P4-24-C

 1811





cere-
_yy vs.; _
KG* \>.

ccc?Sr
ccc- —
( «&-..C«xc.
6. > c fe <x

/ -<< CCC (C
   C. («fC
		<<3
	/ "^jKp	•Cfi
		


>«%**«












<&-«<*&.• CO
. .5««-c'_ «



-««rcc  <c;
 .< <rc >t
 -*  <«< ,«
 ,c «~c  c
 ' *rc  c
 ■r err  c

 <-c<r  <
- ccc  (
«. <"CC -  <
  c.rc
Jfrcc '
Star 
NATIONAL LIBRARY
NLM 00551122 b
i
I:
life
Surgeon General's Office
^mmmm i
■:h; u,
r„...£>c
No..'VA..//.../     i
NLM005591226 
 
 
CLINICAL  LECTURE
ON A CASE OF
PROGRESSIVE  MUSCULAR  SCLEROSIS.
DELIVERED  MAY 13, 1871.
BY
        WILLIAM  PEPPER,  M.D.,
                      'it
Lecturer on Clinical Medicine in the University of Pennsylvania