miliary lesion, and under certain conditions  they
become opalescent  or granular,  swell  up, burst their  albuminous
sheaths, and swim around iu masses.  Bevan Lewis gives  the same
explanation of their origin as that which  he  offers  for miliary scle-
rosis.
   In insanity there is frequently a granular disintegration  of nerve-
cells, so that  they become  swollen and  more  spherical, lose their
homogeneity, and  show  granular formation, whilst the protoplasm
and  nucleus tint  but faintly with  carmine or aniline  dyes.   The
nucleus often  shares in  the degeneration, becoming  angular  or dis-
torted, whilst the ordinary pigment of the cell,  which is usually col-
lected  at  its base,  becomes diffused, and the cell takes on a  yellow
hue.  The lateral  processes aud the apex,  too, are affected, and
dwindle and disappear;  but, curiously enough,  the process  from the
base generally remains,  although it  may be swollen and without a
miliary sheath.  In  many cases, too, the cells are  totally disinte-
grated, their site being marked by a granular mass.  The bloodves-
sels  also partake of the  change.   The perivascular spaces become
enlarged with fatty granules and  deposits of hsematin, and the ves-
sels  are generally  atheromatous and covered  with fatty  granules.
The cerebral  parenchyma around  the cells and the vessels is, as a
rule, full  of fatty  granules.  The  first description of this  granular
degeneration was given by Major.  It is especially frequent iu senile
atrophy.
   Pigmentary or fuscous degeneration of the nerve-cells is frequently-
found in epileptic insanity and general paresis.   In order to estimate
this, however, an acquaintance is needed with  the  usual amount of
pigmentation  of the  nerve-cells, the gray matter of the brain and
spinal  cord.   A fresh  cell of the cortex, examined  in a section pre-
pared by the microtome, presents at one of the inferior angles or along
the base a small collection of golden-yellow pigment, from which a
number of dark amorphous granules are scattered; and, although this
pigment is surrounded by a protoplasm, it is  yet quite distinct from
the latter, and it often encircles the nucleus concentrically.  In  the
pathologically pigmented cell, however, the whole cell becomes tumid,
and  instead of being  elliptic, is of  pyriform  or spheroidal contour.
The pigment is greatly increased in  quantity.  The cell protoplasm
stains intensely with aniline blue-black, and, if subjected to this dye for
more than a very short period, the unpigmented protoplasm and the
nucleus become obscured.  At the same time  the pigmented portiou
is entirely unaffected by  aniline  or carmine dyes, and becomes  of a
bright yellow or brownish-yellow, and  has a rough, granular look.
The nucleus is deeply stained by the usual reagents.  As  the pigmen-
tary degeneration proceeds, other changes ensue.  The nucleus, prob-
ably from retraction of the unaffected protoplasm, is drawn toward 
606
MENTAL DISEASES.
the apex, or laterally, or even toward the base.   This nucleus  may
be  pigmented, but  it usually loses the oval contour and becomes
more or less irregularly  angular.  The staining by aniline may7 grow
to be less evident.   The lateral  process  may dwindle or disappear.
The pigmented area appears to be separated from the rest of the cell
by a capsule of more deeply stained material, aud at this  period there
may be one or more highly retractile spots in the nucleus.   Finally,
there is a general shrinking of the cell, or the cell may  be  filled by
a somewhat bright, translucent, colorless  material, its  outline  may
be so faint as  to cause it to  be easily overlooked, and vacuoles  may
appear.   The granular  pigment in  fresh  sections  is unaffected by
ether, alcohol, caustic soda, or fuming nitric acid.  When  the  cells
are well  advanced in degeneration,  this pigment may be decidedly
darkened with a  one per cent, solution  of osmic acid, and a small
portion of fatty matter may thus be evidenced.
  Bevan Lewis has called attention to au arrest  in development of
the nerve-cells in certain  cases  of epileptic idiocy and  imbecility,
especially in the second aud third  layers of the cortex.   These de-
generated cells are normal so far as regards contour and branching,
but degenerated by the granular, pigmentary, or  fatty conditions of
their  contents, and  they are completely unaffected by the staining
reagent employed.   That it is not a  retrogressive process is  main-
tained by Bevan Lewis,  because he thinks that if the granular,  pig-
mentary, or fatty condition were a  diseased process, this would be
progressive and  result in complete disintegration, and also because
the nucleus of these cells is usually displaced, so that instead of being
at the junction of the apex  process  of the cell, it is often  pressed and
flattened against the sides.
  The formation of vacuoles in nerve-cells is always associated with
granular  degeneration, although granular degeneration   may  exist
without vacuolation.   Vacuolated nerve-cells are met with  in senile
atrophy and in chrouic alcoholism.   The cell contains oval or sphe-
roid bodies, colorless and lustrous, highly refractile, unaffected by any
staining reagent, and  in some cases, when the  refractile quality is
wanting, the contents of the vacuole will be seen to have escaped by
rupture.  It has been suggested that this coudition of vacuolatiou is
due to  defective  oxidation, inasmuch as  it occurs in phosphorus-
poisoning, which induces a fatty degeneration from increased meta-
morphosis of albumin, but chiefly from interference with the oxidation
of the tissues through  destructiou of  the red blood-corpuscles.   The
experiments of Voit,  Bauer, Popow, Danilo, Kreyssig,  and Flesch
upon dogs and rabbits also  indicate that  phosphorus and arsenic pro-
duce a granular degeneration and  vacuolation of the ganglion-cells
of the spinal cord.   Flesch and  Trzebinski attribute the change to
the  reaction of chrome-preparations,  and the latter states  that the
lesion was never  observed  by him  in fresh preparations, although
Lewis flatly contradicts them both.   In some cases the nucleus alone
is vacuolated,  which occasionally occurs in the small, angular cells of
the second layer of the cortex, and in one case  sketched by Bevan
Lewis the change was so extensive that almost every cell was affected. 
THE PATHOLOGY OF INSANITY.
607
\Yhether it is important or not to make a distinction between vacuo-
latiou of the cell and vacuolation of the nucleus is at  present unde-
termined, but Bevan Lewis thinks that there is a difference in  the
pathogenesis of each lesion,  because he regards it as improbable that
defective oxidation  should affect only one layer of nerve-elements,
and  this the smallest, as it seemingly does  in vacuolation of  the
whole cell, so that  here  presumably the  cause is in some textural
change in the cell itself or its connections.
  Some  extremely  valuable  and interesting  observations upon  the
blood of the insane have been made by Macphail, and to this essay
the prize and the bronze medal of the Medico-Psychological Associa-
tion  of Great Britain were justly7 awarded in  1884.   Examining a
number of cases of general paralysis, epilepsy, dementia, and many-
unclassified  cases of insanity, he arrives at the conclusions that while
there is no evidence that ansemia in  itself is the  cause of  insanity,
yet an ansemic condition of  the blood is undoubtedly7 iu  many cases
intimately associated with mental disease ; that the blood in the de-
mented class of asylum patients is  deficient  in hsemoglobin and  in
hsemocytes, and that deterioration progresses  as age advances ;  that
the blood of patients known to be addicted to masturbation is dete-
riorated  in  a marked degree; that the blood is  below the normal
standard in general  paralysis, and  the deficiency is greater in  the
active and completely paralyzed stages of the disease than in the in-
tervening  periods  of inactivity and quiescence; while there  is a
deficiency in the quality of the blood of epileptics, the  decrease is
not  so pronounced as in ordinary demeuts  at the  same age;  that
prolonged and continued doses of bromide of potassium do not cause
deterioration in the quality  of the blood ; that prolonged attacks of
excitement have a deteriorating influence on the quality of the blood ;
and  that the blood of the average number of patients  on admission
is considerably below the normal standard.   He  also found that in
those who recovered  the quality of the  blood was improved during
residence in the asylum, and that on discharge it was not much below
the normal  standard. There was also a close connection between gain
in weight, improvement in the quality of the blood, and mental re-
covery ;  and while there was a definite improvement in the condition
of the blood during mental couvalesceuce in all cases, the  improve-
ment was both more pronounced and more rapid  in those who  had
had  tonic treatment.  He found four tonics to be most  efficacious,
either alone or in combination, in restoring the quality of the blood,
and  these were in order of their value :  iron and quinine, iron alone,
strychnine,  and malt-extract.   Arsenic was of little value as a blood
tonic in these cases, and quassia and cod-liver oil did not give satis-
factory results. 
CHAPTER   VII.
                        MELANCHOLIA.

  Definition.   Melancholia is a  form of insanity in which  there
is  a profound melancholy, the cerebral  reflexes are lessened and
attended with great mental  distress, aud there  is often a suicidal
impulse.
  Clinical History.   Melancholia may  be divided into  four
forms :
       1.  Simple melancholia;
       2.  Agitated melancholia, or melancholia agitata;
       3.  Hallucinatory melancholia ;
       4.  Melancholia with stupor.
  The simple form may, in its slighter degrees, bear an almost indis-
tinguishable  resemblance to  au ordinary depression of spirits, and
yet, even in the slighter cases, there is a peculiar visage of mingled
woe, shadowy mental dulness, and distrust, that is instantly detected
by  an experienced eye.  Relatives and  friends, so  intimately ac-
quainted with the patient as to be competent to notice  mental shades
of difference, will observe something wrong, although  they cannot
always define it.  Even  in these slighter degrees the mental reflexes
are attended with  mental pain ;  in  other words,  any  impression
coming to the cortex  from without is painful.  The sights, sounds,
and sensations that were wont to give  pleasure now cause pain.  Wife,
children, other relatives, friends, pleasant sights, harmonious sounds,
agreeable  odors, savory  savors—all produce  mental distress.   The
most  agreeable or mirthful object  cannot reach the  mind without
metamorphosis, in its passage through the  melancholiac  cortex, into
something mournful.   It is almost impossible, therefore, to make the
patient smile. There are certain symptoms of great  diagnostic value
in this simple melancholia, as I  have discovered, viz.: a peculiarity
of the melancholia, an obstinate insomnia, and  peculiar sensations
(to  which I have given the name of the post-cervical ache) in the back
of the head aud neck, or at the vertex, or up and  down the  spine.
With these I shall deal more in  detail a little further on.  Iu this
simple melancholia the  memory is usually maintained,  although at
the acme of the disease in some cases  there may be a  slight impair-
ment, so that the  events of this period are afterward remembered
mistily.  The reasoning  faculties, so far as the melancholia permits,
are usually intact, so that the patient  can  reason well enough except
as the painful mental reflexes warp the mind by converting all  sen-
sations into  painful ones    Simple melancholia is  usually without
hallucination or illusion, except in the most marked types, and even
then the hallucinations or illusions last only a short time. 
MELANCHOLIA.
609
  In hallucinatory melancholia  the  melancholy is  much  more  pro-
nounced.  The patient has, in addition to the painful mental reflexes
distressing hallucinations and illusions.  He lives in a realm of terror!
Not only does the diseased cortex make painful the myriad ordinary
sensations travelling in from the various sensory structures of the
body—retina, ear, tongue, nostrils, skin, mucous membrane, genitalia,
viscera—but it converts them into hallucinations and illusions of the
most terrifying character, and according to the degree of the melan-
choliac cortical transforming  power is the amount of mental distress
manifested by the patient.  Some break out with  occasional  excla-
mations of suppressed agony, as, " My God, I cauuot stand this any
longer."   Others  will tell you, with tears streaming down their

                              Fig. 171.
Melancholia agitata.
cheeks, that they  have committed the unpardonable sin, and  that
they are  damned  in the eyes  of God and  man.  Some will have
paroxysms of great distress.   Others will  be in constant agitation,
wringing  their hands,  praying,  beseeching, tears streaming down
their cheeks, incoherent, perhaps violent (melancholia agitata). (Fig.
171.)
  Melancholia with stupor is a form  in which the stupidity comes
early in the disease, and it is to be distinguished by this feature, as
well as by the degree of the melancholia, from the slight temporary
stupidity  which sometimes supervenes in convalescence from  the
other forms of insanity.  In this  form the patient  sits mute,  mo-
tionless, almost  expressionless (melancholia  attonita; angedonnerte
Melancholie of the Germans). , (Fig.  172.)  Occasionally there are
slight cataleptoid  symptoms.   The silence may at times be  broken
by some muttered expressions of mental distress.   When the patient
                              39 
610
MENTAL DISEASES.
is addressed, it is evident that he is confused mentally, and he will
look at  one with a bewildered expression.   Little as the face indi-
Melancholia attonita.
cates  it, however, these cases are tormented by the most frightful
mental  terrors, and the patients will  afterward speak  of this period
with  horror when they have retained memory of it.   Fortunately, 
MELANCHOLIA.
611
however, in this melancholia with stupidity, as well as in hallucina-
tory melancholia, the memory is generally impaired throughout the
worst periods of the disease.
  In any of these forms the patient may have certain vague distress-
ing sensations in the prsecordia, causing great fear, and  sometimes
productive of sudden outbreaks of violence.  (This is the so-called
prcecordial fear of the Germans.)  These sensations are probably
ordinary prsecordial sensations, as of palpitation from intestinal reflex
or functional cardiac trouble; and when we consider how apt they are
to cause alarm in the perfectly sane, we can imagine with what terror
they will inspire a melancholiac as they are transmitted to  his woe-
producing  cortex.  All cases subject to this prsecordial fear  are dan-
gerous.
  All these forms of melancholia have  certain peculiarities  in  com-
mon, namely :
       Suicidal tendencies;
       Violent outbreaks;
       Self-limiting or developmental tendencies;
       Occasionally prsecordial  fear.
  The slighter  the  melancholia, the  less will be the mental distress,
and, therefore, the less will be the suicidal tendency; but  even in
the slightest cases  these patients cannot be trusted, because a suicidal
impulse may develop suddenly, and it is  precisely in these milder
cases that the  most deliberate and carefully planned suicides occur.
A patient of this mild type, whom I saw many years  ago in consul-
tation, was regarded by his  family as entirely harmless, yet one day
when his daughter left  him for a moment to go  into an adjoining
room, he slipped out, walked over two miles  to  the  park, around
which he tramped for fully an hour, until he had selected,  with ex-
cellent judgment, about the most secluded spot in the  grounds, then
tore up his shirt, made a  rope of it, and hung himself to a branch
of  a tree.  Another patient, although occasionally  agitated,  was
thought to be so harmless that  former precautionary measures were
abandoned.  She had consented quite cheerfully to go  to an asylum,
as the  family means were limited, and had made  her  arrangements
quietly and docilely.  Just  before starting her mother attempted to
lecture her, in  a mild, motherly way,  upon the necessity of being
more cheerful, when she became greatly excited, suddenly drew out
a wisp of paper from her axilla, took the end of a match from under
her long  finger-nail, where she had secreted it, lit  the  paper, and set
fire to her  nightgown, sustaining a frightful burn  on the  thigh  and
abdomen.  Under proper treatment, however, this suicidal  impulse
soon disappears from the milder forms.
  Violent outbreaks of a homicidal nature are usually  only observed
in the graver forms, as  in  the agitated melancholia and the melan-
cholia with stupidity.
  The milder forms of melancholia can be distinguished from neur-
asthenia  by means  of the three symptoms to which  I have  called
attention, namely, the peculiar facies, the insomnia,  and the  post-
cervical ache.  The fades is something  that cannot be represented 
612
MENTAL DISEASES.
by a photograph, as I have already  said, because the very act of
consciously looking at an  object, as iu having a  photograph taken,
disturbs the slight unconscious  play of the muscles that makes the
expression.  In very marked cases of this form, however, the fades
will be so pronounced that it is apparent to anyone, as in a recent
well-known case that figured in the courts, in which the question of
shamming  was brought  up, and  concerning which  I was asked
whether it was not  possible for an actor  to assume  the patient's ex-
pression ; to which  my answer was that while an actor might assume
it for a  short period of time, it would be beyoud human powers of
imitation to continue it for days and weeks, much less months.  This
peculiar facies is made up of an expression of gloom and  suspicion.
The post-cervical ache is  the name which I have given to  a peculiar
complex of sensations that  these milder patients usually7 experience,
generally in the occiput and in the upper part of the neck, although
in exceptional cases the sensation may extend up to the vertex and
even over  to the brow, or in  the  other direction down  the whole
length of the spinal cord.   The sensation varies so from  patient to
patient that it is impossible to give  it  an accurate name, as one will
call it an ache, another a pain, or a thrilling sensation, or a frightened
feeling, or a creeping, or a throbbing, or an  uneasiness, and so on
through all the gamut of sensory perceptions.  In 175 cases  of this
disease which  I have examined all three symptoms were  present in
54 per cent., whilst in 18 per cent, the post-cervical ache was lacking
and the insomnia was absent in only ten cases.  The insomnia varies
greatly in degree.   In some cases it may be so great that the  patient
will only obtain an hour  or two of sleep for months, while in others
it may merely cut off half an hour of slumber, or  even occur from
time to  time, or for a short period at the onset.  Usually  it persists
for months after  the other symptoms have  disappeared, and if not
properly treated,  it may last for years; indeed, I attach so much  im-
portance to this symptom that I never consider a patient cured until
the tendency has been thoroughly eradicated.  In  some few happy
cases, however, it disappears with promptness, and  does not  return.
It has been objected to my discovery of these three symptoms  that
they are not always present, and that even if they are, one or more
of them are often found  in other mental diseases.  To the first ob-
jection I would answer that I have yet to see the first case of indubit-
able simple melancholia in  which two of these three symptoms have
not been present, and I think that  my  opportunities of seeing  such
cases are sufficient  to warrant me  in  attaching a value  to this fact.
In reply to the second objection, my critics do not seem to understand
the very simple  fact that I do not claim for these three  symptoms
separately the diagnostic value which  I do  claim for them when
grouped together.  We should  never forget that just as we have so
many letters in our alphabet, from which in varying combination are
formed the different words that constitute our language, so have we
so many symptoms in medicine which can be readily catalogued, and
from the varying combination  of which we  make our  diagnoses of
the different diseases ; and that just as the individual letter  is of small 
MELANCHOLIA.
613
importance, so is the individual symptom of relative insignificance.
In addition, it should not be forgotten that melancholia, the disease,
is not melancholy, the mood.
  These milder forms  of melancholia are self-limited, lasting from
three mouths in  the very mild cases that are properly treated, to
nine and twelve  months  or even longer in the severer cases, espe-
cially in those occurring in  elderly  and broken-down individuals.
All these forms of  melancholia have a slight developmental  ten-
dency, so that it is not always possible  to prognosticate the gravity
of the disease until it has been established  for several weeks.
  Causation.  The causes of melancholia are—
       Heredity;
       The emotions;
       Mental and physical overstrain ;
       Surgical operations ;
       Inanition ;
       Pelvic disease;
       Intestinal derangement;
       Febrile diseases;
       Parturition ;
       Derangement of abdominal viscera ;
       Diabetes.
  Although melancholia is sometimes of hereditary origin, it occurs
much more frequently without heredity ; and even in the cases where
there is heredity this may consist of melancholia itself, a predisposi-
tion to insanity, or a neurotic tendency.
  The emotions are, if I may judge by my own  experience, by far
the most frequent of all the causes of melancholia.   This is contrary
to the general belief,  which is that one of the diagnostic signs ot
melancholia is the causelessness of the melancholy; but I can confute
this with many cases from my case-book.   One of the most typical
cases that I ever saw was caused in a  mother  by the  death of  her
only  child, whilst  another followed directly upon the death of a
friend, another because of jealousy of her husband, and so on.
  Mental and physical  overstrain  is a frequent cause, and this fact
also contradicts the  belief in the causelessness of melancholia.   In-
deed, I think  that the two most frequent causes of this mental dis-
ease are mental and  physical  overstrain and the emotions.
  Surgical operations  occasionally cause melancholia.  I  have not,
however, thought  it proper to classify the cases of  melancholia  fol-
lowing operations in a  separate chapter, for they differ in no wise
from melancholia from  other causes.  It is a curious fact,  too, as I
shall have  occasion to  point out, that surgical operations will some-
times relieve melancholia.
  Inanition is a rare cause.
  Pelvic disease in the female is frequently causative of melancholia.
It is a great mistake, however, for  gynecologists to  assume, as they
so often do, that relief of pelvic lesions will of itself cure the melan-
cholia.  This  will sometimes happen, but it is much more frequently
the  case that the melancholia must  itself be treated, and it  will often 
614
MENTAL DISEASES.
disappear iu  spite of the persistence of the  pelvic lesion which has
been causative of it.
  Intestinal  derangement often causes melancholia; and the most
frequent of these intestinal lesions is a functional derangement of the
duodenal region or of the small intestine.   It is true of these causes,
as it  is of pelvic  lesion, that relief of them will generally not be
sufficient to disperse the melancholia.   I  made  many failures in my
earlier years  because of my belief that this type of melancholia could
be directly relieved by cure  of  the  intestinal  deraugement,  but a
wider experience has taught me to be very cautious in this matter.
  The febrile diseases will  sometime cause melancholia, too, but
more generally the post-febrile insanity is a  mild form of hallucina-
tory insanity or paranoia.
  Parturition not  infrequently causes melancholia.  It is absurd to
class the insanities following parturition under the  head of puerperal
insanities, for they differ in no wise from the same types of insanity
from other causes.
  Melancholia sometimes follows nephritis or diabetes, but rarely.
  These different  causes, however, are far more prone  to cause the
simple form than they are to  induce melancholia agitata and stupid
melancholia.
  Diagnosis.   The diagnosis is usually easy except at  the outset of
the mild cases, or at the period of a mild onset of the severe cases;
and it is just at  this time, especially in simple melancholia, that the
three symptoms  of the facies, insomnia, aud post-cervical ache are
of enormous  value,  together  with the  fact that in certain  cases
there is a slight  dulness of the cerebral reflex.  It is sometimes stated
that the fact of the melancholia having been  causeless is a diagnostic
symptom; but this is a  great mistake, because, as I have already
stated, melancholia, of  all  the mental  diseases, is  most prone  to
develop after a great emotional  shock, such  as  the loss of some one
very dear to  the patient, or  business reverses, or  some great cause
for  worry  and  anxiety.   But  even  in  these cases the  sadness  is
usually greater—is, so to speak, more morbid—than is warranted by
the cause.  In the severer cases the hallucinations, delusions, stupor,
cataleptoid symptoms,  agitations, prsecordial fear, and the  violent
outbreaks will make the diagnosis very certain.
  Melancholia is to be differentiated from—
       Sadness due to grief or anxiety ;
       The initial  depression of mania ;
       Hypochondria;
       Hysteria;
       Katatonia;
       Insanity of doubt;
       Periodical insanities;
       Primary  or secondary  dementia ;
       Eudarteritic insanity of middle life ;
       General paresis ;
       Grave brain-disease, such as  tumors, intracranial syphilis,
         disseminated sclerosis, and meningitis. 
MELANCHOLIA.
615
   Sadness from grief or anxiety seldom makes a patient so mechanical
and lethargic as does true melancholia.  Great shock of a mental nature
may stun  a patient for a certain period, but it will be usually succeeded
by a certain outbreak of tears or manifestation of grief, and about such
a person there is  not the quiet unreasoning melancholy of a melan-
choliac, nor is there apt to  be marked insomnia, and never any post-
cervical ache or the dull cerebral reflex.
   The initial impression of a mania is usually not  a true melan-
choly, but is of the nature of depression of spirits, such  as we con-
stantly see at the outbreak of some sickness, and  it differs entirely
from the facies and behavior of a melancholiac.  Besides, the super-
vention of mania, usually in a few days, will make the matter plain.
   A hypochondriac seeks relief, constantly talks about himself and
his woes,  and rushes from  physician  to physician; but the melan-
choliac is reserved, quiet,  asks for no treatment, and is frequently
very  much averse to it.
   Hysteria may simulate melancholia quite closely for the time being;
but the caprice in the symptoms, the other signs of hysteria, and the
overdoing, so to  speak,  of the simulation,  will make the diagnosis
easy to any good.observer  who has ever observed a melancholiac.
   Katatonia can  be readily differentiated by its commingled  symp-
toms of marked catalepsy aud great stupidity.
   The insanity of doubt   may  sometimes have  conjoined with it
slight melancholic tendencies,  but even then  the constant repetition
of certain vague fears that  nothing can satisfy, together with the ab-
sence of the facies, insomnia, and  post-cervical ache, will make the
diagnosis  plain.
   A periodical insanity can, of course, be only diagnosed when it has
returned once or  twice, but the circular  form, in which melancholia
immediately precedes mania, can  be  suspected from this very fact;
moreover, the melancholia  is not accompanied by the three symptoms
jnst spoken of, if I may judge by my  experience in a few cases.
   Primary and secondary dementia can be readily recognized  by the
silliness of the patient, either  coming primarily or being secondary
to some brain disease.   Insanity occurring  in  people of middle age,
usually associated with chronic endarteritis, cardiac hypertrophy, and
chronic interstitial  nephritis, is very seldom a true melancholia, but
usually consists of depression of spirits alternating with more or less
capricious  and confused acts, outbreaks of  temper,  and  eccentric
conduct.   ( Vide chapter on " Dementia.")
   General paresis of the insane, or paralytic dementia, is to be dis-
tinguished by the unequal pupils, the  lingual, facial, and  bodily
tremor, the extravagant delusions, the imperfect speech, and finally
the paretic symptoms.
   Any gross brain disease may  of course produce depression of spirits,
but it would  be  inexcusable  to  confound  this with a true melan-
cholia, and the symptoms of these gross brain diseases will be found
in their proper chapters  under  the head of" Tumors," " Intracranial
Syphilis," " Multiple Sclerosis," and  " Meningitis." 
616
MENTAL DISEASES.
  Prognosis.   Prognosis  is good  iu  simple  melancholia  and  in
the milder forms of hallucinatory melaucholia, except in the aged,
when it is usually exceedingly intractable.   It is doubtful in melan-
cholia with stupidity.   Melancholia agitata oocurring in slight de-
gree with simple melaucholia is of good prognosis,  although the
disease will be prolonged  by it.  When  it occurs alone, however,
and is severe from the start, it is of doubtful prognosis.  The dura-
tion of the disease varies from a  few7 weeks to two or three years, the
average being about nine months in the curable cases.
  Treatment.  All these cases of melancholia should  be isolated,
either in their own house or in an asylum.  It is a great mistake to
have them travel or force them to seek amusement, as is so often done
in the early  stages ; for these efforts at amusement are extremely
painful  to  the  patient  at this excitable though melancholy period,
whilst they may be beneficial in the later stages of convalescence,
when the painful mental  reflex has become much more healthy.
The simple form of melancholia  may be readily treated at home, in
a boarding-house, or a hotel, if proper watch can be kept upon the
patient, either by some member  of the family or by a  nurse.   This
is also true of the milder forms of hallucinatory melancholia, but the
severer cases of this form and most cases of melancholia with stu-
pidity are best treated in an  asylum, unless the means of the patients
are so ample  as to enable them  to employ one or two nurses for a
year or more.
  Opium is  the  best of all drugs  for the direct treatment of the
melancholia.    I use only the aqueous  extract of opium, made up
into carefully triturated tablets.   One-eighth of a grain is  taken once,
twice, or even  three times a day, according to the severity of the
melancholia and  the susceptibility of the patient.   Great care  must
be taken to have the opium pure.   It  must never be bought  hap-
hazard  in  the  shops, but  should  be obtained  from  some  reliable
source and then analyzed.   Morphine  will  sometimes answer the
purpose as well,  although  frequently it excites the  patient and con-
stipates, which  latter symptom is comparatively infrequent with the
opium.   To overcome the  restlessness that  is often so prominent a
feature, the bromides should  be employed, preferably of potash or
sodium, usually giving  from twenty to  thirty grains at  bedtime in
the milder cases, or oftener in the severer ones.
  The great  plague of the melancholiac is  insomnia, and to overcome
this the  following drugs may be hsed, the choice being indicated
by  the  order in which they are named : Sulphonal, chloralamid,
urethan, paraldehyde, chloral hydrate.  Of sulphonal the dose should
be thirty grains, repeating it in an hour if necessary.  It should be
finely powdered, as it is very insoluble  at the  best, and  given in a
cup of chocolate, milk,  or beef-tea an hour  before  bedtime.   But it
is best in the compressed tablets.  The dose of chloralamid  should
be  10 to  30 grains, in  the  form of compressed tablet or an elixir.
Urethan is very soluble, and can be given iu 10- to 20-grain doses.
Paraldehyde is best administered in a mixture, the dose being 1 to 2
drachms.   Chloral  hydrate is probably the best of all these  hyp- 
MELANCHOLIA.
617
 notics, but  is very apt to be depressing, and melancholiacs have a
 strong teudency to form  the chloral-habit.   The initial dose should
 never be beyond 10 grains, and it should only be repeated cautiously.
   In the form  of melancholia which  is caused  by  intestinal  de-
 rangement  the  latter  should  always  be carefully treated.   The
 best treatment  is usually the  dilute muriatic  acid, 20 drops  three
 times a day in a wineglass of water after meals, together with an
 occasional dose of calomel, 3 to 5 grains at bedtime, to be followed
 in  the  morning  by  a laxative, such  as  two teaspoonfuls of  the
 sulphate  of magnesia,  or a glass of Hunyadi or Rubinat. When
 this treatment has been continued for about a week, it will generally
 be  found  advantageous to give 2 grains of salol three times daily,
 one hour after meals, in the  form of tablet triturate, capsule, or a
 pill, together with 3  grains of a  reliable preparation of paucreatin.
 Constipation  should  be carefully overcome in this form by means of
 the aloetics and the laxatives which have been spoken of in Chapter
 IX., under " Neurasthenia."
   If the general health of  the patient is  depressed,  it should be
 carefully remedied by attention to the measures that have been ad-
 vocated under  " Neurasthenia ;" although rest is usually not at all
 applicable in  a  case  of melancholia, as  the  melancholiac is usually
 too restless to submit  to  it.   In all cases,  however, rigid  isolation
 of  the patient should  be maintained, for it  must  be remembered
 that these  melancholiacs  have, combined with  their  melancholia,
 a high degree of nervous irritability, so that I  have frequently seen
 relapses brought on by a  disregard of this precaution.   No attempt
 should ever be made  to amuse a melancholiac, for every well-mean-
 ing endeavor of  this  kind simply increases the nervous erethism and
 fails entirely of its effect.  Wherever it is possible  to  do so, I put
 patients of  this class  in charge of a trained nurse, because  they are
 more easily controlled by strangers than they  are by  their own
 family; besides which, it is almost impossible to make the family
 realize that a person who  can  converse  intelligently  and whose
 memory is so little impaired should not be made the recipient of all
 the little  carking cares that have no effect upon a well person but
 that simply aggravate the melancholia.  When a nurse is in charge
 of a patient the  family  should be excluded  entirely.   Indeed, in
 many cases  of pronounced melaucholia in which the family relations
 are sources of  worry and anxiety, I positively refuse to treat the
 patient unless this isolation can be obtained.
  These cases of melancholia, especially of the frequent simple type,
 are very prone to relapse, aud  they should be  carefully kept under
 treatment until this tendency has been obliterated.  Even  after this
 there will be a marked disposition to insomnia,  and the peculiar sen-
 sation to  which  I have given  the  name of the post-cervical  ache
 will continue for years.   The  tendency to insomnia  is always a
 source of anxiety to  me, but  the continuance  of the  post-cervical
 ache is a matter which I regard very lightly, and I always instruct
 my patients when they leave me to return promptly if the obstinate
insomnia should again supervene.  The post-cervical ache is often a 
618
MENTAL DISEASES.
very distressing symptom,  inasmuch  as the sensations, which  are
generally slight, may become actual pain at times.   For an exacerba-
tion of this post-cervical ache the best remedy is that  to which  my
attention has  been called  by Dr.  Bauduy, of St. Louis, namely,
phenacetine, 5 to 10 grains of which will often act like a charm.  I
am sorry to say, however, that the effect of this is only temporary.
A much more permanent effect upon the  ordinary less sensations
can be obtained by galvanization of the brain.  The current should
be  applied every day or every second day  in the manner that has
been described upon page 123, a current of 2 to 3 milliamperes being
used, this being continued at first for three minutes and afterward for
five.
  I desire also to impress upon my reader the necessity of not per-
mitting the  patient to know the nature  of the  medicines  that are
given.   It will be  very difficult  usually to prevent him from recog-
nizing  the  bromide of potash,  because  most intelligent people are
familiar with its  taste.  But  I never  give a  prescription to the
patient for  the opium and morphine or the hypnotics.  I send these
prescriptions myself  to the  pharmacist, mark them, " no copy or
repetition," and I  never deal with a pharmacist who will not respect
this injunction.  In the many cases, however, that I have  treated I
have never yet seen the habit formed of taking  these drugs.  At
first I  thought that this was due to my precautions, but I have since
come to believe that there is a curious law at  work in these indivduals
which  prevents the person who really needs  hypnotics from forming
the habit for them, just as the late Dr. Austin Flint used to say that
he had never seen  an inebriate made in his series of several hundred
cases by his constant habit of ordering large doses of alcoholic stim-
ulants  in tuberculosis.  Nevertheless, I would  again  strenuously
advise  the physician to take the precautions which I have  done.   I
do not believe that a single one of the  hundreds of patients whom I
have treated has the faintest idea of what medicines have been given
him.   They are  frequently very inquisitive, but I tell them bluntly
that, as they can  know nothing of the  action of drugs,  it is not
proper that  they should be informed, and I never have any further
trouble
  Melancholiac females are almost always worse  at the  time of the
menstrual period,  and its approach can generally  be detected by the
increased restlessness, deepened  melancholy,  and  disturbed  sleep of
the patient.   In all cases, therefore, the  patient should  be kept* in
bed as  much as possible until the menstrual flow has been well estab-
lished.   She should be watched very carefully at  this time, and in
some pases  the dose of medicine should be temporarily increased,
diminishing it again in a few days.
  Surgical  operations  upon the pelvic organs of the female, espe-
cially in cases where the melancholia has been seemingly caused by
lesion of these, will often have a remarkably beneficial effect if done
at the proper stage of the disease.   The patient should have entered
upon the stage of convalescence and the withdrawal of the medicines
should  have begun.  In some cases, too, a tardy convalescence will be 
MELANCHOLIA.
619
affected in a marvellous way for the better by au operation upon the
female pelvis even when there is no lesion of it; so that I often have
my gynecological friends operate upon some slight abrasion of the os,
curette the uterus, or do some minor operation iu these cases.  This
last observation, however, is more applicable to cases of insanity and
hallucinatory mania than to those of melancholia.
  The question of committal of a  case of melancholia is  often one
that involves a great responsibility.  My rule is never to  commit a
patient who can  be  treated at home, for I am  no believer in the
asylum treatment of curable  cases  of insanity.  In melancholia, as
well as in many other forms of mental  disease, the perceptions and
the memory are frequently unimpaired or but slightly affected, aud
the patient either has a full realization of the fact that he  or she is
in au  asylum, or they will in the course of time  awaken  to such a
realization.  The nurses of a lunatic asylum are never so efficient as
the trained nurses whom we are now fortunate in possessing iu such
numbers, nor are they  of as high a class in poiut of refinement and
education.   Even if they were, they are under no such stimulus or
oversight as wheu they are watched by the keen and anxious eyes of
an affectionate mother, daughter, relatives, or by an attending physi-
cian.   Besides, the convalescence  of patients in  a lunatic  asylum
simply brings them  face to face with what  is generally regarded—
whether justly or not—as oue of the horrors of life, namely, a luna-
tic asylum.   Then, too, however slight  their mental  affection may
have been, the fact that they have been  committed to  a lunatic asy-
lum clings to them  through life.   Like Lady Macbeth's  " damned
spot," that would  not out, it too frequently blasts their career, whilst
a severe attack of mental  disease treated at  home is lightly regarded
by the laity under some such soothing euphuism as brain fever.  Nor
do I believe that the stage of convalescence can fail to be retarded
by the constant contact with lunatics.  For all these reasons  I never
commit a patient to  an asylum, as I have said, if he  or she can be
treated at home.   The question of whether the latter can be  done
will be determined by  the degree of insanity, the probable duration
of it,  the environment of  the patient, and his or her circumstances. 
CHAPTER  VIII.
                            MANIA.

  Definition.   Mania is a form of insanity in which the cerebral
reflexes are increased and attended with great mental pleasure.
  Clinical History.  The prodromata of mania are vague and
indistinct, and consist of symptoms pointing to reflex cerebral irrita-
tion, such  as  restlessness,  vague forebodings,  eccentric  conduct  or
words, flushing or pallor of the face, disturbed  sleep, and depression
(not melancholia).   It is not  always easy to  distinguish these  pro-
dromal symptoms  from moodiness  or  depression  due to many ail-
ments, though generally something that is done or said will be so at
variance with  the  patient's character as to excite  the  suspicion of
some watchful female, wife, sweetheart, or mother, or even of some
intimate male friend or business associate.   The impressions of  such
witnesses, even  though they cannot always  bear radical  analysis,
should never be disregarded.
  The forms of  mania are—
       Simple mania;
       Hallucinatory  or delusional mania.
  In the simple  form of mania the patient talks, acts, and  feels like
a person  who is slightly under the influence of some stimulant.  The
mental operations are quickened, and they  are  pleasurable.  The
mental condition  is the very  antithesis  of that of melancholia, for
whilst  it is impossible  in the latter to excite  a pleasurable emotion,
it is almost  impossible to make  a  maniac melancholy.  To such a
patient the world seems roseate-hued.  He laughs, he jests,  he is pos-
sessed of an infinite good humor,  at the  same time that his remarks
and repartee are  smarter and clever than  is his  wont.   His physical
activity is also  increased, and he is restless.   Careful observation
will, however, make it very evident that  this increased  mental and
physical  activity is unreal.  A slight mental confusion  may be de-
tected.   The eye may have a dull and heavy expression, or there may
be a weary look, the face being oddly at variance with the pungent
promptness  of the conversation.   In this simple mania delusions,
illusions, and hallucinations are usually entirely absent, or slight; in
the  latter event  the patient  has  seemingly some vague, dimly per-
ceived  delusion or hallucination,  whose  unreality he himself recog-
nizes, or out of which he can be readily reasoned for the  time being.
  In hallucinatory or delusional mania the hallucinations and delu-
sions are not only much more marked, but the increase of mental and
physical activity is apt to  be greater, and the  patient becomes con-
fused and incoherent.   In the cases running a  subacute course  from
the  beginning, however, the incoherence and  mental confusion  may 
MANIA.
621
almost or entirely disappear, whilst the hallucinations and delusions
persist.
  Mania  may be  acute, subacute, or chronic.   The  acute  form is
generally one of great excitement.  The patient talks incessantly, and
is in incessant motion.   He  is seemingly violent, and may be pro-
voked by a trifle to the most outrageous  act.  His  cerebral reflexes
are enormously  exaggerated, but he is  not inherently  violent, and
can  be easily controlled by an  expert  attendant, differing in this
respect from  the patient with  the acute  delirium of alcoholism, of
gross brain disease, or of delirium grave.   The subacute type is that
usually assumed by simple mania.   The chronic form  is usually pre-
ceded by the acute, rarely by the subacute.
  The tendency of mania to develop is  slight.  Patients generally
show the worst of their complaint in the first week or two.
  Duration.   The duration of simple  mania under proper treat-
ment will be from  three to six  months, but  hallucinatory mania
usually lasts about eighteen months, and  sometimes for years.
  Causation.  The causes of mauia are  very much the same as
those of melaucholia, although the emotions, the intestinal derange-
ments, and diseases of the female pelvis do not play so prominent a
part.  Mental and physical  overstrain, febrile  diseases, parturition,
surgical  operations, and inanition are, however, of about the same
relative importance.
  Prognosis.   The prognosis is good in simple mania.   In all the
different forms the favorable factors are : subacuteness, moderate in-
crease of cerebral  reflexes, slightly defined  delusions and hallucina-
tions, and  a reasonable proportion between the delusions, hallucina-
tions, and  illusions and the mania.  Predisposition to insanity is not
by any means an unfavorable symptom.
  Diagnosis.   Mania is to be differentiated from—
       Toxic stimulation of alcohol, opium,  cocaine,  and can-
          nabis indica;
       Delirium grave;
       Meningitis, of traumatic, cerebro-spinal, or aural origin ;
       Pyeluria;
       Delirium from organic brain disease;
       Post-febrile  delirium from peritonitis, typhoid, typhus,
          scarlatina, rubeola, etc.;
       Epileptic insanity;
       Hysterical insanity;
       General paresis;
       Periodical  insanity.
  Toxic stimulation of  alcohol,  opium, cocaine, and cannabis indica
or hasheesh  should be  readily  differentiated by the  history of the
case.
  Delirium grave can be distinguished by the greater  violence of the
patient, alternating  with entire lucidity,  and by the ansesthesia and
self-mutilation that  so  often occur.  The delirium  of meningitis is
usually mild in  form, and attended by a hebetude not seen in mania,
besides which there  will be the  history of the trauma, or the symp- 
622
MENTAL  DISEASES.
toms of cerebro-spinal meningitis, or an aural trouble precedent to
the delirium.
   It will sometimes happen  that pyeluria will induce a vague, mild
mania,  which may be entirely misinterpreted if the urine is not  ex-
amined.  I have seen two such  cases for which the certificates were
filled out for committal  to  a lunatic asylum, but which recovered
under ordinary treatment of the pyeluria.
   The delirium of organic brain disease needs only to be alluded to.
   Hallucinatory insanity following peritonitis, typhoid fever, typhus
fever, scarlet fever, rubeola, etc.,  should  not be  confounded with
idiopathic  mania, as each has  an  entirely different  prognosis, and
the treatment is often very different.
   It not infrequently happens that the periodicity of the mania inci-
dental to a periodical insanity will be overlooked, and this should be
borne in mind in any case of mania.
   Epileptic and hysterical insanity need only to be mentioned.
   It is  possible that a general paresis may commence with symptoms
of acute mania, and  this should always be remembered.  It is often
impossible to make a diagnosis at first.  A tremor of the tongue and
facial muscles is often present in mania, and must not be confounded
with that which may take place in general paresis.   The safest rule
is to wait for the lapse of a  few weeks, and  then the persistency of
the facial and lingual tremor, a  remitting  irregularity of the pupil,
and  evident dementia, will make the diagnosis of general paresis ex-
tremely probable.
   Treatment.   The treatment of mania should be  by means of
the hydrobromate or hydrochlorate of hyoscine, bromide of potash,
hypnotics when necessary,  isolation, and  attention  to the general
health.
   The most effective drug at our disposal for controlling the restless-
ness  of  mania is the hydrobromate or hydrochlorate of hyoscine,
which has the great  advantage of not depressing, even when given
in large and  continued doses.  The dose at first should be y^-g- grain,
in the form of tablet triturate.   This should  be  given two or three
times a  day, or, if necessary, even every three or four hours.  Bro-
mide of potash, gr.  10  to 20, should be administered with it, the
dose  being given  two or three  times daily,  as  may be necessary.
Usually in these cases of mania  the insomnia is  not profound, and
can be met by the two drugs just mentioned and by attention to the
nutritiou.  If, however, it should be necessary to employ hypnotics,
the best is either sulphonal or chloralamid,  the former in doses of 10
to 20 grains at bedtime in tablet triturates or in  a powder given in
a cup of chocolate, beef-tea, or milk ; the latter in tablet triturate or
elixir.  If the patient should refuse to take medicines, they can  be
often given  in food.  The tablet  triturates of  hyoscine  made for
hypodermic purposes can  be readily dissolved in  milk or beef-tea.
The bromide of potash can  be sprinkled  over the  food just as ordi-
nary salt is.  The  hypnotics can  be dissolved in a cup of milk, beef-
tea, or cocoa.  Great attention should be paid in these cases of mania
to the condition  of  the general  health.  Abundance of nourishing 
MANIA.
623
food,  especially large quantities  of milk, should be regularly and
systematically given.   Alcoholic  stimulants in moderate  quantity
should also be employed, best in the form of milk punch or egg-
nog.  Sedulous  attention should  be paid to  the condition of the
bowels and skin.   These  cases should be rigidly isolated, and they
will always be best handled by trained nurses, for  the reason that,
like all the other insane, they are more controllable  by strangers
than by relatives.   It is  almost  impossible to obtain any degree  of
rest in mania  until the disease has been gotten well under control.
At this period, however, it is always well to insist upon  the patient
lying in bed  for at least  twelve  hours out of the twenty-four and
resting two or three hours during the afternoon.   The same  attention
should be paid to the menstrual period of women as has been advised
in "Melancholia," and the same considerations will obtain  about com-
mittal to a lunatic asylum. 
CHAPTER  IX.
                          KATATONIA.

  Definition.   Katatonia is a cerebral disease, with cyclical symp-
toms ranging in  succession from primary melancholia to mania, stu-
pidity, confusion, and dementia, one or more of these stages being
occasionally absent, whilst convulsive  aud  cataleptoid  symptoms
accompany the mental changes.
  History.   This remarkable disease, about which there has circled
a considerable warfare, was first described by Kahlbaum in 1874, and
to-day, twenty-one  years  afterward, alienists  are  hopelessly divided
in opinion as to whether the author's claims to have  discovered
a new clinical type are warranted or not.  As described by Kahl-
baum, katatonia is  a cyclical insanity, passing through five different
stages  respectively  of melancholia, mania, stupor, and  intellectual
feebleness, with  connected delusional conceptions  that are  slightly
logical,  often incoherent  (confusional  insanity),  and, last  of  all,
dementia.  Each stage is extremely variable in  duration,  and in
each  may be  observed   alternating  depression  and excitement.
Most frequently mania  follows  the initial melancholy, or  melan-
choly with stupor  may  take  the  place of mania, and  in cases of
this latter kind it  will be often found that  there has been mania
in preceding years.  It may happen  in rare instances that the melan-
cholia with stupor  is  the first stage, occurring most frequently after
violent  physical or mental  shocks, such as intense  fear, trauma-
tism, etc.   In other cases, after a stupor of short duration, there is
again a period of excitement or melancholy, which is again succeeded
by  the stupor, with or without mania.   Occasionally, in  the midst
of a long stage of  mania, lasting for a  week or a month, there will
be intermingled some days of stupor, or, more rarely still, the stupor
alternates with  a condition of confusional insanity.   The termina-
tions are in dementia, cure, or death.  The different stages of melan-
cholia, mania, stupor, intellectual enfeeblement, and dementia offer
nothing special in their symptoms; but the stage of exaltation, what-
ever it may be,  has certain characteristics, being either of the type of
melancholia agitata, or most violent excitement, or an insauity with
logical and fixed delusions that we  should nowadays  call paranoia.
There are other symptoms that  Kahlbaum  claims as  peculiar to
katatonia.  First, there  is a theatrical, so-called pathetic  manuer of
the patient, often as of a person declaiming, or of oue acting a tragical
or religious part, the  patient declaiming or reciting constantly, with
gesticulations, but  incoherent  in all that is  said.  Secondly, there
is a tendency  to the repetition of words and phrases without sense or
connection, but  pronounced as if the patient were speaking in public, 
KATATONIA.
625
 and to this symptom Kahlbaum has given the name of verbigeration.
 This verbigeration  may, in the course of the disease, pass gradually
 into  the  silly loquacity of the ordinary dement or the rapid succes-
 sion  of  ideas of mania.   Thirdly, there is often observed a  re-
 markable tendency to make use of diminutives, of  which, it may be
 remarked, in  passing, the German language contains a larger quantity
 than any other modern tongue.  With  these mental symptoms are
 associated certain marked physical ones.  Often in the stupor, less
 frequently in  the other stages, there is a cataleptic condition of the
 extremities, and convulsions are frequently observed of a choreiform,
 epileptiform, or tetaniform nature.   There is never  auy motor paral-
 ysis, but  occasionally some ansesthesia has  been  observed,  whether
 apparent  or real  is  a  question, and also frequently hyperesthesia,
 while localized occipital headache is said by Kahlbaum to be charac-
 teristic.   Among  other symptoms  of inferior diagnostic value that
 have been noted by Kahlbaum may be mentioned oedema of the lower
 extremities, occasionally of the lids, cutaneous desquamation,  ano-
 rexia, fetid breath, constipation, and chlorosis.  Phthsis  is very fre-
 quent in  this  disease, although Kahlbaum has found it rare in other
 forms of mental disorder, and it  is probably  for  this  reason that
 pneumonia is  more  frequent  in the fatal cases than it is in general
 paralysis.
   The list of  causes  that have been offered by Kahlbaum throws  no
 light upon the disease at all, and  consists only of such etiological
 factors as are found in almost every serious affection.   Kahlbaum
 claims that there have beeu epidemics of  katatonia,  and that the so-
 called convulsionnaires were katatoniacs; but as these mental or hys-
 terical epidemics are claimed by the votaries of so many other dis-
 eases, we  may well pass over  this assertion in silence.
   As regards  the pathology, Kahlbaum institutes a  comparison with
 general paralysis.   He  believes that in the onset there is  a condition
 of stasis  in all cerebral vessels, with  serous exudation, leading  to
 softening  of the  cerebral tissue without  retraction, but with forma-
 tion of exudations upon the interior surface and upon the membranes,
 particularly at the  base.   In the more advanced cases there are a
 retraction of tissue and  an organization of the exudates.   The arach-
 noid is always affected,  particularly where it stretches from the pons
 to the medulla oblongata behind the fourth ventricle, although the
 exudation  may  extend  along  this  same  membrane  upward to the
 fissure of Sylvius and  the second and third frontal convolutions,
 which Kahlbaum would have us regard as a possible explanation  of
 the mutism observed in the stage of stupor or of the verbigeration.
 Pulmonary and intestinal tuberculosis are very constant accompani-
 ments.
   Upon the publication of Kahlbaum's memoir, the question at once
 arose  as  to whether  a  new clinical entity had beeu discovered, or
 whether a  description had been given of  different forms of insanity
complicated with cataleptic and convulsive symptoms. Almost every
large  meeting  of alienists  in Germany has had  this question before
it  for solution, and  a formidable literature upon  this subject has
                                40 
626
MENTAL DISEASES.
 accumulated.   In support of Kahlbaum's claims are ranged Hecker,
 Brosius, Neisser, Schiile, and Neuendorf, in Germany; Etoc-Demazy,
 in France ; Spitzka, Hammond, and Kiernan, in America.   Those
 denying Kahlbaum's claims are Arndt, Westphal, Tigges, Von Rein-
 ecke, Krafft-Ebing, and Tamburini.  The  opponents of Kahlbaum
 maintain that there is no such form of disease as he describes under
 the  name of katatonia  or insanity of tension (Spannungs-Irresein),
 or that  the  main  symptoms are found in other forms of insanity.
 Fink  has reported three  cases  of  hebephrenia  closely resembling
 katatonia.  Krafft-Ebing  and  Ritti  range this disease under the
 head of circular insanity.  Tamburini has cited a number of cases
 of melancholia attonita  with  cataleptic symptoms; and a  large
 number of observations of melancholia with stupor complicated by
 cataleptic symptoms have been published  by Angelucci,  Wiggles-
 worth, Voisin,  and Wagner.   There can be no question that the
 somatic symptoms in katatonia,  upou which Kahlbaum lays so much
 stress, are found in many other forms of insanity,  and  hysterical
 neuro-muscular hyper-excitability is very frequent in catalepsy and
 in choreiform, tetaniform, and epileptiform convulsions.   Catalepsy-
 has  been described also by  Morel and S6glas in paranoiacs, imbe-
 ciles, epileptics, and in melancholia, with or without stupor.   Guis-
 lain  and  Morel had observed ecstasy in many diseases, particularly
 hysteria, long before Kahlbaum wrote; and  others have  seen it in
 melancholia,  in  circular insanity, in  alcoholic intoxication,  hypo-
 chondria, and mania.  Seglas  has  reported contracture in general
 paresis, whilst Knecht has observed a number of the other katatoniac
 symptoms in this latter disease, in which Sage has also noted chorei-
 form movements.   The  verbigeration  has been observed by Vogel-
 gesang and Jastrov/itz in general paralysis ; the stereotyped gestures
 by Brugia and Maezocchi in the same disease, with  or without
 delusion; aud Morel's celebrated gemisseur, or sigher, clasping his
 clothing convulsively with  his left hand, whilst his right  arm kept
 rhythmical time with his right foot  tapping the floor, was a nota-
 ble example of this kind of movement,  although he was evidently a
 case  of paranoia.   The eccentric and declamatory attitudes are ex-
 tremely frequent, as any alienist  knows, in many forms of  insanity.
   From all this it will be seen that the question is as yet under dis-
 cussion, and that only a very  small number of alienists  support the
 claims of  Kahlbaum.
  The treatment of katatonia is not understood, and therefor  a case
 that  seems to be of  this kind  should  be  treated upon the same prin-
ciples as those indicated in the sections respectively upou "Mania"
 and " Melancholia." 
CHAPTER   X.
                    PERIODICAL INSANITY.

   The laws  of periodicity  which  obtain  among all natural  phe-
nomena are, as we should naturally expect,  present as well in insan-
ity ; and to the oldest physicians certain periodicities were well known.
As far back  as 1791 Pinel  wrote upon  periodic  or intermittent
mania.  The alternations of chronic forms of insanity are every-day
matters to hospital attendants, so that orderlies are familiar with the
good  and bad days of patients ; whilst  every general practitioner
knows the periodical  influence of menstruation  upon mental char-
acteristics.   Indeed, it may be said  that  almost  all the phenomena
of health  and disease  have a periodicity that  is exemplified in sleep,
appetite, difference of feelings in the spring, autumn, and winter,
periodical returns of certain diseases such as dipsomania, malaria,
occasionally neuralgia, especially migraine;  and I have seen  as
marked periodicity in cases  of intracranial syphilis as in malaria.
It is  probable that the ancient  notion  of  the moon affecting  the
insane was due  to this  observance of periodicity  in mental dis-
orders,  so  that  from  this idea  may have been  derived  the term
lunacy;  but  the first account  of  periodical  insanity  as  a dis-
tinct  form of mental disease was given by  Falret and Baillarger in
1854.   Curiously enough,  by one  of those singular coincidences
which occur so often  in  the history of medicine, the description of
the same disease was given at the same time by two men, each seem-
ing to have  been perfectly honest in his  publication and without
knowledge of the other's researches.  Emmerich claims that Gries-
inger was the first  to  observe  this form of  insanity,  and that he de-
scribed it in his book in 1845 ; but  he gave it no name, speaking of
it merely in passing, so that the credit of the  discovery undoubtedly
belongs to the two Frenchmen.   Baillarger termed it folie a double
forme or formes alternes, whilst Falret denominated it  folie cir-
culate.   Baillarger again  refers to the subject  in 1880.  These
two authors describe a condition of mania followed by melancholia;
but there seems to have been some difference between the two as to
whether or not  there  was a  lucid  interval between the two condi-
tions, or whether the  melancholia immediately followed the mania.
However, it is undoubtedly true, as is said  by Falret's son, writing
in 1890, that  this  lucid interval may or may not be present.   The
essential distinction is  that these two conditions of mania  and mel-
ancholia respectively follow each other, and whether there is a lucid
interval or not is  immaterial.   The  different stages vary greatly,
from  months  to years, and  so may the  intervals, and even  in  the
same attack the different stages will  not  be  of corresponding length. 
628
MENTAL  DISEASES.
The Germans call  these cases  Zirkelwahnsin or zusammengersetzte
Psychosen, whilst they have been called by the French manie melan-
cholique.  Wittkowski described what he called recurrirende Manie
or recurrent mania, an  unfortunate  name, as it does uot serve the
purpose  of designating the  special  form  that he detailed, which
consisted of two attacks of mania separated by a lucid interval.  He
had seen only five cases among one thousand patients, aud  they
ran in this order :  1. Fifteen days of the first attack, thirty days
interval, thirty days  of the  second  attack.   2. Seven days of the
first attack, fourteen days interval, fifteen days of the second attack.
3. Four days of the  first  attack, about one month  lucid interval,
and  about five  weeks  of the second attack.   4. Nine days of the
first attack, thirty-one days lucid interval, eight days of the second
attack.   5.  Ten days of the first attack, eleven days lucid interval,
nine days  of the  second attack.   Recurring  attacks  of mania and
recurrent attacks of melancholia have been frequently described, but
of all the cases on  record none has been erected into distinct types
except those that  have been described by  Baillarger, Falret, and
Wittkowski.   Classifying  cases of  periodical insanity,  therefore,
we may say that there are :
       The circular insanity of Baillarger and Falret;
       The recurrent mania of  Wittkowski;
       Ordinary mania, or melancholia, with periodicity.
   Iu the circular insanity of Baillarger aud Falret neither the mania
nor the  melancholia  is typical, the mania being rather a condition
of excitation and  garrulousness of the degree that  constitutes high
spirits or that would denote great eccentricity, whilst the melancholia
is a condition of depression and low  spirits, and not of the anxiety,
restlessness, insomnia, post-cervical ache,  and  suicidal tendency of
true melancholia.   Some of  the cases of circular insanity  will  do
the most remarkable  things in the condition  of mania, perform the
most  eccentric acts, or manifest the  most erotic tendencies.  Thus,
one patient of mine always  became very restless, would  go out  on
the street and amuse himself  by  pitching  coins to  newsboys and
watching them scramble, was exceedingly gallant, and offered him-
self to a half-dozen women, telling the most marvellous Munchausen
yarns to blind their fancy, becoming witty, loquacious, and  absolutely
irrepressible.  Iu the melancholiac stage all  this is reversed, and the
patient becomes taciturn, sluggish in  movement, moping, inattentive,
listless.    The bodily  weight increases in  the stage  of  mania and
decreases in the  stage  of melancholia, and the appetite follows the
same law.   Indeed, all the  bodily functions are greatly increased in
the stage of mania and greatly depressed in the stage of melancholia,
so that the flushed  face and increased bodily heat of the former stage
merge into the cold extremities and waxy skin of the latter.  The
lucid interval of circular insanity, in my7 experience, is  not a true
lucid interval.  The patient is rather in a state of remission than of
absolute intermission, although the slight difference may only be seen
by one accustomed  to deal with cases of insanity, or by some intel- 
PERIODICAL  INSANITY.
629
 ligent member of the family who can  notice the difference in  men-
 tality.
   These cases of circular insanity are of very evil prognosis, so far as
 complete  cure of the malady is concerned,  although it is sometimes
 possible to cut short  a single attack.
   The recurrent  mania  of Wittowski is a very rare  disease, and I
 myself have  never  seen  a case of it.    All of Wittowski's  cases,
 however,  recovered, but he does not state whether  they had further
 recurrences of the trouble.
   Ordinary recurrent mania and  recurrent  melancholia will have a
 doubtful  prognosis, although not necessarily a hopeless one, and of
 these the  melancholias have the best prognosis.   Clouston is of the
 opinion that the periodicity of  mental  disease is one of the signs of
 an educated race that  is dying out, or, iu  other words, that perio-
 dicity occurs  mainly in what the French call the degenerated.   He
 observed  40 to 46 per cent, of the periodical  cases among 338 of
 various forms of insanity, and of these one-half had monthly period-
 ical changes,  one-third were somewhat irregularly seized,  and the
 remaining one-sixth were entirely irregular.
   Causation.   No  special cause has ever been determined for  peri-
 odical insanity, over  aud  above  the general causes of mental disease.
   Diagnosis.  There is  usually no difficulty in recognizing circular
 insanity with  its  successive stages  of  mania and  melancholia,  one
 either following the other or separated  by a  so-called lucid interval,
 nor should there be any difficulty iu recognizing Wittkowski's recur-
 rent mania, or the other forms of less sharply  marked  periodical
 insanity, when these diseases have gone through their different stages
 of development; but the danger usually is that they may not be
 recognized at the start,  or that some  other form of insanity  may-
 be mistaken for them.    The initial mania  of circular insanity has
 more of eccentricity and odd high spirits about it than are found in
 ordinary  mania;  and in the latter, delusions, hallucinations, and
 illusions are far more frequent, so that a gradually developing mania
 that is more like eccentricity than downright insanity should always
 put us on our guard.   The stage of melancholia following the mania
 is sometimes not recognized, because it is thought to be the necessary-
 depression which precedes convalescence  in  many acute or subacute
 insanities ; but the diagnosis of  periodical insanity should especiallv
 be  made  from  epileptic  insanity,  because as good an  observer as
 Doutrebente was deceived by a case  of  larvated epilepsy, and diag-
 nosed it as circular insanity.
   Treatment.  Some cases of periodical insanity, even of circular
 insanity, can  be very materially  benefited  by treatment  so far as
 regards the individual attack.  Thus, several  authors have spoken—
 and I have myself seen it do good—of the  excellent effect in  the
 mania  of  circular insanity, or in  the  recurrent  forms, of cannabis
indica, the tincture, in ni^xv-oj doses, as often as  may be necessary,
either two or three times a day, or every few hours.   To  this may-
be added with great benefit  the  bromide of potash  in drachm doses.
The sulphate of quinine in large doses, 10 to  60 grains a day, is also 
630
MENTAL DISEASES.
often of considerable benefit, and Baillarger has seen excellent effects
from its continued use for days in  these large doses.  I can confirm
this of my own experience, although I have sometimes had to admin-
ister the bromide of potash with it because of the cinchonism or the
general nervousness that it  induced.   Hyoscine, either the  hydro-
chlorate or the hydrobromate, is also an excellent remedy in doses of
jfa grain twice, thrice, or four  times a day.  The  stage of  melan-
cholia  cannot be treated  so well as the stage of mania;  indeed, I
think  that the treatment of periodical  insanity should be the vigor-
ous treatment of the stage  of mania  with the hope of cutting it
short.   The stage of melancholia can sometimes be  influenced, how-
ever, by the use of opium in the form of the aqueous extract, ^ grain
once, twice, or three times a day, or codeia, in conjunction with the
sulphate of strychnine, fa to fa grain, three times a day, or the sul-
phate  or tannate of quinine  in  tonic doses.  Both  of these  can  be
given  iu the form of tablet triturates;  aud if the patient refuses to
take medicine, the hypodermic  tablet  triturates can be dissolved in
food, such as milk, beef-tea,  or cocoa. 
CHAPTER  XI.
                    FUROR TRANSITORIUS.

  Definition.   Furor transitorius is an outbreak of violent fury,
lasting for a few hours, and terminating in deep sleep, from which the
patient awakes without the slightest memory of what has occurred ;
and never recurring in the same person.
  Clinical  History.  Transitory  fury  has occasionally  vague
and  short prodromal symptoms,  but these  are more frequently
entirely absent.   When they do  occur, they consist of restlessness,
irritability, flushed face, headache, or a sense of pressure and beating
in the head, vague general sensations, malaise, cardiac  irregularity,
vertigo, perspiration, and roaring in  the ears.  They usually last
only for a few minutes before the attack begins.  The onset of this
is sudden, and it is  characterized by  the blindest fury, the patient
smashing  articles of furniture and tearing his own clothes into bits,
at the same time that he howls or growls or murmurs inarticulately,
This attack may last a few minutes or a few hours, when the patient
suddenly becomes quiet, and passes into a deep sleep of hours' dura-
tion, from which  he awakens without the slightest memory of what
has taken place.
  Causation.  The causes of transitory furor are extremely uncer-
tain, but it has been known to occur after  mental or physical over-
exertion, in the puerperal  state, from rapid changes of temperature in
the room or the atmosphere, with indigestion and gastric disturbances,
and  also  from the inhalation of carbonic  acid gas from  an over-
heated stove.
  Diagnosis.   The diagnosis will be  principally from  trausitory
mania and epileptic mania, aud for this I would refer my readers to
the section on diagnosis in "Epileptic  Insanity."
  Prognosis.  The prognosis, so far as the recurrence of the attack
is concerned, is excellent,  because it has never been known to recur
in the same  person.
  Treatment.   Treatment can seldom be  brought to bear, because
the attack is over before the physician  has been called or, the patient
is so violent as  to  render it utterly  impossible to  administer any
medicine; whilst,  on the  other  hand,  it is  of course useless  to do
anything  when the patient has passed into the terminal  slumber.
In case of necessity, however, a hypodermic injection of fa  to fa
grain of Merck's hyoscyamine might be of excellent effect,  I should
think, although I have hitherto never had au opportunity  of essay-
ing it. 
CHAPTER  XII.
                     EPILEPTIC INSANITY'.

   Definition.   Epileptic  insanity is the  insanity  occurring iu
epileptic individuals before  the attacks,  during them, after them,
between them, or taking their place.
   History.   Although insanity in the epileptic has been known as
long as epilepsy itself, and although such  older writers as Esquirol,
Pinel, Brach, Garard, and  Hall, have  described  epileptic  insanity
with some degree of precision, it is yet true that the first really pre-
cise study  of the subject was made by Falret in  1861; but it was
not until 1875 that  the first exhaustive paper  appeared, by Samt;
whilst Hughlings-Jackson in the same year elucidated the matter
with a philosophic catholicity that needed  only fuller clinical detail
to have made it complete.   Since this time a number of writers have
busied themselves with this topic ;  but, with the exception of certain
medico-legal details, nothing has been added to the clinical disquisi-
tions of Falret and Samt.
   Clinical History.   Although Samt enthusiastically advanced
the claim that epileptic insanity had  certain features of its  own by
which it could be recognized without any history of antecedent epi-
lepsy in the patient, his views have yet  met with no  support from
alienists, and, highly desirable as it might be for  medico-legal con-
siderations to be able to diagnose epileptic insanity per se, the fact
still remains that this cannot be done, as in epileptics  the following
forms of mental disorder  have been described :
        Falret's intellectual petit mal and grand mal;
        Stupor, with or without verbigeration and alliteration ;
        Circular insanity;
        Paranoia ;
        So-called larvated  insanity, or insanity taking the place of the
         usual epileptic attacks;
        Chronic insanity;
        Dementia.
   In all these different types there are certain general characteristics,
which, together with  the history of the  epilepsy, serve to demarcate
epileptic insanities from the  non-epileptic varieties, although, as has
been said, they are not absolutely conclusive, merely serving as what
the lawyers call prima facie evidence;  i. e., evidence which points a
certain  way, but which other facts  must  coufirm or refute.   These
characteristics are : the epileptic facies  and character ;  a strong  ten-
dency to automatism, dreaminess, violent outbreaks, seemingly erratic
losses  of memory, and sudden recoveries.  The  epileptic facies is
difficult  to  describe, although it can usually be readily detected by 
EPILEPTIC INSANITY.
633
one accustomed to dealing with this class of patients; but, as nearly
as it can be put into words, it consists  of a  commingled suspicion,
slight dreaminess, and moroseuess.   The automatic acts of the epi-
leptic are akin to those of the somnambulist—indeed, often surpass-
ing those of the latter; and this fact is of very great medico-legal
importance.  I have known an epileptic to  roam  about the city for
days, seemingly acting with perfect intelligence, so that no suspicion
of his real condition was excited, and  yet returning to his normal
consciousness either without any- remembrance of where he had been
or what he had been doing during this  time, or with only fragmen-
tary recollection  of the period.   Many instances  of this  kind are
upon record.   Other epileptics may commit crime  with deliberation,
from motive and with cunning, and Echeverria  has  collected  many
such cases.  Most cases  of epileptic insanity will  have  a  period of
dreaminess in  some stage of the mental manifestations, usually in
conjunction with delusions, and with this is frequently associated the
condition for which Kahlbaum has suggested the name of verbigera-
tion; whilst sometimes a curious alliterative repetition of words is
observed, one patient thus repeating: " I have turn,  turn, turn, turn,
del, del, del, tumbled and delivered----."
   Violent outbreaks are  exceedingly common in the different  forms
of epileptic insauity, and it is an axiom with alienists that these cases
are, next to those of transitory fury, the most dangerous of all classes
of lunatics.  The losses  of memory in epileptic insanity are very
curious, and have led to some terrible mistakes medico-legally, having
been too often  misinterpreted in the courts.  The loss of memory
may be entire, partial, or complete for a time, with  entire restoration.
Thus, a patient may have absolutely no  remembrance of what he has
done at a certain  period when he had perhaps committed a crime, or
he may forget entirely for a time and then afterward have a complete
remembrance of the period, or he may  have only a  partial remem-
brance restored to him, or, what is still more confusing, his partial
or  entire restoration to memory may  again be lost.   Samt gives
some remarkable illustrations  of  these facts.   Another curious
characteristic of the epileptic memory is that a patient losing con-
sciousness  by becoming epileptic, from any of the  numerous causes,
may be deprived of  memory absolutely  for all that  has occurred
after  the loss  of consciousness, and then, coming to  himself, may-
have  his memory sharply resumed from the  time when he lost
it.  Thus, cases of petit mal may stop  in the middle of a sentence,
pass  through  their  attack,  and,  coming  to  themselves,  go on
with  the sentence from  the point where they  left  it off.  Hunter
McGuire, of Richmond,  Va., details a most remarkable case of this
sort, of a negro who  had been wounded in the battle of  Manassas
by a splinter of shell fracturing the  inner table of  the skull.  He
became an epileptic, and remained such for some ten years, when Dr.
McGuire operated upon him, removing the splintered inner  table,
and the  first words that he uttered on recovering from the ether were  :
"Where is the_____regiment?"  thus displaying the absolute lack
of memory for  everything that  had occurred from  the time of his 
634
MENTAL  DISEASES.
wounding.  Sudden recoveries often occur in epileptic insanity, so
that a patieut who has been violent and uncontrollable one day may
be perfectly rational upon the next.  This is a third fact of grand
medico-legal value.
  The iutellectual petit mal of Falret consists of confusion of ideas,
with instantaneous iustinctive acts that are often violent.  These cases
generally begin with sadness or  moroseness without cause, and then
become silent, irritable, and confused.   They are  semi-conscious, of
confused memory, and it is difficult  to enlist their  attention.   They
often  leave  home suddenly and wander aimlessly.   They  consider
themselves wretchedly unhappy, often think that they are persecuted
by their families or friends, and may accuse others  of being the cause
of their anxieties or their  torments.   Any dislike or hatred to an
individual which they may have had in their normal condition may
now become greatly aggravated, aud uuder the influence of some such
motive, or without  it, they may be  guilty of suicide or  some such
crime as theft, arson, or homicide, or may do some violent impulsive
act, such as butting their heads against the wall, smashing things, or
venting their rage upon some innocent individual.   After any one
of these violent acts the patient usually comes to himself, or this may
happen without any such precedent violence.  This condition of petit
mal varies in duration from  a few hours to several days, and may
recur  again  and  again.   The intellectual grand mal of Falret was
known to  the older French writers  as mania with fury (manie avec
fureur).  The onset is usually brusque, although  it may sometimes
have certain prodromata, such as cephalalgia,  vomiting, flushing of
the face, brilliancy of the eyes, alteration of the voice, slight convul-
sive movements of the  face  or  extremities, or sadness, irritability,
and slight excitation.  These prodromata last but a few hours.   An-
other  curious feature of this form is that one attack alway7s closely
resembles  every future attack in the same subject.  The mania is one
of the greatest violence and brutality, so that the patient is very de-
structive to anything and everything about him, at the same time
that he is possessed of terrifying and lively delusions  and marked
hallucinations of hearing, smell,  and especially  of sight.   The hallu-
cinations of sight are very generally of some red  color.   There is a
marked incoherence, however, in the delusions and hallucinations,
which  succeed one another with great  rapidity.  These attacks sel-
dom last more than a few days, and cease  as suddenly as they have
begun, the patients usually returning instantaneously to  their normal
condition,  although  sometimes  there  may be a  short  consecutive
period of slight stupor.  As has been well said by Falret, they awake
as from a  horrible nightmare.
  The stupor of the epileptic  is generally a dreamy, delirious condi-
tion, with occasional automatic acts of  violence, and with verbigera-
tion aud alliteration such as have been  already  spoken of.
  Circular insanity has also been described in epileptics ; but it is an
exceedingly  rare condition, and  many  cases of so-called circular in-
sanity in the epileptic have been  simply the intellectual grand mal of
Falret, succeeded by more profound  stupor than usual. 
EPILEPTIC INSANITY.
635
  Guauck  has observed a  spurious  form of  paranoia  to  occur  in
epileptics ;  but his cases and the few which I have seen should really
be called paranoioid insanity, inasmuch as they have a much shorter
duration than the ordinary cases of paranoia, whilst the ideas  of
persecution  and self-exaltation  are less defined than in the  latter
disease.
  The so-called larvated insanity of Morel was claimed by him to
be a form of epilepsy of the type of intellectual grand  mal, taking
the place of the regular epileptic paroxysms as a sort of equivalent.
Hughlings-Jackson, however, believes that all these are  preceded by
attacks of  ordinary  petit mal which  have been overlooked, and  he
cites cases to  prove  his  assertion.  It  should be  remembered that
petit mal may consist of merely so slight a loss of consciousness as to
constitute scarcely more than  a vertigo, either  without any muscular
movements, or with  very slight twitchings of  the  facial muscles, so
that an attack might very readily be overlooked even by the patient's
family7 or those  immediately surrounding him.  It is well to know,
however, that such cases of mania do occur in epilepsy, and that the
name of larvated or concealed in au excellent  oue, even  though they
are preceded by such slight attacks of petit mal.  These larvated attacks
of epileptic insanity are apt to recur periodically or quasi-periodi-
cally, and they have in several instances been mistaken for periodical
mania.
   Whilst most cases of epileptic insanity are temporary in duration,
varying from a few hours to a few days or weeks, the insanity may
also become chronic aud last for years.
   Dementia is the usual termination  of most cases of severe organic
epilepsy, or of  frequently recurring  different  forms of  epileptic in-
sanity ; but I think that the usual statements as to the  inevitable
tendency of cases of epilepsy to dementia are very much exaggerated.
As has been said in  the chapter upon " Epilepsy," epilepsy is only a
symptom,  and there are many forms which do not tend to true epi-
lepsy at all, such as  the nutritional, the laryngeal, the form associated
with migraine, and  many cases which recur infrequently.
   The medico-legal responsibility of the epileptic has been a question
about which a great deal of confused thinking has been  done.   It is
monstrous to assert  that a person is not responsible  for his or her
acts because he or she is subject to epilepsy.   On the  other hand, it
is equally monstrous to assert that an act done under the influence of
epilepsy should be punished by the law because there has  been evi-
dence  of deliberation and intelligence about it, or because it has been
done with  a motive.  The simple questions in  any given case are:
   1st.  Was the individual in question suffering from  some one of
the many forms of epileptic insanity? or,
   2d.  Had the individual in question had au epileptic attack at such
a time before or after the act committed as to render it probable that
he or she was at the time of the committal of the act under the influ-
ence of epilepsy?                   ,..-,,.       •   •      it
   In either one of these events the individual in question is  undoubt-
edly irresponsible, never mind how great may have been the seeming 
636
MENTAL DISEASES.
deliberation and  intelligence or  the  motive.   It should always be
remembered, as has  already beeu said, that the epileptic individual
may have the most curious  and  seemingly contradictory losses  of
memory, so that he may remember an  act immediately after it has
been committed, lose this memory later, and regain it still later on.
All epileptic criminals, however, are dangerous, and society should
be protected against them, not by their incarceration in a prison, but
by their isolation in au insane asylum.
  Causation.  The causes  of epileptic insanity are the causes of
epilepsy which have been narrated at length in the chapter upon that
subject.
  Diagnosis.   When  a patient has had an  attack  of epilepsy,
either of the type of petit mal  or  grand mal, and this  is succeeded
or preceded by mental  derangement, the  diagnosis is easy enough ;
but more care is required in  reaching a conclusion about the nature
of an insanity or a  criminal act  of  an individual who is  merely
known to be subject to epilepsy, but in whom the insanity or crimi-
nal act has  not  been  preceded  or succeeded  immediately by an
epileptic  manifestation.   In such a case the criteria  which  have
been mentioned will  become of great  diagnostic value, namely : the
epileptic  facies and character,  the tendency to  automatism, the
dreaminess,  the violent outbreaks, the seemingly  erratic losses  of
memory, and the sudden recoveries.   The claim made by7  Samt,
however, that mental aberrations with these characteristics  can be
positively diagnosed  as  epileptic, even though the patient has  had
no attack of petit or grand mal, has not been adopted by alienists in
the twenty-one years that have elapsed since  Samt's   publication,
for the very good reason that non-epileptic  insanities will sometimes,
though rarely, have these features.
  The diagnosis of epileptic insanity should be from—
       Transitory frenzy;
       Acute mania;
       Periodical insanity;
       Hallucinatory insanity;
       Paranoia.
  The patient subject to transitory frenzy has no epileptic manifes-
tations of any kind.   The attack has  never been known to  recur;
indeed, the individuals  subject to it rarely manifest any symptoms
of insanity at any other time in their life.
  The acute mania of the non-epileptic is far less violent, far less
characterized by  brutality,  and  much  more marked by rapid  and
changing  ideation, generally of a  beneficent character, so that when
any violence is done, it is because  of irritation or opposition,  whilst
the onset is not so apt to be sudden, and the convalescence is much
more gradual.
  Periodical insanity is sometimes mistaken for epileptic insanity;
but the diagnosis can be made by the  regular  recurrence without a
history of epilepsy,  the far less tendency to automatism and  vio-
lence, dreaminess, and loss of memory, and the alternation of mania
and  melancholia, with or without a so-called lucid interval  in the 
EPILEPTIC INSANITY.
637
form  known as  circular insanity.  On the other hand,  recurring
epileptic insanity should not be mistaken for periodical insanity, and
the diagnosis can be made by the absence of a history of epilepsy.
  In hallucinatory  insanity the  diagnosis will  be made by the pre-
dominance of the hallucinations  and delusions, and  by the lack of
the history of epilepsy and of the epileptic characteristics.
  Paranoia presents an entirely different picture from that of epilepsy,
although Gnauck has reported  so-called cases of paranoia in epilep-
tics ; but,  as has been said, they differ essentially from the true para-
noiacs, inasmuch as the  delusions of persecution and self-exaltation
are confused and intermingled with  the peculiar lapses of memory,
epilepsy, and the epileptic mental characteristics.
  Treatment.  The bromides do not have the same influence upon
the insane manifestions  of epilepsy as  they do upon  the non-insane
symptoms.  The best drug is usually hyoscine, the hydrobromate or
the hydrochlorate, in doses of jfa grain,  once in  one, two, or three
hours, best given hypodermically.  Cannabis indica  is also a very
useful medicine, and the best preparation to use is the fluid extract in
doses of 5 to 10 drops every  hour or two  until the sample has been
tested.  In some cases  the application of an ice-bag  to the  spinal
column for an hour or two  at  a time has broken short  an attack.
Occasionally brisk purgation with elaterium is of value, using doses
of I grain every two or three hours until the effect is obtained ;  or,
if the patient's  condition be such  that this may act as too much of a
depressant, a brisk saline  will answer the purpose.   I  have also
known  an attack to be broken  up by a powerful counter-irritant,
such as a  large blister somewhere about the body,  or the application
of the actual cautery to the back.  In the  more chronic  forms of
epileptic insanity cannabis indica, in combination with the bromides
(vide Chapter IX., under " Epilepsy"), will be found the best treatment. 
CHAPTER   XIII.
                      DELIRIUM GRAVE.

  Synonyms:  Mania gravis.   Phrenitis.  Typhomania.  Acute de-
lirium.
  Delirium grave is a very rare disease, characterized by furious out-
breaks of maniacal  excitement and violence, with intermissions.  The
patient is extremely7 incoherent, breaks, kicks, screams, talks inces-
santly, has hallucinations that are usually fixed and often very vivid,
and there is generally such ansesthesia that injuries are not felt, so
that one patient actually gnawed off an ungual phalanx of  a finger.
Great insomnia is usually present; the temperature ranges from 100°
to 103°, sometimes  even higher; the pulse is frequent and soft; and
there  is rapid emaciation.   To this excited period usually  succeeds
one of  depression,  almost of collapse, in which the patient lies
quiet, staring, muttering, mute, as  in  the terminal period  of acute
exhaustive diseases.  These conditions of excitement and  depres-
sion  may alternate, and in some cases the depression may not be
extreme, so that the patient may be aware of his condition.   The
disease almost always terminates fatally,  and when  recovery does
occur it is  incomplete, leaving some permanent aberration  of mind
or passing gradually on into general paresis or some form of dementia.
  In cases of delirium grave the pathological lesions are :  great cere-
bral  and  spinal hypersemia, often with oedema;  and  according to
Spitzka,  the cortical  ganglion-cells  are granular or  opaque,  stain
poorly, and their peri-ganglionic spaces, like the adventitial lymph-
sheaths, are literally crammed with the  formed elements of the blood.
This hypersemic  congestion has been  supposed to be due to a vaso-
motor paresis ; but  this, like  most of  the vasomotor theories, is the
purest kind of hypothesis.
  The diagnosis of  delirium grave should  be from—
       Acute mania ;
       Meningitis;
       Transitory furor;
       Agitated melancholia.
  In  acute mania the  patient does  not have  the ansesthesia, and is
not so wildly and uureasoniugly furious, nor has he the intermissions.
  In meningitis  the onset  is more  gradual, the  maniacal outbreaks
are not  nearly so furious, the  delirium is  more apt to be muttering
or mildly vivacious, and there is  often a  characteristic retraction of
the head.
  In  transitory frenzy the outbreak  is more sudden, more like an
epileptic attack, lasts only a few hours instead of a few weeks, and 
*
                       DELIRIUM GRAVE.                    639

the patient is perfectly himself again when  the  attack  is over; so
that there is no  similarity between this disease and delirium grave,
except in the one symptom of the  maniacal outbreak.
   Agitated  melancholia should never be  confounded with delirium
grave, because the agitation is  not a furious  maniacal outbreak, but
is a restless, impulsive act or series of acts in a very melancholy, de-
pressed, often suicidal individual.   I refer  to the differential diaguosis
in this place only because  I have seen several mistakes made.
   The prognosis of delirium grave is exceedingly grave, as there are
very few recorded cases that have not terminated fatally.
   The only treatment for  delirium grave that has been  of any use
has been that claimed by one writer, with  large doses of ergot, which
should be given in the form of the fluid extract, in doses of a drachm
every two hours.   Bromide of potash in  doses of 10 or 20 grains
should also be given every two or  three hours, with hydrobromate of
hyoscine, Tfa grain, at the same intervals during the excited stage.
During the  depressed  stage  the   bromide and hyoscine should be
omitted entirely. I  believe, also, from my experience in a few cases,
that large  doses of the sulphate  of  quinine will be found to be of
great value,  aud I  should  give 20  to  30 grains  iu the  twenty-four
hours, in the form of the tablet triturates or capsule, or, if the  patient
is averse to taking medicine, in solution with au acid ; or the  hydro-
chlorate of  quinine,  hypodermically, as  in  the  following solution
recommended by Hare:

       R.—Quin.  hydrochlorat.......gr. vij.
          Glycerinse      j.....^   f 3ss
          Aquae destillat.   j
    M. ft. sol.
    g.—Warm solution before using it, and do not add acid. 
CHAPTER  XIV.
                  HALLUCINATORY INSANITY.

   Synonyms: Primare Verriicktheit (Westphal).   Hallucinatorische
Verwirrtheit.  Mania Hallucinatoria (Mendel).   Delusional Stupor
(Newington).   Hallucinatorischer Wahnsinn.
   Definition.  Hallucinatory insanity is a form characterized by
quickly changing delusions, hallucinations, and illusions, with  con-
fusion of thought  and alternations of  excitement, depression, and
stupor.
   Clinical  History.   In  hallucinatory insanity  the  patient's
delusions, hallucinations, and illusions are constantly and quickly
changed, and they are sometimes  of a depressed or even terrifying
nature, sometimes gay, sometimes vague in character.   But the char-
acteristic of them  is  a  thronging ideation, so to speak, a constantly
changing  phantasmagoria  of mental  impressions, without logical
connecting link between them, and the delusions are not therefore
logical or  systematized.  The patient,  however, may be calm  and
seemingly  intelligent, although this  calmness  is very readily  dis-
turbed by the nature  of the  hallucinations, illusions, and delusions.
There is a  degree of intelligence, on the one hand, that is far greater
than is witnessed in mania; whilst, on the  other hand, the hallucina-
tions, illusions, and delusions are  infinitely more vivid and shifting
in character.   These  patients, when the disease  is not far advanced,
can give very- accurate and  vivid accounts of their hallucinations and
delusions, of which they retain an accurate memory; but in the severer
types of the disease  there are successive  conditions of excitement
and  stupor from  exhaustion  and speechlessness, and of these the
patient will often afterward have  extremely defective  memory.   In
some cases convulsions  may occur, although these are infrequent.
The convalescence is generally preceded by a mild form of dementia,
although the  patient may recover without this and  by a gradual
diminution of the other symptoms.
   Etiology.  The causes of hallucinatory insanity are—
       Neurasthenia;
       Ansemia;
       Alcoholic and  sexual excesses;
       Many febrile diseases;
       The puerperal condition.
   Much  has been  said of the  febrile  and  the  puerperal insanities,
but the most of them belong to this form, although  the puerperal
condition may produce  also a  pure melancholia  or a  pure mania.
Peritonitis  in the female is  especially apt to be followed by hallu-
cinatory insanity. 
HALL UCINA TOR Y INSANITY.
641
   Duration.   The average duration is five to six months, although
certain cases may run their course in a few days.  The post-febnle
and the menstrual are the shortest in duration, whilst the puerperal
cases  vary very greatly.
   Prognosis.   Prognosis is favorable, if the patients  can be sub-
jected to  proper treatment, and if it is commenced early enough.
Exhausted  individuals, however, or  those  who  have had  previous
attacks, may pass into dementia or die.
   Diagnosis.   The diagnosis of  hallucinatory insanity is from—
       Mania ;
       Melancholia;
       Paranoia;
       The mania of general paresis;
       Delirium tremens.
   In  mania the hallucinations, delusions, and illusions are not nearly
so prominent, the element of confusion is far less, and the latter does
not come  in spells lasting for hours or even a day or two, as in hal-
lucinatory insanity.
   Iu  melancholia there is profound  melancholy, stupor, or melan-
choly agitation, not the thronging ideation, hallucinations, illusions,
and delusions of hallucinatory insanity.
   Paranoia is  characterized  by logical delusions, great  intelligence,
and generally by calmness of manner; and confused hallucinations
and delusions are only present in the exacerbations.
   The mania of general  paresis can  be recognized by the history of
the case and by the accompanying  physical symptoms of tremor,
defective speech, perhaps also by the peculiar  gait, aud the pupillary
abnormalities.
   In  delirium tremens the history of the  case, the hallucinations of
sight  and  hearing, and often the  great excitement,  will make  the
diagnosis.
   Treatment.  The treatment of these cases of hallucinatory in-
sanity should be by means of chalybeates,  quinine, bitter tonics,
abundant  nourishment, and either  alcoholic stimulation  or  the  malt-
extracts.   Not one  grain  of a depressing remedy should be used
unless it is absolutely necessary.  It is my custom to see that these
patients obtain large quantities of food at once, which they especially
need  because of the impossibility in  most  cases of keeping them at
rest, even  in a chair or  on  a lounge.  I therefore satisfy myself
that they  really have three full meals a day, from one to two quarts
of milk in the twenty-four hours, and a pound of beef made into a
strong beef-tea and divided into three equal portions to be taken in
the twenty-four hours.  (Vide " Neurasthenia.")  A careful attention
should prevent these patients from becoming constipated, more espe-
cially  when taking large quantities of food.   The sleeplessness, which
is apt  to be an annoying feature, can be overcome  by means of a milk
punch or eggnog at bedtime.   If  this will not answer, 10 grains of
sulphonal  should be  administered, with  10  grains of  bromide of
potash, at  bedtime in beef-tea  or cocoa or  milk.  If, whilst taking
large quantities of food, the patient still remains excited and unruly,
                              41 
642
MENTAL DISEASES.
3-^5-  grain hydrochlorate or  hydrobromate  of hyoscine should be
given once or  twice a day, and continued, if necessary, day by day.
Hyoscyamine  is a dangerous drug to use in hallucinatory insanity
because of its depressing effect, and  it should therefore seldom be
administered unless the violence of the patient should make it neces-
sary, when grain ^fa of it should be combined with 10 to 15 grains
of potassium bromide, and increased  as circumstances may require.
Opium  in some cases will have a very beneficial effect, but it is an
extremely unreliable drug in this affection;  nevertheless every case
will be a guide to itself, and if the medicine  is not found to produce
improvement it should be dropped.   The aqueous extract is the best
preparation to use, and ^ grain may  be given once  or twice a day.
It is often extremely difficult to get these patients to take medicine,
through perversity or some delusion.  If this  be so, the soluble tritu-
rates of opium and hyoscyamine should be used ; and in giving iron
the carbonate of iron can be mixed with tea, beef-tea, cocoa, or gravy,
a drachm being given three times a day in  this manner, as it is nearly
tasteless.   Quinine and  the  bitter tonics are often very  difficult
indeed to administer, although the tannate of quinine will sometimes
be taken in the form of chocolate lozenges. 
CHAPTER   XV.
                          DEMENTIA.

  There has been considerable diversity of opinion among alienists
as to the clinical forms of dementia aud their prognosis.   Dementia
has come to mean technically the  same  thing as stupidity, and it is
called by this latter name by the French authors.  It may be clinic-
ally divided into two great  types,  namely :
       1.  Primary dementia;
       2.  Secondary dementia.
  The primary dementias may be due to exhaustion of the brain, to
psychical shock, and to mechanical shock.
  That which results from  exhaustion of the brain varies greatly in
degree.  It is what some authors term cerebral asthenia or neurasthenia.
In the slighter forms it may consist of a simple defect in memory show-
ing itself occasionally, and an inability to  concentrate the attention
upon mental problems.   Thus, the patient will find  that he cannot
remember names, events, or faces, aud that his brain refuses to func-
tionate in those delicate mental processes which we call thought.   He
may thus  read over and over again a page that he would ordinarily
have no difficulty whatever in mastering, and yet be unable to rise from
its perusal with a knowledge of what he has read, much less with a
mental assimilation of it.   It is the chronic analogue of what all feel
at times in moments of fatigue; but the  essential clinical difference is
that, while the mental effects of fatigue may be overcome by a sound
night's  sleep  or a few days of change, rest, or diversion, the case of
dementia is unaffected by these lighter remedial measures.  In types
of greater severity there is a tendency to automatic trains of thought
which cannot  be interrupted  by an effort of the will or by ordinary
diversity in the affairs of life.   In the gravest types the whole deli-
cate psychical mechanism of the mind beeomes disarranged, and this
manifests  itself in the emotions, the will-power, and the capacity for
thought.  The perceptions, however, in this form of dementia do_
not suffer in anything like the proportion of the other faculties of
the mind. This may at first sight seem singular,  but, after all,
it is only in  the line of what we know of the physiology of the
brain ; for instance, the experiments of  Miiuk, the German cerebral
physiologist,  have demonstrated again and again that  the exsection
of the auditory  centre from the  cortex of a dog does not impair at
all  the  animal's capacity for  hearing, but does away entirely with
his capacity to understand the  sounds that he hears clearly, as is
evident by the  motion of the head and  the pricking of the  ears.
(See page 40.)  After all, this  is  nothing  more than a singularly 
644
MENTAL  DISEASES.
 sharp demonstration of what, in a less definite way, has been known
 to generations of comparative anatomists—namely, that the cortex of
 the  brain  is the organ of the mind, aud that it takes what we call
 mental  cognizance of all the impressions coming to it from without.
   The  dementia resulting from mechanical or psychical shock is of
 sudden onset and is severe in its manifestations, so that  the patient's
 memory, thought, expression, emotions, and will-power  are often  as
 completely blotted out of existence as  by excision of the whole gray
 matter  of the brain.  Even these cases, however, if closely observed,
 will  be seen  to be receptive of sensations  in  a certain  dull and
 apathetic manner.
   Besides  these dementias from cerebral exhaustion and mechanical
 and psychical  shock, there are certain well-recognized  types which
 almost  all  the writers upon mental affections have been able to define,
 and these are worthy of separate description.   They are:
        1.  Primary, or acute dementia ;
        2.  Hebephrenia;
        3.  Senile dementia;
        4.  Paretic dementia.
   Paretic dementia is so thoroughly well marked as a form, is so well
 understood, and its prognosis aud treatment are so radically different,
 that I shall reserve a separate chapter for it; but the others can best
 be treated  in this connection.

                     PRIMARY  DEMENTIA.

   Synonyms:  Stuporous insanity.  Amentia.   Primary stupidity.
   Definition.  A simple dementia occurring in young adults.
   Clinical History.   This occurs  in young  persons,  as a rule
 under twenty-five years of age.  It is characterized by a high degree
 of stupidity, so that  the patient  does  not speak, makes very little
 volitional effort, cannot be interested in anything, and the  emotions
 are either absent or are manifested erratically.   These individuals sit
 quietly  and stupidly, and when they have convalesced it will be found
 that they have little or no memory of what has  taken  place.   The
 bodily functions are usually depressed,  the pulse is slow, the appetite
 is either lessened or not manifested  at all, although food will  be taken
 often in the same quantities as in health if persuasion be used, the
 action of the  heart is  greatly enfeebled, the temperature is slightly
 lowered, the skin is cold, and oedema of the lower extremities is not
 infrequently observed.   Ptyalism is a frequent symptom.
  Causation.  The causes of primary dementia are :
        1. Heredity;
        2. Masturbation ;
        3. Venereal excesses;
       4. Ansemia;
       5. Overexertion of mind.
  Of all these causes, the only one that  needs to be dilated upon  is
the last—that of mental overexertion.   This, in  my experience, has
been the most frequent  etiological  factor, and, singularly enough, the 
DEMENTIA.
645
majority of cases have been in the male sex, although I am not cer-
tain whether  or not this is a coincidence.   The  mental overexertion
that I have seen has been that of overstudy, either actual or relative.
Ambitious  boys and girls  are set to work to accomplish tasks that
are frequently beyond their power; or even when their mental reach
might  be  sufficient, the regulation of the habits  is so faulty as to
disable them  prematurely by lack  of proper fresh air, exercise, diver-
sion, and  regular  and  systematic habits of study.  In some cases
ansemia has also been  an aggravating factor, but it is a curious fact
that this has  been the exception to the rule, and that while ansemia
is  rich in its pathological effects  in  other directions, it seems to  be
peculiarly infrequent as a cause of this mental type; indeed, most of
the patients of this class are, so far as regards other  than the cerebral
tissues, in good health.
  Prognosis.  The prognosis of primary dementia is usually a good
one, as most of the cases  recover  in  from one to three months, and
some may  even terminate  more quickly.   In  the  infrequent cases
that do not  recover, the primary exhaustion has  either been very
severe,  or there is improper treatment.  Unfavorable cases pass into
a condition of prolonged dementia.
                         HEBEPHRENIA.

   Hebephrenia, or insanity of pubescence, is a mental disease ob-
 served more particularly in the male sex, characterized by a mawkish
 silliness with a tinge of melancholia.   These cases are apt  to be con-
 founded with  hysteria, and they stand upon the border-line in many
 instances  between  insauity and neurasthenia, although  sometimes
 they may become so well marked as to constitute a genuine insanity.
 They are actuated  by silly  semi-delusions,  a mawkish  sentimen-
 tality, caprice, sadness that is not  a  true  melancholia, or  silly out-
 bursts  of hilarity  that are temporary.   In  the lighter  cases  the
 impairment of reasoning power, judgment, and perception is slight,
 but in the graver ones these faculties  may  be markedly impaired.
   Hebephrenia is easily distinguished from mania, melancholia, in-
 sanity, or primary dementia.   It has not the true, continuous,  intelli-
 gent sadness of melancholia, nor the post-cervical ache or insomnia ;
 nor the continuous flow of ideas and  hallucinations and  hilarious
 delusions of mania, nor the restlessness;  nor  the continuous sedate
 silliness constituting  true  dementia; nor  the period  of continuous
 hilarity and good-natured  flow of ideas  and accentuation  of all the
 physical  and  mental faculties of the maniacal stage  in circular in-
 sanity, nor the passage from  this mania into the continuous melan-
 choly or  depressed  condition  which is the second  phase of circular
 insauity.
  The  prognosis of hebephrenia is  good  in  the  slight cases,  but
 unfavorable in the severe ones in the fact that it is apt to be very
protracted. 
646
MENTAL DISEASES.
                      SENILE DEMENTIA.

  At the outset it must be distinctly understood that senile dementia
is something far above mere senility,  being a mental condition that
is clinically demonstrative of well-recognized pathological  lesions.
The mental picture is distinctly one of dementia or stupidity, and it
is not precise to classify under this heading those cases of melancholia
which occur in the aged, the more especially as they have an entirely
different prognosis.   The  mind in its entirety suffers, presenting in
one patient certain symptoms of the mental impairment, in another
another, and in a third a different group; but  however great the
variations may be from case to  case, through them all runs,  to an
expert eye, the unmistakable element of the  dementia or stupidity.
It may be slight or evanescent; but it is there if the history can be
fully obtained.   The judgment, the memory, the emotions, the sen-
sations,  one or more or all  become affected ; but  the clinical demon-
stration of the  impairment may be a shifting one.  To these mental
symptoms may be added paralysis in varying forms.  Cases of senile
dementia may therefore be divided into two  great groups, namely:
Mental  symptoms alone,  and those  which have an admixture of
mental and physical  symptoms.
  In the first group the memory is peculiarly apt to be affected.  A
sharp distinction, however, must be made between the impairment of
memory which occurs in an aged person and the abnormal loss of it
in one who is afflicted with  senile  dementia.   The  characteristic of
the normal senile memory is that it becomes weak for recent events,
whilst it may remain unimpaired for those of the past.  In senile de-
mentia,  however, this loss of memory of recent events becomes
much more marked, and in some cases, although not always, it varies
from time to time.  Thus,  a senile dement may  fail to recognize a
person or a place that ought  to be perfectly familiar to  him, or he
may do  this at certain times and yet have a perfect  memory regard-
ing the matter at others.   For this reason patients of this class are
very apt to lose themselves upon the street, and  I  have known
them to wander hopelessly for hours,  walking and  riding in horse-
cars, in  a city  in which  they had passed their  lives;  or to stare
fixedly without a sign of recognition at the face  of some  near rela-
tive.  The judgment becomes affected  also in the majority of cases,
so that  a  man  or woman  of hitherto clear and appreciative mind
either utterly fails to reach conclusions  or attains to  entirely false
ones. The emotions show a great variability, so that at one  time
without cause the patient weeps, or is morose, or  breaks  out into
violent fits of anger,  or becomes melancholy.  The conduct grows to
be erratic, and eccentric acts  are performed  that  are either without
reason or that are done for trifling motives, or the patient may have
different degrees  of  restlessness, or even wander away from  home.
Delusions are frequent, and they may be either shifting or  fixed.
They may be based upon hallucinations or illusions, or arise without
these.  The delusions are  apt to  be  of the  nature of persecution,
the  patient imagining that he is being robbed or cheated, or that there 
DEMENTIA.
647
is some conspiracy against him, or that his relatives are treating him
badly.   Hallucinations aud delusions are extremely frequent, most
often optical or auditory in their  nature, less frequently olfactory,
and often  based upou false perceptions through the general senses or
through  the sensations  coming from the  thoracic or  abdominal
viscera. Like all the other phenomena of senile dementia, the halluci-
nations and  delusions are apt to  be fragmentary and shifting in
character, varying thus from time to time, although there  are certain
ones that are fixed, and in some rare cases all are of this permanent
nature.  Their variability maybe at times almost startling, and their
significance may escape oue who is not expert in these matters.  Thus,
one patient of mine was taking a trip to Cuba,  and whilst talking
with the captain of the steamer, some three hundred miles from land,
he suddenly said, " Look ! look !"   The captain looked  in the di-
rection he pointed, and saw nothing, and told him so. He exclaimed
excitedly, " Oh yes, don't you see  Johu," his coachman, "out there
with the carriage and horses ? "  The captain got his glass and care-
fully scanned the horizon, but could see nothing,  and yet the patient
persisted for  an hour or more that he had seen his coachman and the
horses  and  the  carriage  three hundred  miles out on  the Atlantic
Ocean.   To  my mind no more definite evidence of an hallucination
could be obtained, and yet an expert was found who was willing to
state that this might have been a mere mistake ! It is often extremely
difficult to make the distinction in these cases between an hallucina-
tion and an illusion, for the reason that it may be difficult to  obtain
the proof as to whether a given faulty perception is really at the start
a faulty perception  or is the transmutation of a correct perception
into an imperfect one.   Nevertheless this distinction  can be  made
at times with great positiveuess.  For example, a certain gentleman
about  whose will  there  was a contest, had  complained vehemently
that there was a bad smell in one of his closets.  The plumbers were
summoned and the plumbing-work  was removed, yet he persisted still
in his  belief that the  disagreeable  odor was  there.   The  plumbers
were again summoned, tore up the closet and were unable to find any
pipes leaking or any dead animal.  Still  the patient insisted upon it
that he noticed the disagreeable odor. So a sanitary expert was called
in from the local Board of Health,  but he could neither find any odor
nor cause for any.   The patient  finally pasted  up  the closet, in a
painfully  laborious way with ordinary newspaper, which he plastered
on with wet flour; and having done this, he declared that the smell had
disappeared.  His naso-pharyngeal passages were carefully examined
at about this time  by a competent laryngologist, and  no cause for the
odor was found in them.  It was, however, testified to that some gas
pipes had beeu leaking in the street at about the time when  the old
gentleman began to complain of the odor in the  closet;  so that the
evidence was about as complete as it could be that a true perception,
namely, of gas in the street, had been pathologically transmuted into
a disagreeable odor in  this closet, and no better evidence  of an illu-
sion can be given.   These patients  are also apt to become extremely
erotic,  and this condition although  usually variable  in  its duration, 
648
MENTAL DISEASES.
may at times  become permanent, and  sometimes even leads to the
most brutal attacks by old men upon women or girls.
   In the second group  of cases of senile dementia, in which the
mental  symptoms just described are conjoined with paralytic  phe-
nomena, the paralysis is  either of the  nature of hemiplegia, mono-
plegia, implication of individual  muscular groups, or, less frequently,
individual nerves.  When hemiplegia  occurs  it is  of the  ordinary
type, causing motor paralysis of the upper and lower extremities and
the lower part of the face, so that the nasolabial fold is weakened or
lost on one side, and of the tongue, causing this organ to deviate to one
side  or the other.   With this hemiplegia may be  conjoined aphasia,
usually of the ataxic form.   When the paralysis is monoplegic, the
upper or the lower extremity alone may be  affected, or  one side  of
the face.  When  individual muscles or muscular  groups are impli-
cated, some of the facial muscles or those of the upper extremity are
most apt to suffer, although any of the muscles of the body may be-
come affected.   Individual nerves are seldom implicated, except the
olfactory, the auditory, and  the  optic.   In examining the olfactory
it must be borne in mind that the sense of smell is often blunted in
the  aged, and that  it can also be obtunded by  naso-pharyngeal
lesions ;  but an absolute anosmia that is  not due to any naso-pharyn-
geal  cause may be regarded as pathological.   The mere blunting of
the sense of sight, too, is  a very general  phenomenon of senility, but
neuro-retinitis, hemianopsia, or  amaurosis is pathological.    It  is
very difficult to examine  the sense of  taste in a case of suspected
senile dementia; but if it is possible to do this, it will sometimes  be
found to be impaired (page 161). With the exception of these cranial
nerves, the paralytic symptoms of  senile dementia are mainly motor
in character, although, as has been said, it is  difficult to  reach  con-
clusions  about sensations  in patients  whose  minds are  affected.
Tremor is  another physical symptom  that  is extremely common,
and  it is situated in  the tongue, the facial muscles, the head and
neck, or the extremities,  most usually in  the  tongue and the facial
muscles.  If this tremor is at all marked, it will render the hand-
writing tremulous and uncertain.   Tremor, however, is so general a
symptom in the aged that, taken by itself, it  is of little value diag-
nostically, but, becomes of enormous importance when it is conjoined
with the other symptoms of this disease.  The speech is  affected  in
various ways,  according to the cause of the  derangement.  Thus, if
the patient be  deaf, it may be low and mumbling or high-pitched ; or
it may have the characteristics of the various forms  of aphasia (page
141); or if the tremor is great,  it  may be muffled,  low-pitched, and
monotonous.
   Prognosis.  Senile dementia  is usually of very unfavorable prog-
nosis, although quite a number of cases cau be treated with such suc-
cess as to make the ordinary changes of senility again become almost
normal.

   For the purposes of the general practitioner but little time  maybe
spent upon the forms  of  secondary dementia, for  reasons which will 
DEMENTIA.
649
appear.   It occurs either during the convalescence from the acute or
subacute forms of insanity, or in the terminal stage of the organic
mental affections, or with grave textural lesions of the cerebrum.

   DEMENTIA, OR MENTAL EXHAUSTION IN  THE  CONVAL-
             ESCENCE FROM CURABLE INSANITY.

   This form ought not really  to be called dementia, not because the
phenomena are not those of stupidity, but rather for the reason that
the term is apt to be misleading.  They are really conditions of cere-
bral exhaustion after an acute or subacute insanity  has run its course,
and they mark the beginning of convalescence.  I simply dwell upon
them because I have so often seen physicians and households thrown
into despair by their supervention, when a more accurate knowledge
would have seen every reason  for hope.  It is not every form of cur-
able insanity that passes through this stage, curiously enough ;  but it
does occur at times, and, as will be seen in the section upon treat-
ment, it calls for no special remedies other than what are  indicated  by
the disease which has preceded it.

                    TERMINAL DEMENTIA.

   Very  different, however, is the form  of dementia which occurs
with certain organic diseases of the cerebrum  in which  insanity has
been one of the symptoms, as  in paralytic dementia, or which occurs
toward the end of a case of brain tumor, cerebral hemorrhage, em-
bolism, or thrombosis, or after a cerebro-spinal meningitis, or a cere-
bral abscess.  This type marks the final stage, and unless  its cause
can be removed—which  is very seldom the  case—the  prognosis is
hopeless.

   Pathological Anatomy of Dementia.  The pathological alter-
ations of dementia are unknown in all the forms except the senile one.
In this the lesions are those of precocious senility, so to speak, con-
sisting of the degenerated vessels, meningitis of the pia, occasionally of
the dura mater, and the textural alterations of the cerebrum resulting
from  these  arterial  and membranous changes.  Atheroma  of  the
vessels is extremely frequent,  as are also miliary aneurisms.   Arte-
rial thrombosis may occur, and also embolism, of  either intracranial
arterial  origin  or from the heart.   Intracranial hemorrhage fre-
quently occurs, being either the result of rupture of one of the larger
vessels  in  which  atheroma is especially  prone to occur, or from
miliary aneurism of the arterioles of the basal ganglia or the cortex.
Softening of the  brain is  frequent, too, induced by  the arterial
changes  resulting in atheroma, miliary aneurism, thrombosis, and
embolism.   It is a question as yet undecided as to whether  cerebral
softening ever occurs without  these precedent arterial changes.  Me-
ningitis  of  the pia mater and the dura is not infrequent.   As  has
already  been said (see chapter on " Paralytic Dementia "), Tuczek 
650
MENTAL DISEASES.
has described loss of the tan gential nerve-fibres in certain cases.  That
alterations in the ganglion-cells of the cortex occur would  seem ex-
tremely probable, but the  nature of them is not as yet thoroughly
understood.  When the ordinary senile changes in the peripheral vas-
cular system and the heart are, as is usually the case, superadded to
these pathological alterations of the cerebrum, it is easy to understand
the mechanism of production of the varied symptoms, both physical
and  mental, of senile dementia.  The whole machinery of the brain is
disarranged, and the symptoms of the disease  are, therefore, as we
have seen, capable of ranging over as wide a field as is covered by the
functions of the senile cerebrum.  The mental symptoms are probably
due to the fact that the frontal lobes are especially affected.  The par-
alytic symptoms arise from  lesions of the motor area (page 139) or the
internal capsule (page 142).  That some of these paralytic symptoms
are permanent, whilst others are temporary, may be dependent upon
two factors, namely, the localization of the lesion and the  nature of
it.   For example, the arterioles of  the pia mater ramifying over the
cortex  anastomose freely with one  another, as we have seen (page
92), so that hemorrhage, thrombosis,  or embolism in one of them
may at first produce considerable impairment of function, which may
disappear  in a short time, as anastomosing vessels  bring in an addi-
tional  supply  of blood  to  the affected part.   On  the  other  hand,
when a terminal arteriole of the internal capsule is  diseased, the area
of territory supplied by it has no  anastomosing vessel to feed it when
its blood-supply is cut off by an embolus or thrombus, so that the
injury primarily inflicted by such embolus or thrombus  remains un-
modified.   Then, too, the extent of the hemorrhage and  the rapidity
of its  supervention, the extent to which  an embolus or a thrombus
blocks up a vessel, and the rapidity with which it does so, are all
factors determining the clinical symptoms of the lesion.  The altera-
tions in the cerebral lymphatic system have been  but little studied,
but  they are probably of  a similar nature to those in paralytic de-
mentia.  (See  chapter on " Paralytic Dementia.")
  Diagnosis.  The diagnosis of the different forms of  dementia is
usually not  difficult.  The element of dementia or stupidity is the
salient factor,  and  it is usually very easy  to obtain the history of
preceding  orgauic disease of the cerebrum or lack of it, so as to dis-
tinguish the primary from  the secondary or terminal dementias.  The
differentiation  is to be made from the following  affections :
       Melancholia;
       Katatonia;
       Delirium ;
       Paralytic dementia ;
       Bromism ;
       Morphinism;
       Cocainism ;
       Alcoholism ;
       Apoplexy;
       Confusional insanity;
       Organic disease of  the cerebrum ; 
DEMENTIA.
651
       Nephritis;
       Diabetes.
  The essence of melancholia is, as the name denotes, melancholy,
whilst that of dementia, as is equally well indicated by the name, is
stupidity.  Herein lies the fundamental difference between the two
diseases.  ^ In  certain grave cases of melancholia, as in the attonita
form, or  in that occurring in the senile, there is such a degree of
taciturnity as almost at times to be mutism, and to a superficial ob-
server this may seem like  dementia; but careful observation will
elicit evidences of memory and perception and reasoning  power but
slightly impaired.   It is a very common mistake to call melancholia
occurring in the aged senile dementia.   Practically, the difference is
great, because the prognosis and  the  treatment of the two diseases
are entirely different, and so are the medico-legal bearings.   More-
over,  the  senile melancholic often has a  very pronounced suicidal
tendency which is seldom present in the senile dement.
  The succession  of symptoms in katatonia covers a range that  is
never seen in  any of  the forms of dementia, and this alone should
make the diagnosis an easy one.
  In  delirium there is a dream-like condition with hallucinations and
illusions, and  usually a history7 of preceding  febrile disturbance, and
the temperature is generally increased  during a certain course of the
mental manifestations.
  Paralytic dementia may be  difficult at times to distinguish from
senile dementia,  but  the former disease  occurs in  much younger
adults, rarely, indeed, in the aged; the paralytic attacks are more of
isolated muscles  and  muscular groups  rather than  hemiplegia, and
its delusion of grandeur, which is frequent, is never observed in senile
dementia.
  Bromism may produce very great stupidity, and has often  led to
a diagnosis of dementia.  The distinctiou, however, is easily made
by the history of  the  bromides having been given in large doses,
by  the disagreeable breath, the dilated  pupils, and  the loss  of the
pharyngeal reflex that is normally observed  in tickling  the  throat
with a spoon or a  feather.
  Morphinism will sometimes induce conditions simulating dementia
when overdoses have been given or when the drug has been suddenly-
withdrawn. In such instances the history will enable one to make the
diagnosis.  Where this is absolutely lacking, as in ambulance cases,
the contraction of the  pupil may throw light upon the matter, when
it is  markedly contracted.   When the pupil, however,  is widely-
dilated, as  in  certain  cases  of morphinism under the  circumstances
described, the  diaguosis may become a difficult one, and  time alone
can make it.   Indeed, it is not always safe to rely upon the contrac-
tion of the pupil, for this may be due to lesions within the eye itself.
When there is any doubt about  the matter,  sharp interrogation of
the  patieut will often  bring out  the  truth,  as very  few morphine-
fiends have any hesitation about confessing to their vice rather than
suffer the torment of abstinence.
  In  a suspected  case of cocainism the sensibility of the nostrils 
652
MENTAL DISEASES.
and the throat should be tested, as they may retain a certain degree
of ansesthesia if the cocaine has been  taken through them.  If no
information can be obtained in this way, or through the history of
the case, it will not be safe to attempt a diagnosis  until  the effect  of
several  doses of cocaine has been tried.  If this does not immediately
disperse the  stupidity, it can be definitely said  that the dementia is
not due to cocainism.
   In  a case of dementia from alcoholism the history  is very im-
portant.  If this is lacking, the urine  should be  tested for alcohol,
and the condition  of  the  facial capillaries should  be carefully ob-
served.  If they are  dilated  in the usual  way,  and  there  is the
alcoholic odor of the breath, the diagnosis is easy.   In some cases  of
alcoholism, however, there may be great facial pallor, and in such
an event the odor of the  breath may be  the only factor for diagnosis.
If no data can be obtained from the history, breath, dilatation of the
facial capillaries, or alcoholic urine, the diagnosis  should be held  in
abeyance for the time beiug.
   By apoplexy in  this sense are  meant the  phenomena which are
included in the chapter upon " Hemorrhage,  Embolism, and Throm-
bosis."  In dementia suspected to be from these causes the evidences
of paralysis should be carefully sought  for.   It should  be observed
whether the cheeks blow out symmetrically7 on the two sides in expi-
ration;  or if the respiration is not  sufficient to expand the cheeks,
the patient should be pinched or pricked with a pin, aud during the
resulting cry it should be carefully observed whether the facial mus-
cles contract  equally upon the two sides.  The attitude of each upper
and lower extremity should be  carefully studied so as to see whether
there  is more muscular flaccidity than in the corresponding member
or members of the opposite side; and the foot and the hands should
be pricked with a pin upon the two sides to see whether the resulting
movement is equally free in all.  The  knee-jerk should  be carefully
tested upon  the two sides, and it will often  be found to be lost  or
exaggerated  upon the  paralytic  side.  If it is possible to make the
patient  protrude the tougue, note should be taken  as to whether this
protrudes straight or deviates to one side.
   In functional insanity  the element of dementia is manifested rather  *
in the acts than in the conversation, and there is never such a degree
of stupidity as obtains in primary dementia,  or such a degree of agi-
tation as is seen in hebephrenia.
   In all cases of dementia organic diseases of the cerebrum  should
be carefully  excluded.   To this end it should be ascertained  that
there  has  been no  symptom of abscess, either idiopathic, proceeding
from  middle or  internal ear  trouble, or from  venous  thrombosis;
that there is  no paralysis of motion or sensation; that there has been
no injury  to  the skull; or that  there has been no symptom  of intra-
cranial  tumor or meningitis.
   The diagnosis  from nephritis is  easily made, because a nephritis
that is  sufficient to produce a mental condition  simulating  dementia
will  show large amounts of albumin and the different varieties of
casts  in the  urine.   It  must  be  remembered,  however, that small 
DEMENTIA.                        653
amounts of albumin and  a  few hyaline  casts, even a few epithelial
ones, are not sufficient for a diagnosis  of  nephritis as a cause of de-
mentia.  The crucial test  in this  particular will usually be the esti-
mation of the urea, for if this  is far below the normal  the dementia
may be set down as of nephritic origin.
   In  diabetes  the  diagnosis is also made with ease, as in a case of
dementia from this cause there would be found a  high specific gravity
of the urine and large amounts of sugar.
   Treatment.  The treatment  of the  dementias will vary, neces-
sarily, according to the type.   It  may at  once be said that the termi-
nal dementias  are  uot treatable; that is, those  which indicate the
terminal stage of organic disease of the cerebrum.
   The  primary  dementias resulting  from exhaustion of the braiu,
emotional disturbance or mechanical shock, should be treated by abso-
lute isolation  and such measures as may  be iudicated by the general
nutrition of the patient and the circulation.  If the patient has been
in good health, nothing more may be needed than complete  isolation
and rest.  This  should be carried out by putting the patient to bed,
and excluding all  but  those  in immediate attendance upon him or
her.  Where it is possible to do so, it is always best to  have a trained
nurse iu these cases, as in  this  way old associations are absolutely
excluded;  and besides this  the  neatness, the noiselessness, the tact,
the professional nonchalance and  coolness of the trained nurse can
never be attained by an  anxious member of the family.  If this
isolation in charge of a trained nurse can be carried out away  from
home, it is almost  always productive of better results.  The robust
patient may need little  more than this isolation and care, continued
 for a few  days, perhaps  a  week or  two.  At the end of this time
 short walks or drives, or  some gentle means of diverting the mind,
 such  as some form of  light reading, may be mentioned.   It is the
 greatest folly in the world, however, always productive of bad effects,
 to attempt to divert these cases by relatively energetic amusements,
 such as going to the theatre, travelling, or matters of that sort.
 They will do far better always with the absolute mental and physical
 rest.   As  time  progresses, other gentle  means  of diversion should
 be devised, always taking care, however, to err  on the side of too
 much rest rather than too little, watching carefully the effect of each
 new  outlay of energy, and not repeating  it if the patient  becomes
 restless or more listless.
   Should the patient, however, be ansemic  or exhausted, or in a poor
 physical condition, with poor appetite and defective circulation, much
 more energetic and  elaborate  measures should be taken.  The treat-
 ment then&should become  the same as  in neurasthenia, and the reader
 should carefully study  what  has been  said  on pages 463 et seq.
 There  may be, however, a slight difference needed in  the treatment,
 in the fact that these cases of dementia will do best if a cardiac stimu-
 lant  is  employed  early iu the treatment, and  sometimes it may be
advisable  to use it from the very start.   If the stupidity is very
 profound  and  the  circulation is poor, an  alcoholic stimulant should
be resorted to, varying according to the needs of the case from an ounce 
654
MENTAL DISEASES.
and a half to three ounces of whiskey in divided doses iu the twenty-
four hours.  It is often surprising to see how well these patients will
bear this large amount of alcohol; and in some instances I have even
given with benefit as much as 8  to  10 ounces in twenty-four hours,
although  this is  scarcely ever necessary except in those who have
been accustomed to the use of alcohol.  If the alcoholic stimulant
acts well, a special cardiac stimulant will not be necessary.   In some
instances, however, especially in those who have been extremely tem-
perate, alcohol will cause considerable restlessness without any coinci-
dent improvement in the mental symptoms; and when this is the case
it should  be either discontinued entirely or reduced to a small quan-
tity, and the sulphate of strychnine administered  in its place.  The
dose of this  should be from fa to fa grain  three times a day, best
in the form of tablet triturates of a reliable firm, as in them the dose
is exact, whilst iu a solution it may vary with the evaporation of the
fluid or from the carelessness of the person giving  it.  Some patients
cannot take strychnine because of the disagreeable griping produced
by it in  the  unstriped muscular fibres of the intestine, and when
this occurs, digitalis should  be substituted, 10 drops three times daily
of a freshly made and reliable  tincture, or  one  grain  of the solid
extract in pill-form at the same intervals, or three drops of a reliable
fluid extract.   When  the  patient has  been restored to such mental
health as to make it  seem as if he or she were in the usual condition
of mentality, a vacation of two or three months should always fol-
low, as it too often  happens that return to the ordinary course and
associations of life  at this period  will  bring  about a relapse.  It  is
at this time  that travel  becomes of  great value if undertaken with
due regard to  comfort and avoidance of fatigue.
  In primary dementia the same treatment should be applied.
  In  hebephrenia  it is not  always necessary, however, to advise rest
to the same  extent, although  isolation should be carefully main-
tained.  It is extremely important  in  cases of hebephrenia to take
the patient away from home and surroundings and put him or her
in charge of a trained nurse, because many of these cases are those
of young  adults who have  never had any self-control and who have
never been taught it  by parents or relatives; furthermore, these indi-
viduals will always do better with strangers.   In some  of them the
agitation aud restlessness are so great that they may call for the admin-
istration of a cerebral sedative, and the best of these are the  bromide
of potash and the hydrobromate of  hyoscine.  The  former should
be given in doses of 20 to 30  grains pro re nata, and the latter in the
same way in doses of gr. T^.  Usually 20  grs. of bromide  of pot-
ash once or twice a day or ^ gr. of  the hydrobromate of hyoscine
as often, wiH be sufficient;  or, if either dose alone does not quiet the
patieut sufficiently, it may be well to  combine the  two drugs  in the
above dosage.   These cerebral sedatives, however, should not be used
except  when  necessary to restrain the  restlessness that is  sufficient
to weaken the patient, for any less degree of agitation  will be best
overcome  by treatment of  the  disease  itself.   Hyoscyamine should
never be used in these cases,  for it is a  dangerously depressing drug 
DEMENTIA.
655
in many instances, and the disagreeable dryness of the mouth and
dilatation of the pupil which it produces are apt to increase the de-
mentia.
  Senile dementia should be treated upon the same principles as the
primary type.   In many instances, however, the rest should be more
absolute.
  There is  no necessity of sending these cases  of dementia to an
asylum, for  not only can nothing more be done for them there than
at home, but generally far less is attempted, and in the curable cases
the associations  of an asylum are extremely disadvantageous when
the stage of convalescence has been reached, whilst the stain of hav-
ing been  in such an institution may constitute a serious obstacle in
their after-life. 
CHAPTER  XVI.
                  CONFUSIONAL INSANITY.

  Definition.   Confusional insanity consists of a slight stupidity
that is characterized by incoherence and  confusion of ideas rather
than by true dementia, without  emotional disturbance.
  It is  often confounded with  true dementia, but  the  difference is
that the  dement is positively stupid, whilst in  this form of mental
disease there is a stupidity that is inherent  rather to the ideas and
the actions than to the general appearance.  For example, a woman
afflicted with this  form became widely known several years ago by
her action in kidnapping the child of  well-known people.   She was
finally found living at a hotel  in  a neighboring city with  the girl
whom she had abducted.   She could see nothing wrong in what she
did, was very  much  surprised that anybody had found fault with
her, claimed that she had taken  the  child only because  she took a
fancy to it, had treated it very kindly, had not attempted in any way
to conceal herself, aud had made no attempt whatever to obtain any
pecuniary reward.  After a long conversation with her, during which
I  elicited these  facts,  she started  to leave the room,  and calmly
lifted a Bible as she  passed by a table, and was walking off with it,
when I stopped her and called her attention to the fact that the book
did not belong to her.  She made no attempt to conceal her intention
to take it, but  placidly remarked that people took her  things, and
she did not see why  she could not  have theirs.  Conversation with
her upon  general topics would not have evidenced any mental aber-
ration except to one  skilled in the  examination of deranged minds.
This woman was a type of this  form of insanity.  In some cases the
memory is blurred, but usually it remains intact.  Rarely there are
hallucinations  and delusions, both being usually  varied and non-
characteristic, except that delusions of identity  are  common.   The
speech is sometimes confused, although this  has been the exception
in the cases I  have seen, and there is no  tendency to extravagance,
but rather to irrelevancy and incoherence.
   The prognosis of  these cases is usually good, although, when the
attacks are frequent or when the patient is much debilitated, the dis-
ease may become chronic.
   The diagnosis is readily made, and the affection is to be distin-
guished  from  dementia,  mania,  general  paresis,  melancholia, and
insanity of pubescence.   (See Part III., Chapter III.)
   The treatment is to be along  the  same line as in dementia.   (See
Chapter XV.) 
CHAPTER  XVII.
                          PARANOIA.

  Synonyms: Verrucktheit.  Primare Verriicktheit.  Chronic  de-
lusional insanity.   Delirants chroniques.   Monomania.   Reasoning
mania.
  Definition.   Paranoia is a form of mental disease characterized
by logical or systematized delusions of persecution and self exaltation,
without excitement of emotion or idea or impairment of memory.
  History.  The word paranoia is derived from  the  Greek word
napavoia, which was a classical term denoting insanity used by some
of the best Greek authors, such as iEschylus, Arrianus,  Plato, Aris-
totle,  Lucianus, and Plutarch ; but it does  not seem to have been
used by any modern writers until it was employod by Vogel in 1764
as a collective  name for some nine different forms of mental dis-
ease.   In 1818  Heinroth  also  made  use of  it to denote certain
secondary states of exaltation with fixed  delusions and  exaggerated
feeling  of personality,  although  the  first use of the word in its
modern meaning is  due to Mendel.  The evolution of our present
knowledge of this form of insanity is due primarily to the observa-
tion of the  French alienists  of fifty years ago, then to that of the
Germans, whilst in  recent years the Italians have  added very con-
siderable material, and  at present the French  are again interesting
themselves in the subject.  Singularly enough, in this scientific dis-
cussion that has been  one of the most interesting and critical of
modern psychiatry, the English  and the Americans have  borne but
a small  part, with one or  two notable exceptions.  The germ of
paranoia was first detected by the great Esquirol in his chapters
upon  monomania, with  ideas  of grandeur.   Griesinger in 1845 next
described the combined or successive  delusions of persecution and
grandeur.   In  1852  Morel detected what he termed the systemati-
zation,  or,  in  more Anglo-Saxon terms, the  logicality of  the
delusions.   With this the  picture of the disease was drawn  in its
essentials, so that  the  discussion from  the days of Morel  to  the
present time has waged around the important but relatively  sub-
sidiary queries  as to whether the  malady is hereditary and chronic
or secondary to pre-existent insanities,  or whether it is primary and
can occur acutely  and  non-hereditarily.   Griesinger,  in  his  first
description, in 1845, was of the opinion that it was always a disease
secoudary to mania and melancholia, but twenty-two years afterward
he admitted that Snell was correct in his statement that it was always
a primary disease.   Snell, however, himself described in 1873 a form
secondary to melaucholia,  mania,  and epilepsy, and at the present
time most of the French and Italian authors are agreed  with him in
                               42 
658
MENTAL DISEASES.
the belief that there are both a primary and a secondary variety.  The
question  of heredity has  undergone quite as revolutionary a  trans-
formation.   The earlier authors were very positively  of the opinion
that  paranoia was always  a hereditary disease in the sense  that it
occurred  in those who were predisposed to insanity or to neuroses by
heredity, and even at the present day some of the best-known alien-
ists are still of  this way of thinking; but  in 1878, in his celebrated
Hamburg discourse, Westphal described an acute form and initiated
a literature upon that point, in which his views have been espoused
by Leidesdorf, Koch, Jung, Schiile, Merklin, Morcelle, Marie, Ton-
nini,  Buccola,  and others,  so  that some  recent  authors, especially
Werner,  have gone so  far as to include under the heading of acute
paranoia many cases of puerperal, post-febrile, alcoholic, morphinic,
and  cocainic insanity, and  the semi-insane neuroses, such as folie de
doute,  fear of certain localities  (agoraphobia, claustrophobia, topo-
phobia),  dipsomania, pyromania, kleptomania, certain homicidal and
suicidal impulses, certain belonephobias, certain morbid impulses to
collect pins, onomatromania, certain morbid impulses to gather fig-
ures (arithmomania), and finally an almost laughable  form described
by Magnan  in certain old maids who have the characteristic old-maid
love for  cats, and to which he gives the magniloquent name of folie
des anti-vivisectionistes.   In France of late years  Magnan  has taken
some peculiar views of the subject,  which  have met with but partial
acceptance even in his own country.  He claims  that the chronic
delusioual insane have been described in two phases of the evolution
of their  mental disease, aud  that to these two phases  has been given
the name of paranoia,  so that systematized delusions of persecution
aud  grandeur are but stages in chonic delusional insanity;  but as
the terminal stage of the cases he describes is dementia, and as very
few  cases of true paranoia  pass into dementia, it is obvious that his
description does not tally with  the facts in this particular, whilst the
acute cases of paranoia usually recover.   From this review it will be
apparent that there is a mental disease characterized  by delusions of
persecution and self-exaltation, and that this disease may be hereditary
or non-hereditary, chronic  or acute, primary or secondary.
   Clinical History.   Paranoia may be divided  into, first,  the
primary, and secondly, the  secondary form.
   The primary form may be acute or  chronic, and  both the acute
and the  chronic may be hallucinatory.
   Acute primary  parauoia  begins with a delusion  of persecution
which may be infinite in   its  variety.  At first this harasses and
vexes the patient,  and may even cause doubt  in  his own  mind as to
the  genuineness of the delusive phenomena; but as  time passes he
becomes more  and more convinced  of the  reality of the delusions,
and it becomes correspondingly difficult to reason with him about
them.   He lives in an atmosphere  of suspicion—everything around
him has a covert meaning, and  " trifles light as air  become as proof
of Holy Writ."   Indeed, Shakespeare's description of Othello's jeal-
ousy is an excellent picture of what is often  seen in  alcoholic para-
noiacs.  People are watching him, he thinks, on the street, and in the 
PARANOIA.
659
public conveyances; somebody coughs as he passes by, and imme-
diately he believes that that cough has some secret meaning; a match
lies before his feet as he goes along the street, and he checks himself
and  goes  around  it, convinced that there is some design about it;
his wife fastens a handkerchief in the window to dry, and he rushes
headlong  to  the  conclusion that this  is a signal set for some para-
mour ; or a headline in the paper, a bill-poster on the street, a sign
over a store, a casual glance from a passer-by, an advertisement, may
have a fantastic meaning lurking in it to his  distorted perceptions.
As time  passes these  delusions become more and more fixed.  The
patients reasou about them calmly, perhaps, and they differ from the
delusions  of melancholia and mania in the fact  that any agitation in
the patient is produced as the consequence of these delusions, and the
excitement does not precede the delusions.   The delusions are thus
always bound together in a chain of false logicality, in which, how-
ever, the  morbid  element is plain to  the experienced observer.   As
the delusions become  more and more fixed, there gradually arises a
question  in the morbidly logical mind of the  patient as to why he
should be thus persecuted, and out of this, in a natural enough way,
gradually grows the delusion of self-exaltation, or what  the French
somewhat magnificently term the delusion of grandeur.   The patient
then  becomes in his own estimation a person  of importance, either
because of his station in the  world,  or because  of his personal
attributes.  Thus, Dougherty, the would-be lover of a well-known
actress, who believed  that he had  been persecuted and wronged
because of his love for  her, stated to  me  calmly and  with a half-
deprecatory smile that he had been the handsomest man in the world
before he  had been broken up by confinement and anxiety.  Another
patient told me in a smiling, modest way that he was persecuted be-
cause he was possessed of a certain secret way of polishing wood, in
which his skill was greater than that of any other living  man.  An-
other believes that he is watched, and that his food is poisoned because
he has certain business secrets, the disclosure of which would be very
damaging to Jay Gould, the great American  arch-millionaire,  the
monetary anti-Christ to  hordes of diseased minds and  many  sane
ones.  Another imagines  that he is a great man in the estimation
of the world because he has made great scientific discoveries, which
his rivals are  trying  to  discover; and  so on through a myriad
phases, infinite as the mind of man in its various degrees of culture
and  imagination, these patients  have many delusions of self-impor-
tance.  The  judgment, the reasoning power,  and  the  memory  of
these paranoiacs are remarkable, indeed, often startling, so that they
are almost certain to impress the lay observer  and  many physicians
also as being; perfectly sane except upon certain  points.   One unedu-
cated man outlined to me the most remarkable theory of the action
of the mind upon the muscles,  embodying  in  all its essentials  the
views of the most advanced neurologists of the present time regard-
ing the motor centres of the cerebrum ;  whilst a woman of this class
was  brought to me by  her lawyer, who was  a perfect believer in her
sanity and who told me the most connected story of the wrongs that 
660
MENTAL DISEASES.
she had suffered at the hands of relatives, all of which were proved
to be entirely false in the light of subsequent developments ; and a
little Methodist minister once came under my care who  calmly nar-
rated to me the most circumstantial account of proofs of his  wife's
infidelity, so connected  and so circumstantial as to stagger me for the
time being,  the more especially as he maintained them  with great
distress of mind when  brought face to face with his wife, and when
I  told him frankly that he must be either perfectly sane or else have
a delusion and be insane, he promptly and calmly admitted the force
of the argument, aud  was entirely  willing to  wait for the test of
time, which, however, showed incontestably that he  was insane.  I
have seen a patient of this class  take the witness-stand to demon-
strate  his own  sanity,  answer questions  with perfect readiness and
logical sequence, stand  unscathed an analytical  cross-examination,
stagger judge and  jury, afterward point out the logical errors of the
trial, and yet in the next breath  say something that would evidence
a firmly rooted delusion. These  patieuts write letters coherently and
well;  indeed, often undertake literary work ; and at one time in the
Utica  asylum in New York  State a magazine was conducted with
considerable skill by a number of patients of this class.  Yet, under-
neath  all this seeming good judgment and logicality, the delusions
and the false judgments based  upon the delusions keep surging to
the surface.   The loss  of the ethical sense, too, in these patients is
remarkable, and this symptom  is one upon which writers have  not
laid by any  means  the stress  that  its  importance  and frequence
deserve.  They will tell you of  some brutal act that they have done
with the utmost calmness and the most perfect apparent  recognition
of the  nature and  quality of the act and its consequences.  Thus,
this man Dougherty, to whom I have already alluded, told me very
calmly that  when  he had been  committed to the asylum twice, and
found that he had no redress, he made up his mind that the system
of committing  people  to asylums was defective; that he sought for
a  long time  for the  best means of correcting the evil, and that he
came reluctantly to the conclusion that a  revolution, as he expressed
it, was the only effective  remedy, so that he determined to kill  the
physicians who committed him, the judge  who had indorsed the com-
mitment, the commissioners of lunacy who had approved of it, the
officers of the  asylum  to which he had been committed the second
time, the local commissioners of charity in whose charge the asylum
was, and the State commissioners of charity who had visitatorial power
over all the asylums of the State.  He armed himself with two re-
volvers and proceeded to the Flatbush Lunatic Asylum, where he shot
a young assistant physician, Dr. Lloyd, backed  out  of  the asylum,
keeping everyone at bay with his two revolvers, and proceded on the
horse-cars to the Brooklyn Bridge, a distance of some seven miles, to
cross over to New  York, where  he had proposed to go  on with his
murderous work; but fortunately he was arrested on the bridge  at the
instance of another physician who had followed him.  He said that he
was very reluctant to kill Dr. Lloyd, because he knew that  the latter
was a  young man whom  his  parents had  educated  at  considerable 
PARANOIA.
661
sacrifice, and because he was the only son ; but he steeled his heart to
the deed by reflecting upon the necessity of the revolution which he
was thus to inaugurate.  He also said that he  had at first intended to
shoot the cook of the institution, but second  thought convinced him
that people might  think that there was an element of  spite in this
which would detract from the moral effect of  the deed.   I remarked
at this point  that I thought myself that it would have been rather a
small affair to  kill the cook,  whereupon he quickly rejoined, with a
chuckle, " Oh, if you  had eaten the food that that d—d scoundrel
cooked, you  would have  wanted to  kill him,  too !" and laughed
heartily.  Nothing could impress upon him the enormity of his deed
or of the plan that he had in mind.   This is a typical illustration of
the cold-bloodedness, or, to speak more accurately, the loss  of the
ethical sense, which is a prominent symptom in these patients.   Their
delusions, indeed, approach the nearest of all  the insane delusions to
the fixed and erroneous beliefs of the saue, for they will reason about
them logically up  the last point  of being convinced, and  it may
happen that in the earlier stages of the disease it may be possible to
convince  them for the time  being of the falsity of their opinions.
Between their delusions  and  the fixed beliefs of the sane, however,
there lies this great difference, namely, that the latter do not have the
predominant delusion of persecution mingled sooner or later with
that of self-exaltation.   In  a  scientific sense, therefore, these patients
are  not responsible.  Even the dictum of Anglo-American  juris-
prudence, which is embodied in the statute of the State of New York
declaring  that a man shall be held responsible for his acts if he knows
the nature and the quality  of his act and the consequence thereof,
does  not  make these patients responsible, because while they may,
parrot-like, state  that  they know the  nature  and quality of the act,
and what  the  punishment will  be  for it, it is very evident  to the
most superficial observer that they do not really appreciate what they
are doing  because of their  lack of ethical sense  aud because of the
manner in which the mind as a whole is warped by the fixed delu-
sions of persecution and self-exaltation.  It is  quite another ques-
tion, however, as to whether  these patients should be  punished by
law.   There can be no question that they are very dangerous lunatics,
and they should  certainly be  put under restraint  for such time as
to make it certain that they are really cured.
   These patients  are  generally subject  also to paroxysms of excite-
ment, sometimes  arising from their  delusions,  sometimes .entirely
independent  of the latter, and in these periods of excitement they are
apt to  become confused and incoherent,  although such phases are
usually temporary.
   The chronic form of simple paranoia may either be  preceded by
the acute  form, or it may be chronic  and  gradual from the very
onset   Under this chronic form are  to be found what Sander called
original paranoia,  litigious paranoia (paranoia querulantium),  moral
insanity erotomania, and  the inventorial and the sexual paranoia.
The truth of the matter is  that classification of this  kind is an end-
less task  for the  delusions of paranoiacs are as various as are the 
662
MENTAL DISEASES.
different sensations, and  the  metamorphoses of these delusions with
the hallucinations that occur in the classes of which we have yet to
speak are simply chaotic.   Nevertheless, the litigious, the moral, and
the original forms deserve a more precise description because of their
frequency.
   Litigious paranoia is generally to be found in those who have a
neurotic heredity.   The onset is gradual, and it is usually caused by
some loss of property or injury of reputation, out of which arise the
delusions.  These patients press from suit  to suit without regard  to
whether they win or are  defeated, and are never-euding  nuisances,
often dangerous ones,  to juries  and judges.   A case of Buchner's
formed an association of the  oppressed;  another  began a crusade for
the liberation of the supposed  insane  from the  asylums; another,
being  temporarily committed to  prison, organized an association of
the murderers, whom he regarded as deprived of their rights as citi-
zens, and cheerfully wrote to my friend, Dr. Hammond,  that he, the
patient, was now president of the Murderers'  Club, and that false
witnesses would hereafter be dealt with in a summary way that was
much  more in  consonance with justice  than  the tardy processes of
the courts.
   Moral insanity or moral paranoia  is invariably found among those
who have a neurotic heredity.  In these cases the moral defect  may
begin in early youth and continue throughout life.  The acts of these
individuals are usually without motive, although, when  the passions
or prejudices  of people  have been  aroused, they may  seem to  be
nothing more than the  deeds of rogues;  but the useless  theft  of
small  articles by a person who is abundantly able to pay for them,
the obtaining of money upon false pretences by an outlay far greater
than is represented by the money thus obtained,  without estimating
the loss of time aud labor, the utter lack of appreciation of the con-
sequences evidenced  by the act,  and very frequently its stupidity,
are all very evident to the dispassionate or unprejudiced and experi-
enced  observer.  I have  known a patieut of this class spend ten
dollars to  swindle  a poor woman out of a dollar, or lose a position
worth hundreds of dollars  a month  by obtaining  a few dollars  by
false pretences, or cheat a person by7  false representations into buying
a  farm that he could have made infinitely more money by retaining.
In all these cases of moral insanity  that I have seen, however, there
is, if not  continuously, at least paroxysmally, the delusion of perse-
cution and self-exaltation.
   The original paranoia of Sander occurs in  those who are heredi-
tarily neurotic, or who present anatomical signs of degeneration, such
as cranial deformities, and defects of development, as stuttering, left-
handedness, total loss of muscular sense, absolute  lack of any sense of
humor, etc.   This is an infrequent form.  It  generally begins at
puberty, although  the earlier youth may  have presented vague and
indefinite signs of  eccentricity, such as a peculiar  reserve, coldness
of manner, suspicious attitude, visionariuess, a vague something that
impresses people with the idea that the patient is peculiar.
   Acute hallucinatory paranoia is, as the name denotes, accompanied 
PARANOIA.
663
by  hallucinations,  often  illusions, which are at  times  extremely
yivid and detailed with a picturesqueness  that portrays the mental
impressions they have made.  This form occurs most* frequently in
the inanition succeeding acute febrile disorders, such as typhus  and
typhoid, iu  the  puerperal condition, in peritonitis, after operations,
and many cases have beeu seen after the recent epidemics of influ-
enza.  Alcoholism, morphinism, and  cocainism are also not infre-
quent causes.  This  hallucinatory paranoia may  also occur in  a
chronic  form.
   Secondary paranoia is seldom seen, if I  may judge by my own
experience, and when  it occurs, it is generally after  mania and melan-
cholia,  passing,  however, either into  convalescence, dementia, or a
relapse  of the original mania or melancholia.   It has been claimed
that it sometimes occurs after some of the other insanities, but this I
have never seen.
   These paranoiacs constitute the most dangerous class of the insane,
especially in the acute and chronic simple form ; and the deeds which
they commit are the dangerous  ones of a deluded  patient who is yet
possessed of all the  intelligence that can make a, deed dangerous.
The history of the world is full of the brutal murders that have been
committed by this class, and all the educational means of modern civili-
zation, such as the newspapers, the magazines, and books, which go to
educate aud elevate the minds of the sane,  have an equally powerful
but perverted effect upon  these warped intellects.  They are as much
the enemy of the sane as the wild beast is the enemy of man.   Their
delusions are so fixed and their intellects otherwise are so keen  that
there can be no truce between them  and the  sane.  They live in a
world of their own, and the sane appear to them as abnormal as they
appear  to the sane.  Out  of their delusion of persecution necessarily
grows the necessity of action to protect themselves from the perse-
cutors ;  the  logic of events continually presses them on, however
sluggish and cowardly they may naturally be; they are irritated and
harassed  and vexed  and  troubled  into aggressiveness, and,  like
Mahomet, they enforce their  opinions  with  the sword.   In  this
respect  they differ radically from the melancholiac, who  passively
suffers  the injury that he believes is  being done him,  and which he
attributes to some fault or sin  of his own, and not, like the para-
noiac, to the persecution of others ; and their delusion of persecution
is entirely different from that of  the case of mania, who is  simply
terrified by it and proceeds to no  logical or connected  act, but only
occasionally to an impulsive one.
   Prognosis.   The  prognosis in the  cases of  acute  simple  and
acute hallucinatory paranoia is generally good, for the disease usually
terminates in recovery, infrequently in a chronic condition,  and
very seldom in  dementia.   In the chronic cases, however, the prog-
nosis is very unfavorable, especially in those of a neurotic heredity
and in the original form of Sander.
   Etiology.   The causes of paranoia are :
        Heredity;
        Traumata; 
664                   MENTAL DISEASES.
       Mental and physical exhaustion ;
       The puerperal condition ;
       Febrile diseases, such as typhus and typhoid ;
       Surgical operations;
       Epilepsy;
       Alcoholism ;
       Morphinism;
       Cocainism.
  These causes need not be gone into in detail, as they are considered
in the historical portion of this chapter or in other chapters.
  Diagnosis.  The diagnosis of paranoia should be from—
       Mania;
       Melancholia;
       General paresis;
       Hallucinatory insanity.
  In mania there is an acute or subacute ouset, the delusions are but
slightly systematized, whilst  the  emotional condition of hilarity  is
excessively well marked, and there is a larger degree of motor rest-
lessness than is ever seen in paranoia.
  In simple melancholia the  delusions may sometimes  be so logical
as to puzzle us temporarily, especially when  they take the nature  of
persecution ; but in  a very short time there will  supervene the
suicidal impulse, the  confusion of mind, and the profoundly melan-
choliac condition.  In  the simple  form  of melancholia, too, the in-
somnia, the post-cervical ache, and  the characteristic facies, of which
I have elsewhere spoken, are symptoms not observed in paranoia.
   In general paresis the dementia is a prominent feature throughout
the disease,  the delusions are always stupid and illogical (unsystem-
atized) ; there are also the physical symptoms of pupillary inequality,
abnormal pupillary reflexes, and tremor of the tongue, facial muscles,
and limbs.
   The great rush of ideation in hallucinatory insanity, with the utter
lack of coherence in the sequence of ideas,  is the direct  reverse  of
the logical and emotionless delusions of the paranoiac, whilst the va-
riations in  the former disease from motor  and  mental excitement  to
depression or exhaustion and obstinate taciturnity are also a feature
that is not observed in the latter disease.
   Treatment.   The treatment of paranoia should vary accordingly
as it is acute or chronic.  In the acute cases any causes of inanition
should be removed at once; and in the post-febrile cases occurring
after typhus and typhoid fever and influenza, nourishment, alcoholic
stimulants,  and  rest  are generally all that is  needed, and narcotics
should not be employed at all,  or used very carefully.   The feeding
in these cases should  be far in  excess of what is normally taken  by
the patient, if it  is possible to  give this amount of food, and I am
never  satisfied  unless I can have the patient take at least three full
meals  a  day, with a  pound of  beef made into  a strong beef-tea, and
two quarts of milk.   Potassium bromide, hydrochlorate  or  hydro-
bromate of hyoscine,  opium, and hyoscyamine are the best drugs with
which to control  the delusions and  hallucination in  the  cases that are 
PARANOIA.
665
not due to marked inanition, and even in these they may be sparingly
employed if large quantities of food and stimulation do  not answer
the purpose.   The dose of bromide of potassium should never exceed
20 grains, three times a day.   The hydrochlorate or hydrobromate
of hyoscine in doses of T^ grain once or twice, or  even in  robust
individuals three times a day, is an  exceedingly useful drug in con-
trolling the restlessness and the delusions, aud the great advantage
of it  is that  it  can, if  necessary, be given  for weeks at a time in
hardy individuals.  Hyoscyamine is an excellent drug in  many cases
for overcoming  the motor excitement and the tendency to  violence,
and it is often  useful in combating the hallucinations; but it is apt
to be very depressing in its effect and  should only  be used tempo-
rarily, care being taken even then to  see that it does  not produce re-
tention of urine or even strangury.   Opium, in the form  of the solid
opium or as an aqueous extract, is  often extremely useful in cases
in  which hyoscine or  hyoscyamine  have failed,  and sometimes  in
combination with them.   The solid  opium should be given in doses
of  1 grain once or twice a day, and  the aqueous extract in  a dose
of ^ graiu, once to thrice daily, but  care should  always be  taken to
employ a perfectly reliable preparation of opium, as  there are many
worthless and  cheap specimens upon the market.   Morphine  I have
almost discontinued  using for the last few years, because of its un-
reliableness in this class of the insane.   In  many cases of  this kind
the patients will refuse to take medicine, and then  it may become
important  to  give it without their knowledge,  which can usually
be  readily done, for the drugs can  be  easily dissolved in  a  cup of
soup, cocoa, coffee, or any other liquid, or otherwise mingled with the
food.   In  some violent cases it may be necessary to administer the
hyoscine, hyoscyamine. or opium hypodermically.   In all  the acute
cases, however, this treatment should, if possible, be supplemented
by  several weeks of rest in bed, and I know of nothing  that will
quiet the patient better  than this.  The chronic cases should be com-
mitted to an asylum unless  it is possible to guard the  community
thoroughly against them by proper attendance at home.   They are
too dangerous to be at large, and the  most harmless of them may
at any moment  do some violent deed, as iu the  case of the  bomb-
thrower  Norcross, who exploded ten pounds of dynamite in  a busi-
ness office in this city. 
CHAPTER  XVIII.
                   PARALYTIC DEMENTIA.

  Synonyms: General  paralysis of the insane.  Progressive general
paralysis.   General paralysis.  General paresis.  Paralysis of  the
insane.  Paralytic dementia, or Dementia paralytica.  Paretic  de-
mentia.  Allgemeiue progressive  Paralyse der Irren.   Paralytische
Blodsinn.    Allgemeine  progressive  Gebirnlahmung.    Paralysie
generale progressive.  Periencephalite chronique diffuse.  Demence
paralytique.
  Definition.   Paralytic dementia is a cerebral disease of chronic,
remittent  type, characterized by  dementia  of very gradual onset,
usually merging into mania or melancholia, generally with stupid and
expansive delusions, and accompanied by tremor, ataxia, pupillary
alterations, aud eventual paresis.
  History.   The first description was given by Bayle in 1822, who
considered it to be au arachnitis.  From this period until  the early
'50's the main treatises were by Frenchmen; but in 1854 Erlen-
meyer, a German, wrote upon it,  and from that time to the present
it has  been considered by the writers of every civilized  nation, a
catalogue of whose names  would fill pages.
  Clinical History.  Although many diseases of the brain have
been falsely diagnosed as paralytic dementia,  and although the future
will undoubtedly make it evident that some cases of what we now
regard  as this malady are really  essentially  different affections, it is
entirely possible at  the present day to make a positive  diagnosis of
the  one clinical entity.   When we come to consider the  pathological
anatomy of the disease, we shall find that paralytic dementia consists
of molecular alterations that  affect the cerebrum as a  mass, and this
fact should at the outset make us realize clearly that the symptoms,
both mental and physical, are  co-extensive  with  the  cerebral  func-
tions, so that there is scarcely any one symptom to be  found in other
diseases of the brain which cannot be found  in this, differing only in
the  manner of grouping.  Authors are at  variance as  to the number
of stages,  but in my experience these are in the main as  follows:
       The prodromal;
       Maniacal or  melancholiac;
       The demented.
  But  there are many exceptions  to this rule in which only the first
and second stages are observed.
  The  prodromal stage.  This may extend over months or years, and
the  mental and physical symptoms are remittent and insidious.  The
mental symptoms consist  of alterations in character  that  are often
vague  and transitory,  or  of intensifications of pre-existing mental 
PARALYTIC DEMENTIA.
667
traits.   The patient becomes eccentric, and performs some act that is
so causeless and so entirely at variance with his usual behavior as to
puzzle those acquainted with him.  One patient of mine, for example,
who had been newly married, brought home a rose to his wife, gave
it to her affectionately, seated himself  before his mirror to brush
his hair, then, suddenly rising, slapped  her face, and nonchalantly
went about his dressing as if nothing  had occurred,  without any
word of explauation, seemingly unaware that he had done anything
out of the way.   Another, who was a cautious business man, went to
a firm of brokers and engaged recklessly in  speculation.  Another
became very suspicious of his  family without cause, although he had
hitherto been of a jovial aud kindly disposition.  On the other hand,
a naturally frugal  man  becomes  penurious; a generous man grows
extravagant;  one who is reticent becomes still more silent, and a
talkative individual is converted into a loquacious one;  and thus we
witness a deepening of all the innumerable shades of character.   At
the same  time—often, indeed, at the very first—there is a change in
the finer ethical sentimeuts, which lie on most civilized human charac-
ters like the bloom upon the peach, indicative of the highest culture,
and varying in each individual with the social station, sex, age, race,
and nationality.   So that a kind father or husband becomes brutal
or seeks the society of loose women, or a chaste and  modest woman
gives rise to remark, or an affectionate son or daughter  becomes dis-
obedient, disrespectful, or thoughtless.  Contemporaneously with these
mental alterations, physical ones are observed, often so slight as to
escape other eyes than  those of the trained observer.   Among the
earliest of these  are tremor, and  speech and  pupillary alterations.
The tremor is generally in the tongue and in the facial muscles, occa-
sionally also in the extremities.  It is best observed in the former by
causing the patient to protrude the organ slowly, when the lingual
muscles are seeu to be agitated by a series of slight  fibrillary move-
ments.  In the latter the tremor is  best  seen by causing the  patient
to speak, when the facial muscles of the lower part of the face,  espe-
cially at the angles of the mouth, will  twitch with  slight muscular
twitches that are intermingled with tremor.  The speech-defects are
best made evident either by a slurring over aud indistinctness in the
pronunciation of certain words or of consonants and labials, or by
a combination of these  two  peculiarities.   Frequently, however, a
patient who can  pronounce  individual  words  distinctly will  slur
over these  same words when he  pronounces  them  in  the context
of a sentence or  in ordinary  conversation.   The pronunciation  of
the letter "r"  is  apt to  be  especially difficult, particularly to a
Frenchman or a German, with whom the  "r" is either guttural or
prolonged, although this defect can  almost  invariably be observed
even in the Euglish-speaking races.   A good test of this is to get the
patient to pronounce such  a sentence as " riding cavalry brigade,"
or  better still  the same words  in  German, " reitende Cavallerie-
Brigade," with the full German guttural intonation, or the sentence,
"round'about  the rough and  rugged rocks the ragged rascal ran."
When  the tremor is slight in the extremities it can best be detected 
668
MENTAL DISEASES.
in the hand, by causing the patient to extend the arm at full length
at right-angles from the body and then lightly supporting the fingers
upon  the palm  of the  examiner's  hand, when  a  delicate muscular
tremor will be made evident,  like the throbbing of a small engine.
Tremor in the lower extremity may be detected by having the patient
sit down  and  extend the  lower extremity at right-angles from the
body, and then  lightly supporting the heel with the examiner's palm,
when the foot and toes will be seen trembling with fibrillary tremor
that  is  usually more distinct and  coarser than is observed in the
fingers.   The pupillary  alterations are to be noted  in the size of the
pupils, their marginal contour, and  the reaction of the iris to light,
consensual or  cutaneous  stimulation,  and  accommodation.   The
pupils in about  one-half of my cases have beeu dilated,  my observa-
tions thus agreeing with those of Bevan Lewis, and whilst the mod-
erate-sized pupil  is next in frequency, the contracted pupil is infre-
quent.  In about one-half of my cases one pupil was larger  than
the other.  These were also about the same figures  in Bevan Lewis's
patients, but whilst he  states that the right pupil was  generally
the largest, this has  not been constant in my cases, as  in the same
case sometimes the one pupil and sometimes the other  would  be the
larger.  This pupillary inequality is a symptom that is very apt to
escape observation, inasmuch as it may be temporary, lasting  only
for a few days or weeks  at a time;  indeed, in oue  patient of mine,
about whom there was a question of diagnosis, this inequality was not
observed by me for  upward  of some three weeks, and was  finally
detected by my assistant  during my absence from town, but I did not
see it myself for several  weeks afterward. The pupil may be perfectly
immobile  or excessively sluggish in reaction to light, tested by a
strong light and focal illumination  of the eye by a  convex lens, and
in some cases this sluggish reaction  may be followed by  wide dilata-
tion ; or the pupil may be sluggish, or it may not react with accommo-
dative movements of the eye; or it may fail to respond or respond
sluggishly upon stimulating the skin by the electric brush,  by pinch-
ing, or  by a pin.   It  is usually the smaller  pupil  which  fails  to
react consensually, or with the light-reflex, and the  consensual move-
ments generally occur when there  is impairment of the light-reflex,
although the light-reflex  may  be  impaired  whilst  the consensual
reflex may be  active.  The  knee-jerk  in this  prodromal  stage is
abnormal  in a majority  of cases, being sometimes exaggerated, some-
times slight, sluggish, or absent.  Transient urinary incontinence is
also  au occasional symptom  of the prodromal stage.  Whilst all
these symptoms that have  been enumerated are more or less constant,
varying slightly in inteusisy, perhaps, there are yet apt  to be parox-
ysmal exacerbations,  when the mental defects, the speech-alterations,
the tremor, and the  pupillary abnormalities  are increased,  and the
face becomes congested or pale, sometimes also the extremities. These
exacerbations last from one to several days.   As time goes on, these
symptoms increase in frequency and intensity, and  the ataxia which
has constituted the speech defects becomes  manifest  in the upper
extremities.  It  will best be made evident by getting the patient to 
PARALYTIC DEMENTIA.
669
write his name, or by having him close his eyes, swing his arm from
his  side, and quickly bring the  tip of his index-finger to touch the
tip of his nose (page 171).  The muscular strength  at  this time is
usually unimpaired, as can  be demonstrated  by testing the strength
of the  facial muscles or  the  grasp of the  hand;  but  in some few
cases, even in this prodromal  stage, the paresis may  be observed in
some of the muscles of the  face,  more especially  in a flattening or
sluggish movement  of the  muscles making the naso-labial fold, in
slight  deviation  of the tongue,  in a  loss of power in  one eyebrow
or one  side of the  brow, or even in imperfect action of one  upper
eyelid.
  These prodromal symptoms are of vast importance, especially in a
medico-legal sense, for it is by means of them that an  early diagnosis
can  be  made and much suffering frequently saved to the patient, his
relatives, and  his business interests.   Suddenly or gradually they
will merge into the second stage.
  In the maniacal or melancholiac stage the patient has superadded
to the  other symptoms a mania or a melaucholia,  each with certain
peculiarities distinguishing  it from other manias and melancholias.
In the mania of paralytic dementia there is almost  invariably a cer-
tain stupidity tingeing the delusions and the hallucinations, so that
the  former  are  illogical, and  with this stupidity is mingled an ex-
pansiveness or exaggeration of idea giving rise to the so-called deli-
rium of grandeur.  The patient,  for example, may  say that he owns
all  the theatres' in  the United  States or all  the steamboats, that he
will make his physician a present of a million, that  he is the most
powerful  man  in the  world,  and so  ramble on in this extravagant
strain;  but when you ask him how it is possible that he can be worth
all this when his circumstances are known to be far inferior to what
he claims them to be, he reiterates his assertion without attempting
to reason about it.   In this respect he affords a marked contrast with
the paranoiac who  may have  the same grand conceptions, but will
have any number of settled and fine-spun reasons with which to lend
them plausibility.   It is this air  of stupidity or  dementia tinting
the delusions and hallucinations that is so especially characteristic of
the paralytic dement and gives one of the names to the disease. The
mania   usually becomes violent, and  in some exceptional instances
becomes so  violent  as to lead to a fatal  termination by exhaustion.
The melancholia  of  the paralytic dement is not accompanied by ob-
stinate  insomnia, or post cervical ache, but  there  are often suicidal
tendencies, and the  delusions  and  hallucinations are the depressed
ones characteristic of ordinary melancholia.  In some  few instances I
have observed illusions in paretic dements, but it is very difficult to
determine this in such cases.   In both  the melancholia  and the
mania  paroxysms of terror are characteristic, coming on  frequently
without external cause.
  This second stage, of mania or  melancholia, may, however, as I
have already said, be wanting in certain cases, in  which there is a
simple  dementia throughout; but if present, it usually merges into
the third stage, of dementia. 
670
MENTAL DISEASES.
  Although there is a  certain element  of stupidity throughout  all
three stages in the paralytic dement, this stage of dementia proper
is marked  by downright  lack  of mental faculty to a greater o*- less
degree, so that the patient becomes  stupid or  childish, talking and
acting foolishly, at the same time that he may be difficult to restrain
temporarily.
  Throughout all  these  stages  of paralytic dementia there may
occur epileptiform or apoplectiform attacks; i. e., slight loss of con-
sciousness,  with or without convulsions, localized  or generalized, or
losses of consciousness  varying from mere  syncope to downright
coma, with paralysis that may be hemiplegic  or monoplegic in dis-
tribution or affecting speech.   Usually toward the  end of the first
stage, or during the second, paresis affecting at first the lower extremi-
ties begins to appear, showing itself at first only in  the paroxysmal
exacerbations, and gradually increasing  in degree until in the later
stages it may become complete paralysis of  the upper and  lower
extremities.  In  some  cases, however,  the paretic symptoms  are
among the earliest, and it  is by no means infrequeut  to find an  initial
tremor, pupillary alterations, and  defects in speech accompanied  by
a paresis of one  side  of the face and  tongue, or  to note that the
patient, even at this early stage, has a distinct paresis over and above
his ataxia.
  Certain of the  symptoms have peculiarities that are at times  of aid
in diagnosis, and which should, therefore, be considered in detail, such
as affection of smell, sight, hearing, tact, paiu, muscular  sense, and
temperature.
  Voisin claimed that the sense of smell was always defective  in the
initial stage of general paresis, but in this he has not been  borne out
by the later writers,  and  my experience  leads  me to state unquali-
fiedly that he is mistaken, for I have yet to see the  first case of this
disease in which the sense of smell was affected in  the early stage,
although  I have occasionally seen it  affected in cases of cerebral
syphilis  simulating  general  paresis.  In  the later  stages, as most
writers  are uniform  in stating, it is certainly  impaired; but this is
rather due to the mental impairment than to any particular lesion of
the olfactory apparatus itself.
   The sense of sight is sometimes affected in a  peculiar way, first
described by Fuerstner.   The defect is usually in one eye, especially
the right.   Single letters are recognized, and the patient can name
them; but when  combined in a word they are not recognized,  and it
is the same with  simple objects.  This is really nothing more  than a
variety of the mental blindness which has been elsewhere described
in this work.   The ophthalmoscope is of but little  diagnostic use in
general paresis, for it is in only a small  proportion of cases that any
lesion is found,  generally of  the nature of a primary optic-nerve
atrophy, and many of these are those which are associated with spinal
symptoms, although it can be observed in pure cerebral cases.  As the
symptom,  however, is not usually7 observed until the disease is well
established, it generally has but slight value in the question of  differ-
ential diagnosis. 
PARALYTIC DEMENTIA.
671
  Hearing is occasionally over-acute at the onset.   Word-deafness
(vide page 140) is observed also at times.
  The sense of pain is generally  acute in the first stage of general
paresis, and there are apt to be hypersesthesia and neuralgia.  Sander
calls attention to the fact that au  onset of migraine in an individual
in the fourth decade of life, without a precedent history either personal
or hereditary, is of great  diagnostic value, and  I think he is right.
Ansesthesia is a usual accompaniment of general paresis when the dis-
ease is well marked, and occasionally even in the early stage.  In six
cases of Mendel's in which there was marked ansesthesia there was
also a spinal  lesion ; but the former has occurred in cases of mine in
which  there were no spinal symptoms whatsoever, and it is not neces-
sary that there should be such.   This ansesthesia  in the later stages
may become very great.  Mickle  relates an  instance of a patient
chewing his right forefinger  as if it had been a  piece of tough
food, so that it became  gangrenous  and was amputated without any
general or local ansesthesia, the patient gazing stupidly at the opera-
tion without the least concern or evidence of pain. Baillarger relates
a similar case of amputation, and Lines tells how a  patient seized a
live coal and kept it in his hand long  enough  to produce a severe
burn.  I have seen ansesthetical  phenomena almost similar to this in
several instances, and in one case  that  had just passed out of the
initial stage  into an attack of mania the ansesthesia was so complete
that a large, jagged  wound caused by the patient thrusting his  hand
through a plate-glass  window  was dressed without the slightest
sensibility being  manifested.  This tendency to ansesthesia should
always be borne in mind when general paretics are made to bathe in
warm water, and it  is often an explanation of the so-called parboiling
accidents occurring in asylums and creating so  great a  furor in the
sensational newspapers of the day.   Fulgurant and stabbing  pains
may, of course, be met with iu the cases in which the disease is com-
 plicated with tabes.
   Etiology.  The causes of paralytic dementia are—
        Sex ;
        Age;
        Heredity;
        Occupation ;
        Social position;
        Other insanities;
        Cranial  traumata;
        Climate, locality, and race ;
        Syphilis;
        Alcoholism ;
        Food aud other poisons ;
        Spinal disease.
   Women are much less frequently attacked than men, and a careful
 analysis of  statistics made by  Mickle has shown that about four
 males are attacked to one female.   It is probable that this difference
 between the sexes is largely due to  the greater  exposure and tension
 of men in life and their greater  tendency to dissipation and errors of 
672
MENTAL DISEASES.
hygieue and diet, although it must not be forgotten  that  the female
is throughout life the more viable organism.
  It occurs chiefly between thirty and thirty-five, although excep-
tionally it may occur after or before these dates, sometimes as late as
sixty and occasionally as early as six.
  Heredity of  paralytic  dementia has been  rare in my experience,
although neurotic heredity has obtained in most cases.
  The military and  naval life are said to be conducive to paralytic
dementia.   Thus, the disease was frequent among the soldiers of
Napoleon the Great, and Mickle found many cases in the regiments
of the English Guards.
  Mickle states that of 64,642 persons admitted to the insane asylums
of England and Wales, 5.91 per cent, of the private admissions
were general paretics, whilst of the pauper admissions  8.21 per cent.
were  such.   Laehr found  only three  cases  of paralytic dementia
among 786 females of the better classes, and Jung asserts that 31.8
per cent, of the'males of the better class were paralytic dements, but
only one out of 109 females.  In the French army, so Colin main-
tains, three-fourths of the cases  of insanity in the officers were due
to paralytic dementia.
  There can be no doubt that the ordinary psycho-neuroses  of long
duration can sometimes  merge into paralytic dementia, and this has
been especially observed in cases of hallucinatory insanity by Marcg
and Calmeil, the former's cases having lasted  respectively three, four,
five, and six years, and the  latter's thirteen.  At  the  same  time it
must be borne in mind that this  causation is rare.
  There can be no doubt that cranial trauma acts in certain  cases as
a cause.
  There are many curious facts  about climate, locality, and  race in
the causation of paralytic dementia.   It is said to be extremely infre-
quent in Ireland, many of the large  public asylums having no case
of it, and only 2 to 3 per cent, of the  admissions to the Dublin Asy-
lum consist of this disease, whilst it is almost unknown in the Belfast
institution, where, it is stated  by Mickle, " the population is chiefly
of Lowland Scotch origin, aud really of Saxon blood, while the Celts
of Wales, Cornwall, and the Scotch Highlands have a considerable
share of the disease."  Yet  the  Celts of the  south of Scotland are
rarely affected by  it.   In the south  of France the  disease  has in-
creased during  the last two generations.  It is said not to have been
recognized in this country until 1843, and then by Dr. Luther Bell.
According  to  Dr. Workman, there was not  a single case in 1853,
when he entered the Toronto Asylum ; but from January, 1865, to
July, 1875, there were 72 deaths. The percentage is different in the
different provinces of Germany, in different parts of Belgium, in the
counties of England, and in the different States of Italy.  In  Cuba it
is infrequent.   In Portugal  the percentage is about 3 per cent, of all
the  insanities.   In Constantinople, judging by the institution on the
Asiatic side in Scutari, which was visited by Mendel, the disease was
relatively frequent, and increasing in  number  according to the state-
ment of the superintendent.   It  is stated that in Rio Janeiro, Brazil, 
PARALYTIC DEMENTIA.
673
there were 11 cases in 297 insane.  In Cuba it occurs much oftener
among the negroes than with the native whites.  In Australia it is said
to be frequent.
   In a most excellent and painstaking monograph written in  1889 by
Morel-Laval lee and Belieres the subject of the relationship of syphilis
to paralytic dementia is most exhaustively considered, and the authors
show very decidedly that syphilis is admitted by competent observers
in all the countries of Europe to be a frequent cause of this disease,
although there is no means of differentiating these cases from others
of non-specific origin.  These writers also demonstrate very conclu-
sively7 that there is a disease closely simulating paralytic dementia, and
designated by Fournier  as  syphilitic  pseudo-general paresis, which
may be induced by focal lesions of the cortical or subcortical regions
of the cerebrum, or by syphilomata, causing fusion of the cerebral
membranes, and-leading secondarily to cortico-meningeal infiltration.
Some forty-six cases are carefully collated and detailed  to  illustrate
these conclusions.  Although the authors do not offer any tangible
means of  differentiating syphilitic pseudo-paresis,  yet  a  study of
their cases will show  that in every case there was a precedent history
of cerebral syphilis, and in my cases this was also shown.   The dura-
tion of the disease maybe said to be from three to five years, although
cases have been narrated that ended in a few months, and others that
lasted many years.
   Diagnosis.   It should  be remembered that general paresis is
really  a gradual dementia, complicated  by stupid delusions, often
expansive  in  nature, by  pupillary alterations, by motor symptoms
that are ataxic in  the initial stage and paralytic  in the  later,  by
general tremor  that  causes a peculiar pronunciation,  and by the
supervention, in  many instances, of a mania or melancholia upon
the initial symptoms.  The  malady7 is,  therefore,  really a chronic
dementia of a peculiar type, with physical symptoms.   The pupillary
myosis, or dilatation, or inequality, or reflex alterations, the tremor of
the tongue and facial muscles, and the peculiar pronunciation, asso-
ciated with mental alteration  that is vague and stupidly eccentric, the
tendency to paroxysmal exacerbations, lasting a day  or two or more,
in which all the symptoms are exaggerated, and  flushing or pallor
are superadded—all these make a picture in the early stage that is seen
only in this  disease,  although there may be a certain  resemblance
to it  in others.    When to  these  symptoms are joined delusions
of grandeur, the diaguosis becomes very easy;  but even when the
dementia has not been interrupted by any markedly expansive delu-
sions the diagnosis  can be made by consideration of the foregoing
facts.   When to these symptoms of the initial stage have been joined
a mania or melancholia, of gradual  or sudden onset, the diagnosis is
still more easy, aud in every case of melancholia  or mania  the pre-
cedent history should be carefully obtained.
  The diseases from  which general paresis should  be differentiated
are—
       Disseminated  sclerosis;
       Paralysis agitans;
                                43 
674
MENTAL DISEASES.
       Cerebra syphilis;
       Primary dementia;
       Secondary dementia;
       Melancholia or mania;
       Katatonia;
       Paranoia;
       Alcoholism;
       Bromism;
       Lepto-meningitis cerebri.
  The diagnosis from disseminated sclerosis is not always easy, and
the diagnosis from a meningitis of the pia mater is sometimes equally
as difficult.  Usually, however, in disseminated  sclerosis the mental
symptoms are not so pronounced at the beginning.  There is not the
same  degree of ataxia, there is more apt to  be  nystagmus and the
pupillary alterations characterizing general  paresis,- and the tremor
precedes the mental symptoms by a period of months or years.   Nor
is there in disseminated sclerosis the tendency to paroxysmal exacer-
bations which  is seen  in  most cases of general paresis.  In dissemi-
nated sclerosis, too, the tremor in the early stage  is  usually of the
intentiont-ype, and this is rare in general paresis.
  Paralysis agitans  is  easily differentiated  from  general  paresis
because of the peculiar bent attitude, the slow, deliberate speech, in-
stead  of the stuttering, scanning enunciation of the general paretic,
by the lack of mental symptoms, except  some dulness in the later
stage, by the lack of  marked  pupillary alterations other than those
belonging to old age, and by the absence of  any paroxysmal exacer-
bations, although cases of paralysis agitans  may have apoplectiform
attacks.
  I feel quite  positive, although I am aware that I hold my opinion
alone against most authors, that cerebral  syphilis  can in most cases
be diagnosed  by means of the  symptoms to which I have called
attention, namely, quasi-periodical headache and insomnia, both head-
ache and insomnia ceasing upon the supervention of any paralytic or
convulsive symptoms; and when a cerebral disease characterized by
these symptoms, preceded or  not  by a history of specific  infection,
passes into dementia resembling general paresis, the diagnosis can be
made in the larger number of instances.  In some, however, in which
the history of these inititial symptoms  is wanting,  the diagnosis can-
not be made.
  Primary  dementia occurs  in  individuals  who  are younger than
general paretics, and the dementia is of an entirely different character,
the patient acting sillily and talking incoherently aud foolishly, whilst
the onset of the dementia is sudden as compared with the very grad-
ual and insidious onset of the  first stage of general paresis.  It must
be remembered,  too, that  the dementia  of general  paresis  is  only
vaguely manifested in the earlier stage, whilst that  of primary de-
mentia comes  on  full-blown, so to speak.  In primary dementia, too,
the ataxia, the pupillary alterations, the  apoplectiform  and epilepti-
form attacks, all are wanting.
  The secondary dementias are always, as the term  implies, secondary 
PARALYTIC DEMENTIA.
675
 and terminal conditions of different forms of insanity;  but the pre-
 vious history should make it plain in every instance that the previous
 insanity has not been  of the nature of general paresis.
   Every case of melancholia or  mania should have  the  previous
 history brought carefully to  the light, so  that the melancholiac or
 maniacal stage of a  general paresis  may  not  be  mistaken for an
 initial melancholia or  mania.
   Katatonia may in some cases be mistakeu for general paresis, but
 a careful examination  of the  patient and the history will make the
 differential  diagnosis easy.  Katatonia is a  cyclical disease, passing
 through a variety of mental phases, interrupted by choreiform, epi-
 leptiform, and cataleptoid attacks, and characterized by verbigeration.
 General paresis, on the other hand, is a chronic dementia of a remit-
 tent and insidious type, varied occasionally by demented agitation or
 demented depression without verbigeration, occasionally with  apoplec-
 tiform and epileptiform attacks, but seldom or  never with  catalep-
 toid symptoms.  In katatonia, too, the pupillary inequality and the
 pupillary reflex-alterations  are  wanting, as are also the ataxia, the
 tremor, the peculiar speech, and the eventual  paresis.
   Cases of  paranoia that have expansive delusions may be mistaken
 for general  paresis ; but the resemblance between the two diseases is
 too superficial to lead  to more than temporary mistake.  The delu-
 sions of the  paranoiac  are always reasoning and logical within certain
 limits, whilst those of the general paretic are stupid and non-logical.
 The paranoiac may have occasional tremor of tongue or facial mus-
 cles ; but so  far is he from  evincing the dementia of the general
 paretic that  he is abnormally7 keen and  acute, and in him are lacking
 the ataxia,  the characteristic pupillary alterations, the tremor, the
 tremulous speech, the  epileptiform or apoplectiform  attacks, and the
 terminal paresis.
   Some cases of alcoholism bear a strking  resemblance  at first sight
 to general  paresis, especially those which I have found  on the post-
 mortem table to consist of opacities of  the pia mater and congestion
 of the cerebral substance.  The diagnosis can be made  by means of
 the alcoholic history, the relatively acute onset of the symptoms, the
 tendency of the delusions to be keener and more logical than those
 of general paresis, and  to partake of the character of suspicion, es-
 pecially of marital infidelity.  It must  be borne in mind, however,
 that prolonged alcoholism of itself produces a genuine general paresis,
 and that these cases of which  we are now speaking are  simply cases
 of acute alcoholism.
  Bromism may, to a careless observer, simulate general  paresis;  but
 the distinction can be  readily made by obtaining the history, by the
 fetid breath, by the acne, by the excessive stupidity without delusions,
 by the lack  of any other pupillary alterations than dilatation, by the
 lack of ataxia and tremor, by thick, muffled speech rather than a
tremulously scanning  one, and by the early onset of general weak-
ness that may simulate paresis.
  Prognosis.  The prognosis  of general  paresis  is a  very serious
one although undoubtedly competent observers, such as  Minot, have 
676
MENTAL DISEASES.
put on record cases of cure.   I have never seen one, but I have wit-
nessed remissions of considerable duration, and  it should always be
borne in mind that these may occur in any case.
  Pathology.   We are just beginning nowadays to obtain a clear
insight into the pathological alterations of the cerebral tissues in this
disease.  Until recently striking results of morbid alterations  have
been  described and have passed  as  explanatory  of  the  textural
changes, although they  have  in reality been the terminal results of
a long series of microscopic alterations that  have themselves eluded
our ken.  This has been due, in the main, to two causes : first, our
lack of complete  knowledge of the histology of the  cerebrum; and,
second, to our defective  hardening-methods.   The marvellous bi-
chromate of silver stain, first discovered  by Golgi and  subsequently
applied by the genius of Cajal (vide pp. 17 et seq.), has now,  how-
ever, revolutionized our knowledge of the  marvellous mechanism of
the brain ; whilst the method of so-called " control" experiments—
i. e.,  investigations of  normal tissues by the same method—has
brushed away many descriptions of deceived investigators.   There is
a difference of opinion among cerebral pathologists, for instance, as
to whether paralytic dementia primarily begins in  the  bloodvessels
and  their lymphatic appendages, or whether its onset is to be found
iu the nerve-fibres aud the nerve-cells.  As a matter of fact, this is
an idle strife of words,  because there  have been  put on record no
pathological observations capable of proving that all the fine medul-
lated nerve-fibres of the cortex, such  as are described by Cajal and
his followers, have been thoroughly examined, for the simple reason
that the staining-fluids  used  in the pathological cases will not stain
all this network of fibres, and  it is therefore impossible to say that
authors who have described  only vascular lesions in the early cases
may not,  however  conscientious and truthful they  may have  been,
have overlooked certain degenerations in these nerve-strauds. Then,
again, Binswanger has demonstrated that all the hardening-methods
alter the original  structure of the cell, whilst Frommann positively
maintains that the so-called conservative solutions,  such as absolute
alcohol and chromic acid, often entirely destroy these bodies.   Nor
is this all, for certain alterations described as pathological have been
shown to be due to immediate post-mortem change.  Thus, Zacher
describes  with great particularity certain  microscopical details  in
nerve-fibres, which he would  have us  regard as the earliest signs of
the disease, such as irregular  nodules, varicosities,  brittleness, nor-
mal  axis-cylinders shown through  transparent   medulla,  atrophy,
irregular curved  shape, and  final disappearance, observed especially
in the tangential fibres and the sublying strands ; and yet Binswanger
has ruthlessly demonstrated the same  appearances in the brain of a
man who had been beheaded !   In spite of the difficulties of the histo-
logical technique,  however, it can now be said that the changes affect:
       1.  The nerve-fibres;
       2. The nerve-cells;
       3.  The neuroglia and  the vessels ;
       4.  The membranes. 
PARALYTIC DEMENTIA.
677
  In 1880 Tuczek thought there was a progressive  disappearance
of nerve-fibres from the anterior, basal, medial, and lateral portions
of the cerebrum,  as  far back as  the anterior central  or ascending
frontal convolutions, the gyrus rectus, at the base of the brain (Figs.
14 and 18), being also implicated in some  acute cases.   The  fibres
involved were those which are known as the tangential fibres of the
cortex,  as well  as the superradiating  and  interradiating fibres.
(See Fig.  29, page 53.)  In these  cases, in  addition to a decrease  or
disappearance of the nerve-fibres, there was an increase or fibrous
transformation of the interstitial tissues, with an abundant develop-
ment of abnormally large spindle or Deiters' cells.   Tuczek claimed
that these pathological appearances were pathognomonic of Paralytic
Dementia, aud he holds this view  to the  present time; but whilst
the facts  to which he first called  attention have  been abundantly
confirmed, his interpretation  of them has  not met  with the same
happy fate, as the same fibres are frequently wanting in other  forms
of mental  disease.  Thus, Zacher, examining  the  brains of twelve
paralytic dements, endorsed Tuczek's statements ; but in three brains
of ordinary paralysis, two of paranoia, and  three of senile dementia,
he  found  the same peculiar  disappearance of nerve-fibres, as did
Keraval and Targoula in secondary dementia, Emminghaus in post-
febrile dementia, Jendrassik in tabes dorsalis without mental impair-
ment, and  Greppin in several cases of what he calls post-melancholiac
dementia ; whilst Kostiurin, examining the  brains of twelve perfectly
sane people, varying  in  age from sixty-five to eighty-eight years at
death, observed a considerable loss of tangential fibres in the parietal
lobe.  Greppin, moreover, could not find any lack of the intracortical
nerve-fibres in a case of paralytic dementia  of nine  months'duration.
Indeed, Fischl points out  that there are great physiological differ-
ences in the number and calibre of the cortical  nerve-fibres,  and that
a sufficient regard has not been paid to these physiological conditions.
Binswanger,  who  has lately made  the most thorough  study of the
pathological  data  about this disease, believes that it is only possible
to reach  conclusions  as  to the disappearance of fibres in the upper-
most, or  tangential layer (Fig. 29, page 53), and the interradiating
fibres, whilst the findings in the superradiating fibres are uncertain ;
but there  can be  no question that the bloodvessels are implicated
at an early stage, although, as has already been said, there is a doubt
as to whether they are at first affected.  These  changes in the vessels
are in the  nature of a hyaline  degeneration.  By them is induced a
fluctionary and  passive  hypersemia, and the  outflow, through the
wall of the  bloodvessels,  of numerous red and  white blood-cells.
Probably because of a certain  amount of  destruction of tissue,  as
well as of  the transudation, there soon follows a  dilatation of the
extra-vascular lymphatic system, and the veins become distended with
red blood-cells, although, curiously enough, white blood-cells have
not been  observed within them.
  The alterations  in the basic and connective-tissue substance of the
brain as well as in the vessels, have been of great interest, inasmuch
as upon the termination of them rests the question  as to whether the 
678
MENTAL DISEASES.
disease is really primarily an interstitial encephalitis.  At the outset
there is great question as to how much  of what  was formerly re-
garded  as  basic  and  connective-tissue substance was  really nerve-
processes which have been shown to exist by the newer  methods.
Different authors have attached different meanings  to the increase in
the number of free nuclei, the appearance of spindle-cells,  the alter-
ation of the  basic substance into thickened  and fibrous tissue, and
the proliferation and thickening of the neuroglia.   The older writers
regarded these appearances as due to a true inflammatory process, be-
ginning in the bloodvessels, the nerve-elements being terminally im-
plicated.  In an elaborate  paper upon this  subject, as far back as
1880, Binswanger demonstrated  that  there were varieties of nuclei
coming from the different structures of the cerebrum, viz., from the
smooth muscles  of the vessels, the neuroglia, the ganglion-cells, the
adventitial  sheaths, the  pericellular spaces,  and  also  certain  free
nuclei  which  are found strewn throughout the cerebrum.   Some of
these color readily, whilst others do not, the former being generally
the smallest.  These nuclei  are  irregularly distributed in  the white
and gray substances, vary greatly in number  in different individuals
and in different  portions of the cerebrum, and are more numerous in
advanced age.  In addition to these facts, investigations by Lubimow,
Witkowski,  His, Gierke, Golgi, Cajal, Kolliker, and Retzius, have
only served, as  has already been said, to create great doubt as to
what the  so-called basic  and connective-tissue substance is, and this
uncertainty has  naturally reflected itself in the observations as to the
nature of  paralytic dementia;  as a  consequence of which nothing
more can be definitely said than that the neuroglia  is sometimes atro-
phied and sometimes proliferated, whilst the spindle-cells in the mid-
dle  and deeper  layers aud the cortex  are  not  increased in number
except in the later stages.
   Cionini  has found  the gray matter of  the cortex  diminished in
thickness, especially in the central convolutions aud the frontal brain,
partially also in  the  occipital lobe.  It would therefore  appear that
a certain amount of  cortical substance must have beeu  destroyed,
and what  has remained has become  more compressed, whilst the
physiological spaces around cells and bloodvessels  have widened.
   At the same  time there begins an active proliferation (generally
regarded as reparative) in the endothelial adventitia of the  arterioles,
capillaries, and  veins, leading to a thickening of these structures and
proliferation of the endothelial nuclei.   A portion of these new forma-
tions also undergo a hyaline degeneration  at a later stage.   In some
vessels the process of proliferation even implicates the true wall of
the  vessel.   By these  means the lumen  becomes  narrowed, and iu
later stages even obliterated.  A new formation of vessels is doubt-
ful,  although Bevan Lewis thinks he has seen it.  The iutra-adven-
titial lymph-spaces  are only affected  in  places, separated from the
media, and containing red  and white blood-cells, coagulated lymph,
and amorphous and finely granular pigment; but white blood-cells are
only found occasionally;  indeed, the presence in large masses of the
latter  is regarded by some authors, notably by Binswanger, as an 
PARALYTIC DEMENTIA.
679
indication of the course of the disease, for he believes that they are
seldom found in the intra-adventitial lymph-spaces iu large number
in slowly progressive cases with paralytic intercurrences, whilst they
are present in those with chronic and frequently repeated venous con-
gestions.  The extra-adventitial lymph-space, together with the peri-
cellular space, is very generally dilated.   In the former is also found,
though in a less degree, white and red  blood-cells, fibrinous coagula,
and pigment;  but  in  the lymph-spaces of the  cortical substance
itself, as well as in the  pericellular spaces, no distinct increase of the
lymphoid elements has  been observed.  True inflammatory or exuda-
tive processes  may  be added to  these  alterations with  the further
progress of the disease, and they are demonstrated clinically by som-
nolence and irritative  and paralytic phenomena;  and if death then
occurs,  there may  be  marked infiltration  of both the extra-  and
intra-adventitial lymph-system, although it has been demonstrated, on
the other hand, that these inflammatory changes may be wanting, the
clinical phenomena then being probably due to the obstructed flow of
the lymph-stream produced by the dislocated cerebral pressure.   In
the later stages of the disease the pia mater  plays an important part.
In the early stages this membrane  is only  moderately affected  over
the convexity of the  hemisphere, particularly in  isolated places  in
the frontal lobes, being thickened and proliferated in its endothelial
nuclei;  but with the course of time the thickening and nuclear  pro-
liferation of the endothelial  adventitia of  the other vessels extend
to the similar structures in the pia; and these hypoplastic processes
of the pia are regarded as an extension of the proliferation of the
vessel-sheath to the endothelial membrane.  Partial adhesions of the
pia to the connective tissue lead in places to imperfect obliteration of
the epicerebral spaces,  this being observed in the region of the ves-
sels going to the cortex, as well as in the portions of thickened  pia;
and this is due to an increased growth  of the pial connective fibres
and of the  endothelial septa coming from the pia  and traversing the
epicerebral  space.  There are thus induced au obstruction in the flow
of the lymph-stream, and a stasis in the lymph-spaces of the connective
tissue, as well as those in the deeper portions of  the cortex.   It is
not difficult to understand that this altered lymph thus obstructed  in
its flow should coagulate cerebral tissue which has been already de-
stroyed. These changes do not seem to differ in kind, whether the case
be chronic or relatively acute, except in the rapidity of their  progress.
A certain number of the violent cases  are  fatal  because  of the ex-
haustion  produced by the  great  motor excitement,  the  deficieut
nourishment, the pulmonary or intestinal  lesions, etc., rather  than
because of any intensity iu  the  pathological phenomena of the cere-
brum, and, indeed, in  many of them true inflammatory phenomena
are entirely wanting.   These alterations in the tissues  especially
affect the frontal brain, the convolutions of the island of Reil, aud the
parietal lobe, and fiually extend to  the temporal and occipital lobes.
   Discussion of the alterations in the cells has not been  had in this
general description because of the uncertainty regarding them.
 3 The  ganglion-cells  of the  cortex, especially  in the frontal lobe, 
680                   MENTAL DISEASES.
 often possess two or more nuclei, one of them, however, being prob-
 ably the nucleus of a wandering leucocyte.  The body of the cell is
 jagged in places, the space  thus formed  being filled with the nuclei
 of leucocytes, whilst the pericellular spaces are widened, and contain
 one or more leucocytes, as well  as  pale, ovoid nuclei which are
 coarsely granular.  What  these  large ovoid  cells are is uncertain,
 although Binswanger believes that they come from the endothelium.
 They  have often been mistaken for the true nuclei of the ganglion-
 cell.   Many other alterations in  the cells  have been described by
 different  authors.  Thus, Binswanger states that  the nucleolus is
 often swollen, and  contains peculiar white, glittering, irregular lines,
 producing a cracked appearance ; or the place of the nucleoli is taken
 by two to four irregular lump-like large  granules, or the nucleus
 holds  a  large  number of small, dark, distinct  granules, whilst the
 body of the cell is unaltered.  In other cases the same author has
 seen the  nucleus enlarged, puffed, cloudy with granules, or holding
 glittering plates ; or its contour is irregular, or merges with the sur-
 rounding cell-protoplasm, in  both of which instances the nucleolus
 is unaltered.  In other  cases the  body of the cell appears normal,
 but the place of the nucleus has been taken by a loose, finely granu-
 lar mass, and in still  other cells the nucleus has disappeared, being
 replaced by brown  pigment, and the nucleolus  is also gone.   With
 these alterations of the nucleus and the  nucleolus, the body of the
 cell is irregular, bellied, diminished, darkly pigmented, and contains
 small nuclei without nucleoli.   Alongside of many cells thus altered
 are found  others perfectly  intact.   These cellular  alterations were
 observed  in  the  central, the third frontal  and  neighboring convo-
 lutions, and those of the island of Reil. These observations of Bins-
 wanger have  been  confirmed by Liebmann, Zacher, and Bucelski;
 but in certain  investigations  undertaken  by Fischl he found that
 in  some hardening-methods,  notably in  Flemming's,  Ehrlich's,  or
 Muller's solutions, the  nucleoli of the  cells  would disappear  or
 diminish, the place of the  nucleolus would  often  be taken by pig-
 ment,  and its  shape would be altered and the  nuclei would lose
 their sharp outlines, whilst pigmentary collections would almost con-
 stantly be found in  the ganglion-cells.   Nevertheless, as pathological
 he  regarded  pigmentary degeneration with fattiness and entire de-
 struction of the ganglion-cells, and the nuclear and  nucleolar altera-
 tions found in  normal brains  are  seen in a larger  number of cells
 and in many  more places  in pathological instances.  Fischl was
 never  able to  obtain  the  hyaline degeneration  of the cell-body
 (spoken of by  Liebmann and Lubimow)  in alcohol  preparations.
 Binswanger has found the cortical cells diminished in number in the
 early stages and  in the galloping  cases, although this was not very
 marked, and the cells were  often only affected  singly, and in indi-
 vidual groups  in  the frontal  lobe and the central convolutions.
 Friedmann has made some very interesting observations upon the
early alterations in the ganglion-cells of the anterior horn, and  he
states that the  death of the cell  is effected in several ways:   (1)
By a  homogeneous swelling of the cell,  which  is really a  hyaline 
PARALYTIC DEMENTIA.
681
transformation of it, commencing in the centre, whilst a small periph-
eral portion of the cell  may remain intact for  some time, contain-
ing the chromatic substance, and even the nucleus, which latter dis-
appears late,  but yet before the nucleolus ; (2)  by a granular de-
struction  or  fatty degeneration.  In this  the diseased portions are
transformed into a pale, granular mass, as the chromophile substance
disappears.   The first step in this type is the granulation, and not
the fattiness.   Types  1  and 2  are often combined; (3) by sclerotic
degeneration,  which is less  frequent than  the  other forms  in the
acute inflammatory period,  whilst  it  is more  often found in the
chronic cases ; (4)  by the transparent light-cell.   This is a very in-
frequent form, characterized  by the destruction of all but a small
portion of the chromatic  substance, the nucleus often  remaining
intact.  This author  does not believe in the  existence  of simple
atrophy or shrinking of the cell, or in the so-called cloudy swelling;
the first being, according to him, only the result of the homogeneous
degeneration,  and  the latter a combination  of  swelling with the
second  stage  of the  molecular destruction.   These observations,
however,  have not yet been confirmed.   They have led, however, to
a great doubt as to whether  the active inflammatory changes in the
ganglion-cells described by others really occurred, inasmuch as they
have  probably been due to  defective hardening-methods or faulty
observation.
   From these descriptions it can be seen that the  theory of paralytic
dementia  being due to an interstitial encephalitis,  as was maintained
by the older authors, is not warrantable.  Nor is there any confirma-
tion of the views of Bevan  Lewis, who lays great  stress upon the
role played by the connective tissue, for he  would have  us  regard
the connective-tissue  (or spider or Deiters') cells  as playing  the
part of depurative agents,  being, as  he expresses  it, true scaven-
ger-cells.   He maintains that these bodies are auxiliary to the capil-
laries, that they feed  upon  the degenerated  nerve-cells  and fibres,
both of which are converted into granules or oily droplets, and he
even presents many alterations of the condition of these scavenger-
cells at different stages  of the  degeneration  of the  cortex, figuring
them  laden with the products of the disintegration of nerve-cells
and nerve-fibres, and actually at  times  drawing  upon the peri-
vascular sheath with  such force as to distort it.  Nor, in view of
these  newer  investigations, need we attach more  than a relative im-
portance  to certain gross  phenomena which  have been observed  in
the brains of paralytic dements.  Thus, meningeal hemorrhage may
occur on the outer surface of the arachnoid into the subdural  spaces,
and it may be a mere streak of fluid  staining, a coagulation, or a rust-
stained pellicle that may be peeled off, forming one of the varieties of
the so-called arachnoid cysts.   Fuscous degeneration of the cortical
nerve-cells may  sometimes occur.   Spitzka  has  described a cystic
degeneration  of the cortex found either in the gray matter or in both
the gray and white, consisting of minute cavities, varying in size from
a pin-point to a millet-seed. 
682
MENTAL DISEASES.
  Treatment.   The first point to determine iu any case of general
paresis is whether there  has been a history of cerebral syphilis, and
then whether it is possible to cause improvement of the symptoms
by large and increasing doses of the iodide,  or, if the  iodide is
not well borne,  by the  conjunction  with  it  of  mercury.   (See
" Syphilis of the Nervous System.")  If there should be no cere-
bral  syphilis, the use of either  iodide or mercury will be  of  slight
value, simply diminishing the tendency to convulsive and  apoplec-
tiform  attacks and to agitation; but  in  this event the dose need
not exceed  15 or 20 grains three times a day.  The use of large
doses of ergot has sometimes  seemed to me to affect  the disease
favorably.   The  fluid extract  should always  be employed, com-
mencing with | drachm  doses  three times a day, and increasing  to
\ ounce three times a day if the patient's stomach will carry such
a quantity.   Sulphate of quinine, 5 to 10 grains at  bedtime occa-
sionally, with 20 grains  of bromide of potash, has also seemed to me
to be of considerable use.  In the attacks of mania the patient can be
quieted  by means of warm baths, by hyoscyamine, by the bromides,
and  by tincture of veratrum  viride.  In using warm  baths  care
should be taken to test the temperature thoroughly and not allow it
to exceed 100° or 105°,  and the patient's sensations should  never  be
relied upon, as there may possibly be the ansesthesia which  has been
spoken  of, whilst too warm a  bath  may  easily lead  to vesication.
The  crystallized form  of  hyoscyamine  should be used — Merck's
preparation  being  the best in my opinion—and the doses should
vary from fa^ to jfa grain once or twice a day.  I do  not believe,
however, in the large doses, fa to -fa grain, that are sometimes recom-
mended. The combination with a  bromide, the bromide of potas-
sium best, will increase  the sedative effect of hyoscyamine without
increasing its depressing influence, and 10 or 15 grains of the bro-
mide will answer for this purpose.   The tincture of veratrum viride
is sometimes of excellent use in quieting maniacal excitation, in doses
of 5 to 10  drops; but  it should  always be  carefully watched, and
should not be given in cases of cardiac lesion.   Electricity I have
never found of the  least use in cases of  general  paresis, either  the
galvanic, faradic, or static current. 
CHAPTER  XIX.
DEMENTIA PARANOIDES.
  Definition.   A form of insanity characterized by eonfused ideas
of persecution aud self-exaltation  without marked emotional dis-
turbance, rapidly passing into dementia.
  Clinical History.  This is a disease to which  attention has
been called by Kraepelin, and is well worthy of being known because
of its resemblance to paralytic dementia.
  The majority of cases begin with  confused  ideas of persecution,
and these are ushered in  with prodromata of malaise, insomnia, rest-
lessness, and indisposition  to work, but  these  are often exceedingly
vague.   They last for  several  months.   During this  period  of
time  there  is  a  gradual  mental  alteration  denoted  by eccentric
and  causeless acts,  which  are often startling in their disregard
of conventionality or even  morality.   Delusions of exaltation  or
grandeur  next make their appearance,  and, like  those of paralytic
dementia, they are stupid  and illogical  or unsystematized in char-
acter.  Delusions of  hearing are also frequent.   The patient, how-
ever, has no emotional disturbance, but speaks of his delusions and
his auditory hallucinations with  perfect  calmness.  The patients are
usually silent, and speak briefly.  They will  often seem  to have a
dull consciousness of being sick, especially in  the beginning of the
disease, and this at times seems  to be of a hypochondriacal nature,
as they complain of weakness, trembling in the limbs, and difficulty
iu thinking, but  the real appreciation  of their  condition is never
present.   In some cases the delusion of grandeur  is most marked, in
others that of persecution.   The  delusion of persecution is usually of
a startling  nature, such as that the patient has had his head cut  off
by the physician, or that somebody has  opened his abdomen,  or that
mephitic odors have penetrated his  room at night, etc., and these lead
often to violent assaults upon the persecutors.  When the disease is
well established, hallucinations are frequent, and involve the various
senses of sight, hearing, etc.   Although the intelligence may at first
be only slightly impaired, the dementia soon supervenes and pro-
gresses rapidly.   The  mood at  this time is  always an exalted one,
and at night the patients are frequently excitable.  There are, how-
ever no corporeal or so-called  somatic symptoms whatever.  Ihe
progress of the disease is toward  incurable dementia.  The age of the
patients is generally between thirty aud  fifty, two-thirds being in the
former period of life.  The  dementia,  according to  Kraepelin,  is
worse in the younger cases.  .
   Prognosis.   The prognosis of these  cases is always unfavorable,
according to Kraepelin. 
684
MENTAL DISEASES.
   Diagnosis.   Dementia paranoides is characterized by the gradual
supervention of illogical and  stupid  delusions of persecution and
exaltation, without emotional disturbance or somatic symptoms, and
the rapid passage into dementia with marked hallucinations of sight,
hearing, and the general senses.
   Primary dementia is to be distinguished from it by the fact  that
the dementia is a silliness not characterized by delusions of persecu-
tion or self-exaltation, and the delusions are feeble, often difficult to
make out, and the dementia is entirely curable.
   Paranoia is easily differentiated by the exquisite logicality  of the
delusions of persecution and exaltation, by the absence of dementia,
and often by the  changeability of the delusions.   Dementia para-
noides, however, may be mistaken  for paranoia in the initial stage
of depression or exaltation.
   From  paralytic dementia, dementia paranoides is  to  be distin-
guished  by the  earlier age of the patients  affected  by it, by the
absence of somatic symptoms, the greater fixity of the delusions, and
the longer course.
   Hallucinatory insanity is demarcated by the fact that there is  in it
no such dementia as in dementia paranoides, although certain progres-
sive forms of the former disease may be practically indistinguishable
from the latter; indeed, Kraepelin does not feel  sure that there is
not some close relationship between the two types of insanity.
   Pathology.  Nothing whatever is known of the pathology of
dementia paranoides.
   Treatment.   The treatment is unknown, according to the de-
scriber of the disease, Kraepelin. 
CHAPTER XX.
                           DELIRIUM.

   Definition.  Delirium is a dream-like mental condition with ex-
citement, with or without delusions, hallucinations, and illusions, and
occurring during or after some febrile condition  or  from the  action
of a poison.
   Clinical History.  In many cases of delirium  there are pro-
dromata consisting of restlessness,  mental confusion, reflex  excita-
bility to sensory perceptions, irritability, and a mild grade of insomnia,
with  disturbing  dreams.   Hallucinations and  delusions may then
appear, at first fragmentary and vague.  These hallucinations are
especially prone to affect the senses  of sight and hearing, and their
variety is very great.  Under the influence of these  false perceptions,
possibly sometimes from other causes, the  patient becomes more and
more restless and excited.  If the grade  of  the delirium becomes
greater, these phenomena become intensified, and in  the severer types
the mental disturbance may become very great.  In other  cases the
onset is very sudden, and it  may even be without prodromata.  In
still others the delirium throughout is of  a low,  muttering, so-called
typhoid type.
   Etiology.  The causes of  delirium  are to  be  found in  all the
febrile affections, such as pneumonia, bronchitis, pleurisy, peritonitis,
the exanthemata, typhoid fever, typhus, etc.
   Prognosis.   The  prognosis of delirium will depend largely upon
its cause,  the duration of its causative affection, and the condition of
the patient. Taken by itself, however, in any case the delirium adds
to the gravity of the patient's condition.  In a very general way it
may fairly be said that the prognosis is  better the more in propor-
tion the delirium is to the  degree of fever and the better the general
condition of the patieut.  Moreover, the  mild delirious conditions
which occur occasionally after  typhoid, peritonitis,  and some other
febrile affections are usually of good prognosis, provided the patient's
general condition is good, even when they continue for weeks, and
although they may occasionally pass into such other types of insanity
as acute dementia  and  hallucinatory iusanity.   The prognosis  of
similar conditions after typhus  and variola, however, is said  to be un-
favorable.   With these exceptions, the continuance  of the  delirium
beyond a week, however,  is unfavorable, as  is  also its persistence
after the defervescence.
   Diagnosis.  The diagnosis  of delirium is usually made with ease
by the history of the case and  by the presence of the  characteristic
mental condition.   It needs only to be differentiated from :
       Transitory fury, or furor transitorius ;
       Epileptic insanity;
       Delirium grave. 
686
MENTAL DISEASES.
   Transitory  fury  has a very acute ouset, usually without prodro-
mata or very slight ones, and the condition is, as the name denotes,
one of absolute blind, reckless fury, lasting from a few minutes to a
few hours, and being succeeded by a deep sleep, without any memory
of what has occurred.  It is therefore an  entirely different picture
from that of delirium.
   In epileptic insanity there may at times be a  delirious condition
simulating a delirium very closely in its dreaminess.   However, the
history of the epilepsy will make the diagnosis easy when  it can be
obtained.  In certain ambulance cases, however, it may be impossible
to obtain this history for the time being, whilst the mental condition
may continue  for several days, rarely, however, as long as a week;
and  uuder these circumstances time alone can determine the matter.
   In delirium grave there  is an  alternating condition of furious
maniacal  violence with absolute  intermissions, and  this  is entirely
different from the continuous dreamy condition of delirium.
   In cases of muttering delirium, sometimes indeed  in  those of a
more excitable type, it is  well to  search carefully for any lurking
lesion in the pelvic, the aural, and the cranial cavities.  I have known
of a number  of cases of mistaken  diagnosis which close examina-
tion  show7ed to be due to a  pelvic abscess, an aural trouble, a throm-
bosis of the cerebral veins, or an intracranial abscess.
   Treatment.  The treatment of delirium should depend, of course,
largely upon its  cause.  If it is possible to remove this, it should
always be done, as in the case  of a pelvic, aural, or  intracranial
abscess, or by the opening of a thrombosis of a cerebral sinus. In  the
febrile affections the treatment of the disease causing the fever is all
that  can be undertaken.  When the delirium is proportionate to  the
rise  of temperature special  measures should be  adopted if possible
to bring  the temperature  down, and this should  be done over and
above  the general  treatment of the case.   The  measures employed
for this purpose  should be the cold  pack, the  water-coil, and  the
antipyretics.   The  cold  pack  and the  water-coil are  dangerous
measures  except  in robust individuals, and  should be  used with
caution or not at  all.  For my own part, I usually prefer them only
as a  last resort in cases in which the antipyretics have  failed and  in
which  also it is  evident that  the  delirium  rises and  falls with
the temperature-curve.  The best antipyretics are the  coal-tar prep-
arations, and of these the least dangerous is acetanilide in doses of 4
grains  twice or three times daily.  Even in using these the pulse
should be very carefully watched,  and if it is  seen to flag, alcohol
and cardiac stimulants should be immediately employed.   Whiskey
is the best of alcoholic stimulants, aud it should be given with a free
hand in whatever doses may seem necessary, varying from two ounces
to as much as 12 ounces in the twenty-four hours.   The condition
of the  pulse should be the guide as  to the dose, as should also be  the
previous habits of the patient, for those who have been accustomed to
alcoholic stimulants will of course take more in sickness than the tem-
perate.  If the alcoholic stimulant does not properly affect the pulse,
the sulphate of strychnine or digitalis should be administered.  The 
DELIRIUM.
687
strychnine should be  given in doses of gr. -fa pro re nata;  that is,
three times in the twenty-four  hours, or every two or three hours.
In some cases, however, in which the strychnine induces disagreeable
griping of the intestines, digitalis may be used, either in the form of
a reliable  fresh tincture, ten drops pro re nata, or one grain of the
solid extract, or three drops of a  fluid extract, or digitaline.   The
nourishment in all these cases should be pushed as much as possible.
Of course, it  is impossible  to give exact directions for every case,
because these  will vary so much.  In all cases, too, great care should
be taken to have the bowels move freely at least once  a day, and a
good plan  is to give -fa grain of  calomel every hour or two until the
bowels do act properly. The condition of the skin should be carefully
looked after also, and  it should be kept moist and gently perspiring.
Cerebral sedatives should never be used in delirium if they can be
avoided, for they are always drepressing, and they very often event-
ally increase the mental trouble.   When it is absolutely necessary to
give  them, as from  the extreme restlessness of the patient,  they
should be administered very carefully.  The best are the bromide of
potash  and the hydrobromate of hyoscine, the former  in doses of
20 or 30 grains, the latter  jfa grain.  These may be  given either
alone or in combination, always according to the varying condition—
indeed, it is a good rule, when possible, for a physician never to, order
a dose without having satisfied himself of the effect of the previous
one.  I have  seen more than one case of perfectly curable delirium
depressed into a fatal  condition  by the reckless use of these cerebral
sedatives.
   When the  delirium occurs after defervescence or in the stage of
convalescence  of the  febrile affections  the keynote of treatment  is
combined stimulation, rest,  and nourishment.    The warning that has
already been  given  against cerebral  sedatives should  be repeated
here with double emphasis, and it may truly be said that it is very sel-
dom necessary to use either bromide  of potash or hyoscine except occa-
sionally at bedtime, to secure a restful night, and even then these drugs
should  be  given in combination with some alcoholic or cardiac stimu-
lant, such as an ounce or two of whiskey or fa grain of strychnine.
Much more useful, however, is  the administration of quinine, iron,
malt-extract,  and food.  The following prescription is one that I
have found  so useful in these cases as to make it almost a matter of
routine with me to prescribe it:

         R.—Quin. sulph........gr. ij.
            Ferri. sulph. exsic.......gr- J-
            Strychnise sulph.......gr- sV
  M. ft. capsul. no. j.  Mitte xv.
  S.  One three times daily after meals.

   If the iron in this prescription shows a tendency to constipate, for
it may  be  substituted  four  grains of ferratin.  Should the constipa-
tion  still  persist, gr. fa of aloin may be combined with each dose.
The malt-extracts should be given regularly  after each meal in full
doses.   If the patient does not dislike the peculiar taste and  odor of 
688
MENTAL DISEASES.
a fresh malt-extract, it is always best to give one of these, as they are
rather more reliable than the imported alcoholic  preparations.  The
food should be of the most nourishing  description, and if there  is
difficulty in taking full meals it should be given frequently in smaller
quantities.   The rest should be absolute, most or all the time being
spent in bed until the delirium has entirely disappeared.  Again and
again have I seen relapses  brought on in these cases by making
patients walk or taking  them  out to drive before they had  fully
recovered. 
CHAPTER   XXI.
                            IDIOCY".

  Idiocy is a condition of congenital mental defect that is technically
distinguished from that of  later years, which is  known as dementia.
The symptoms are simply those of lack of development, and this may
vary very much in degree,  from downright lack of mind to different
conditions of imperfect mental activity, so that one idiot may sing well,
another play like a master, as did the celebrated Blind Tom, or another
may be startlingly weather-wise, or another may even be a clairvoyant,
and so on.   The causes of idiocy are chiefly those lesions which have
been described in the chapter upon the cerebral palsies of childhood,
namely:  porencephalitis, hemorrhage, traumata, etc.  Besides these
there may be other causes : imperfect development of the cerebrum and
cerebellum as a whole or  in portions;  lack or imperfect development
of the corpus callosum; hydrocephalus, congenital or acquired; local
or diffused encephalitis, which may be  primary or secondary to acute
processes;  meningitis ; and in some rare cases cerebral hypertrophy.
Besides all these causes Lannelongue has advanced the idea that mauy
more cases of idiocy than have been supposed are due to premature
ossification of the fontanelles and synostosis.  For many years  this
supposition has been advanced by different pathologists.   Virchow
and Welker have supposed that many abnormalities in the shape of
the skull might be due to lack of development of the bony tissue from
an  inhibition due to inflammatory changes in  the  sutures, whilst
Gudden has assumed that it might be caused by insufficient nutrition
of the  cranial bones  from early obliteration of their nutrient vessels.
Meyer has demonstrated that  in  some cases rhachitis can cause the
same defect.  If the  lack of development of the skull is bilateral and
symmetrical, so-called microcephaly results. If the vertex of the skull
is undeveloped, whilst the basal bones attain their proper size, the so-
called Aztec type of  skull results, a variety of microcephaly.  Gratio-
let has pointed out certain cases with a very small skull of thick bones
and synostosis at the vertex, whilst the cranial bones at the base were
mainly cartilaginous, the petrous bone and the ethmoid being larger
than normal, and the fossa of the cerebellum being unusually capa-
cious;  so that the cerebellum, medulla  oblongata, and the spinal cord
were largely developed, while the surface of the cerebrum was scarcely
more convoluted than in  the ourang-outang.  Idiots of this class are
extremely vivacious, and Griesinger compares them to birds.  These
cases have a pointed nose that is  beaked, and small, low, and short
heads.   In the cases of  cretinism  that are seen endemically in  the
Alps of Switzerland there is frequently found to be early ossifica-
                                44 
690
MENTAL DISEASES.
tion of the cranial bones, and in these the nose is sunken and broad,
the eyes wide apart, the cavities  of the eyes  broad but not deep,
prominent cheek  bones and jaw  as in the so-called prognathism.
With these different varieties of arrested  cranial development often
goes lack of development of the bones of the body and limbs.  Lanne-
longue, however, asserts that it is  the  premature ossification of the
fontanelles, especially, that is the cause  of many cases of idiocy, and
he has therefore proposed that the skull should be liberally removed
over each hemisphere so as to allow abundant space in the develop-
ment of the cerebrum.  This operation  is known  as  craniectomy.
The objection to Lannelongue's view is  that, as has been seen, arrest
of cerebral development producing idiocy may result not only from
pathological  lesions  in the intracranial  contents themselves, but also
from  lack of bony development in the bones at the base,  and in
either of these  cases it would be worse than useless to remove the
skull at the vertex.   In the second  place, the operations that have
been done upon  cases of idiocy at Lannelongue's suggestion have not
shown any  beneficial  results.  Dr. R. S. Newton has collected for
me thirty-nine cases in which Lannelongue's operation has been done.
Temporary improvement is often seen, and  the  overwrought  minds
of parents and  relatives are very apt to  exaggerate the amount of
this;  but no case of permanent improvement has  been  put upon
record.   Nevertheless, I think that an operation is warrantable in
suitable cases.  If, for instance, a child has developed up to a certain
age, and has then gradually ceased to do so, and if  there have been
no symptoms of an intracranial lesion, or if the shape of the skull is
such as to indicate a deformity such as we have described  as being
due to lack of development of the cranial bones of the vertex, then I
believe that it is fair to perform a craniectomy.   Even then, however,
it should be borne in mind  that a porencephalitis may have occurred
without marked  symptoms.   Even  if it does no good, the operation
should do no harm, and as there is a possibility that the future may
enable us to diagnose suitable cases, I  can see  no objection  to the
procedure; but a craniectomy, eveu  when  done antiseptically, is  a
very dangerous operation, as  the childish  braiu  does not stand the
shock of the operation nearly as well  as the adult cerebrum,  so that
the number of deaths has been large from this cause.  The operation
must therefore be regarded as one of last resort. 
GLOSSARY.
  Aba'sia.   Unsteadiness of gait.   From a, privative, and facie, a step.  See
Astasia abasia.
  Acromegaly.  A disease characterized by enlargement of the extremities
and of the face.  From anpov, extremity, and /ikyac, great.
  JEsthesiom'eter.  Instrument for measuring the degree of tactile sensibility.
From aiotino-ic, sensation, and fiirpov, measure.
  Agorapho/bia.  Fear of open  spaces.  From  ayopa, market or open place,
and <j>60oc, fear.
  Agraphia.  Loss of ability to  write.  From  a, privative, and ypa<j>u,  to
write.
  Allochei'ria.  A perversion of sensibility, in which an impression made on
any part seems to be felt on the other side.  From alloc, another, and xup,
hand.
  Amyotrophy.   Atrophy of a muscle.  A form of lateral sclerosis is called
amyotrophic, on account of the progressive muscular atrophy characteristic
of it.  From a, privative, jive, muscle, and  rpofn, nourishment.
  Ance'mia.  A condition of debility characterized by diminution in the ratio
of red corpuscles in the blood.  From av, privative, and  atfia, blood.
  Anozsthe' sia.  Privation of sensation ;  paralysis  of sensibility.  It may be
general or local.   From av, privative, and aiadrjoic, sensation.
  Analge'sia.  Absence of pain.   From  a,  privative, and alyog, pain.
  Anapeira/tic.  Relating to  spasms of inco-ordination  in muscles caused
by repeated  exercise, as in writers' cramp.  From  avaneipao/iai, to attempt
again.
  Ank'le cWnus.   A series of  uniform spasmodic contractions of the ankle-
joint produced by continuous stretching of its extensor muscles.  From kIovoc,
tumultuous movement.
  An'ode.  The positive electrode or pole of a galvanic battery.   From ava,
upward, and ofioc, a way.
  An'sa lenticula'ris.  Tract of nerve-fibres extending from crusta to lentic-
ular  nucleus, and passing under the optic thalamus.  From ansa, a loop;
lens,  a lentil.
  Anthropophagy.  Cannibalism.   From avdpuKoc, man, and <pdyu, to eat.
  Anticyclone.  A period of blue skies, bright sunshine, high barometer, and
slight atmospheric motion.  Painful forms of neuralgia occurring especially
at that  time are  called anticyclon'ic.  From anti, opposite to, and cyclone
(nvKlog, a circle).
  Ape-hand.  Complete atrophy of the thumb-muscles, noticed in progressive
muscular atrophy.
  Apha'sia.   Impairment of  or loss  of speech, resulting from  apoplexy, 
692
GLOSSARY.
 embolic softening of the brain, neoplasms, or other cause.  From a, privative,
 and (pv/J-t, to speak.
   Arboriza/tion   Tree-like appearance of nerve-fibres,  as in the cerebrum
 and cerebellum.   From arbor, tree.
   Arc'uate fi'bres.  Fibres  in the medulla oblongata which  pass from the
 anterior median  fissure to  the olivary body and cerebellum.  From arcus,
 arch.
   Argyll''-Rob''ertson pu'pil or sign.  Small pupil which fails to  respond to
 light, but not to efforts at accommodation; absence  of pupil reflex, etc.
   Artefacts.   Artificial structures  or  productions.   From ars,  art;  /actus,
 made.
   Asta'sia.  Inability to stand.  From a, privative, and io-tv/m, to stand.
   Asta/sia  aba/sia.  A  condition of defective automatic  co-ordination,  im-
 pairing the power of standing or walking.   From d, privative, and hrnfii, to
 stand;  d, privative,  and haaic, step.
   AsteWion.  Point of meeting of the lambdoid, parieto-mastoid, and occipito-
 mastoid sutures in the skull.  From aster, a star.
   Astheno/pia. Weakness of sight.  From aadevrjc, weak, and o\p, the eye.
   Atax'ia or At'axy.  Disorder: applied especially  to muscular inco-ordina-
 tion.  From d, privative, and ragig, order.
   Ath'etoid move/ments.  Irregular movements, such as are seen in athetosis.
 The term  athetoid is applied  to a  form of chorea  characterized by alow,
 gradual, worm-like movements of the fingers and toes.  From aderog, without
 fixed position.
   Athetosis.   Inability to retain the fingers and toes in  any one position.
 From aderog,  without fixed position, from d, privative, and ridnfii, to place.
   At'rophy.  Decrease  in size with  corresponding loss of power.   From d,
 privative, and rpo^n, nourishment.
   AuWa.  A sensation like that of a vapor or emanation preceding an epileptic
 or hysterical seizure.  From aura, a vapor.

   BaciVli.   Micro-organisms, made  up of cylindrical or  oval cells,  which,
 when connected, form  rods or cells, many of  which are pathogenic.  From
 baculus, a rod; bacillus, a small rod.
   Bacte/ria.  A genus  of Schizomycetes, which include micro-organisms that
 were at one time classed with  the infusoria.  They include micrococci, sar-
 cinae, bacteria proper,  bacilli, vibriones, spirochsetse, and  spirilla.  From
 fianTTipiov, a small stick.
   Base'dow's disease.   Exophthalmic goitre.   From Von  Basedow, who de-
 scribed it.
   Bell's paVsy or paralysis.  Paralysis  of the facial nerve.  From Sir Charles
 Bell, who described it.
   Belonepho'bia.   Morbid dread of  pins and needles.  From fielovn, a pin,
 and (j>o6og, fear.
   Blepharospasm.  Spasm of the orbicularis  palpebrarum muscle.  From
 j31e<j>apov, eyelid, and anac/iog, spasm.
   Brachycephalic.  Having a short  head.   From Spaxvg,  short, and  netpaln,
 head.
   Breg'ma.   Point of junction of the coronal and  sagittal sutures.  From
Ppexu, to moisten. 
GLOSSARY.
693
  Bul'bar paral'ysis.   Motor paralysis, with muscular atrophy, affecting the
motor cranial  nerves and attached muscles, especially the hypoglossal nerve,
and certain filaments of the facial and of the spinal accessory.   From bulbus,
medulla oblongata, and paralysis.

  Cais'son disease.  A series of symptoms dependent upon  working in com-
pressed air, as in a caisson or diving-bell.  Sometimes called diver's paralysis.
  CaVcar a/vis.   The hippocampus minor.  Lat., a bird's spur.
  Cal'carine.   Pertaining to the hippocampus minor; as calcarine fissure, a
groove on the occipital lobe corresponding to the hippocampus minor. From
calcar, a spur; calcar avis, the hippocampus minor.
  Carpholog/ia.   The generally delirious action of gathering flocculi (" pick-
ing the bedclothes"), significant of extreme cerebral irritability, in low fevers,
etc.  From napipog, flocculus, and leyu, to gather.
  Cat'alepsy.  State of suspended consciousness and volition, with rigidity of
voluntary muscles.  From /card, down, and  la^avu, to fall,  to seize.
  Cath'ode.   Negative pole or electrode of a galvanic battery.   From  Kara,
downward, and  66og, a way.
  Caud/ate nu'cleus.   That portion  of the  corpus striatum which is within
the ventricle; the lenticular nucleus forming the other portion.  From cauda,
a tail.
  Cellulif 'ugal cur'rents.  A term applied to nervous currents which flow out
of the cell through the axis-cylinder processes.  From  cellula, a small  cell,
and fugio, to flee.
  Cellulip''etal cur'rents.   A term applied to nervous currents which flow into
the cell through the protoplasmic processes.  From cellula, a small  cell, and
peto, to seek.
  Cen'lres.  The chief or central points of physiological activity, the func-
tions of which can usually be localized.
  Centrifugal fi'bres.  Efferent  fibres, which pass from a  centre to convey
impressions to the periphery.  From centrum, centre, and fugio, to flee.
  Cent rip'etal fibres.  Nervous fibres passing to a centre, as afferent or sensory
fibres.  From centrum, centre, and peto, to seek.
  Cen'trum ova'le.  The oval medullary portion  seen when the hemispheres
of the brain are sliced away.   From centrum, centre, and ovale, oval.
  Cerebel'lum.   That portion of the medullary mass contained in the cranial
cavity which occupies the lower occipital fossae below the tentorium.  From
cerebrum, brain ; cerebellum, little brain.
  Cer'ebro-spi'nal. Relating  to  the brain and spinal cord.  From cerebrum,
brain, and spina, spine.
  Chias'ma.  A crossing or decussation of certain nerve-fibres ; e. g., Chiasma
opticum, the crossing of fibres of the optic nerve.
  Chor'da  tym'pani.   A filament of the Vidian nerve, which enters the tym-
panum.  From  chorda, cord, and tympanum, the drum of the ear.
  Chore'a.  A condition attended with irregular involuntary clonic contrac-
tions of the muscles, one form being known as St. Vitus's dance.  From Xopeia,
a dance.
  Chorema'nia or Choreoma'nia.  Chorea, or St. Vitus's dance, attended  with
convulsive emotions in hysterical or neurotic individuals.
  Cine'ture-feel'ing.  A feeling as if the waist was encircled by a tight girdle
or belt, noticed  in certain nervous affections.  From cinctura,  a girdle. 
694
GLOSSARY.
   Cing'ulum.   A bundle  of fibres lying in the gyrus  fornicatus.   Lat., a
 girdle or zone.
   Claustropho'bia.  Fear of enclosed places.   From Lat., claustrum, an en-
 closed place, and <po$og, fear.
   Glaus''trum.  A layer of gray matter situate between the island of Reil and
 the external capsule.   From claustrum, a barrier (claudo, to shut).
   Claw-hand.   A condition seen in  progressive muscular atrophy, due to
 sinking of the interosseous  spaces on the back of the hand and incomplete
 extension of the terminal phalanges, with contraction of the antagonistic
 muscles.
   Clethropho'bia.  Fear of enclosed or fastened places.  From  Klfjdpov, a bar,
 bolt, and <p6fiog, fear.
   Clon'ic.   A term  employed to designate certain irregular convulsive move-
 ments, in which relaxation alternates with spasm.   From nlovog, tumultuous
 action.
   Coch'lea.  Anterior portion of the internal ear;  its winding form suggest-
 ing resemblance to  a spiral shell.   From mxli-ag, a snail with a  spiral shell.
   Co'ma.   A profound lethargy.  From nufia, a swoon, deep sleep.
   Com'missures.  Bands or cords of nervous matter  connecting different im-
 portant portions  of the cerebrum, cerebellum, etc.  From committo,  to join
 together.
   Conirac'ture.  Persistent and wax-like contraction of a muscle.  From con,
 together, and  traho, tractum, to draw.
   Convolutions.  Smooth  tortuous eminences on the surface of the cerebral
 hemispheres.   From convolvo, to entwine.
   Co-ordina'tion.  The working in harmony of muscles in the performance
 of any function.  From con, together, and ordino, to put in order.
   Coprola'lia.   Involuntary use of obscene words, a symptom in some forms
 of insanity.  From Konpbg, ordure, filth, and laMu, to talk or prate.
   Cor'pora amyla'cea.  Microscopic starchlike bodies found in the brain and
 spinal marrow.  From corpora, bodies, and amylum, starch.
   Cor'pora  mammilla'ria.   Mammillary  bodies or eminences,  forming  the
 bulbs of the fornix.  From mammilla, a small breast; diminutive of mamma,
 a breast.
   Cor'pus callo'sum.  A white medullary band seen on separating the two
hemispheres of the  brain,  which it connects with each other.  From  corpus,
 body, and callosus, hard.
   Cor'pus stria'tum.  Anterior cerebral  ganglion, forming a portion of the
floor of the  lateral ventricle, and now known of two  distinct masses of  gray
matter, the caudate and the lenticular nucleus.   Literally, striated body.
   Cor'tex.  The cortical or gray substance of the brain, seen on the external
parts of the cerebrum and cerebellum.  From cortex, bark.
   Ore'tinism.  A form of idiocy especially prevalent  in the deep valleys of
certain  mountainous  regions of  Europe; commonly accompanied  by an
enormous  goitre.   The name is thought to be derived from  " Chretien,"
Christian, as implying freedom from moral responsibility—sinlessness.
   Cri'ses.  Violent  attacks of pain in the gastric, laryngeal, or iliac regions,
simulating organic disease of those parts ; characteristic of locomotor ataxia.
  Cru'ra.  The peduncles  of the  cerebrum and cerebellum.   From crura,
legs (from their leglike appearance). 
GLOSSARY.
695
  Cu'neus.  Cuneate or wedge-shaped lobule on the surface of the occipital
lobe of the brain.  From cuneus, a wedge.
  Oyrtom'eter.   An instrument for measuring the curve of any portion of the
body.   From nvprog, convex, ixerpov, measure.

  Decussa'tion.   An x-shaped crossing of nerve-fibres or filaments, as of the
optic nerve.  From decussatio, a crossing.
  Demen'tia.  Loss of reasoning power,  or incoherence of ideas.  From Lat.,
de,  out of, and mens, the mind.
  Dendrit'ic.  Tree-shaped, tufted,  villous.  From 6ev6pov, a tree.
  Dichot'omous.  Dividing into  two branches of the same or nearly equal
size; bifurcating.  From  dcxorop-eu, to cut into halves.
  Diple'gia.  Double symmetrical paralysis.  From Sig, twice ; nlvyv, a stroke,
a blow.
  Diplo'pia.   Double vision,  two objects being seen instead of one;  due to
derangement of the axes of vision.   From <Jt-7rAooc, twofold, and  otptg, vision.
  Di'ver's paral'ysis.  See Caisson disease.
  Dolichocephalic.   Having a long head, the antero-posterior diameter being
excessive.  From dolixog, long, and Kecf>a?.rf, head.
  Dor'sad.  Toward the dorsal aspect.  From dorsum, back.
  Dynamom'eter.  Instrument for  measuring the force of muscular contrac-
tions.   From Sbvauig, power, and /usrpov,  a measure.
  Dysozsthe'sia.   Obscured, diminished,  of even abolished sensation, particu-
larly of the special senses.  From  6vg, difficult, and aiodrjoig, sensation.
  Dys'trophy.  Imperfect  or  defective  nutrition.  Progressive  muscular dys-
trophy is a synonym of progressive  muscular atrophy.  From  dvg, with diffi-
culty, and rpofj)?/, nourishment.

  Echola'lia.  A symptom of palmus, consisting of the repetition of words
heard.  From fou, echo, and ?uiMu, to talk or prate.
  Ecs'tasy.  An entranced condition with visions, the body being meanwhile
in a cataleptic condition.   " Out of one's self."   From in, out of, and ordcng,
station.
  Elec'trodes.   Poles of a galvanic battery.   From electricity,  and  66og,  a
way.
  Elecirol'ysis.   Decomposition through the influence of the electric current.
From electricity, and Ivaig,  solution.
  Elec'tro-therapeu'tics  or -ther'apy.  Treatment of  disease by  electricity.
From electricity, and depa-rrEvu, to cure.
  Em'bolism.  Plugging of a vessel with an embolus  (plug) separated from
the interior of the heart or a bloodvessel, and carried along in the circulating
blood until it produces obstruction,  as of a cerebral artery.
  Encephali'tis.   Inflammation of the brain (encephalon).  From tyKtyalog,
the brain, and itis, a suffix denoting inflammation.
  End-bask'ets.   Thick and wavy terminal  ramifications, having the appear-
ance of baskets, surrounding the cells of Purkinje.
  End-bulbs.   Terminal  nerve-corpuscles in the lips, tongue, palate, etc.
  Ep'ilepsy.  A  cerebro-spinal disease in which  the  patient suddenly falls,
with loss of consciousness and convulsive movements of the muscles.   From
tnl, upon, and laufiavo), to  fall, to seize. 
696
GLOSSARY.
  Er'ethism.  Augmentation of the vital  phenomena, through irritation, in
any disease or organ.   From epediC,u, to irritate.
  Er'gotism.  A condition resulting from the excessive use or abuse of ergot
or spurred rye;  of which  vertigo, convulsions, torpor, paralysis, and  dry
gangrene may be symptoms.
  Erythromelal'gia.  A nervous disease characterized  by a circular patch of
redness and swelling,  with pain in the part affected, usually the feet.  From
epv&pog, red, fitlog, a limb, and alyog, pain.
  Exophor'ia.  A tending of the visual lines outward.  From ef, out of, and
tyopiu, to carry.
  Exophthal'mic goi'tre.  A disease characterized by cardiac palpitation, with
rapid pulse; enlargement of the thyroid gland, and prominence of the eyes
or exophthalmus.   From ef, out of, and b^Oalnbg, eye.
  Exophthal'mus.  Abnormal protrusion of the eye.   From  k%, out of,  and
6<{>da?ifj.bg, eye.

  Farad'ic.  Relating to faradization, or  electricity by induction, Faradism.
From Faraday, the celebrated chemical and physical investigator.
  Fenes'tra ova'lis.  Aperture in the inner tympanum.  Lat., oval window.
  Formica'tion.  An itchy  or creeping  sensation, as if ants were crawling
over the surface of the body.  From formica, an ant.
  Fornica'tus.  Arched, as the gyrus fornicatus or fornicate convolution, im-
mediately above the corpus  callosum.   From fornix, an arch.
  For'nix (arch or vault).   Medullary body in the cerebrum, on the middle
line, beneath the corpus callosum and above the middle ventricle.
  Foudroy'ant (Fr.).  Sudden, overwhelming.
  Friedreich's disease.  A hereditary disease, consisting of nystagmus, ataxia,
defective speech,  loss of knee-jerk,  and curvature of  the  spinal  column.
Named from its  describer.
  Fu'ror transito'rius.  An outbreak of violent fury, lasting for a few hours,
and  terminating in deep sleep, from  which the patient  awakes without the
slightest memory of its occurrence, and never  recurring in the same person.
From furor, fury, and transitorius, transient.
  Fur'uncle.  A boil.   Lat., furunculus.

   Gang'lia.  Enlargement or knots in the course of a  nerve, usually belong-
ing to the great sympathetic system.  Plural of ganglion, a knot.
   Geniculate bod'ies.   Eminences situate at the inferior and external portion
of the optic thalami.   From geniculum, a small knee or joint.
   Gi'gantism.   Extraordinary size.  From yiyag, a giant.
   Gir'die-feel'ing.  A feeling as if the waist was encircled by a tight  girdle
or belt, noticed in certain affections of the nervous system.
   Glabel'la.  The part of  the face between  the eyebrows.   From glaber,
smooth.
   Glio'sis.  Sclerosis  with  excavated spaces  in the  gray substance of the
brain, giving rise to  atrophy of the optic nerves and olfactory bulbs,  and
other symptoms  resembling general  paralysis.  From yliog, glue, and  osis,
suffix denoting morbid condition.
  Glo'bus hystericus.  A symptom of hysteria, being a sensation as if a ball
was present in the throat.  From globus, ball. 
GLOSSARY.
697
   Glos'so-la'bio-larynge'al paral'ysis.  A motor  paralysis,  with muscular
atrophy, affecting the motor cranial nerves and attached muscles, especially
the hypoglossal nerve, certain filaments of the facial and of the spinal acces-
sory.  From yluaaa, tongue, labium, lip, and !apvy£, larynx.
   Glos'so-pharynge'al.  Relating to the tongue and pharynx; as the glosso-
pharyngeal  nerve, which  is  distributed to those organs and others  in the
vicinity.
   Grand mal (Fr.).   " Great disease:" applied in epilepsy to the fully devel-
oped fit.
   Graves s disease.   Exophthalmic goitre.  From  Dr. Graves, its describer,
in 1835.
   Gum'ma.  A syphilitic gummy  elastic  tumor formed in the periosteum,
met with in all the important viscera.  From gummi,  gum.
   Gy'rus.   Literally, a ring or circle.  Used in anatomy of the nervous system
to designate any one of certain  convolutions of the brain.

   Hcematomyel'ia.  Spinal hemorrhage. (For definition, see Htvmatorrhachis.)
From atfia, blood, and fivelog, marrow.
   Hasmator'rhachis.   An  effusion  of  blood  about, within, or between the
membranes of the spinal cord, or into the  substance of the cord.   From ac/na,
blood, and paxig, the spine.
   Hebephre'nia.  So-called   insanity of the period of puberty.  From 7767,
puberty, and  <j>pr/v, the mind.
   Heb'etude.  Dulness of intellect or of sense, sometimes noticed in  brain
affections.   From hebes, dull.
   Helicomon'ades.  The micro-organisms  of syphilis.   Discovered by Klebs
in 1878.  From ili^, a spiral, and uovag, a mound.
   Hemianossthe'sia.  Loss of sensation in the lateral half of the body, caused
by lesions of various portions of the central nervous system.  From rjp,i, half,
av, privative, and aiadrjaig, sensation.
   Hemianop'sia.  A deficiency of one-half of  the  visual field.   The term is
applied to  the  crossing  of the  rays of light  in the media and front of the
retina.  From y/ii, half, a, privative,  and a>ip, the eye.
   Hemio'pia.   A deficiency  of  one-half  of the visual  field.  The term is
applied to the condition of the retina.  From v/m, half, oTrro/j.at, to see.
   Hemiatrophy.  Atrophy of one side of the body from impaired nutrition.
From fifu, half,  a, privative,  and rpotyn, nourishment.
   Hemicran'ia.   Headache  of one side of the  head.  From fifu, half, and
upaviov, skull.
  Hemiple'gia.  Paralysis affecting one-half of the body.   From rj/11, half,
and nlriy//, a stroke or blow.
  Hemispheres.  Literally, half-spheres.   A term applied to the upper sphe-
roidal portion of the brain.   From v/u, half, and ofaipa, sphere.
  Hippocam'pal.  Relating to the hippocampus ; as the hippocampal fissure.
From 'nznog, a horse, and na/nrog, a sea-monster.
  Hippocam'pus.  Name  given to two elevations in the  ventricles of the
brain, the hippocampus major and  minor.  From 'iTnrog, horse, and Kxiunog, a
sea-monster.
  Hunt'ington's chore'a.   A form of hereditary chorea in  adults, the symp- 
698
GLOSSARY.
toms of which are peculiar dancing and postural movements  and grimaces,
mental impairment and muscular inco-ordination.
  Hy'aline.   Glassy or transparent.  From valog, glass.
  Hydrocephalus.   A collection of fluid  within the brain;  dropsy of the
head.  From vdup, water, and ae^alfj, head.
  Hydromyel'ia.  Fluid in  the cavities of the spinal cord. From vdup, water,
and fivelbg, marrow.
  Bydropho'bia.  The aggregate of symptoms produced by infection from the
virus communicated by the bite of an animal affected with rabies; excessive
dread of water and difficulty of deglutition being prominent.  See Rabies.
From vdup, water,  and 4>6(3og, fear.
  Hyperacu'sis.  Unusual acuteness or sensitiveness of hearing.  From vwep,
over, and duovcug, hearing.
  Hyperce'mia.  Abnormal accumulation  of blood in the capillaries.  From
virep, over, and di/na, blood.
  Hyperidro'sis.   Excessive  sweating.  From  vizep,  excessive, and ISpug,
sweat.
  Hy'pertrophy.  Overgrowth from superabundant nutrition, with deficiency
of waste.  From virep, over, and rpotpr), nourishment.
  Hyp'notism.  An artificial condition of suspended sensation, consciousness,
and  will-power, produced, by various  methods, by  another person, as by
suggestion, so called.  From vwvog, sleep.
  Eypochon'dria.   Morbid fears;  formerly supposed to have their origin in
the region of the hypochondrium.
  Hypoglos'sus.  The hypoglossal nerve,  distributed  to  muscles connected
with the tongue and hyoid bone.   From vko, under, and yluaaa, tongue.
  Hyste'ria.  A morbid  emotional condition reputed to have its seat in the
uterus.   From varipa, the uterus.
  Hys'tero-ep'ilepsy.  Hysteria associated  with epileptiform convulsions and
other nervous symptoms.

  lnco-ordina'lion.  Lack of correspondence between  mental manifestations
and muscular  action, as in locomotor ataxia,  etc.  From in, not;  con, to-
gether ; ordino, to put in order.
  lnfundib'ulum.  Literally, a funnel  A funnel-shaped collection of gray
matter attached to the pituitary body.  From in, in, and fundo, to pour.
  Inhibit'ion.  Action of restraining  or prohibiting, as of nervous influence
to muscles to which such nerves are supplied.  From inhibeo, to restrain.
  In'ion (" occiput'').  The occiput or the occipital protuberance.
  Insom'nia.  Sleeplessness.  From in, not, and somnus, sleep.
  In'sula cer'ebri.  The island  of Reil, in the brain.  Insular signifies re-
lating to the isle of Reil.  From insula, island, and cerebrum, brain.
  Intercalate.   To insert;  to place between.  The term  Intercala'turn is ap-
plied to the locus  niger.   From inter, between, and calo, to place.
  Intracra'nial.  Within the cavity of the skull, as  intracranial syphilis, in-
tracranial hemorrhage, etc.   From intra, within, and upaviov, skull.

  Jaw jerk.  A motion, produced by tapping the jaw  while the mouth  is
open ; it is diminished or absent in some nervous diseases. 
GLOSSARY.
699
  Kaiaton ia.  A form of insanity characterized by mania, melancholia, and
cataleptic symptoms, manifested in alternation.  From  /card (intensive), and
rdvog, tension.
  Kenopho'bia.  Same as  Agoraphobia.   Fear of open  spaces.  From nevbg,
hollow, empty, and Qdfiog, fear.
  Knee-jerk.  Motion produced by tapping the patellar  tendon while the leg
is placed loosely over the opposite knee;  increased or diminished in nervous
diseases.


  Lagophthal'mus.   A partial or complete paralysis of the orbicular muscle
of the eyelid, preventing closure.  From layug, the hare,  and bqOalfiog,  the
eye.
  Lamb'da.  The junction of the lambdoidal  and sagittal sutures, a point
from which measurements are taken in craniological examinations.  From
the  Greek letter A.
  Lan'drys paral'ysu.  Acute  ascending paralysis, characterized by motor,
or almost entirely motor, paralysis  of  the lower  extremities, then  of  the
trunk, upper extremities, neck, and face.  Described by Landry in 1859.
  Lar'vated.  Hidden or obscure: applied by  Falret to a form of epilepsy
without petit mal, or in which it  is very slight; epilepsie larve (Fr.).  From
Lat., larva, a mask.
  Lemnis'cus.  A bundle of fibres in the pons and crus  cerebri, appearing
superficially as a  triangular band, winding obliquely  around the superior
peduncles from the  funiculus  olivarius to the corpora quadrigemina.   Lat.,
a ribbon.
  Lentic'ular.  Having the shape of a lens or lentil, as the lenticular ganglion.
From lens, a lentil;  lenticula, a small  lentil.
  Lep'to-meningi'tis.  Inflammation of the pia mater.  From leirrbg, thin,
slender, and itis, suffix denoting inflammation.
  Leucocythce'mia.  Increase of leucocytes with decrease of red corpuscles in
the blood.  From levubg, white, avrog, cell, and al/ua, blood.
  Lim'bic lobe.  A lobe which  surrounds  the corpus callosum.  From limbus,
a border.
  Ling'ula.  A thin lobule of gray matter derived from the anterior border
of the cerebellum and blended with the valve of Vieussens.  Diminutive of
lingua, tongue.
  Lithce'mia.   The presence of uric acid (sometimes called lithic acid) in the
blood.  From lidog, stone, and  alua, blood.
  Localiza'tion. Specification  of a certain part or structure  as a centre of
physiological functions or processes, or of pathological actions.  From locus,
a place.
  Locomo'tor atax'ia.  A chronic morbid condition of the spinal  cord,  at-
tended with loss of power of co-ordination of voluntary muscular movements,
lightning-pains, absent tendon-reflex, etc.  From  locus, a place, and moveo,
motum, to move; a, privative, and ra^cg, order.
  Lo'cus cazru'leus.   A dark-brown or bluish spot in the floor of  the fourth
ventricle; also, a collection  of large, dark, pigmented  cells  in the region
behind the posterior quadrigeminal bodies.  From focus, place, and cceruleus.
blue. 
700
GLOSSARY.
  Lordo'sis.   Curvature of bones generally, but especially  of the  vertebral
column forward, sometimes due  to paralysis of the muscles of the spine or
of the abdomen.  From lopduaig, curvature.

  Ma'nia.  A form of aberration of mind  characterized by acute mental
excitement and exaggerated nervous action.  From navia, madness.
  Mar'ie's malady.  Acromegaly.  After Marie, who first described it.
  Mas'ochism (Krafft-Ebing).  A sexual perversion in which a  member of
one sex takes pleasure in being dominated by the other, as when the male has
sensuous delight in submitting to humiliating and degrading acts  from the
female.  From Sacher-Masoch, a novelist who wrote on this subject.
  Massage (Fr.).  Friction and manipulation of the body.  From  Fr., masser,
to shampoo.
  Masseur (Fr.).  A man who practises massage.
  Masseuse (Fr.).  A woman who practises massage.
  Mas'toid.   Nipple-shaped.  The projection on the temporal bone behind
the ear is called the mastoid process.  From fiaarbg, nipple, and eldog, like.
  Medul'la oblonga'ta.  The prolongation of the spinal cord upward into the
cranium.  From medulla, marrow, and oblongatus, prolonged.
  Med'ullated fi'bres.  Nerve-fibres covered with a medullary sheath.  From
medulla, marrow.
  Megacephal'ic.  See Mesocephalic.  From ueyag, great, and ne<j>alv, head.
  Melanchol'ia.  Melancholy; supposed by the ancients to be  caused  by
black bile.   From fielag, black, and xolv, bile.
  Meniere's disease.  A complex of symptoms, of which vertigo is the chief,
occurring with lesions of the  external,  middle,  or internal  ear.  After
Meniere, who first described it.
  Meningi'ti*.  Inflammation of  the meninges of the brain and cord.  From
fiijviyi;, membrane, especially that enveloping the  brain  and cord; the pia
mater; and  His, suffix denoting inflammation.
  Menin'go encephali'tis.  Inflammation  of  the  brain  and  its  membranes.
From p.T?viyz, membrane, eynetyalog, brain, smclitis, suffix denoting inflammation.
  Menin'go-myeli''tis.   Inflammation of the spinal cord and  its membranes.
From p-r/viy^, membrane, fivelog, marrow, and itis, suffix denoting inflammation.
  Mes'merism.  A form of hypnotism.  From  the name of its  originator,
Mesmer.
  Mesocephal'ic.   Term employed to designate a skull whose capacity is be-
tween 1350 c.cm.  and 1450 c.cm. (being  determined by filling the skull with
shot poured  into it through the foramen magnum).   If less than  1350, the
skull is said to be microcephalic;  if over  1450,  megacephalic.  From peaog,
middle, and ne^alr), head.
  Mi'crobe.   Microbes are minute  unicellular  organisms  (schizomycetes).
The class includes the micrococcus, bacillus, spirillum,  etc., commonly known
as bacteria.   From fiiupbg, small, and /3log, life.
  Microcephalic.  See Mesocephalic.  From /uxpog, small, and ne^al?], head.
  Migraine (Fr.).  Pain in the temporal or orbital region of one side of the
head; sick  headache.  Abridged  from Hemicrania.   From i)p.i,  half, and
npaviov, skull.
  Mil'iary an'eurism.   Aneurism of the smallest arteries, of the cerebellum
especially.  From milium, millet, and dvevpvapa, dilatation. 
                              GLOSSARY.                          701

  Milliam'pere.  A measure of electricity, one-thousandth part of an ampere.
rrom mille, a thousand,  and ampbre, unit of strength  of electro-magnetic
current shown  by force of one volt through one ohm.   From the name of a
French scientist.
  Milliampereme'ters.   Instrument for measuring  minute  electricity, as by
milliamperes (which see).  From milliampere, and u^pov, measure.
  Monoma'nia.   A form of mental aberration formerly supposed to be con-
fined to one subject of delusion.  From fiovog, alone, and /xavia, madness.
  Monople'gia or  monople'gic paral'ysis.  Paralysis  limited  to one organ or
part, caused by circumscribed lesions. From fiovog, single, and irlriyrj, stroke.
  Morphinoma'nia  or  Morphioma'nia.   A  morbid  craving  for  morphine.
Mania from the use of morphine,
  Morvan's disease. A disease commencing with neuralgia, which is followed
by paresis and analgesia, finally by one or more whitlows, with  necrosis of
the phalanges.   From Morvan, who  described it in 1883.
  Myeli'tis.   Inflammation of the spinal cord.  From /uvelbg, marrow,  and
Ms, suffix denoting inflammation.
  Myodt'rophy.  Atrophy of a muscle.   From pig, muscle, a, privative, and
rpoipn, nourishment.
  Myopath'ic at'rophy.  Progressive  muscular atrophy.  From  uvg,  muscle,
and ivatiog, disease; a, privative, and Tpo<pr/, nourishment.
  Myosclerot'ic paral'ysis.  A chronic disease, usually called pseudo-muscular
hypertrophy or progressive muscular sclerosis, causing paraplegia and great
increase in the size of the limbs.  From p.vg, muscle, and culripog, hard.
  Myo'sis.   Contraction  of the pupil.  From fivu, to close the eyes, and osis,
suffix denoting morbid condition.
  Myoton'ia.  Thomsen's disease.  Painless tonic contraction of  voluntary
muscles, lasting several seconds at a time, and thus interfering with loco-
motion and other  movements.  From fivg, muscle, and rdvog, tension.
  Mysopho'bia.  A morbid fear of being unclean.  From fivaog, uncleanliness,
and (pofiog, fear.
  Myxozde'ma.   Gelatinous infiltration of the skin, usually accompanied by
dulness of the senses, slow monotonous speech, and cretinoid aspect.   From
fivi-a, mucus, and  oWrjfia, a swelling.

  Na'sion.  Craniometrically the median point of the  naso-frontal suture.
From nasus, the nose.
  Necrophilism.   Insane sexual  desire for a corpse.   From veupbg, a corpse,
and (pileu, to love.
  Ne'oplasms.  New formations or growths, as tumors.  From veog, new, and
Tvlaa/ua, growth.
  Neural'gia.  Pain  felt over the  distribution of a nerve, usually  without
fever.  From vevpov, a nerve, and alyog, pain.
  Neurasthe'nia.  Nervous exhaustion.  From vevpov,  a nerve, and dcOeveia,
weakness.
  Neuri'tis.  Inflammation of a nerve.   From vevpov, a nerve, and  itis, suffix
denoting inflammation.
  Neuroglia.  A  reticular substance  lying between  the  ganglionic cells and
nerve-fibres in the brain and cord.   From vevpov, a  nerve,  and ylia, bird-
lime, glue. 
702
GLOSSARY.
   Neuro'ma.  A tumor composed of nerve-tissue.  From vevpov, a nerve, and
 oma, suffix denoting tumor.
   Neu'ron.  A nerve.   The cerebro-spinal cord.  From the Greek, vevpov, a
 nerve.
   Neuro'sis.  Nervous  disease without specified  lesions.   From  vevpov, a
 nerve, and osis, suffix denoting morbid condition.
   Neurot'omy.  Section or division of a nerve.  From vevpov, nerve, and to/m/,
 incision.
   Night-ter'rors.  A sudden attack of terror in sleeping children, as if of some
 impending danger.
   Notomyeli'tis,   Inflammation  of the spinal cord.  From vurog,  back,  and
 fivelog, marrow.     ,
   Nu'cleus.  The deep origin of a nerve;  a group  of cells forming central
 termination of a nerve or bundle of  nerve-fibres.  From nucleus, a kernel.
   Nystag'mus.  Involuntary rapid movements of the eyeball. From vvaTayp.bg,
 nodding of the head, slumber.

   Oinoma'nia.  Dipsomania; passion for wine.  From olvog, wine,  and fiavia,
 madness.
   Ol'ivary bodies.  Oval protuberances on the lateral surface of the medulla
 oblongata.  From oliva, an olive.
   Oper'culum.  Literally, a lid or cover.  A triangular eminence covering a
 considerable portion of the island of Reil.
   Ophthalmoplegia.  Paralysis of  ocular muscles.  From  6cj>dal/xbg, eye,  and
 nlriyrj,  stroke.
   Oti'tis. Inflammation of the ear.  From ovg, ear, and itis, suffix denoting
 inflammation.

   Pachymeningitis,  Inflammation of the dura mater, its chronic form causing
 thickening of  this membrane. From naxk, coarse, thick, uyviy%, membrane,
 and itis, suffix denoting inflammation.
   Pain'ful points.  Points  on a  neuralgic  surface, particularly sensitive to
 pressure.
   Pal'mus (adj. palmo'dic).  "The twitches."   Convulsive tic.   A nervous
 affection characterized by twitching, by involuntary imitation and readiness
 to perform any act directed, however objectionable, and by a tendency to the
 use of  indecent words.  From walfiog, twitching, palpitation.
   Papillitis.  Inflammation of the papilla or optic  disk.  From papilla, a
 nipple, the optic disk, and itis, suffix denoting inflammation.
   Paracentral lob'ule.   Area between the calloso-marginal and  paracentral
 sulci on the  median surface of the cerebral hemispheres.  From irapa, beyond,
 and  nevrpov, centre.
  Parcesthe'sia. Morbid perversion of sensibility, as in numbness, etc.  From
 -apa, beyond, and aiadijaig, sensation.
  Paral'ysis.   Impairment or complete loss of power of  motion or of sensa-
tion, or of both.  It may be general  or local.  From rrapa, beyond, and Ivu,
to loosen.
  Paramyoclonus.  Convulsive tremor in symmetrical muscles, the spasms
ceasing during sleep.   From  Trapd,  beside, beyond, p.vg, muscle, and  nUvog,
disturbance. 
GLOSSARY.
703
  Paramyoton'ia.  Tonic muscular spasm.  From rcapa, beside, beyond, p.vg, a
muscle, and rovog, tension.
  Paranoi'a.  Unsoundness  of  mind;  crankiness.  From  wapdvoia, fatuity,
madness (Trapd, beside, beyond, and vovg, the mind).
  Paraphasia.  Aphasia of conduction. Substitution of words which do not
express the meaning intended to be conveyed.  From Trapd, beside, beyond.
and acacia, aphasia.
  Paraple'gia.   Paralysis  of the lower  extremities.   From Trapd,  beside,
beyond, and irl?iyn, stroke.
  Par'esis.  Impairment of motor power. Partial paralysis.  Sometimes used
synonymously with general paralysis.   From naptvpi, to relax.
  Park'inson's disease.  Paralysis agitans, or shaking palsy.  After Parkinson,
who first described it in 1817.
  Par vag'um.   The pneumogastric nerve.  From par, pair, and vagus, wan-
dering.
  Pathognomon'ic.   Characteristic of the disease.  From nadog, disease, and
yiyvuonu, to know.
  Pe'duncles.  Mainly  used to  denote  the  three  cerebellar processes, the
superior, the middle, and  the lower, connecting the cerebellum  with other
portions of the brain.  From Lat., pedunculus, a small foot.
  Perimys'ium.  The areolar tissue of  striated muscle.  From nepi, around,
and /xvg, a muscle.
  Periph'eral.   Relating to the periphery  or circumference, as peripheral
nerves.  From wepifepei-a, circumference.
  Phreni'tis.  Inflammation of  the brain or its membranes, or the series of
morbid  symptoms  associated with it.  From <pprjv, mind, and itis,  suffix de-
noting inflammation.
   Petit mal (Fr.).   "Slight disease:"  applied in epilepsy to  the initial symp-
toms of the fit.
   Pe'trom.  Hard; resembling stone;  as petrous portion of temporal  bone.
 From -irerpa, a rock.
   Pluricord'onal cells.   A variety of many-column cells of the spinal cord,
having long axis-cylinders.  From plus, many, and (Fr.) cordon, cord.
   Pneumogas'tric.  Relating to  the lungs and stomach.  The pneumogastric
 nerve is so called because it is distributed chiefly to the organs of  the  chest
and abdomen.  From Tvvevp.uv, lung, and yaarnp, stomach.
   Pol'io-encephali'tis.   Acute inflammation of the cortex, affecting chiefly the
 motor  region.  From irolibg, hoary, gray, kytctyalog, the brain, and  itis, suffix
denoting inflammation.
   Poliomyeli'tis. Inflammation of the gray matter of the spinal cord.   From
wo?ubg, hoary, gray, nvelog, marrow, and itis, suffix denoting inflammation.
   Polycesthe'sia.  Abnormal sensibility, in which a  touch impressed at a
single point is felt at two  or more points.   From ™lvg, many, and aio^ig,
sensation.
   Pons  Varo'tii.  An eminence at the upper portion of the medulla  oblongata
 and at the base of the brain.  First described  by Varolius.  From pons, a
bridge.                                    .  .     „ ,      ,
   Porencephaly.  A defect of structure consisting of abnormal passages in,
 or absence of, any  part of the cerebrum.  From irdpog, a passing over, bridge,
and eyne^alog, the brain. 
704
GLOSSARY.
  Prcecen'tral.  In front of the centre.  A term applied to a special convolu-
tion and fissure of the brain.   From prce, before, and centrum, centre.
  Prcecu'neus.  A  quadrate lobule  on  the median surface of the cerebral
hemisphere, in  front of the cuneus.  From proz, in front  of, and cuneus, a
wedge.
  Pro'cess.   A prolongation or eminence.  From Lat., processus, a going for-
ward.
  Prosopalgia, Prosoposal'gia.   Facial neuralgia.   From npdawrrov, the face,
and alyog, pain.
  Pro'toplasm.  A substance common to all organisms and essential to all the
phenomena of life.   It is semi-translucent,  viscous,  and without  visible
structure.   From npurog, first, and irldo~o-u, to mould.
  Pseu'do-mus'cular hy'pertrophy.  A chronic disease causing paraplegia and
great increase in size of the lower limbs, and occasionally of the upper limbs.
From ipevdrjg, false, musculus, muscle, virep, over, and rpofjj, nourishment.
  Psych'ical cells.  Name given by Cajal to certain cortical cells.  From fuxn,
the soul or mind.
  Pter'ion.  In craniotomy the region in which the extremity of the great
wing of the sphenoid approaches the frontal, parietal, and temporal bones.
From -Krepov, a feather or wing.
  Pto'sis.   Drooping of the upper  eyelid, from paralysis of the levator pal-
pebrse muscle or induration of the eyelid.  From Tzruoig, a falling.
  Pul'vinar.  The posterior eminence of the optic thalamus.  From pulvinus,
a cushion.

   Quadrigem'inal  bodies.  Four rounded  eminences under the corpus cal-
losum;  the optic lobes.  From quadrigeminus, fourfold.

  Ra'bies.   Canine madness, or hydrophobia of animals; hydrophobia being
rabies  manifesting itself in the human being.  From Lat., rabies, madness
or fury.
  Raph'e.  (More correctly rhaphe.)  A line, ridge, or seam in the middle
line.  From patyr), a suture.
  Raynaud"s disease.  An affection  consisting of paroxysmal  attacks  of pain,
pallor, coldness, numbness, and ansesthesia  of the  lower extremities, and a
gangrenous condition of the toes.  After  Raynaud, who described it.
  Reac'tion of  degenera'tion.  Alteration  in the response of  a nerve and
muscle to the galvanic and faradic current, caused by lesion of such nerve
and  muscle.
  Re'flexes.  Reflections by an efferent nerve of impressions that have been
carried to a nervous centre by an afferent nerve.   From re, back, and flecto,
flexum, to bend.
  Reinforce'ment.  A term applied to augmentation of reflex response, when
muscular action or stimulation  operates at the same time on different parts
from those embraced in the reflex circle.
  Rest'iform bod'ies.   Two peduncles or medullary projections from each side
of the upper extremity of the medulla oblongata.  From  restis, a rope, and
forma, shape.
  Rhachialgi'tis.   A badly compounded word (literally, inflammation of pain 
GLOSSARY.
705
 in the spine), denoting what is sometimes called  "spinal irritation."   From
 PaXlS, spine, alyog, pain, and itis, suffix denoting inflammation.
   Rhe'ophore.   Any substance conducting  the  electric  current; usually the
 electrodes held by, or applied to, the patient.   From peog, current, and <po&G>}
 to carry.
   Rhe ostat.  An instrument which regulates  the  current  of electricity or
 measures its resistance.   From peog, a current, and lottou, to stand.
   Rom'berg's sign or symp'lom.  Uncertain, swaying gait, in the dark or
 with the eyes closed.  After Romberg, who first described it.

   Sadis'mus.  A condition that is the opposite of Masochismus,  which  see.
 In sadismus a member of one sex takes sensual delight in  exercising force
 upon one of the other sex.  From the name of  the  Marquis de Sade,  a
 prurient writer.
   Sagit'tal.  A term applied to a groove, sinus,  suture, etc., of the skull, from
 the arrow-shaped appearance.   From sagitta, an arrow.
   Saltato'ric.  Of a jumping, jerky, or dancing character.  From Lat., sal-
 tator, a dancer.
   Sclero'sis.  Induration or hardening of tissues.  From anlripbg, hard.
   Somnam'bulism.  Sleep-walking.  From  Lat., somnus, sleep,  and ambulo,
 to walk.
   Spasm.  Involuntary muscular contraction ; a convulsion.  From owaapog,
 act of drawing.
   Spasmod'ic.  Relating  to or characterized by spasm, as spasmodic diseases.
 From cirao-fiog, act of drawing.
   Spas'tic.  Relating to contraction.   From airaaTinbg,  contracted.
   Sphyg'mograph.   Instrument for automatically recording the rate and force
 of the pulse.  From a<j>vy/iog, pulsation, and ypd<j>u, to write.
   Spini'tis.  Inflammation of the spinal cord ; myelitis.  A hybrid word, from
 spina, the spine, and itis, suffix denoting inflammation.
   Sta'tus epilep'ticus.  A condition, sometimes  fatal, in  epilepsy, when one
 fit follows another in rapid, continuous, and regular succession.  From status,
 state, and kizllafifiavu, to seize upon.
   Slepha'nion..  Point at which the coronal sutures and  temporal lines cross.
 From cre^avn, the crown.
   Stri'ce acus'ticce.   Transverse white lines on the inferior portion of the floor
 of the fourth ventricle, which are associated with the roots  of the auditory
 nerve.
   Subslan'tia ferrugin'ea.  A collection of large,  dark,  pigmented cells on
 the fasciculi teretes of the fourth ventricle of the brain. From substantia,
 substance, smdferrum, iron.
   Substantia ni'gra.  A tract of cerebral gray matter between the crusta and
 tegmentum, consisting of numerous pigmented nerve-cells of irregular shape.
 From substantia, substance, and nigra, dark.
   Subthal'amic.   Under the optic thalamus, as the subthalamic body.
   Syph'ilis.  A  specific  infectious venereal disease.  Perhaps  from c^ldu,
to debase, humble, disgrace ; some authorities consider the derivation to be
from avg, swine, and QiXtu, to love.
  Syphilo'ma.  A  syphilitic  tumor, as a gumma or syphilitic gummy tumor
of the brain.  From syphilis, and oma, suffix denoting  tumor.
                                   45 
706
GLOSSARY.
  Syringomyel'ia.  See Syringomyelitis.
  Syringomyelias.  The formation of a fissure  or  cavity in the cord.  From
cvpiyt;, a  hollow tube, pipe, pve2.bg, marrow, and itis, suffix  denoting inflam-
mation.

  Ta'bes.  A wasting away ; emaciation.  From Lat.,  tabeo, to waste away.
  Ta'bes  dorsa'lis.  Literally, dorsal wasting; a synonym for  progressive
locomotor ataxia.  From tabeo, to waste away,  and dorsum,  back.
  Tachycar'dia.   Abnormal rapidity of the heart's  action.  From raxvg, quick,
and mpdia, the heart.
  Tegmen'tum.   The postero-superior portion of the crura cerebri.  Lat., a
covering.
  Telangiectasis.  Dilatation of  the extremities  of bloodvessels  or  of the
capillaries.  From rehog, the end, ayyeiov, a vessel,  and huraaig, extension.
  Ten'don-re'flex.  Reflex contraction of a muscle, caused  by percussion of
its tendon.  See Reflex.
  Tetanil'la  (diminutive of tetanus).  Tonic, bilateral, intercurrent, usually
painful spasms  of certain  muscular groups, without  loss  of consciousness.
From reravog, distention, convulsion, cramp.
  let'anus.  A  disease characterized by rigidity, with paroxysms of tonic
convulsions; lockjaw.  From reravog, distention, convulsion, cramp.
  Tet'any.   See  Tetanilla.
  Thal'ami op'tici.  Two masses of nervous matter at  the base of the brain,
from which  the optic nerves have a partial origin.  From  dalapog, bed, and
oirrmog, relating to sight.
  Ther'mo-asthesiom'eter.  A registering instrument with which  to test the
temperature-sense.  From Geppn, heat, aiaQrioig, sensation, and perpov, measure.
  Thermom'eter, cer'ebral.   Instrument to determine  and  register the tem-
perature  of  different regions of the skull.  From Qepprj, heat, uerpov, measure,
and cerebrum, brain.
  Thom'sen's disease.  See  Myotonia.  From Dr. J. Thomsen,  of Schleswig,
who, in 1876, first described it in his own case.
  Thrombo'sis.   Obstruction of any portion of the circulatory apparatus, as
of the brain, by a coagulum.  From thrombus,  a clot.
  Tic (Fr.).   Spasmodic action; twitching.
  Tic douloureux.  (Literally, painful tic.)  Painful twitching from neuralgia
of branches of the fifth pair of nerves.
  Tituba'tion.  A reeling, stumbling, staggering gait, as in cerebellar disease.
From titubo, to stumble or totter.
  Ton'ic spasms.  Rigid muscular contractions without relaxation.  From
rovog, tension.
  TopoaVgia.  A name given to pain in different regions which are not ana-
tomically or physiologically  delimited.  From   ronog, a  place,  and d'kyog,
pain.
  Traum'atism.   The condition of the organism produced  by a wound or in-
jury.   From rpavpa, a wound.
  Trigem'inus, or Trigem'inal nerve.   The fifth pair of nerves, which divides
into three branches.  From tri, in composition  three, and gemini, double;
triplets. 
GLOSSARY.
707
  Tris'mus.   Lockjaw:  a spastic closure of the lower jaw.  From rpcapog,
gnashing of the teeth.
  Troph'ic.   Relating to nutrition.  From rpo^, nourishment.
  Trophoneuro'sis.   Failure in nutrition due to impairment of nervous action.
From rpoyti, nourishment, and vevpov, a nerve.
  Typho'ma'nia.   A disease characterized by furious outbreaks of maniacal
excitement  and violence, with  intermissions.  Also,  condition of lethargy
and delirium in typhus.   From rv<i>og, stupor, and pavia, madness.

  Un'cinate or  Uncina'tus (Lat.).  Hooklike, hooked, furnished with hooks,
as uncinate convolution  or gyrus of the brain, which terminates  in a hook-
like process. From uncus, a hook.

  Vag'abond pains.  Wandering pains,  of a stabbing and  fulgurant kind,
symptomatic of locomotor ataxia.
  Vag'us.   See Par vagum.
  Ve'lum  interpos'itum.   A vascular  membrane reflected from the pia mater
into the interior of the cerebrum through the transverse fissure.  From  velum,
a veil, and interpositus, placed between.
  Ve'lum  medulla're.  A term variously applied to  the valve  of  Vieussens,
the medullary  strip  associating the medulla  and the cerebellum,  and the
small posterior valve of the  cerebellum.   From velum, a veil, and  medulla,
marrow.
  Ven'trad.  Toward the belly; anterior to the vertebral  column.  From
venter, belly, and ad,  to.
  Ven'tricles.  Five cavities in  the interior of the brain, known as  the  two
lateral, the middle, the fourth, and the fifth ventricles.  From ventriculus, a
small belly.
  Verbigera'lion.   The repetition by an insane person of one word or sentence
or sound,  but without sense or sequence.  From verbigero, to talk.
  Ver'mes.  Two medullary projections at the surface of the cerebellum, the
vermiform processes.  From vermis, a worm.
  Ver'tebral.  Of or pertaining to a vertebra.  Having vertebra?. Vertebrate.
From vertebra, a spinal bone (verto, to turn).
  Ver'tigo.  Dizziness.   From Lat., verto, to turn.
  Ver'ligo, au'ral.  See Meniere's disease.   From verto, to turn, and auris, the
ear.

  Waller'ian law.   A law that a nerve degenerates in the direction in which
the impulse is normally conveyed by it.
  Wrist-drop.  Paralysis of the  muscles of the forearm, induced by lead-
poisoning.
  Wry-neck. Contraction of the muscles of the region of the neck, gener-
ally of one side, causing a fixed position of the head on that side. 
 
INDEX.
  ABDOMINAL reflex, 169
    Abducens nerve, 84, 85
Abscess, cerebral.  See Cerebral Abscess.
Accessory nerve of WilUs, 85
Acclimation, headache from, 497
Acoustic nerve, 88
    nuclei, 88
    striae, 86, 88
Acromegaly, 555
    causes of, 555
    clinical history of, 555
    diagnosis of, 557
    duration of, 557
    partial, 559
    pathology of, 557
    prognosis of, 559
    treatment of, 559
Actinomyces, intracranial, 331
Adenitis as a cause of neuritis, 194
Adenoma, intracranial, 331
.ffisthesiometer, 163,164, 583
Affenhand, 250
Agraphia, 41
    centre for, 139,140,141
    localization of, 41, 43
    motor centres for, 41, 43
Agoraphobia, 589, 658
Aiguille cache, 164, 583
Air-conduction of sound, 161
    electric, 112
Alcoholic coma, 508
    dementia, 652, 671, 672
    habit, 200, 566, 570
    insanity, 567, 658
    mania, 568, 621
    melancholia, 568
    multiple neuritis, 567, 570
    paralysis, 286, 566. 567
    paranoia, 567, 568, 658
    paresis, 567
    pseudo-general paresis, 567
    treatment of alcoholism, 572
Alcoholism, 200, 566, 570.  See also Alcoholic.
    alcoholic treatment of, 572
    a cause of locomotor ataxia, 261
        of neuralgia, 184
    coma of, 508
    cures for. 572
    dementia from, 652. 671, 672
    diagnosis of,  286,  569, 675
    headache from, 496
    multiple neuritis  of, 567, 570
    pathology of, 568
    prognosis of, 567
    symptoms of, 566
    treatment of, 569
    tremor of. 527, 567
    vertigo of, 494         .            ...
AUgemeine progressive Gehirnlahmung, bbb
    Paralyse der irren, 666
Allocheiria, 263
Amaurosis, tobacco, 335
Ambiguous cells  of Andriezen, 55
Amentia, 644
American gout, 188
Ampere, 107
Amputation, neuroma after, Jii
Amyotrophic lateral sclerosis, 241  258, 277, 356
Amyotropnische lateralsclerose  277
Anaemia as a cause of neuralgia, 182,186
    cerebral, 354, 457
Anaemia cerebral, in insanity, 602
    headache from, 496
    neuralgic, 182,186
    with neuritis, 202
    spinal, 354
    vertigo of, 494
Anaesthesia, detection of, 165
    disassociated, 285, 286, 287
Anaesthetic area, 583
    leprosy, 286
    zones, 262, 263
Analgesia tract, 264
Analgesic paralysis, 286
Analgesics, 188
    in neuritis, 200, 201
Anapeiratic neuroses, 469
Anatomy of brain, 34
    of nervous system, study of, 19
Andriezen, ambiguous cells of, 55
Aneurism as cause of myelitis, 225
    cerebral, 331
    miliary, of cerebrum, 306
Angedonnerte Melancholie, 609
Angina pectoris, 460, 563
Angioma, intracranial, 331
Angio-sarcoma of  brain, 330
Angular gyrus, hemorrhage in. 310
Ankle-clonus,  168,  275
Anode, 106, 127, 235
Ansa lenticularis, 70
Anthropophagy, 595
Anti-cyclone,  421
Anti-cyclonic neuralgia, 290
Antiseptic surgery of the brain, 339
Antrum, disease of, as cause of neuralgia,
  183
Ape-hand, 250
Apertures, Mierzejewski's, 341
Aphasia, ataxic, centre for, 141
    centre for, 141
    of conduction, 41, 141
    of interrupted  conduction, centre for, 139
    localization of, 38, 43
    motor, 40,  43
       centre for,  139,141
    seat of, 96
Apoplectic cicatrix, 307
    coma, 309
    cyst, 307              i
    dementia,  652
Apoplectiform attack, 309
    dementia,  670
Apoplexy.  See Hemorrhage.
    of the newborn, 321, 323
Aqueduct of Sylvius, 64
Arachnoid cyst, 601
Arborization, 25
    of association-fibres of cerebellum, 51
    of cerebellum, 74, 76
    of fibres from posterior root, 31, 32
    of motor area,  47
Arched convolution, 37
Arcuate fibres, 48
Area, anaesthetic, 583
    motor.  See Motor.
Argyll-Robertson pupil, 224, 261
Arithmomania, 658
Arm, motor points of, 131
Arrow-markings, 196
Arsenicism, chronic, 261
Artefacts, 76, 303, 603 
710
INDEX.
Arteries or Artery, anterior root, 239
           spinal, 97
        cerebellar, 97
        of cerebrum, 89, 96, 306
        diseases of, cerebral hemorrhage from,
          308
        fissural, 239
        lenticular, 92
        median, 97
        optic, 92
           hemorrhage from, 92
        postero-internal optic, 91
        posterior spinal, 97
        radicular, 97
        spinal, 239
        vertebral, 97
Ascending convolutions, 35
    frontal convolutions, 35, 37
    paralysis, acute, 205, 240, 243
    parietal convolutions, 35, 37
Association-fibres of cerebellum, 49
        of white matter of brain, 48
Astasia-abasia, 529
Asterion, 97, 98
Asthenia, cerebral, 643
    nervous.  See Neurasthenia.
Asthenopia, 156
    ocular, 536
    of ocular muscles, 156
Ataxia, 171
    of combined sclerosis, 280
    hereditary.  See Friedreich's disease.
    hysterical motor, 529
    locomotor.  See Locomotor ataxia.
    motor, 172, 261, 262
    progressive spastic, 279
    static, 172, 261, 262
    tests for, 172
    toxic, 271
Ataxic aphasia, 141
    paraplegia, 279, 545
        diagnosis of, 549
        hereditary, 545
    paramyotone, 304
Athetoid chorea, 353, 419
    movements, 349, 353, 419
Athetosis, 319, 351
    causes of, 352, 353
    diagnosis of, 349. 353
    double, 351
    pathology of, 352
    post-hemiplegic, 353
    prognosis of. 353
    treatment of, 353
Atrocious pains, 261
Atrophische Spinallahmung, 230
Atrophia musculorum lipomatosa, 299
        progressiva, 240, 249
Atrophic method of study of nervous  system,
      19
    paralysis  of children, 230
Atrophie musculaire progressive,  249
    primitive des noyaux moteurs, 292
Atrophy, fibrillary, 255
    muscular, 257
    myopathic, 249
    of nervous matter, 603
    of optic nerve, 157, 261, 262, 389
    progressive muscular.  See Progressive mus-
      cular atrophy.
    of tongue in bulbar paralysis,  293
Audition, 62,  159
Auditory labyrinth, 540
    nerve, 88
        lesion of, 160
    tract, central, 89
Aurae, epileptic, 398
Aural vertigo. See Meniere's disease.
Auto-hypnotism, 514
Axis-cylinders, 31, 32
    histology of, 25
    of motor area, 46
    of a nerve, 18
    process, 18
       current through, 18
       of motor area, 44
Axo-Leclanche cells, 113
  BACILLUS or  BACTERIUM  of diphtheria,
         490
       Klebs-Loeffler, 490
       in Landry's disease, 243
       in meningitis, 361
       of Nicolaier, 475
       of syphilis, 378
       of tetanus, 475
       in tubercular meningitis, 369
Barometric disturbances as causes  of chorea,
             421
           of neuralgia, 183
Base of brain, 37,152
Basedow's disease, 560
Baskets,  terminal, 75, 77
Battery or batteries, cells of, 105
       faradic.  See Faradic and Faradism.
       galvanic.  See Galvanic.
       method of applying, 123
       portable, 113
       stationary, 115
       wires of, 117
Battledore hands, 555
Bedsores in myelitis,  224, 228
Beef-tea, formula for, 467
Bell's palsy, 206
Belenophobia, 658
Beschaftigungs-Neurosen, 469
Bichromate of silver  staining, 17, 28
Binding-posts of batteries, 114
Birth-palsies, 317
Blepharospasm, 156
Blindness, mental, 41, 43, 670, 676
    of retina, 63
    word-, 41, 43
Blood-globules in insanity, condition of, 607
    syphilitic changes of, 377
    white, 197
Bloodvessels of cerebrum, 73, 89, 306
Blue-line, 398
Body or Bodies, olivary, 73
       of Luys, 70
       quadrigeminal, 60-70, 146, 152
       restiform, 67, 72
       starchy, 217
       striated, 103,146
       subthalamic,  62, 70
Bone-conduction of sound, 161, 209
Bones, traumatic diseases of, 574
Bouquet of pyramidal cells, 53, 54
    of pyramidal cells of motor area, 45, 46
Brachycephalic skull, 98
Brain. See Cerebrum and Cerebellum.
    abscess of.  See Cerebral abscess.
    actinomycosis of, 331
    adenoma of, 331
    anaemia of, 354, 457
    anatomy of, 34
    aneurism of, 331
    angioma of,  331
    angio-sarcoma of, 330
    antiseptic surgery of, 339
    arteries of, 89-96,  307
    base  of, 37
       lesion of, 152
    bloodvessels of, 89, 306
    cancer of, 331
    -centres, injuries to, as a means of study, 19
    cholesteatoma of, 331
    circulation of, 306
    composition of, 19
    congestion of, 354
    convolutions of, 34, 35, 58
    cysto-sarcoma of, 330
    disease of, 56
    enchondroma of, 331
    fibro-glioma of, 330
    fibroma of, 331
    fibro-sarcoma of, 330
    fissures of, 34-37, 60, 100-103
    fcetal, pathological conditions of, 321, 324
    galvanization of,  117, 125, 498
    glio-sarcoma of, 330
    glioma of, 57, 330
    gray  matter of, 43
    gumma of, 330
    hydatid cysts of, 331 
INDEX.
711
Brain, hyperaemia of, 354
    hypertrophy of, 457
    infantile, diseases of,  321
    lipoma of, 331
    lympho-sarcoma of, 330
    melano-sarcoma of, 330
    multiple sclerosis of,  334
    myxo-glioma of, 330,  331
        -sarcoma of, 331
    myxoma of, 331
    neuroma of, 331
    osteoma of, 331
    parasitic cysts  of, 331
    plexiform angio-sarcoma of, 330
    psammoma of. 331
    pseudo-enchondroma of, 331
        -fibroma of, 331
        -sarcoma of, 331
    railway, 577, 579
    sarcoma of.   See Sarcoma.
    sclerosis of, 334
    softening of,  in insanity. 602, 604
    surgical operations on, 336
    syphilis of.   See Syphlis, Intracranial.
    temperature of, 174
    thrombi in, 331
    tubercle of, 329
    tumor, diagnosis of, 184, 461
        traumatic, 575
    white matter of, 48
 Bread-crumbling position, 520
 Bridge of Varolius, 61, 210
 Broca's centre, 96
 Bromism, 651, 675
 Bronzed skin, 561
 Brow-ache, 182
 Bulbar paralysis, 292, 293
        progressive, 292
 Burdach, column  of.  See Column of Burdach.
  CAISSON disease, 246
       causation of, 247
       clinical history of, 246
       diagnosis of, 249
       pathology of, 248
       prognosis of, 248
       treatment of, 249
Caissons, rules for workers in, 249
Cajal, method of staining, 17
   sensory motor tract of, 32
   staining nerve-cells of, 17
Calcarine fissure, 37
Calloso-marginal fissure, 37
Canals, central,  of spinal cord, 84
   circular, of labyrinth, 73
Cancer, intracranial, 331
   of brain, 331
   on nerves, 211
Capsule, endotheUal, of ganglionic cells, 30
   external, 60
   internal, 58
       lesions of, 145
Carcinoma, intracranial, 331
   on nerves, 211
Caries, spinal, pain of, 185
   vertebral, 289
Carphologia, 566
Catalepsy, 513, 516
Cataplexy, 513, 515
Cathode, 106, 128, 235
Caudate nucleus, 57, 61         .
Cauterization in locomotor ataxia, 274
Cautery, electric, 106
   galvanic,  106                .
CeU or Cells, ambiguous, of Andriezen, 55
        Axo-Leclanche, 113
        of battery,  105
        chloride of silver 113
        column-, of spinal cord, 27, 29. 78
        commissural, 26 27
           of spinal cord, 27. 29, 30
        connective-tissue, 197
        cortical connections oi, oi
        Daniell, 107
        Deiters', 32, 217
        Edison-Lalande, 113, 114
Cell or Cells, epithelial, 32
           transformations of, 33
       fusiform, of molecular layer, 44
       of galvanic battery, 112
       ganglionic, 30
       Grenet, 113
       Law, 113
       Leclanche, 113
       many-column, of spinal cord, 28, 30
       of Martinotti, 47
       nerve.  See Nerve-cells.
       neurogliar, 32
       nuclei of,  32
       pluricordonal,  of spinal cord, 28, 30
       polymorphous, of motor area, 46
       psychical, 46
       of Purkinje, 72, 74
       pyramidal, of motor area, 44
       retinal, 87
       root-, of spinal cord, 27
       sensory, of Golgi, 54
       spider-, 32
       spinal cord, 27
        Stammers', 113
       star-shaped, 74
            of molecular layer, 44
       triangular, of molecular layer, 44
 Cellulifugal currents, 18, 52
    fibres, 24
 Cellulipetal currents, 18, 52
 Central auditory tract, 89
    canal of spinal cord, 64
    ganglia of corpus  striatum, 103
 Centre for agraphia, 139,140,141
    for aphasia, 141
        of interrupted conduction, 139
    Broca's, 96
    in the convolutions, 38, 43
    cortical, 38, 43, 139, 140
    heat, 103, 146
    mind, 142
    motor.  See Motor.
        aphasia, 139, 141
    for muscular sense, 139
    optic, 87
    for pain, 139
    of speech, 40, 43
    for touch, 139
    vasomotor, of medulla oblongata, 405
    for vision, 139,140, 150
    for word-blindness. 139, 140, 141
        -deafness, 139, 140, 141
 Centrifugal fibres of posterior root, 30
 Centripetal fibres of posterior root, 30
        of white matter, 48
 Centrum ovale, 57, 81
        lesions of, 142
        tumors of, 336
 Cerebellar arteries, 97
    column, direct, 79
    disease, diagnosis of, 271
    tract, sensory, 73
    vertigo, 327
 Cerebellum,  See also Brain and Cerebellar.
    anatomy of, 34
        and functions of, 72, 73
    and cerebrum, connection between, 73
    arborization of, 74, 76
    association-fibres of, 49
    bloodvessels of, 89
    co-ordination by,  73
    disease of, diagnosis of, 281
    fibres from spinal cord to, 77
    functions of cortex  of, 73
    granular layer of, 74, 75
    hemispheres of, 72
    hemorrhage in, 310
    histology of, 73
    inhibitory powers of, 73
    lesions of, 149
    molecular layer of. 74
    motor tiacts from, 73
     nervous currents through, 76
     peduncles of.  See Peduncles, cerebellar.
     tumors of, 336
     white substance of, 74, 76
 Cerebral abscess, 372 
712                                   INDEX.
Cerebral abscesses, causes of, 372
        diagnosis of, 373
        localization of, 373
        operation for, 373
        pathology of, 372
        prognosis of, 373
        symptoms of, 372
        treatment of, 373
    anaemia, 354, 602
    aneurism, 306, 331
    arteries, posterior, 91
    asthenia, 643
    circulation, 306
    disease, diagnosis of, 425
    emboli, composition of, 308
    exhaustion, dementia from, 644
        after insanity, 649
    hemorrhage. See Hemorrhage, intracranial.
    hyperaemia, 354
    inflammation, 602
        localization of, 38, 43
    neurasthenia, 643
    palsies of childhood, 312, 315
           causation of, 315
           contracture in, 316
           diagnosis of, 316
           diplegia in, 316
           history of, 315
           motor paralysis of, 316
           mutism in, 316, 319
           pathology of, 321
            prognosis of, 325
           speech-defects in, 316
            symptoms of, 316
           treatment of, 325
    porosity of Golgi, 325
    sinuses, thrombosis of.  See Thrombosis.
    syphilis.  See Syphilis, intracranial.
    temperature, 145,174, 373
    thermometer, 373
    thermometry,  145, 174, 373
    tumors, 186, 461, 575
    veins, thrombosis of, 321, 324
    ventricles, hydrops of, 367
 Cerebritis, focal, 602
 Cerebro-spinal axis, hemorrhage in, 310
    epidemics, 225
    meningitis. See Meningitis.
    nervous svstem, diseases of, 354
    syphilis, 260, 271, 288, 381, 384
 Cerebrum.  See Brain and Cerebral.
    anatomy of, 19, 34
    arterial supply of, 306
    arteries of cortex of, 92
    association-fibres of, 48
    bloodvessels of, 89
        and cerebellum, connection between, 73
    cortex of,  arteries of, 92
        yellow softening of, 94
    diseases of, 315
    fibres from spinal cord to, 77
    fissures of, 34,101
    functions  of, 43
        of cortex of, 73
    ganglia of, 57
    gray matter of, organ of mind, 55, 644
    inflammation of, 602
    localization of lesions in, 139
    miliary aneurism of, 306
    pyramids of, 66, 67
    ventricles of, 57
 Cervical pachymeningitis, 285
    sympathetic, affections of, 563
Chiasm of acoustic striae, 88  '
    optic nerve, 61, 87
Childhood, brain-diseases of, 321
Children, atrophic paralysis of, 230
    cerebral palsy of, 312, 315
    convulsions of, 316
    essential paralysis of, 230
Chloral, hypnotic action of, 501H
Chloralamid, hypnotic action of, 501
Chloride of silver cell,  113
Choked disk, 157, 328
Cholesteatoma, intracranial, 331
Chorea, 418
    athetoid, 353, 419
Chorea, barometric influences on, 421
    causes of, 422
    chronic, 342, 419, 421, 429
    chronica progressiva, 342
    clinical history of, 419
    development of, 422
    diagnosis of, 271, 392, 425, 461, 527
    duration of, 421
    electric, 429
    epidemic, 418
    ereditaria, 342
    eye-strain in, 422
    fibrillary movements of, 419
    functional, 353
    galvanization in, 428
    germanorum, 418
    hemiplegic, 319
    hereditary, 342
    history of, 418
    Huntington's, 342
        causes of, 343
        clinical history of, 344
        dancing movements of, 345, 349
        diagnosis of, 334, 348
        etiology of, 343
        heredity in, 343
        history of, 342
        pathology of, 346
        prognosis of, 348
        symptoms of, 344
        treatment of, 351
    hysterical, 350
    infection as cause of, 425
    magna,  418
    major, 350
    micro-organisms in, 424
    paretic, 419
    pathology of, 423
    post-epileptic, 419
    post-hemiplegic, 352, 419
    of pregnancy, 419, 421
    prognosis of, 426
    relapse  of,  421
    rheumatic, 420
    rhythmic, diagnosis of, 350
    simulation of, 420
    spastic,  319
    Sydenham's, 334, 343, 348, 392, 419
    traumatic, 575
    treatment of, 426
    tremor of, 527
    violent, 420
Choree chronique, 342
    clinique hereditaire, 342
    de l'adulte, 342
    vulgaire chez les veillards, 342
Choreomania, 418
Chvostek symptom in tetany, 480
Choreomania, 418
Cicatrix, apoplectic, 307
        neuralgia in, 183
Cincture-feeling or sensation, 214, 240, 263
Circle of Willis. 89, 90
Circuit, closing, 235
    opening, 235
    short, 116
Circular canals of labyrinth, 73
    insanity, 626, 627, 632, 634
Circulation, cerebral, 306
Circumcision for reflex nervous  disorders, 536
Cingulum, 49
Clark, column  of. 24, 27, 29, 72, 265, 267, 280
Claustrophobia, 589, 658
Claustrum,  60
Claw-hand, 251, 277
Climbing-fibres, 76
Clonus, ankle-, 168, 275
    foot-, 168
Closing, negative, 127,128, 235
    positive, 127, 128, 235
Clots in cerebral sinuses, 358.  See  Thrombosis.
Clownishness of epilepsy, 398
Cocainic insanity, 658
Cocainism, diagnosis of, 651
Cochlear nerve, 88
Coil, Dubois-Reymond, 115
    secondary,  110 
INDEX.
713
Colic, lead-, 393, 394
    pain of, 180
n^ii^S1 of axis-cylinder process, 18, 25
Co loid degeneration in insanity, 604
Color-sense, tests of, 154
Coloring-method, study of nervous system, 19
Column or columns, anterior, 21, 22
           pyramidal, 21
        of Burdach, 21, 24, 26, 72, 77, 266, 267
           lesions of, 280
           nucleus of,  72
        -cells of spinal cord, 27, 29, 78
        of Clark, 24, 27, 29, 72, 265, 267
           lesions of, 280
        direct cerebellar, 21, 79
        fundamental, 78
           of spinal cord, 21
        of Goll, 21,  72, 78,  265, 266, 267
           nucleus of, 72
           lesions of, 280
        of Gowers,  21, 79, 264
           lesions of, 280
        lateral, 21
           limiting, 22
           pyramidal,  21
        of Lissauer, 21,  77, 265, 267
        pyramidal, 21, 81
        of Tiirck, 81
        of spinal cord, 77
           sensory path through, 78
        Spitzka-Lissauer, 21, 77, 265, 267
 Colvin uuit, 122
 Coma, 507
    alcoholic, 508
    apoplectic, 309
    from cerebral hemorrhage, 508
    diabetic, 508
    epileptic,  507
    hemicranial, 507
    from intracranial growth, 329
    nephritic, 507
    syphilitic, 380,  383
    traumatic, 507
    treatment of, 507
 Commissural cells, 26, 27, 29, 30
        of spinal cord,  27, 29, 30, 271
    fibres of cerebellum, 51
        of cerebrum, 51
        of spinal cord,  51
        of white matter, 48
 Commissure, anterior, 51, 72
    posterior, 70
    of spinal cord, 26
 Comparative  anatomy in  study of nervous
  system, 19
 Compression-myelitis, 225, 264
    of spinal cord from traumata, 292
 Consciousness, double, 297, 399
 Concussion myelitis, 225
    of spinal cord, 289, 577
 Conduction, aphasia of, 41, 141
    -bone, 161, 209
    interrupted, 139
 Confusional insanity, 652, 656
 Congestion of the brain, 354
    spinal, 355
 Conjugate deviations of eye, 156, 309
 Constant current, 107, 111, 112
 Constipation from sphincter-paralysis, 224, 229
 Contiguity, connection of cells by, 25
    nervous connection by,  77
 Continuity, connection of cells by, 25
    nervous connection by,  77
 Contraction, electric, 126,171
    muscular, 169
    myotatic, 169
 Contracture. 169, 275, 277
    in cerebral palsies, 316
    in disseminated sclerosis, 389
 Connective-tissue cells, 197
 Converters, 117                „   _
 Convolution or Convolutions.  See Gyrus.
        angular, 36     .
            hemorrhage in, 310
        arched,  37
        ascending,  frontal, 35, 3-
            parietal, 35, 37
Convolution or Convolutions, centres in, 38,
         43,140
       fornicate, 37
       hemorrhage in, 310
       hippocampal, 37
       localization of functions in, 38
       of the brain, 34, 35, 58
       occipital, 36
       relation of, to sutures, 99
       supply of blood to, 95
       supramarginal, 36
       temporal, 36
       uncinate, 37
Convulsionnaires, 625
Convulsions, causes of, 140
    epileptic, simulation of, 407
    from intracranial growth, 328
    hysterical, 440, 445
    hystero-epileptic, 440
    localized,  140
    monoplegic, 140,143
    of children, 316
    primary, 140
    syphilitic, 380, 383
Convulsive tic, 350, 429, 431
Co-ordination, cerebellum the organ of, 73
    muscular, 171
Coprolalie, 429, 430
Cord, spinal.   See Spinal  Cord.
Cornua, anterior, myelitis of, 205, 213, 230
    of gray matter, 20
Cornu ammonis, 37
Corona radiata, 81
Corpora amylacea, 217
    quadrigemina, 60-73, 146,152
       peduncle of, 72, 73
Corpus callosum, 37, 51, 57
       artery of, 89
    striatum, central ganglia of, 103
       lesions of, 146
Corpuscles, nerve-, 32
    sensitive,  of Golgi, 47
Cortex of brain.   See also Cortical.
    centres in.  See Cortical  Centres.
    hemorrhage into, 310
    of cerebellum, functions of, 73
    of cerebral cortex, motor zone of, 73
    of cerebrum, functions of, 73
    organ of the mind, 55 644
    tumors of, 336
Corti,  ganglion of, 88
Cortical cells,'nervous connections of, 52
    centres, 38, 43, 139,140
       affections of, 295
       localization of, 97
       of vision,  150
    lesions, as causes of mental disease, 56,140
       localization of, 139
    reflex, pupillary, 152
Cramp, piano-forte-players',  469
    seamstresses', 469
    smiths', 469
    telegraphers', 469
    violin-players', 469
    writers', 469
Cranial bones.  See Skull.
    nerves, 84
       motor nuclei of, 84, 86
       origin of, 65
       peripheral tract of, 84
       sensory, 86
           origin of, 80
           tract of, 86
       syphilis of, 377
       topography of, 97, 373
       tract of, H4
Craniectomy for idiocy, 690
Cranium.  See Cranial and Skull.
Cremaster reflex, 169
Cretinism, sporadic, 550, 551
Crises, gastric, 261, 275
    laryngeal, 261, 275
    nephritic, 261, 275
Crura cerebri, 60
Cuneus, 37
    cortical centre of vision, 140
    hemorrhage into, 311 
714
INDEX.
 Cuneus, lesions of, 151
 Current, cellulifugal, 18, 52
     cellulipetal, 18, 52
     collector, 109
     constant, 107, 111, 112
     continued, 105
     defective, causes of, 115
     Edison, 117
     effect on resistance of skin, 121
     electric, 106,107
     faradic, 109
        and galvanic, compared, 126
     galvanic, 105, 109, 111
     induced, 109,110
     induction, 109,110
     interrupted, 105,109,110
     negative, 106
     nervous, cellulifugal, 18
        cellulipetal, 18
        transmission of, 30
     positive, 106
     secondary, 110
     -selector, 114
     voltaic, 105,109, 111
 Cutaneous reflexes, 169
 Cylinders, axis-.  See  Axis.
 Cyrtometer, 101
 Cystitis in myelitis, 229
 Cyst, apoplectic, 307
     arachnoid, 601
     hydatic, intracranial, 331
     parasitic, intracranial, 331
 Cystosarcoma of brain, 330


   DANCE, ghost, 418
     Messiah,418
     of St. Anthony, 418
     of St. Guy, 418
     of St. John, 418
     of St. Modesty, 418
     of St. Vitus, 418
     plague, 418
 Daniell cell, 107
 Deafness, mental, 40, 43,159
    word-.  See Word-deafness.
 Decussation of nerve-fibres in spinal cord, 81
    of sensory paths, 80
    tegmental,  of Porel,  70
       of Meynert, 70
 Degeneration, fatty, 197
    of ganglion-cells in paralysis," 294
    partial, 255
    of posterior column, 266
    quantitative reaction of, 129
    reaction of, 105, 128, 185, 195, 235, 256
    spinal, syphilitic, 271
 Degenerative lesions, in study of nervous sys-
  tem, 19,21                               J
 Deglutition, impaired, in bulbar paralysis,

Deiters* cells, 32, 217
    histology of nerve-cells, 18
    nucleus, 73
Delirants chroniques, 657
Delirium, 685
    acute, 638
    clinical history of,  685
    diagnosis of, 651, 685
    etiology of,  685
    grave, 621, 638
       diagnosis of, 638,  686
       lesions of, 638
       prognosis of, 639
       symptoms of, 638
       treatment of, 639
    muttering, 686
    of grandeur, 669
    of meningitis, 621
    post-febrile, 622, 687
    prognosis of, 685
    treatment of, 686
    tremens, 566, 621
       diagnosis of, 569, 641
       symptoms of, 566
       prognosis of, 567
       treatment of, 569
  Delusional insanity.   See Paranoia.
     mania, 620
     stupor, 640
  Delusions, 586
     hysterical, 461
     of grandeur, 657, 659, 683
     of persecution, 657, 658, 683
     primordial, 586
     systematized, 657
     unsystematized, 664
  Demence paralytique, 666
  Dementia, 643, 669, 689
     &cut6 644
     alcoholic, 652, 671, 672
     apoplectic, 652
     apoplectiform, 670
     diabetic, 653
     diagnosis of, 615,  650, 674
     epileptic, 633
     from cerebral exhaustion, 644
     from organic disease, 652
     in convalescence, 649
     nephritic, 652
     neurasthenic, 653
     of functional insanity, 652
     paralytic, 380, 475, 575, 666
        affections of senses in, 670
        alcoholic, 672
        apoplectiform, 670
        clinical history of, 666
        diagnosis of, 615, 651, 673, 684
        epileptiform,  670
        etiology of, 671
        maniacal stage of, 669
        melancholiac stage of, 669
        pathology of,  676
        prodromal stage of, 666
        prognosis of, 675
        pupillary alterations of, 668
        syphilitic, 673
        treatment of, 682
     paranoides, 683
        clinical history of, 683
        diagnosis of, 684
        treatment of, 684
     paretic, 303, 333, 442, 644, 666
     pathological anatomy of, 649
     post-melancholiac, 677
     primary, 643, 644
        diagnosis of, 674, 684
        treatment of, 653, 654
     secondary, 643, 648, 674
     senile, 644, 646
        paralysis of, 648
        symptoms of, 646
        treatment of, 655
        tremor of, 648
     from shock, 643
     terminal, 649, 653
     treatment of, 653
Developmental study of nervous system, 19
Diabetes as cause of neuralgia, 184
Diabetic coma, 508
    dementia, 653
Diseases of nervous system, 17, 439, 472, 493,
  531
Diamine in tetanus, 475
Diffuser, electric, 107
Digiti mortui, 451, 563
Diphtheritic paralysis, 488
        bacillus of, 490
        clinical symptoms of, 488
        diagnosis of, 490
        electricity in, 490, 492
        faradization in, 492
        gymnastic exercises in, 492
        history of, 488
        massage in, 491
        micro-organisms of, 490
        multiple, 489
        of the palate, 489
        pathological anatomy of, 489
        prognosis of, 490
        treatment of, 490
Diplegia, 315, 316
Diploe, hemorrhage from, 339
Diplopia, 156 
TNDEX.
715
Dipsomania, 658
Disk, choked, 157, 328
Disseminated sclerosis.  See Sclerosis
Diver's paralysis, 246
Dolichocephalic skull, 98
Dubois-Reymond coil, 115
Dysaesthesia in myelitis, 214
Dynamometer, 173
Dystrophy, chronic muscular. 249
  EAR-DISEASE a cause of meningitis, 240, 360
    external, diseases of, 538, 542
    internal, diseases of, 538, 542
    middle, diseases of, 161, 538, 542
       nerves to, 209
    pain in, 504
Earth, zero potential, 106
Echolalie,  429, 430
Ecstacy, 511
Edison current, 117
       Lalande cell, 113,114
Electric air, 112
    cautery, 106
    chorea, 429
    current, 106
       measurement of, 107
       regulation of, 107
    diffuser, 107
    lighting, 117
    shock, 108
    sparks, 112
Electricity, 105, 113.  See Electrification,  Elec-
      trization, Faradic. Galvanic, etc.
    applications of,  in disease, 105, 130
    in bulbar paralysis, 295
    diagnostic uses  of, 125
    in diphtheritic paralysis, 490, 492
    dosage of, 107
    effect of, on nervous centres, 20
    faradic.   See Faradic, Faradism, and Far-
      adization.
    frictional, 105,112
    galvanic, 105-112  See Galvanic, Galvanism,
      and Galvanization.
    instruments of,  105
    in lead-poisoning, 396
    in locomotor ataxia, 273
    in multiple neuritis, 206
    in neuralgia, 190
    in neurasthenia, 468
    in neuritis, 201
    in progressive muscular atrophy, 259
    static, 105,112
    as test of pain, 165
    unit of, 107
    voltaic, 105-112.   See Galvanic. Galvanism,

Electrification of the body, 106
    negative, 106
    positive, 106
Electrization of  special muscles  and nerves,
  130
Electro-motive force, 106
Electro-therapeutics, 107
Electrodes, 107,117
    interrupting, 122
    various forms of, 117
    wetting of, 121
Electrolysis, 107
    rheostats for, 117
Eleventh nerve, 85
Emboli, 308, 311
    intracranial, 306
    pigment, in cerebral vessels, 308
Embolus, 72                           1Q
Embryological study of nervous system, 19
Emprosthotonus, 477
EncephaUtis, congenital, of Virchow, 321, 323
    infantile, 321
    traumatic, 574       .
Enchondroma, intracranial, 331
End-baskets of Kolliker, 75, 77          .
Endarteritis a cause of cerebral hemorrhage,
  307
Entartungreaction,  235
Endothelial capsule of ganglionic cells, 30
Epidemic defined, 483
Epilepsia saltatoria, 418
Epilepsie, 397
    larve, 399
Epilepsy, 397
    causation of, 401
    clownish ness of, 398
    coma of, 507
    diagnosis of, 406, 425, 488
    grand mal, 397
    history of, 397
    idiopathic, 406
    Jacksonian, 401
    larvated, 399
    laryngeal, 397. 493
    lesions of, 402
    major, 397
    masked, 399
    minor, 397
    modus operandi of, 404
    operations for, 408
    organic, 401
    ovariotomy for, 534
    pathology of, 402
    pathological anatomy of, 402
    peripheral irritation in, 408
    petit mal, 397
    procursive, 397
    prognosis of, 407
    pupil in, 400
    saltatory, 418
    simulation of, 407
    spinal, 168
    symptoms of,  397, 406
    syphilitic, 380
    traumatic, 575
    treatment of, 408
    trephining for, 468
    types of, 397
    with migraine, 400, 412, 418
 Epileptic aurse, 398
    coma, 507
    convulsion, simulation of, 407
    dementia, 633
    insanity.  See Insanity, Epileptic.
    pigmentary degeneration in, 605
    migraine, 400, 412, 418
    stupor. 632
 Epileptiform dementia, 670
 Epithelial cells, 32, 33
    corpuscles, 32
 Epizooty, 482
 Ergotism, chronic, 261
 Erotic fetichism, 597
 Erotomania, 661
 Erythromelalgia. 564
 Essential infantile paralysis, 205, 230, 575
 Etat crible, 355
 Exhaustion, cerebral, 644, 649
 Exophoria, treatment of, 418
 Exophthalmic goitre, 560
    diagnosis of, 561
    galvanization in, 562
    pathology of, 561
    prognosis of, 562
    symptoms of, 560
    treatment of, 562
 Exophthalmus, 560
 Expression, defects of, 141
 External capsule, 60
 Extravasations of blood, spinal, 240, 245
 Eye, conjugate deviations of, 156, 309
    examination of, 154
         with ophthalmoscope, 157
    movements of, 154
    muscles of, 154
         asthenopia of, 156
         lesions of, 147
    nerves distributed to, 154
    paralysis of muscles of, 154,156, 296
 Eyeballs, oscillation of, 156
 Eye-strain, headache from, 496
    in chorea, 422
    neuralgia from, 182
    pain of, 502
    vertigo from, 494 
716
INDEX.
  FACE, motor points of, 130
    Facial hemiatrophy, 519
       nerve, 84,85
           branches of, 209
           distribution of, 209
           lesion of nucleus of, 207, 210
           motor points of, 210
           neuritis of, 210
           neuroma of, 211
           palsy, 295
           paralysis, 295
           spasm, 186
       tropho-neurosis, 295
       type of infancy in muscular atrophy,
         250, 252
Fallsucht, 397
Falret's intellectual grand mal, 632, 634, 635
       petit mal, 632, 634, 635
Faradaic electricity.  See Faradic.
Faradic battery, 110, 111, 115. See Faradization.
       compared with galvanic battery, 111
    current, 109
       compared with galvanic, 126
    electricity, 105,109, 111.  See Electricity and
      Faradization.
Faradism, 105,109, 111. See Electricity, Faradic,
  and Faradization.
Faradization.  See Electricity and Faradic.
    in diphtheritic paralysis, 492
    in diseases of sympathetic, 565
    in lead-poisoning, 396
    neuralgia, 190
    in night-terrors, 513
    in neuritis, 201
    in progressive muscular atrophy, 259
Fascicular sclerosis, combined, 279
Fasciculus, inferior longitudinal, 49
    posterior longitudinal, 66, 68
    solitary, 87
    sub-callosal longitudinal, 49
    superior longitudinal, 49
    uncinate, 49
    vertical, 49
Fatty degeneration, 197
Fear of localities, 589, 591, 658
    of pollution, 589
    prsecordial, 611
Ferrier, localizations of, 39
Fetichism, erotic, 597
Fibres, arcuate, 48
    clintbing-, 76
    commissural, of cerebellum, 51
       of cerebrum, 51
    garland-shaped, of Stilling, 49
    medullated, of the brain, 47
    mossy, 76
    optic, 62
    parallel, 77
    of Stilling, 49
    tangential, 48, 52
Fibrillary atrophy, 255
Fibro-glioma of brain, 330
    sarcoma of brain, 330
Fibroma,  intracranial, 331
Fibromata of nerves, 211
Fifth nerve, 86
Fifth pair, sensory root of, 66
Figures, mania for, 658
Fingers, dead, 451, 563
Fissural artery, 239
Fissure or Fissures, anterior occipital, 103
       of the brain, 34,100
       calcarine, 37
       calloso-marginal, 37
       cerebral, 34,100
       of the cerebrum, 34, 100
       frontal, 35,101, 102
       interparietal, 36
       longitudinal, 35,101
       parietal, 36,102
       parietoocciptal, 36, 37,102
       praecentral, 35,102
       of Rolando, 34,101
       of Sylvius, 34, 60, 101
       temporal, 36,102
Fleau de la danse, 418
Flechsig, developmental studies of, 19,21
Flexion, forcible, in neuralgia, 192
Flexor muscles, contracture of, 170
Foetus, brain of, lesions of, 321, 324
Folie a double forme, 627
    a formes alternes, 627
    circulaire, 627
    des anti-vivisectionistes, 590, 658
    de doute, 590, 615, 658
Folly of doubt, 590, 615, 658
Foot-clonus, 168
    -jerk, 168
Foramen of Magendie, 341
Forcible flexion in neuralgia, 192
Forearm, motor points of, 132
Forel, tegmental decussation of, 70
Formication in  myelitis, 214
Foudroyant neuralgia, 183
       pains, 261
Fracture, as cause of myelitis, 225
    neuralgia after,  183
    of skull, diagnosis of, 312
    of veretebrse, 289
Frenzy, transitory, 631, 636, 638
Frictional electricity, 105,112
Friedrich's disease, 261,271, 545
       causes of, 546
       diagnosis of, 349, 548
       lesions of, 546
       pathology of, 546
       prognosis of, 549
       Romberg symptom in, 545
       symptoms of, 545
       treatment of, 549
Frontal convolutions,  35, 37
    fissures, 35,101,102
    lobe, involvement  of, in mental disease,
      142
Fulgurant pains, 261
Fulminating pains, 261
Functions, localization of.  See Localization.
Fundamental column, 78
    tract of anterior column, 22
Furor transitorius, 631, 638
Fury, mania with, 634
    transitory, 631, 636, 638
Fuscous degeneration in insanity, 605
Fusiform  cells  of molecular  layer  of  motor
      area, 44
    lobe, 37
    lobule, hemorrhage in, 310
  GAIT, spasmodic, 275
    spastic, 275
Galvanic batteries, 105, 109,110, 111, 112
    battery compared with faradic battery, 111
       cells of, 105-112
    cautery,106
    current, 109, 111
       compared with faradic, 126
       reaction of nerve to, 127
    electricity, 105,112  See Galvanism and Gal-
         vanization.
       definition of, 109
       regulation of, 109
Galvanism.  See Galvanic Electricity and Gal-
  vanization.
Galvanization, cerebral, 117,125, 498
    in chorea, 428
    in diseases of sympathetic. 564
    in exophthalmic goitre, 562
    in headache, 498
    in hysteria, 445
    in lead-poisoning, 396
    in locomotor ataxia, 273
    in melancholia, 618
    in multiple neuritis, 206
    muscular response to, 129
    in neuralgia, 190
    in neurasthenia, 468
    in neuritis, 201
    in occupation-neuroses, 472
    in palmus, 434
    in paralysis agitans, 528
    of peripheral nerve, 125
    in progressive muscular atrophy, 259
    of spinal cord, 117,125 
INDEX.
717
Galvanization in wry-neck, 437
Galvano-caustic, 106
Galvanometer, ill
Ganglia, basal, 57
    central, of optic thalamus, 103
    of cerebrum, 57
    excision of, in neuralgia, 192
Gaughon-cells, functions of, 500
        of motor nuclei, degeneration of, 294
Ganglion of Corti, 88
    Gasserian, removal of, 192
    of Scarpa,  88
Ganglionic cells, 30
Garland-shaped fibres of Stilling, 49
Gasserian ganglion, removal of, 192
Gastric crises, 261, 275
Geastkerne, 195
Gelatinous substance, 264, 265
General paralysis, 666
        of insane, 666
        progressive, 666
    paresis.  See Paresis, general.
Geniculate bodies, 60
    body, lateral, 61
        middle, 61
Genital irritation  as  cause  of neuralgia,
  183
Genito-urinary diseases, reflex  symptoms of,
  535
Gennari, layer of, 52
Genu, 59
    recurvatum, 236
Gerlach's study of nervous system, 19
Ghost liance, 418
Gigantism, 558
Girdle-feeling or sensation, 214, 240, 263
Glabella, 97, 98
Gland,  pineal, 70
Glioma of brain, 330
        telangiectatic, 330
Gliomata, cerebellar, 284
    in syringomyelitis,  283
    on  nerves, 211
Gliosis, 268, 284
Glio-sarcoma, intracranial, 330
Globus hystericus, 438
Glosso-pharyngeal nerve, 84-87
    nucleus, lesion of, 295
Glossy  skin, 185, 195
Goitre, exophthalmic.  See Exophthalmic.
Golgi, cerebral porosity of, 325
    method of staining, 17, 34
    sensitive corpuscles of, 47
    sensory cells of, 54
Goll, column of, 21, 72, 78, 265, 266, 267, 280
Gout, a cause of neuralgia. 181
    American, 188
    treatment of, 188
    vertigo of, 494
Gowers, column of, 21,  79, 264, 280
Grand mal, 397
        intellectual,  of Falret, .632, 634, 635
Grandeur, delirium of, 669
    delusions of, 657, 659, 683
Granular layer of cerebellum, 74, 75
Gray matter of cerebrum, cells of, 18
        cornua of, 20
        functions of, 19
        histology of,  43
        horns of, 20
        location of. 19
        origin of cranial nerves from, 65
        organ of mind, 55, 644
        of spinal cord,  77
Graves's disease, 560
Grenet cell, 113

rrowSTntmcmnial.   See Intracranial.
Gudden's study of nervous system, 19
Gumma of  brain, 330

g?SSS58i?SSXS: fo? nervous symptoms,
  533
Gvrus   See Convolution.
    angularis, 36,140
    fornicatus, 37
    hippocampi, 37
  HAAB, pupillary reflex of, 152
    Haematorrhachis, 245
Haematomyelia, 245
    wahnsinn, 640
Hallucinations, 586
Hallucinatorische Verwirrtheit, 640
Hallucinatory insanity.  See Insanity,  halluci-
     natory.
    mania, 620, 640
    melancholy, 609
    paranoia, 658, 662
Hand-battledore, 555
    -grasp, 173
    -type of muscular atrophy, 250
Head, neuralgia of, 178
Headache, 495
    acclimatic, 497
    alcoholic, 496
    anaemic, 496
    ataxic, 497
    causes of, 495
    dyspeptic, 497
    from eye-strain, 496
    galvanization in, 498
    hemicranial.  See Migraine.
    intracranial, 497
    from intracranial growths,  327
    lithaemic, 496
    of locomotor ataxia, 497
    nephritic, 496
    ocular, 496
    prognosis of, 497
    recurring, from intracranial growth, 323
    reflex, 496
    sick 411
    syphilitic, 185, 380, 497
    treatment of, 497
    varieties of, 495
Hearing,  relation of posterior  quadrigeminal
     body to, 62
    tests for, 159
Heat-centre, 103,146
    localization of, 103
Hebephrenia, 600, 645, 654
Helicomonades, 377
Hemianaesthesia, 152, 439
    hysterical, 576
    from lead-poisoning, 393, 394
    treatment of, 445
Hemianopsia, 41, 43, 63, 140,147,150
    from intracranial hemorrhage, 311
    localization of, 41, 43
    motor centres for, 41, 43
Hemiataxia, 319
Hemiatrophy, facial, 519
Hemicrania.  See Migraine.
Hemiopia, 41, 63, 150
    homonymous, 151
    tests for, 159
Hemiplegia, 315
    bilateral, in cerebral palsies, 316
    from cerebral hemorrhage,  85
    double, 315
    from lead-poisoning, 393, 394
    syphilitic, 379, 382
Hemiplegic chorea, 319
Hemispheres of cerebellum, 72
    cerebral, 35, 37, 72
        bloodvessels of, 94
Hemorrhage in angular gyrus,  310
    in  cerebellum, 310
    cerebral, 306.  See also Hemorrhage, intra-
     cranial.
    in  cerebro-spinal axis, 310
    in  convolutions of motor area, 310
    in  cortex, 310
    in  cuneus, 310
    diploic, 339
    extradural, 245, 289
    in  fusiform lobule, 310
    intracranial, 306, 309, 574
        causes of, 306
        clinical symptoms of, 308
        coma of, 508
        diagnosis of, 311
        electricity in, 314
        faradism in, 314 
718
INDEX.
Hemorrhage, intracranial hemiplegia from, 85
       location of, 309
       of the newborn, 321, 323
       prognosis of, 310
       surgical treatment of, 313
       symptoms of, 306
       traumatic, 574
       treatment of. 313
       trephining in, 313
    in internal  capsule, 60, 309
    intradural, 289
    in Ungual lobule, 310
    meningeal, 245
       in occipital lobe, 310
    from optic arteries, 92
    spinal, 240,  245
       diagnosis of,  246
       meningeal, 245
       prognosis of, 246
       treatment of, 246
    in temporal convolutions, 310
Hereditary ataxia, 261, 271, 545
    ataxic paraplegia, 545
    chorea, 342
    neuralgia, 181
Heredity a cause of locomotor ataxia, 261
    neurotic, 181
■i':"' paraplegia, 545
Hermaphroditism, sexual, 596
Herpes zoster, 563
Hidden needle, 164, 583
Hippocampal convolution, 37
Hippocampus major, 37
Holtz machine, 105,112
Homicidal impulses, 658
Homonymous hemiopia, 151
Homosexuality, 596
Horns, anterior,  myelitis of, 205, 213, 224, 225,
      230, 320
    of gray matter, 20
Huntington's chorea.   See Chorea,  Hunting-
  ton's.
Hydatid cysts of brain, 331
Hydrocephaloid state, 370
Hydrocephalus, 340. 360
    acquired, 340
    acute, 340
    causes of, 341
    chronic, 340
       internal, 341
    compression for, 342
    congenital, 340
    diagnosis of, 342
    external, 340
    internal, 340
    primary, 340
    prognosis of, 342
    secondary.  340
    subdural, 340
    surgical treatment of, 342
    symptoms of, 341
    treatment of, 342
    ventricular, 340
Hydromyelus, 282
Hydrophobia, 245, 482.   See Rabies.
    diagnosis of, 443, 485, 488
    incubation  of, 484. 486
    false, 484
    microbes in, 487
    micrococci  in, 487
    nomenclature of, 482
    Pasteur's inoculation in, 443, 486
    spasms of, 487
    symptoms of, 487
    virus of, 485
Hydrops of cerebral ventricles, 367
Hydrosyringomyelitis,  282
Hyperacusis, 209
Hyperaemia, cerebral, 354
Hyperplastic neural growths, 210
Hypertrophic cervical  pachymeningitis, 285
    paraplegia of infancy, 300
    pulmonary osteo-arthropathy, 558
Hypertrophy of brain, 457
    pseudo-muscular.  See Pseudo-muscular.
Hypnotics, 500
Hypnotism, 514
Hypnotism, auto-. 514
    history of, 514
    in hypochondria, 446
    in morbid fears, 591
    in occupation-neuroses, 472
    production of, 515
    symptoms of, 515
    therapeutic value of, 518
Hypnotization, 515
Hypochondria, 446
    diagnosis of, 291, 446, 615
    hypnotism for, 446
    sexual, 446
    suggestion in, 446
    treatment of, 446
Hypochondriacal insanity, 446
Hypoglossal nerve, 84, 86
Hypoglossus, lesion of nucleus of, 294
Hysteria, 226, 437
    causes of, 437
    clinical history of, 438
    contortions of, 441
    convulsive symptoms of, 438, 440
    diagnosis of, 286, 392, 426, 460,  488, 615
    galvanism in, 445
    major, 440
    melancholic, 442
    mental symptoms of, 438
    motor symptoms of, 438, 440
    neurasthenic, 442
    prognosis of, 441
    sensory symptoms of, 438, 439
    simulating myelitis, 241
    stages of, 441
    traumatic, 575
    treatment of, 443
    visceral symptoms of, 438, 440
Hysterical chorea, 340
    contortions, 441
    convulsions, 440,.445
    delusions, 461
    dyspepsia, 440
    hemianaesthesia, 576
    insanity, 399, 439
    motor ataxia, 529
Hystero-epilepsy, 398,  407, 440
TDIOCY, 689
1  causes of, 690
    surgical treatment of. 690
Illusions, 586
Impressions, how conducted, 18
Impulses, morbid, 589
Inco-ordination, motor, of chorea, 349
    muscular, 171, 271
Indigestion, headache from, 497
Induced current, 109, 110
Induction, 110
    current, 109
Infantile brain, diseases of, 321
    encephalitis, 321
    spinal paralysis, 230
Influenza as a cause of neuralgia, 183
Infundibulum, 62, 64
Inion, 97,98
Innervation of nerve-cells. 223
Insane, cerebral thermometry in, 176
    general paralysis of, 666
    paralysis of, 666
Insanity, alcoholic, 567, 568, 658
    anaemia of brain in, 602
    arrested development in, 606
    atrophy of nervous matter in, 603
    blood-changes in, 607
    cerebral thermometry in, 174,176, 373
    chronic, 600
        diagnosis of, 462
    circular, 626, 627, 632, 634
    classification of, 585
    cocainic, 658
    colloid degeneration in, 604
    confusional, 652, 656
    cranial changes in,  600
    delusional, chronic. See Paranoia.
    of doubt,  590, 615, 628
    epileptic,  399, 600, 632 
INDEX.
719
Insanity, epileptic, causes of, 636
       clinical history of, 632
       definition of, 632
       diagnosis of, 636, 686
       history of, 632
       medico-legal relations of, 635
       paranoia, 635
       treatment of, 637
    facies of, 599
    functional, 652
    fuscous degeneration in, 605
    granular disintegration in, 605
    hallucinatory, 637, 640,  664
       alcoholic, 567, 568
       causes of, 640
       clinical history of, 640
       definition of, 640
       diagnosis of, 567, 637, 641, 663, 684
       duration of, 641
       prognosis of, 641
       treatment of, 641
    hypochondriacal, 446
    hysterical, 399, 439
    illusions of, 586
    intermittent, 627
    larvated, 632, 635
    membrane-changes in,  600
    miliary sclerosis'in, 603
    moral, 661, 662
    morphinic, 658
    paranoioid, 635
    pathology of, 600
    periodical, 615, 627
        causes of, 629
        diagnosis of, 636
        treatment of, 629
    pigmentary,  degeneration in, 605
    post-epileptic, 575
    post-febrile, 658
    of pubescence, 600, 645, 654
    puerperal, 600, 658
    recurrent, 627
    sclerosis in, 604
    simulation of, 598
    softening of  brain in, 604
    stuporous, 644
    syphilitic, 380
    tension, 626
    traumatic, 574
    vacuolation of cells and nuclei in, 606
    varieties of, 585
    vascular changes  in,  601
 Insomnia, 500
    causes of, 500
    from drugs, 507
    from foods, 507
    from fevers, 505
    from insanity, 505
    from organic lesions, 506
    from pain, 501
    from passions, 501
    in intracranial syphilis, 185
    melancholic, 616
    neurasthenic, 505
    syphilitic, 506
    treatment of, 500
 Insufficiency of recti muscles, 156
 Insular sclerosis, 387
 Intention-tremor, 388, 526, 586
 Internal capsule, 58
        hemorrhages into, 60, 309
        lesions of, 145,152
 Interparietal fissure, 36
 Interrupted currents,  109, 110
 Intracranial angioma, 331
    actinomyces, 331
    adenoma, 331
    cancer, 331
    cholesteatoma, 331
    embolism, 306
    enchondroma, 331
    fibroma, 331
    gliosarcoma, 330
    growths, 270, 311, 320, 326, 370
        causes of, 326
        clinical symptoms of, 326
        coma from, 329
Intracranial growths, convulsions from, 328
       diagnosis of. 311, 320, 332, 370
       etiology of, 326
       localizing symptoms of, 329
       operations for, 306
       pathology of, 329
       prognosis of, 334
       surgical treatment of. 336
       treatment of, 335
       trephining for, 338
       varieties of, 329
    headache, 497
    hemorrhage. See Hemorrhage, intracranial.
    hydatid cysts, 331
    lesions, vertigo from, 494
    lipoma, 331
    myxoglioma, 331
    myxoma, 331
    myxosarcoma, 331
    neoplasms, 209
    neuritis, 194
    neuroma, 334
    operations, 336
       antisepsis in, 339
       drainage in, 339
    pain, 502
    parasitic cysts, 331
    syphilis.  See Syphilis, Intracranial.
    thrombosis, 306, 312, 331, 357, 544
    tumors.  See Intracranial Growths.
Island of Reil, 36, 60
       as a centre, 141
 JACKSONIAN epilepsy, 401
v   Jars, Leyden, 112
Jaw-jerk, 167, 275
Joint-neuroses, vasomotor, 563
Joints, abnormally flexible, 235
    contracted, 235
Jumpers, the, 429
Juvenile type of muscular atrophy, 250, 252
  KAKKE, 203
    Katatonia, 624
       diagnosis of, 615, 651, 675
       history of, 624
       pathology of, 625
       treatment of, 626
Kenophobia, 589
Kinderlahmung, spinale, 230
Klauenhand, 251
Klebs-Loeffler bacillus, 490
Kleptomania,  658
Knee of internal capsule, 59
    -jerk, 167
       in myelitis,  215
       reinforcement in, 167
Kolliker, end-baskets of, 75, 77
    nucleus magnocellularis of, 79
    reflex-motor tract of, 32
Kolvin unit, 122
Krause, respiratory tract of, 87
T ABYRINTH, auditory, 540
L  circular canals of, 73
    comparative anatomy of, 542
    disease of, 161, 538, 540
    functions of, 540
    tonus, 540
Labyrinthine disease, vertigo from, 538
Lagophthalmus, 206, 209, 295
Lambda, 97
Landry's disease or paralysis, 210, 223, 238, 243
           bacillus in, 243
           causes of,  244
           diagnosis of, 244
           pathology of, 243
           prognosis of, 245
           treatment of, 245
Larvated epilepsy, 399
    insanity,  632, 635
Laryngeal  crises, 261, 275
    epilepsy.  397, 493
    vertigo, 398, 493 
720
INDEX.
 Latah. 429
 Lateral column of spinal cord, 21
     limiting column, 22
     pyramidal column, 21
     sclerosis, primary, 295.  See Sclerosis.
 Lateralsclerose, amyotrophische. See Sclerosis,
   lateral.
 Law cell, 113
 Layer of Gennari, 52
 Lead cachexia, 393
     -colic, 393, 394
     -line, 383
     -palsy or paralysis, 174, 240, 393, 394
        wrist-drop in, 174, 240, 394, 396
     -poisoning, 392
        blue line from, 293, 394
        cerebral symptoms of, 393, 394
        colic from, 393, 394
        diagnosis of, 334,  396
        electricity in, 396
        hemianaesthesia from, 393, 395
        hemiplegia from, 393, 395
        neuritis from, 395
        paralysis from, 393, 394
        pathological lesions of, 395
        prognosis of, 396
        symptoms of, 393
        treatment of, 396
        wrist-drop from, 174, 240,  394, 396
     -tremor, 526
 Leclanche cell, 113
 Leg, motor points of, 134
 Legal ohm, 122
 Lemniscus, 66
     lateral, 68, 89
        nucleus of, 69
     medial, 79, 89
 Lenticular arteries, 92
 Lenticulo-optic arteries, 91
     -striated arteries, 91
 Leprosy, anaesthetic, 286
 Lepto-meningitis, 360
     cerebri, 392, 675
 Lesions of base of brain,  152
     cortical, 140
     of cuneus, 151
     localization of.  See Localization.
     subcortical, 140
 Leyden jars, 112
 Ligaments, traumatic diseases of, 574
 Lighting, electric, 117
 Limbic lobe, 37
 Lime-metastasis, 308
 Limiting membrane, 32
 Line, lead-, 383
 Lingula, 64, 66, 67, 72
 Lingual  lobe, 37
     lobule, hemorrhage in, 310
 Lipoma, intracranial, 331
 Lipomatous myoatrophy,  299
 Lissauer, column of, 21, 77, 265, 267
 Lithaemia, 448
    treatment of, 188, 417
 Lithaemic neurasthenia.  See Neurasthenia.
    headache, 496
    paraesthesia, 226
    urine, 458
    vertigo, 493
 Lithoidosis, 455
 Lithuria, 455
 Lobe, fusiform, 37
    limbic, 37
    lingual, 37. 310
    occipital, 36, 103,310
    parietal, 35, 36
    temporal, 36,102
Lobule, lingual,  37, 310
    paracentral, 37
    parietal, 35, 36
Lobus infundibuli, 557
Localities,  fear of, 589, 658
Localization.  See Motor Centres.
    anatomical, of neuralgia,  182
    of aphasia, 38, 43
       of conduction, 41
    of areas of function, 38, 43
    of aural lesions, 494
 Localization, cerebral, 38, 43
     of cerebral lesions, 139
     of convulsions, 140
     of cortical centres, 97, 139
     of functions, 38, 43
         by Ferrier, 39
         in spinal cord, 82
     of heat-centre, 103
     of hemianopsia, 41, 43
     of lesions in cerebellum, 139
         in cerebrum. 139
         in spinal cord, 139
     of mental blindness, 41, 43
         deafness, 40, 43
     of motor aphasia, 40, 43
     of muscular sense, 41, 43
     of paralysis, 38, 525
     of paraphasia, 41, 43
     of sense of pain, 41, 43
        of sight, 38
        of taste, 41, 43, 162
        of temperature, 41, 43
        of touch, 41,  43
     of word-blindness, 41, 43
        -deafness, 40, 43
 Lock-jaw.  See Tetanus, Tetany, and Trismus.
 Locomotor ataxia, 172, 213, 260, 261, 262, 264
        alcohol as a cause of, 261
        anatomy of parts in, 264
        causes of, 260
        cauterization in, 274
        clinical history of, 261
        diagnosis  of,  205, 269, 281, 285, 288, 333,
          349, 462, 548
        electricity in, 273
        galvanism in, 273
        headache of,  497
        histological lesion of, 268
        history of, 260
        hysterical, 529
        massage in, 273
        non-pathognomic symptoms of, 262
        pathognomic symptoms of,  261
        pathology of, 264
        progressive, 172, 213,  260
        prognosis of, 272
        rest in, 273
        suspension in, 274
        symptoms of, 261
        syphilis as a cause of, 260
        traumatic, 575
        treatment of,  272
Locus caeruleus. 66, 86
Loeffler, bacillus of, 490
Longitudinal fasciculus, 49, 66, 68
    fissure, 35,101
Lordosis 235
    lumbar, in pseudo-muscular hypertrophy,
      301
Lower extremity, neuralgia of, 180,191
Lumbago, 179
    strictural, 443
Lumbar lordosis, 301
Lunacy.  See Insanity.
Luys, body of, 70
Lympho-sarcoma of brain, 330
Lyssa, 482
Lyssophobia, 485
   MARIE'S disease or malady, 555
    Magnet, 110
Magnetic current, 110
Main-en-griffe, 251
Malaria as a cause of neuralgia, 182
Malformation in study of nervous system, 20
Malingering in contracture, 171
    in epilepsy, 407
    in sense of pain, 165
       touch, 164
    in temperature-sense, 166
    in traumata of cord, 291
Mammary reflex, 169
Mania, 439,  620
    alcoholic, 566, 568,  621, 641
    a  potu, 566, 568, 621, 641
    causes of, 621 
INDEX.
721
Mania, clinical history of, 620
    delusional, 620
    diagnosis of, 615, 621, 636, 641, 604 674
    duration of. 621
    gravis, 638
    hallucinatory, 620, 640
    intermittent, 627
    melancholic, 628
    meningitic, 622
    of paralytic dementia, 669
    periodical, 627
    for pins, 658
    prognosis of, 621
    puerperal, 658
    pyeluric, 622
    reasoning, 659
    recurrent, 628
    simple, 620
    treatment of,  622
    with fury, 634
Manie avec fureur, 634
    melancholique,  628
Manipulations of massage, 135
Many-columned cells  of spinal cord, 28, 30
Markings of Schmitt,  196
Martinotti, cells of,  47
Masochismus, 596
Massage, 135
    in diphtheritic paralysis, 492
    in locomotor ataxia, 273
    in myelitis, 228
    in neurasthenia, 466
    in pseudo-muscular hypertrophy, 304
    manipulations of, 135
    technique of,  135
Masseur or masseuse,  qualifications of, 136
Mastoid cells, disease  of, 542
Masturbation, 593
Median arteries, 97
Medulla oblongata, 61
        anatomy of, 34
        bloodvessels of, 89
        diseases of, 213
        lesions of, 149
        relation of,  to spinal cord, 65
        vasomotor centre of, 405
Medullary sheath, 197
Medullated fibres of brain, 47
Melancholia, 608
    agitata, 609, 639
    alcoholic, 568
    attonita, 609
    causes of, 613
    clinical history of, 608
    of dementia, 669
    diagnosis of. 442, 462, 611, 614, 641, 651,
      674
    galvanization in, 618
    hallucinatory, 609
    headache of, 496
    hysterical, 442
    insomnia of, 616
    mania of, 628
    prognosis of, 616
    simple, 608
    symptoms of,  611
    treatment of,  616
    with stupor, 609
Melancholy.  See Melancholia.
Melano-sarcoma of  brain, 330
Membrane, limiting. 32
Meniere's disease, 161
    diagnosis of, 312, 493, 491, 538, 542
    pathology of,  538
    prognosis of, 542
    symptoms of, 538
    treatment of,  513
    trephining for, 544
Meningeal hemorrhage, spinal, 24n
Meningitis, cerebral, 360
    cerebro-spinal, 225, 240, 363
        causes of,  364
        clinical history of, 364
        diagnosis  of, 320, 366
        etiology of, 364
        history of, 363
        pathology of, 365
664,
Meningitis, cerebro-spinal, prognosis of, 366
       symptoms of, 360
       treatment of, 366
    delirium of, 621
    diagnosis of, 366, 638
    from ear-disease, 240
    gummatous, 327, 329
    mania of, 622
    microbes in, 361, 369
    pain in, 502
    of pia mater, 392
    simple.  See Meningitis.
    suppurative, 360
       causes of, 360
       diagnosis of, 320, 362, 370
       etiology of, 360
       pathological anatomy of, 361
       prognosis of, 363
       symptomatology of, 364
       treatment of, 363
    syphilitic, 327, 329, 370
    traumatic, 240, 320
    tubercular, 329, 360, 367
       clinical symptoms of, 367
       bacilli in, 369
       diagnosis of, 320, 366, 369, 373
       etiology of, 368
       history of, 367
       micro-organisms in, 369
       pathology of, 368
       prognosis of, 369
       treatment of, 371
Meningo-cerebritis, pathology of. 601
    chronic, 602
Meningo-encephalitis, infantile, 240, 321
Meningo-myelitis, 217
    purulent, 225
Mental blindness, 41, 43, 670, 676
    deafness, 159
       localization of, 40, 43
    diseases, 585
       cortical lesions in,  142
    disturbance from intracranial growth, 328
    impairment in cerebral palsies, 316,319
Merzejewski's apertures, 341
Mesmerism, 514
Mesocephalic skull,  98
Messiah dance, 418
Metallic poisoning, tremor of, 392, 526
    tractors of Perkins, 515, 571
    tremor, 392, 526
Meynert, study of nervous system, 19
    tegmental decussation  of, 70
Microbic nervous diseases,  473
Microcephaly, 689
Micro-organisms.  See Bacillus.
    of chorea, 424
    of diphtheria, 490
    of diphtheritic paralysis, 490
    in meningitis. 361
    of syphilis, 377
    of tetanus, 475
Micturition, hasty, iu sclerosis, 275
Middle-ear, disease of, 161
Migraine, 156, 411, 495, 496
    causes of, 413
    coma of, 507
    diagnosis of, 413, 460
    epileptic, 400, 412,418
    pathology of, 413
    prognosis of, 413
    treatment of, 414
Miliary aneurism, cerebral, 306
    sclerosis in insanity, 603
Milliampere, 107, 110, 116
Milliamperemeter, 107,110,116
Mind, centre of, 142
    organ of, 55, 644
Miryachit, 429
Molecular layer of cerebellum, 74
       motor area, 44
Monomania, 657
Monoplegia in myelitis  of anterior horns, 231
Monoplegic convulsions, 140, 143
    paralysis, 139, 140, 143
Moral insanity, 661, 662
Morbus comitialis, 397
46 
722
INDEX.
Morbus, sacer, 397
Morphia-habit, 200
Morphinic insanity, 658
Morphinomania, 200, 566, 572
Morphiomania, 200, 566, 572
Morvan's disease, 285, 286
       pathology of, 564
Mossy fibres, 76
Motor aphasia, 40, 43
       centre for, 139,141
    area, 39, 40, 43,139
       arborizations of, 47
       cells of, 44
       layers of, 44
       of cortex, 80
           lesions of, 208
           layers of, 44
       lesions of, 139
    ataxia.  See Locomotor Ataxia.
       hysterical, 529
    centres.  See Localization.
       for agraphia, 41, 43
       for arm-muscles, 38, 43
       for articulate speech, 40, 43
       for face-muscles, 38, 43
       for head-muscles, 38, 43
       for hemianopsia, 41, 43
       for laryngeal muscles, 38, 43
       for leg-muscles, 38,43
       for paraphasia, 41, 43
       for word-blindness, 41, 43
       for word-deafness, 40, 43
    columns of spinal cord, 23
    cranial nerves, 84, 86
    fibres, 59
       from cortex, 80
       of posterior root, 30
       of spinal cord, 23
    impressions, how conducted, 18
    inco-ordination of chorea, 349
    nerves, peripheral, 80
       polar changes in, 235
           formula of, 235
    paralysis, from myelitis,  214
    points of arm, 131
       of face, 130
       of facial nerve, 210
       of forearm, 132
       of leg, 134
       of thigh, 133
       of trunk, 131
    symptoms, tests of, 154, 290
    tissues, conduction through, 18
    tract of Cajal, 32
       from cerebellum to periphery, 73
       of Kolliker, 32
       lesions of, in children, 324, 325
    zone of cerebral cortex. 73
Mucin-poisoning in tetanus, 481
Multiple cerebro-spinal sclerosis, 387
    neuritis.  See Neuritis.
    neuroma, 211
    paralysis in diphtheria, 489
    sclerosis, 334, 387
Muscles, cortical centres for, 39, 43
    diseases of, 299
    electric stimulation  of, 126
    ocular.  See Eye.
    reflex, 166
    traumatic diseases of, 574
    of upper-arm, type of, 232
    voluntary, tonic spasms  in,  304
Muscular atrophy, 257
       progressive.   See Progressive Muscular
          Atrophy.
    click, 170
    contraction, 169
       electric, 126
           paradoxical, 171
       myotatic, 169
    co-ordination, 171       ,
    diseases, 299
    dystrophy, chronic,  249
    hypertrophy, diagnosis of, 303
    inco-ordination, 271
       test of, 171
    jerk, 166
Muscular, paralysis, pseudo-hypertrophic, 299
    pseudo-atrophy, 254
    pseudo-hypertrophy, 257, 259
    response to galvanism, 129
    sclerosis, progressive, 299
    sense, centre for, 139
       conveyance of, 73, 80
       impairment of, 165
       localization of, 41. 43
       motor centres for, 41,43
       test of, 165, 584
    strength, 173
       tests of, 173
    tonus, 168
    wasting of palsies, 816
Muskelatrophie, 277
Mutism in cerebral palsies, 316, 319
Muttering delirium, 686
Myelin, 196
    changes in, 197
    development of, 19, 22
Myelitis, 213
    acute, 213
    alterations of spinal cord  in, 216
    from aneurism, 225
    of anterior cornua  or horns, 205, 213, 224,
             225, 230, 320
           causes of, 236
           changes of temperature in, 236
           chronic, 241
           diagnosis of, 239, 258, 278, 320
           electrical changes in, 233
           electricitv in, 242
           etiology of, 236
           faradism in, 242
           galvanism in, 242
           gymnastic exercises in, 242
           history of, 230
           initial stage of, 230
           massage in, 242
           paralytic stage of. 231
           monoplegia in, 231
           pathology of, 237
           prognosis of, 237
           treatment of, 241
    ascending degenerations from, 220
    bedsores in, 224
    causes of, 215
    central, 575
    chronic, 215, 273
    cicatrization in, 218
    compression, 225, 264
    concussion, 225
    cyst-formations in, 217, 218
    cystitis in, 229
    degeneration from, 218, 220
    diagnosis of, 224, 244, 278, 281, 288, 333
    diffuse, 240
    duration of, 215
    dysaesthesia in, 214
    electricity in, 228
    formication in, 214
    from fracture, 225
    general diffuse, 213
    history of, 213
    hysteric simulation of, 241
    knee-jerk in, 215
    massage in, 228
    paralysis from, 214
    paraplegia from, 214
    pathology of, 216
    peri-ependymal, 218
    from Pott's disease, 225
    prognosis of, 223
    reflexes in, 215
    rest in treatment of, 226
    sclerosis of cord in, 216
    secondary degenerations from, 220
    sphincter-paralysis in, 224
    symptoms of, 214
    synonvms of. 213
    syphilitic, 216, 227
    terminations <>f, 218
    transverse, 213, 240, 575
       diagnosis of, 285, 288, 320
    traumatic, 215, 290, 291, 575
       treatment of, 291 
INDEX.
723
Myelitis, treatment of, 226, 292
    from tumor, 225
Myoatrophy, lipomatous, 299
Myopathic atrophy, 249
Myositis, traumatic, 574
Myosclerotic paralysis, 299
Myotatic contractions, 169
Myotonia.   See Thomsen's Disease.
Mysophobia, 590
Myxina glutinosa, nervous system of, 31
Myxcedema, 550
    cause of, 551
    clinical history of, 550
    diagnosis of, 554, 558
    etiology of, 551
    history of, 550
    pathology of, 551
    prognosis of, 554
    thyroid extract in, 554
        gland in, 553
    treatment of, 554
Myxoglioma, intracranial, 330.331
Myxoma, intracranial, 331
Myxomata on nerves, 211
Myxosarcoma, intracranial, 331


   NARES, examination of, 162
    Nasion, 97
Neck, neuralgia of, 179
Necrophilism,  595
Needle, hidden, 164, 583
Negative closing,  127,128
    current, 106
    opening, 127, 128
    plate, 106
    pole, 106
Neoplasms, extradural,  287
    intracranial.  See Intracranial Growths.
    intradural, 287
Nephritic crises, 261, 275
Nephritis as cause of neuralgia, 184
    coma from, 507
    dementia from, 652
    diagnosis of, 461
    headache from, 496
    head-symptoms of, 332
    reflex symptoms of,  533
    vertigo in. 494
Nerve or Nerves, abducens, 84, 85
        accessory of Willis, 85
        acoustic, 88
        auditory, 88, 160
        avulsion, 192
        -cells, anatomy and functions of, 17-19
            histology of, 25
            innervation of, 223
            peripheral appendages of, 18
            staining of, 17
            vacuolation  of, 607
        cochlear, 88
        corpuscles, 32
        cranial.  See Cranial Nerves.
        diseases of, as causes of neuralgia, 183
        -division, 192
        eighth, 88
        eleventh, 85
        excision of, 192
        to  the eye. 154
        facial.   See Facial.
        fibromata on, 211
        fifth, 86
        fixations of, 19
        hypoglossal, 84,  86
        mixed, axis-cylinder of, 195,196
        myoxomata on,  211
        neuromata on, 210, 211
        ninth, 84, 86
        oculo-motor, 84
        olfactory, 87
        optic, 87
        origin  of,  19
        pain in, 178
        peripheral, diseases of, 178
        pneumogastric,  86
        reaction to galvanic current, 127
        -regeneration after neuritis, 198
Nerve or Nerves, -resection, 192
           intracranial, 193
       rupture of, 192
       -section, 192
       seventh, 84, 85
       sixth, 84, 85
       -stretching, 192
       third pair of, 84
       trigeminal, 84-87
       trochlear, 84, 85
       -trunk neuromata, 210, 211
       -tumors, 210, 211
       vestibular, 73, 88
       of Willis, accessory, 85
Nervous centres, artificial irritation of, 20
       connective tissue of, 32
       effect of electricity on, 20
    current, 18, 30
       through cerebellum, 76
    diseases.  See Nervous System, diseases of.
       microbic, 472
       reflex, 531
    exhaustion, 448
    prostration, 448
    symptoms of diseases, 493
    system, anatomy and physiology of, 17, 26
       cerebro-spinal. 17, 26, 354.
       diseases of, 17, 439, 472, 493, 531, 562
       functions of, 19
       histology of, 17
       method of studying, 19
               by atrophic method, 19
               by coloring method, 19
               by  comparative  anatomy
                method, 19
               bv congenital arrest of develop-
                    ment, 20
                  malformation, 20
               by continuous sections, 19
               by continuous developmental
                method, 19, 23
               by embryological method, 19
               Flechsig's, 19,21
               Gerlach's, 19
               Gudden's, 19
               Meynert's, 19
               by pathological  anatomical
                    method, 20
                  physiological method, 20
               by physiological method, 20
               by secondary degeneration
                method, 20, 22
               Turck's, 20
               by vivisection. 20
       railway injuries of, see Railway brain,
         Railway injuries and Railway spine.
       syphilis of, 227, 282, 289, 335, 373
       traumatic  diseases of, 573
    weakness, 449
Neural disease, neuralgia from, 183
    growths, hyperplastic, 210
Neuralgia, 178
    from alcoholism, 184
    anaemic, 182, 186
    anatomical localization of, 182
    anticyclonic, 290
    antral, 183
    barometric disturbances causing, 183
    causes of, 181
    cervical, 179
    cervico-brachial, 179
       -occipital,  179
    in cicatrix, 183
    clinical history of, 178
    dental, 182
    from diabetes. 184
    diagnosis of, 184
    dorso-intercostal, 179,183,190
    electricity in, 190
    from eye-strain, 182
    faradism in, 190
    femoral, 179
    forcible flexion in, 192
    foudroyant, 183
    after fracture,  183
    functional changes in, 180
    galvanism in, 190 
724
INDEX.
Neuralgia, from general causes, 186
    generalized, 181
    genital, 183
    gouty, 181
    of the head, 178
    hereditary, 181
    from hysteria, 184
    from influenza, 183
    intracranial, 178,182
    from local causes, 186
    of lower extremity, 180,191
    lumbar, 179,186
    lumbo-abdominal, 179
    malarial, 182
    molecular changes in, 180
    of the neck, 179
    from nephritis, 184
    from neural disease, 183
    neurasthenic, 181,188
    from neuromata, 183
    neurotic, 413
    occipital, 190
    ovarian, 183, 191
    pain of, 178, 501, 502
    pathology of, 180
    phrenic, 179
    from poisons, 183
    from pressure, 191
    prognosis of, 185
    recurrent, 181
    sciatic, 186
    from sewer-gases, 184
    surgical procedures in, 192
    from stricture, 179
    as a symptom, 184
    syphilitic, 182, 381
    from temperature-changes, 183
    toxic influences as causes of, 183
    traumatic, 183, 575
    treatment of, 186, 188
    trigeminal, 178, 182, 189, 270
    of trunk, 179, 190
    from tumors of nerves, 183
    of upper extremity, 180,191
    uterine, 183,191
    vaginal, 183
    visceral, 180,186, 191
Neuralgic neuroses, 413
Neurasthenia, 226, 448
    autopsies of cases of, 457
    a cause of neuralgia, 181
    causation of, 453, 458
    cerebral, 643
    clinical history of, 449
    dementia from, 653
    diagnosis of, 459
    electricity in, 468
    galvanism in, 468
    history of, 448
    with hysteria, 442
    insomnia of, 505
    lithaemic, 188, 449
       asthenic cases of, 463
       causation of, 458
       diagnosis of, 334, 384
       impaired vision in, 450
       massage in, 466
       neuralgic, 451
       pathology of, 454
       pseudo-neuralgias in, 451
       sthenic cases of, 463
       symptoms of, 449
       treatment of, 418, 463
       uric acid in, 455
       urine of, 451
       vertigo of, 450
    massage in, 466
    morbid impulses in, 589
    neuralgia of, 188
    nomenclature of, 448
    pathology of, 454
    prognosis of, 459
    reflex, 449
    rest in, 465
    sexual, 446
    simple, 452
    traumatic, 290, 291, 442, 463, 575, 579
 Neurasthenia, treatment of, 418, 445, 463
    vertigo of, 450, 493
 Neurectomy, 192
 Neuritis, 150, 180,193
    acute, 195
    with anaemia, 202
    analgesics in, 200, 201
    causes of, 193
    cauterization in, 202
    chronic, 195, 240
    clinical symptoms of, 194
    diagnosis of, 193, 205, 240, 244
        by electricity, 129
    electricity in, 201
    facial, 210
    faradism in, 201
    galvanism in, 201
    impaired sensation in, 194
    interstitial, 198
    intracranial, 194
    from lead-poisoning, 395
    of mixed nerves, 194, 240
    multiple, 199, 202, 225, 280, 564
        alcoholic, 567, 570
        causes of, 203
        clinical history of, 203
        diaguosis of, 204
        epidemic, 203
        etiology of, 203
        history of, 202
        paralysis in, 204
        prognosis of, 204
        syphilitic, 381
        treatment of, 205
    of nerve-fibres, 198
    of nerve-trunk, diagnosis of, 255
    optic, 184, 328
    pain of, 185, 194
    parenchymatous, 198
    pathology of, 195
    peripheral, 173, 225, 269
    prognosis of, 198
    regeneration of nerve after, 198
    sciatic, 199
    subacute, 195
    surgical procedures in, 202
    symptoms of,  185
    syphilitic, 381
    traumatic, 193, 199, 574
    tonics in, 202
    treatment of, 188, 199
 Neuroglia, 283
 Neurogliar cells, 32
    sclerosis, 283, 404
 Neuroma, 194, 210
    after amputation, 211
    as cause of neuralgia, 183
    causes of, 211
    cauterization of, 212
    clinical history  of, 211
    diagnosis of, 212
    excision  of, 212
    of facial  nerve, 210, 211
    false, 210
    intracranial, 331
    multiple, 211
    nerve-trunk, 210, 211
    of optic nerve, 211
    painful, 210
    plexiform, 210, 211
    of pneumogastric nerve, 211
    prognosis of, 212
    stump, 210, 211
    surgical procedures for, 212
    of sympathetic nerve, 211
    syphilitic, 212
    tendril, 210, 211
    treatment of, 212
    of trigeminal nerve, 211
    true. 210
Neuro-muscular diseases, 299
    -retinitis, 157,159
Neuron, 18
Neuroses, 397
    anapeiratic, 469
    -joint, vasomotor, 563
    neuralgic, 413 
INDEX.
725
Neuroses, occupation-, 469
    semi-insane, 658
    traumatic, 484, 579
Neurotic neuralgia, 413
Neurotomy, 192
Nicolaier, bacillus of, 475
Night-terrors, 513
Ninth nerve, 84, 86, 87
Nodes of Ranvier, 195, 196
Nodus cursorius, 103
Notomyelitis, 213
Noyaux de l'arboration,  196
    fondamentaux, 196
    of Ranvier, 195, 196
    vaginaux, 196
Nuclei, acoustic, 88
    of cells, 32
    of cochlear nerve, 88
    of cranial nerves, 84, 86
    of cranial nerves, sensory, 86
    sensory,80
    vacuolation of, 607
Nucleus, accessory, of cochlear  nerve, 8
    ambiguous, 86
    bean-shaped, 58, 61
    caudatus, 57, 61
    of column of Burdach, 72
    cuneatus, 72,77, 78,80
    dentatus, 72, 73
    Deiters', 73
    globosus, 72
    glosso-pharyngeal, lesion of, 295
    gracilis, 77, 78, 80
    hypoglossal. 87
    of hypoglossus, lesion of, 294
    of lateral lemniscus, 69
    lenticular, 58, 61
    magnocellularis diffusus, 79
    reticularis tegmenti, 79
    red, 70
    of spinal accessory, lesion of, 294
    superior central, 79
    tegmenti, 72, 73
    trapezoid, 88
    of vaeus, lesion of, 294
Numbness of fingers, 205
Newborn, apoplexy of, 321, 323
Nystagmus, 147, 156, 297
    in disseminated sclerosis, 389


   OCCIPITAL convolutions, 36
    fissure, 103
    lobe, 36,103
        hemorrhage in,  310
    neuralgia, 191
Occupation-neuroses, 469
        galvanism in,  472
        hypnotism in, 472
        symptoms of, 470
        treatment of, 472
Ocular asthenopia, 536
    headache, 496
    muscles, asthenopia of, 136, 536
        external, 154
        insufficiency of,  536
        lesions of, 147
        pain, 502
        paralysis of, 154,155,156, 296
Oculo-motor nerve, 84
Odors, effect of, on nerves of smell,  161
Ohm, legal, 122
    Paris, 122
Oinomania, 566         .
Olfactory fibres, impressions on, 161
    nerve, 88
    tract, 88
Olivary bodies, 73
Onomatomania, 658
Opening, negative, 127,128, ^do
    positive, 127, 128, 235
Operculum, 39
Ophthalmoplegia, 147
    causation of, 297
    diagnosis of, 298
    exterior, 296
    lesions of, 298
] Ophthalmoplegia, pathology of, 298
     prognosis of, 298
     progressive, 296
     symptoms of, 296
     treatment, 298
 Ophthalmoscope, 157
 Ophthalmoscopic examination, 157
 Opisthotonus, 476, 479
 Opium-habit, 200
 Optic arteries, 92
     centres, primary, 87
     chiasm, 61
     fibres, 62
     nerve, 62, 87
        atrophy of, 157, 261, 262, 389
        course of, 150
        neuroma of, 211
     neuritis, 184, 328, 383
     radiation, 60
     thalamus, 57, 61, 64, 103
        lesions of, 146
     tract, 62, 87
 Orbicularis palpebrarum, spasm of, 156
 Orchestromania, 418
 Orthotonus, 477
 Osteoma, intracranial, 331
 Osteo-arthropathy, hypertrophic  pulmonary,
   558
PACHYMENINGITIS, 360
L     cervical hypertrophic, 285
Pain, acute. 502
    atrocious, 261
    aural, 504
    centre for, 139
    chronic, 502
    of colic, 180
    conduction, retardation of, 263
    electricity as test for, 165
    fulgurant, 261
    fulminating, 261
    in infectious disease, 502
    in influenza, 502
    intracranial, 502
    localization of sense of, 41, 43
    malingering in sense of, 165
    in meningitis, 502
    neuralgic, 501
    ocular, 502
    pelvic, 502
    peritoneal, 502
    pleuritic, 502
    pneumonic, 502
    rheumatic, 502
    sense of, motor centres for, 41, 43
    stabbing, 261
    subacute, 502
    syphilitic, 502, 506
    tests for, 164
       of sense of, 583
    vagabond, 261
Painful points, 178
Palate, diphtheritic paralysis of, 489
Palmodic spasms, 430
Palmus, acute, 430, 432
    diagnosis of, 350, 433
    facial, 430
    galvanism in, 434
    general, 430, 431
    pathology of, 434
    prognosis of, 433
    with pseudo-melancholia,  430, 432
    therapeutics of, 434
Palsy.  See Paralysis.
    Bell's, 206.
    birth, 317
    cerebral,  of children.   See Cerebral Palsy.
    facial. See Paralysis, facial.
    scriveners', 469
    shaking,  519
Papillitis. 158
Paraesthesia, lithaemic, 226
    in myelitis, 214
Paracentral lobule, 37
Paradoxical muscular contraction,  171
Paraldehyde, hypnotic action of, 501 
726
Parallel fibres, 77
Paralysie atrophique, 230
    generate progressive, 666
    musculaire progressive de la langue, du
      voile de palais, et des levres, 292
Paralysis.  See Palsy and Paresis.
    acute ascending, 205, 240, 243
    agitans, 519
       causes of, 521
       clinical history of, 519
       diagnosis of, 349, 391, 526, 674
       electricity in, 528
       etiology of, 521
       history of, 519
       localization of lesion in, 525
       pathology of, 523
       pigmentation in, 524
       prognosis of, 522
       sclerosis in, 523
       symptoms of, 519
       treatment of, 527
       tremor of, 519
    alcoholic, 286, 566, 567
    analgesic, 286
    atrophic, of children, 230
    bulbar.   See Paralysis, Glosso-labio-laryn-
      geal.
    cause of talipes, 235
    cerebral, of children.   See Cerebral Palsy.
    diphtheritic.  See Diphtheritic.
    diver's, 246
    essential, of children, 205, 230, 575
    extensor, 174
    facial, 206
        causes of, 207
        diagnosis of, 208, 295
        prognosis of. 207
        symptoms of, 206
        the tongue in, 206
        treatment of, 210
    flexor, 174
        of leg, 271
    general, 666
        of the insane, 666
    glosso-labio-laryngeal, 292
               diagnosis of, 295
               electricity in, 295
               faradism in, 295
               galvanism in, 295
               history of, 292
               pathology of, 294
               progressive, 296
               prognosis of, 294
               symptoms of, 292
               treatment of, 295
    hemiplegic.  See Hemiplegia.
    infantile, essential,  205, 230, 575
        spinal, 230
    of the insane, 666
    labio-glosso-laryngeal, 207, 210
    Landry's, 210, 225, 238, 243
    lead-, 174, 240,  393, 394
    from lesion of internal capsule, 146
    localization of, 38, 525
    monoplegic, 139,140, 143
    motor, from myelitis,  214
    multiple, in diphtheria, 489
    from myelitis, 214
    in myelitis of anterior horns, 231
    multiple, in diphtheria, 489
    in multiple neuritis, 204
    of muscles of eye, 296
    myosclerotic, 299
    of oblique muscles of the eye, 155
    of ocular muscles, 154
    palatal, 489
    progressive bulbar, 292
        general,  666
    pseudo-hypertrophic muscular, 299
    of recti muscles of the eye, 155
    reflex, 216, 226
    of sacro-spinal muscles, 236
    of senile dementia, 648
    spastic spinal, 275
    of sphincter, 224, 229
        pupillse, 297
    spinal, general subacute ascending, 203
INDEX.
Paralysis, syphilitic, 379
    of third nerve, 154                      .
Paralytic dementia,.  See Dementia, paralytic.
    rabies, 245
Paralytische Blodsinn, 666
Paramyoclonus multiplex, 435
Paramyotone, ataxic, 304
    congenital, 304
Paranoia, 637, 657
    acute, 658
    alcoholic, 567, 568, 658
    chronic, 658, 661
    clinical history of, 658
    diagnosis of, 641, 664, 675, 684
    epileptic, 632, 635
    etiology of, 663
    hallucinatory, 658, 662
    history of. 657
    litigious, 661, 662
    inventorial, 661
    moral, 662
    original, 662
    primary, 658
    prognosis of, 663
    querulantium, 661
    secondary, 658, 663
    sexual, 661
    treatment of, 664
Paranoiac, 663.   See Paranoia.
Paranoioid insanity, 635
Paraphasia, localization of, 41, 43
    motor centres for, 41, 43
Paraplegia, 315
    ataxic, 279, 545
    in cerebral palsies, 316, 318
    hereditary, 545
    hypertrophic, of infancy, 300
    from myelitis, 214
    in myelitis of anterior horns, 231
    senile, 525
Parasitic cysts, intracranial, 331
Paresis.  See ralsy and Paralysis.
    alcoholic, 567
    analgesic, 286
    general, 567, 666
        diagnosis of, 442, 461, 664
        of insane, 615
        lesions of, 54
        mania of, 622, 641
        traumatic, 573
        seat of, 44
    pseudo-general, 381
        alcoholic, 507, 570
        syphilitic, 673
Pareso-analgesia, 286
Paretic chorea, 419
    dementia, 303, 333, 442, 644, 666
Parietal fissure, 36,102
    lobe, 35, 36
    lobule, 35, S6
Parieto-occipital fissure, 36, 37,102
Paris-ohm, 122
Parkinson's disease, 519
Par vagum, 84-87, 294
Pasteur's virus, 443, 486
Pathological-anatomical study of nervous sys-
   tem, 20
Physiological study of nervous system, 20
Patellar tendon-reflex,  167
Peduncles, cerebellar, 67, 72
         lesions of, 72, 73, 149, 281
    of corpora quadrigemina, 72, 73
    of pons, 72, 73
    superior, 72
Pelvic organs, application of electrodes to, 121
    pain, 502
Periarteritis, a cause of cerebral  hemorrhage,
   307
Periencephalite chronique diffuse, 668
Perimeter, 159
Peripheral irritation, reflex, 86
    motor nerves, 80
    nerves,  diseases of, 178
         galvanization of, 125
         lesions of, 150 .
         motor, 80
         neuritis of, 225 
INDEX.
727
Peripheral nerves, syphilis of, 381, 384
    neuritis, 173, 269
    organs,  development of, 19
    tract, antero-lateral, 264
       of cranial nerves, 84
Periphery, course of nerves to, 71
Perkinism, 515, 571
Peritoneal pain, 502
Peroneal type of muscular atrophy, 250.252
Persecution, delusions of, 657. 658, 683
Pes cavus, 235
Petit mal, 397
       intellectual, of Falret, 632, 634
Phrenitis, 638
Physiological method in study of nervous sys-
  tem, 20
Pia mater, meningitis of, 392
Piano-forte-players' cramp, 469
Pigment emboli in cerebral vessels, 308
Pigmentary degeneration in insanity, 605
       in general paresis, 605
Pineal gland, 70
Pins, dread of, 658
    mania for, 658
Plague dance, 418
Plantar  reflex, 169
Plaque jaune, 94
Plate in galvanism, 105
    negative, 106
    positive, 106
Pleurothotonus, 477
Pleuritic pain, 502
Plexiform angio-sarcoma, intracranial, 330
    neuromata, 210, 211
Plexus,  protoplasmic, of motor area, 46
Plica polonica, 483
Pluricordoual cells of spinal cord, 28, 30
Pneumogastric nerve, neuroma of, 211
Pneumonic pain, 502
Points douloureux, 178
    painful, 178
    sensitive, of skin, 164
Poisoning as cause of neuralgia, 183
    lead-.  See Lead.
    metallic, tremor from, 526
 Polar changes in motor nerves, 235
         formula of, 235
    progression, alteration of, 129
    reaction, alteration of, 129
 Pole, negative, 106
    positive, 106
    progression of, 128
 Polioencephalitis, 315
    infantile, 321, 322
     superior chronica, 296
 Poliomyelitis, anterior, 230, 244, 279, 288
    traumatic, 575
 Pollution,  fear of, 589
 Polyaesthesia, 263
 Polymorphous cells of motor area, 46
 Pons Varolii, 61
         bloodvessels of, 89
         lesions of, 148, 210
         peduncle of, 72, 73
 Porencephalitis, 315, 321, 323, 690
 Porencephaly, 315, 321, 323, 690
 Porosity, cerebral, of Golgi,  325
 Positive closing, 127,128
     current, 106
     opening, 127,128
     plate, 106
     pole, 106
 Post-cervical ache, 505, 60S
         insanity, 575
     -epileptic chorea, 419
     -febrile insanity, 658
     -hemiplegic athetosis, 353
         chorea, 352, 419
         tremor, 319              „ na„
 Posterior column, degeneration of, 266
     external optic artery, 92
     internal optic artery, 91
     roots, anatomy of, 31
         of spinal cord, 31, 32, 77
             tracts of, 31. 32
     sclerosis, 264
     spinal artery, 97
Postero-lateral sclerosis, 278
Potentials in electricity, 106
    zero, 106
Pott's disease as cause of myelitis, 225
       diagnosis of, 289
       pain of, 185
Praecentral fissure, 35,102
Praecordial fear, 611
Praecuneus, 37
Pregnancy, chorea of, 419, 421
Pressure-neuralgia, 191
Primare verriicktheit, 640, 657
Primary dementia.  See Dementia.
    stupidity, 644
    wire, 110
Processes of nerve-cells, 18
Prognathism, 690
Progressive bulbar paralysis, 292
    general paralysis, 666
    locomotor ataxia.   See Locomotor ataxia.
    muscular atrophy, 240, 249
           causes of, 257
           diagnosis of, 258, 278,  285, 303, 443,
             462
           electricity in, 259
           facial type of infancy, 250, 252
           galvanism in, 259
           hand-type of, 250
           history of, 250
           infantile type of, 295
           juvenile type of, 250, 252
           massage in, 259
           orthopaedic treatment of, 259
           pathology of, 256
           peroneal, 250
           prognosis of, 259
           rest in, 259
           sclerosis, 299
           surgical treatment of, 259
           symptoms of, 250
           traumatic,  575
           treatment of, 259
           type of,  252
    muscular sclerosis, 299
    muskelatrophie, 249
    spastic ataxia, 279
 Projection-fibres of cerebrum, 56
    of white matter, 48
 Pronunciation, impaired, in bulbar paralysis,
   293
 Prosopalgia, 206
 Protoplasmic branchletsof pyramidal layer, 46
    plexus of motor area, 46
    processes, 18
         of motor area,  44
 Psammoma, intracranial, 331
 Pseudo-apoplexy, 329
    -atrophy, muscular, 254
    -contracture, traumatic, 578
    -enchondroma, intracranial, 331
    -fibroma, intracranial, 331
    -general paresis. See Paresis.
    -hypertrophic muscular paralysis, 299
    -hypertrophie der muskeln, 299
    -hypertrophy, muscular, 257, 259
    -melancholia with palmus, 430
    -meningitis, 330
    -muscular hypertrophy, 299
            causation of, 302
            clinical history of, 300
            diagnosis of, 303
            electricity in, 303
            faradism in, 303
            galvanism in,  303
            history of, 300*
            massage in, 304
            pathology of, 302
            prognosis of, 303
            treatment of, 303
     -neuralgia, rheumatic, 451
     -sarcoma, intracranial, 331
 Psychical cells, 46
 Psycho-neuroses, 438
 Pterion, 97
 Ptosis, 261, 262
 Pubescence, insanity of, 600, 645, 654
 Puerperal insanity, 600, 658 
728
INDEX.
Puerperal mania, 658
Pulvinar, 61,70
Pupil, Argyll-Robertson, 224, 261
    examination of, 154
    state of, in epilepsy, 400
Pupillary alterations in paralytic dementia, (
    cortical reflex, 152
    reaction, tests of, 154
    reflex of Haab, 152
       Wernicke's, 152
Purkinje, cells of, 72, 74
Pyeluria, mania of, 622
Pyramidal cells, bouquet of, 53, 54
       of motor area, 45, 46
    columns, 21, 81
    layer of motor area, 45, 46
    tract, 82
Pyramids of cerebrum, 66, 67
    of medulla oblongata, 81
Pyromania, 590, 658
  QUADRIGEMINAL bodies, 60-70
        lesion of, 146, 152
Quantitative reaction of degeneration, 129
    study of nervous system, 20
   RABIES, 245, 482.  See Hydrophobia.
     furious, 487
    paralytic, 245
 Radiation, optic, 60'
 Radicular arteries, 97
 Railway brain, 577, 579
    injuries, 225, 573.  See Traumatic Diseases.
        disease caused by, 574
        objective symptoms of, 581
        organs affected by, 574
        simulation of, 583
        subjective svmptoms of, 581
    spine. 290, 573, 579
 Ranvier, nodes of, 195, 196
    noyaux of, 195,196
 Raynaud's disease, diagnosis of, 564
        pathology of. 564
        prognosis" of, 564
        treatment of, 564
 Reaction of degeneration, 105,128, 185,195, 235,
      256
    polar, 129
 Reasoning mania, 659
 Recti muscles of eye, paralysis of, 155
        insufficiency of, 156
 Recurrent mania, 628
 Recurrirende manie, 628
 Reflex or Reflexes, abdominal, 169
        cremaster, 169
        cutaneous, 169, 215
        headache, 496
        mammary, 169
        motor tract of Kolliker, 32
        muscles, 166
        nervous disorders, 531
           symptoms of, 532
               in anaemia, 537
               circumcision for, 537
               in ear diseases, 537
               in eye affections, 536
               in genito-urinary diseases, 535
               in intestinal disorders, 536
               in lithaemia, 536.  See Neuras-
                 thenia.
               in leucocythaemia, 537
               in nephritis, 533
               in pelvic diseases, 533
                      ovariotomy for, 533
        neurasthenia, 449
        paralysis, 216, 226
        patellar tendon, 167
        plantar, 169
        pupillary, 152
           cortical, 152
        skin, 169
        spinal, 168
       tendon.  See Tendon-reflexes.
Refraction, errors of, 418, 536
Reil, island of, 36, 60
Reil, island of, as a centre, 141
Reinforcement in knee-jerk, 167
    method of, 261
Resistance, unit of, 122
Respiratory tract of Krause, 87
Restiform body, 67, 72
Rest in neurasthenia, 465
    in progressive muscular atrophy, 259
Retina, blindness of, 63
    cells of, 87
    in cortical lesions of, 151
    inflammation of, 157
    lesions of, 157
    tests of condition of, 154
Retinitis, 157
    albuminuric. 157
Retropulsion. 520
Rhachialgitis, 213
Rheophores, 117
Rheostat, 108,115, 116
    carbon, 117
    in electrolysis, 117
    water, 117
Rheumatic chorea, 420
Rheumatism, chronic, diagnosis of, 558
    pain of, 502
Rhythmical sounds, effect of, 541
Rickets, diagnosis of, 342, 558
Risus sardonicus, 476, 479
Rolando, fissure of, 34,101
    substance of, 27
Romberg's symptom, 172, 262, 349, 545
Root-cells of spinal cord, 27
Roots of spinal cord, 77
Root-trunks, 26
    -zones, 22
       anterior, 265
       middle, 265
Rubbing in massage, 135
QACRO-SPINAL muscles, paralysis of, 236
U Saint Anthony's dance, 418
Saint Guys dance, 418
Saint John's dance or disease, 418
Saint Modesty's dance, 418
Saint Vitus's dance, 418
Salivation, in bulbar paralysis, 294
Saltatoric spasm, 435
Saponification, 197
Sarcoma of brain, 330
       angiolithic, 330
       round-celled, 330
       telangiectatic, 330
   of nerves,  211
Scarpa, ganglion-cells of, 88
Scheidenkerne, 195
Schmitt, markings of, 196
Schiittellahmung, 519
Schwann, sheath of, 196
Sciatic nerve, pain in, 180
       rupture of, 192
Sciatica, 180
   nerve-stretching in, 192
   treatment of, 191
Sclerose en plaques desseminees, 387
   laterale amyotrophique, 277
Sclerosis, amyotrophic lateral, 241, 258, 277, 356
           clinical history of, 277
           diagnosis of, 277, 285
           duration of, 277
           pathology of, 277
           prognosis of, 277
           treatment of, 277
   of brain, 334
   combined, 356
           of  the cord, 279
           ataxia of, 280
           diagnosis of, 280
           lesions of, 279
           prognosis of, 280
           symptoms of, 280
           treatment of, 280
   of cord in myelitis, 213
   disseminated, 271, 276, 387
       atrophic granular, 604
       causes of, 390 
INDEX.
729
Sclerosis, disseminated, clinical history of, 388
        contracture in, 389
        diagnosis of, 285, 391, 425, 526, 549, 674
        history of, 387
        pathology of, 387
        prognosis of, 391
        speech of, 389
        symptoms of, 388, 390
        treatment of, 392
        tumor of, 350, 388
    fascicular combined, 279
    in insanity, 603, 604
    insular, 387
    lateral, 213, 271, 356
        diagnosis of, 281
    miliary, in insanity, 603
    multiple, 334, 387
        of the brain, 334
        cerebro-spinal, 387
    neurogliar, 283, 404
    in paralysis agitans, 523
    posterior, 264
    postero-lateral, 278
    primary lateral, 275
            clinical symptoms of, 275
            diagnosis of, 277
            duration of, 276
            history of, 275
            pathology of, 276
            prognosis of, 277
            reflexes in, 276
            treatment of, 277
    progressive muscular, 299
    of spinal cord, 213, 279
 Scriveners' palsy, 469
 Seamstresses' cramp,  469
 Secondary coil, 110
    current, 110
    wire, 110
 Section of nerves, 192
 Seguin, signal symptom of, 140
 Senile dementia, 644,  646,648, 655
    paralysis, 648
    paraplegia, 525
 Senility, 646
 Sense, muscular, conveyance of, 73
 Senses, affections of, in dementia, 670
    localization of.  See Localization.
    tests of.  See Tests.
 Sensitive corpuscles of Golgi, 47
 Sensory cells of Golgi, 54
     cerebellar tract, 73
     columns of spinal cord, 23
     cranial nerves, 84, 86
            origin of,  80
     fibres, 59
         of posterior root, 30
         of spinal cord, 23
     motor tract of Cajal, 32
     nuclei, 80
         of cranial nerves,  86
     paths, decussation of,  80
         of nerve-fibres, 78
         of spinal cord, 80
     symptoms, tests of, 154, 290
     tissues, impressions through, 18
     tract, central, 86
         of cranial nerves,  86
 Serum-therapy in tetanus, 479
 Seventh nerve, 84, 85           .
 Sewer-gases as causes of neuralgia, 184
 Sexual hermaphroditism,  596
     hypochondria, 446
     metamorphosis, 597
     neurasthenia, 446
     perversion, 593
 Shaking-palsy, 519
 Sheath, medullary, 197
     of Schwann, 196
 Shock, dementia from, 513
     electric, 108

' i^^'g?Migraine.
 Siemen's unit, 122

 llual-svmpfom of Seguin, 140
  llrver bicarbonate, staining by, 17, 28
Silver chloride cell, 113
Sinuses, cerebral, thrombosis of.  See Throm-
     bosis.
    intracranial,  thrombosis of.  See Throm-
     bosis.
Sixth nerve, 84, 85
Skin, anaesthetic points on, 164
    bronzed, 561
    glossy, 185, 195
    -reflex, 169
    resistance of,  121
    sensitive areas of, 163
    wetting of, 121
Skull.  See Cranium.
    American, 98
    bones of, thickening of, 342
    brachycephalic, 98
    condition of,  in insanity, 600
    criminal, 99
    dimensions of, 98
    dolichocephalic, 98
    European, 98
    fracture of, diagnosis of, 312
    in idiocy, 690
    mesocephalic, 98
    pathological, 99
    race-characteristics of, 98
    shape of,  98
    sutures of, 99
    thermometry of, 177
    topography of, 97, 340, 373
    types of, 98
 Sleep, theory of.  500
 Smell, test of, 161
 Smiths' cramp, 469
 Sodismus, 597
 Sodomy,  594
 Softening of brain in insanity, 602, 604
    of the cord, 213
        in myelitis, 216
    white, of the cord, 213
    yellow, of cortex, 94
 Sohlenkerne, 196
 Solitary fasciculus, 87
 Somnambulism, 509, 511
 Somnolency, from intracranial growth, 329
 Sound, air-conduction of, 161
     bone-conduction of, 161
 Spade-like hands, 555
 Sparks, electric, 112
 Spasm, clonic.   See Clonus.
     facial, 186
     palmodic, 430
     saltatoric, 435
     tonic, in voluntary muscles, 304
 Spasmodic gait,  275
 Spasmotoxine in tetanus, 475
 Spastic ataxia, progressive, 279
     chorea, 319
     gait, 275
     spinal paralysis, 275
 Speech, articulate, motor centres for, 40, 43
     centre of, 40, 43
     defects of, in cerebral palsies, 316, 319
 Sphincter-paralysis, constipation from, 224, 229
     pupillae, paralysis of, 297
 Spider-cells, 32
 Spinal accessory, lesion of nucleus, 294
     anaemia, 354
     arteries, distribution of, 97, 238
     artery, anterior, 97, 238
        posterior, 97
     caries, 289
        pain of,  185
     concussion, 577
     congestion, 355
     cord, anaemia of, 354, 457
        an atom v of, 20
        cells of, 27, 28,  30
        central canal of, 64
        column-cells of, 27, 29, 78
        columns of. See Columns.
        combined sclerosis of, 279
        commissural cells  of, 27, 29, 30, 271
            fibres of, 51
        commissures of, 26
        composition of, 19 
730
INDEX.
 Spinal cord, compression of, 292, 293
        concussion of, 277, 289
        cornua of, 20
        course of fibres in, 77
        diseases of, 212, 213
        fibres of, to brain and cerebellum, 77
        galvanization of, 125
        gray matter of, 20, 77
        horns of, 20
        hyperaemia of, 354, 457
        inflammation of, 213
        injuries of, 289
        lesions of, 150, 214
        localization of functions in, 82
            of lesions in, 139
        many-columned cells of, 28, 30
        motor columns of, 20
            fibres of, 23
        oblong, 61
        pluricordonal cells of, 28, 30
        posterior root of, 30, 77
        pyramids of,  21
        root-cells of, 27
        sclerosis of, 213, 279
        sensory fibres of, 23
            tracts of,  21
        softening of, 213
            in myelitis, 216
        syphilis of, 271, 282, 288
        systemic diseases of, 213, 224
        traumata of, 289
            compression from, 292
            operations for, 292
        tumors of, 287
            diagnosis of, 288
            operation for, 289
            prognosis of, 289
            symptoms of, 288
            treatment of, 289
        white matter of, 20
    degeneration, syphilitic, 271
    epilepsy, 168
    hemorrhage.  See Hemorrhage, spinal.
    irritation, 448
    lesions, vertigo from, 494
    meningeal hemorrhage, 245
    neoplasms, 287
    paralysis, infantile, 230
        spastic, 275
    reflexes, 168
    syphilis, 271,  282,  288, 377, 381, 384
    tuberculosis,  289
    tumor, 226
        pain of, 185
        traumatic, 575
    vertigo, 494
Spinale Kinderlahmung, 230
Spinallahmung, atropische, 230
    spastische, 275
Spinalparalyse,  spastische, mit  Muskel-
  atrophie, 277
Spine, railway-, 290, 573, 579
Spinitis, 213
Spitzka-Lissauer column, 21, 77,  265, 267
        tract, 265
Squeezing in massage, 135
Stabbing-pains, 261
Staining,  bichlorate of silver, 17, 28
    nerve-cells, method of, 17, 28
Stammers cell, 113
Starchy bodies, 217
Star-shaped cells, 44,  74
Static ataxia, 172, 261, 262
    electricity, 105, 112
Stations for cerebral thermometry, 174
    frontal, 174
    occipital, 174
    parietal, 174
    vertical, 174
Status epilepticus, 441
Stephanion, 97
Stilling, fibres of, 49
Strabismus, 156
    convergent, 156
    deorsumvergens, 156
    divergent, 156
    sursumvergens, 156
 Stratum zonale, 62
 Streptococci of diphtheria, 490
 Stretching of nerves, 192
 Striae acusticae, 86, 88
 Striated arteries, 91
    body, 103,146
 Stricture, urethral, neuralgia from, 179
 Striking, in massage, 135
 Stroking, in massage, 135
 Strongylus tetracanthus, 483
 Stump neuromata, 210, 211
 Stupidity, primary,  644
 Stupor, delusional, 640
    epileptic, 632
    of melancholy,  609
 Stuporous insanity,  644
 Subcallosal longitudinal fasciculus, 49
 Subcortical lesions, 140,143
 Subdural fluid, 340
 Subpineal space, 70
 Substance of Rolando, 27
 Substantia ferruginea, 66
    nigra, 70
 Subthalamic body, 62, 70
 Suggestion, psychical.  See Hypnotism.
 Suicidal impulse or tendency, 611, 658
 Sulcus corporum quadrigeminorum sagittalis,
  69
 Sulphonal, hypnotic action of, 501
 Suppurative meningitis.  See Meningitis.
 Supramarginal convolution, 36
 Surface-temperature, 177
 Suspension in locomotor ataxia, 274
 Sutures, cranial, 97
        points of union of, 97
    of skull, 97
    relation of cerebral fissures to, 100
        of convolutions to, 99
 Sydenham's chorea.   See Chorea.
 Sylvian artery, 60, 89
Sylvius, aqueduct of, 64
    fissure of, 34, 60,101
Sympathetic nerve, diseases of, 194
       neuroma of, 211
    nervous system, diseases of, 563
               diagnosis of, 564
               faradism in, 565
               galvanism in, 564
               prognosis of, 564
               surgical treatment of, 564
               symptoms of, 563
               treatment of, 564
       cervical, diseases of, 563
Syphilis as a cause of neuralgia, 182
    blood-changes in, 377
    cerebro-spinal, 260, 271, 288, 381, 384
    coma from, 380, 383
    convulsions from, 380, 383
    of cranial nerves, 377
    dementia from, 673
    epilepsy from, 380
    headache from, 185, 380, 497
    hemiplegia from, 379, 382
    insanity from, 380
    intracranial, 208, 272, 327, 330, 331, 377,  379
       diagnosis of,  312, 333, 370, 674
       pain of, 185, 502
    locomotor ataxia from, 260
    meningitis from, 327, 329, 370
    micro-organisms of, 377
    from myelitis, 216  227
    of nervous system. 227, 282, 289, 335, 373, 506
           clinical history of, 379
           diagnosis of, 382
           etiology of, 374
           history of, 373
           intracranial, 379
           pathology of, 375
           peripheral, 379, 381,384
           spinal, 271, 379, 381, 384, 385
    neuralgia from, 182, 381
    neuritis from, 381
    neuroma from, 212
    pain of, 502, 506
    paralysis from, 379
    of peripheral nerves, 381, 384
    spinal, 271, 379, 381, 384 
INDEX.
731
Syphilis, spinal, degeneration from, 271, 377
gyphilitic coma, dementia, etc.  See Syphilis.
oyphilomata on nerves, 211
Syringomyelia or Syringomyelitis, 162,282, 287,
         330, 564
       diagnosis of, 258, 284, 285, 289
       gliomatous, 283
       non-gliomatous, 283
       pathology of, 282
       symptoms of, 282


  TABES.  See Locomotor Ataxia.
    dorsalis, 264
       spasmodique, 275
Tache cerebrale, 365
Tachycardia, 563
Tact.  See Touch.
Talipes,  235
    calcaneus, 235
    equino-varus, 235
    equinus, 235
    from paralysis, 235
    varus, 235
Tangential fibres, 44, 48, 52
Tanzplage, 418
Taste, electrical examination of, 162
    impairment of, 209
    localization of sense of, 41, 43,162
    tests for, 162
 Teeth, painful, 182
 Tegmental decussation of Forel, 70
        of Meynert, 70
 Tegmentum, 66
    central field of, 68
    nucleus of, 72, 73
 Telegraphers' cramp, 469
 Temperature.  See  Heat.
     cerebral, 174
         in lesions, 145
     -changes as causes of neuralgia,  183
     localization of sense of, 41, 43
     sense of, 166
         in malingerers, 166
         test of, 154,  583
 Temporal convolutions, 36
     fissures, 36, 102
     lobe, 36,102
  Tendon-reflexes, 166
     absent, 261                   .  ^
     in amyotrophic lateral sclerosis, 277
     in cerebral palsies, 316
     in myelitis, 215
     patellar, 167
     in sclerosis, 276
     in traumata of cord, 290
  Tendril neuromata, 210, 211
  Tenth nerve, 86
  Terminal baskets, 75, 77
     dementia, 649, 653
     fibres of white matter, 48
  Tests for hemianopsia, 159
     for  hemiopia, 159         .
     of impressibility of trigeminus, 161
     of motor symptoms, 154, 290
     of muscular sense, 154,  584
     ophthalmoscopic, 157
     of the senses, 154
         of color, 154
         of hearing, 159
         of pain, 154, 583
         of sensory symptoms, 154, 290
         of sight, 154,157
         of smell, 154
         of taste, 154



     for t^afa^spinal cord, 290
     -tubes for temperature, 16b
  Tetanilla, 479
  Tetanine, 475
  Tetanotoxine, 47o

  TetaanrtTfic1al respiration in, 478
     bacillus of, 475
      causation of, 473
Tetanus, clinical symptoms of, 476
    definition of, 473
    diamine in, 475
    geography of, 473
    intermittens, 479
    mucin-poisoning in, 481
    of newborn children, 472, 478
    parasitic origin ot, 475
    pathology of, 475
    prognosis of, 477
    serum-therapy in, 479
    spasmotoxine in, 475
    surgical treatment of, 478
    traumatic, 473, 478
    treatment of, 477
Tetany, 477
    chronic, 481
    Chvostek symptom in, 480
    clinical history of, 479
    definition of, 479
    diagnosis of, 481
    duration of, 481
    etiology of, 481
    history of, 479
    microbic cause of, 481
    occupations causing, 481
    pathology of, 481
    prognosis of, 481
    treatment of, 482
    Trousseau's phenomenon in, 480, 482
 Thalamus opticus, 57, 61, 64,108
        lesions of, 146
 Thermo-aesthesiometer, 166
 Thermometer, axillary, 166
    cerebral, 174,176, 373
    surlace. 174
 Thermometry, cerebral, 174,176, 373
        diagnosis by, 174
        stations for, 174
    of the skull, 177
 Thigh, motor points of, 133
 Third nerve, anatomy of, 84, 154
        paralysis of, 154
 Thomsen's disease, 304
        pathology of, 305
        prognosis of, 305
        symptoms of,  304
         treatment of, 305
 Thrombosis of cerebral or intracranial sinuses,
      306, 311, 312, 331, 357, 544
     of cerebral veins, 313, 321, 324
     clot in, 358
     infective, 357
     inflammatory, 357
     intracranial, 306,  311, 312, 321, 324, 357, 544
     marasmic, 357
     primary, 357
     surgical treatment of, 360
     venous, 312. 321, 324
 Thyroid gland, enlargement of, 560
         state of, in myxcedema, 553
         treatment by, 554
 Tic, convulsive, 350, 429, 431
     douloureux, 178, 179, 186
         operations for, 192
         treatment of, 191
 Titubating movement, 271
 Tobacco amaurosis, 335
 Tongue, atrophy of, in bulbar paralysis, 293
     impressions on nerves of, 162
 Tonic spasms in voluntary muscles, 304
 Tonus labyriuth, 540
     muscular, 168
 Topoalgia, 185
 Topography, cranial, 97, 373
 Topophobia, 658
 Touch, centre for, 139
     localization of sense of, 41, 43
     malingering in, 165
      sense of, conveyance of, 80
         motor centres for, 41, 43
      sensitiveness of, 163
     test Of, 154.162, 583
  Toxic ataxia, 271
      influences as causes of neuralgia, 183
  Tract, analgesia, 264
      auditory, central, 89 
732
INDEX.
     i Tumors of centrum ovale, 336
          of cerebellum, operation on, 336
          of cerebrum, 186, 461, 575
          of cortex, operation on, 336
          extradural, 287
          intracranial.  See Intracranial Growths.
          intradural, 287
          on nerves, 210, 211
          spinal, 226
          of spinal cord, 287
              pain of, 185
          subcortical, 336
     i Tuning-fork as a test for hearing, 160
    '  Tiirck, column of 81
575           study of nervous system, 20
      Twitches, the, 429
      Typhomania, 638
Tract, antero-lateral peripheral, 264
    central sensory, 86
    cerebellar sensory, 73
    lemnisco-pedal, 69
    olfactory, 88
    optic, 62, 87
    pyramidal, 82
    reflex-motor, of Kbllicker, 32
    respiratory, of Krause, 87
    sensory-motor, of Cajal, 32
    Spitzka-Lissauer, 265

Transitory frenzy, 631, 636, 638
    furor, 631, 636, 638
Transverse myelitis, 213, 240, 285, 288, 320,
Trapezoid body, 88
    nucleus, 88
Trauma as a cause of neuralgia, 183
    cerebral, a cause of meningitis, 361
    of spinal cord, 289
Traumatic chorea, 575
    coma. 507
    dementia, 672
    diseases, 573
        of bones, 574
        of brain, 575
        of ligaments, 574
        of muscles, 574
        of nerves, 574
        of nervous system, 573
        of peripheral nerves, 574
        of spinal cord, 575
    encephalitis, 574
    epilepsy, 575
    essential infantile paralysis, 575
    general paresis, 575
    hemorrhage, 574
    hysteria, 575
    insanity, 574
    locomotor ataxia, 575
    meningitis, 240, 320
    muscular atrophy, 575
    myelitis, 215, 290, 291, 575
    myositis, 574
    neuralgia, 574
    neurasthenia, 290.  291, 442, 463, 575, 579
    neuritis, 193, 574
    neuroses,  484, 575
    poliomyelitis, 575
    tumors of brain and cord, 575
Traumatism,  diseases caused  by.  See  Trau-
  matic.
Tremor, alcoholic, 527, 567
    choreic, 527
    of disseminated sclerosis, 388
    intention-. 388, 526, 586
    lead-, 526
    metallic, 392, 526
    post-hemiplegic, 319
    of senile dementia, 648
Trephining, 100
    for  epilepsy, 468
    for  intracranial growth, 338
    in intracranial hemorrhage, 313
Triangular cells of  molecular layer  of  motor
  area,  44
Trigeminal nerve, 84-87
        impressions on, 161
        neuroma of, 211
    neuralgia, 178, 182, 189,  270
    root, ascending, 87
Trigeminus.  See Trigeminal.
Trional, hypnotic action of. 501
Trismus, 86, 476, 479
    from reflex action, 86
Trochlear nerve, 84. 85
Trophic diseases of the head and chest,  563
Tropho-neurosis, facial, 295
Trousseau's mark, 367
    phenomenon, 480, 482
Trunk, motor points of,  131
Tubercle of brain, 329
Tubercles, painful, 210
Tubercula dolorosa, 210
Tubercular meningitis.  See Meningitis.
Tuberculosis, spinal, 289
Tumors as causes of myelitis, 225
  UNCINATE convolution, 37
      fasciculus, 49
Unit, Colvin, 122
    of electricity, 107
    Kolvin, 122
    of resistance, 122
    Siemens, 122
Upper-arm type of muscles, 232
    extremity, neuralgia of, 180,191
Uricaemia, 448
Urine, Cayenne pepper crystals in, 451
    lithaemic, 459
Urethanef hypnotic action of, 501
Urethral diseases, reflex symptoms of, 535
    stricture, neuralgia from, 179
\7ACUOLES, 257
 \   Vacuolation of nerve-cells in insanity, 607
       of nuclei in insanity, 607
Vagabond  pains, 261
Vagus, lesion of nucleus of, 294
    nerve, 84-87
Valve of Vieussens, 64, 66, 67, 72
Varolius, bridge of.  See Pons Varolii.
Vasomotor centre of medulla oblongata, 405
    diseases of the head and chest, 563
    joint-neuroses, 563             •
    symptoms, diffused, 563
Velum medullare anterius, 64
Venous thrombosis, 312, 321, 324.  See Throm-
  bosis.
Ventral aspect of anterior horns, 20
Ventricles of brain. 57, 63, 74, 71
       hydrops of, 367
Verbigeration, 625, 633
Vermis, 72
Verrucktheit,  657
Vertebrae, caries of, 289
    fracture of, 289
Vertebral arteries, 97
    column.  See Spine, Spinal Cord, Vertebrae,
      etc.
Vertical fasciculus, 49
Vertigo, 493
    alcoholic, 494
    anaemic, 494
    aural.   See Meniere's Disease.
    cerebellar, 327
    from eye-strain, 494
    gouty, 494
    intracranial, 494
    from intracranial growth, 327
    labyrinthine, 538
    laryngeal, 398, 493
    lithaemic, 493
    nephritic, 494
    neurasthenic, 450, 493
    ocular, 494
    prognosis of, 495
    spinal, 494
    treatment, of, 495
 Vestibular nerves, 73,  88
 Vieussens, valve of, 64, 66, 67, 72
 Violin-players' cramp, 469
 Virchow, congenital encephalitis of, 321, 323
 Visceral neuralgia, 180
    sensations, conveyance of, 73 
INDEX.
733
Vision, centre for, 139, 140
    cortical centre of, 150
    examination of defects of, 154
    localization of, 38
    methods of examination of, 154
    relation of quadri-germinal body to, 62
    tests of, 154, 157
Vivisection in study of nervous system, 20
Voice, change of, in bulbar paralvsis, 294
Voltaic  electricity.  See Galvanic, Galvanism,
  and Golvanization.
Vomiting from intracranial growth, 328


    WAGNER, histology of nerve-cells, 18
      Wallerian law, 280
 Wasting, muscular, of palsies, 316
 Watch-test for hearing,  159
 Weight, sense of, 166
 Wernicke's pupillary reflex,  152
 Whip-cord movement, 255
 White matter of the brain, 48
            association-fibres of, 48
            centripetal fibres of, 48
            commissural fibres of, 48
            functions of, 19
            projection-fibres of, 48
            terminal fibres of, 48
     substance of cerebellum, 74, 76
  Willis, accessory nerve of, 85
     circle of, 89, 90
  Wires of batteries, 117
     primary, 110
Wires, secondary, 110
Word-blindness, 41, 43
       centre for, 139,140,141
       motor centres for, 41, 43
    -deafness, 40, 43,161, 671
       centres for, 139,140, 141
       localization of, 40, 43
       motor centres for, 40, 43
Wrist-drop, 174, 240, 394, 396
Writers'  cramp, 469
Wry-neck, 435
       diagnosis of, 436
        galvanism in, 437
        pathology of, 436
        prognosis of, 436
        symptoms of, 436
        treatment of, 436
yELLOW softening of cortex, 94
  ZERO potential, 106
   Zirkelwahnsin, 628
Zone, anterior root, 265
   median. 265
   middle root, 265
Zones, anaesthetic, 262, 263
Zwangshandlungen, 589
Zwangsvorstellungen, 589
Zusammengersetzte Psychosen, 628 
 
 
 
 
 
 
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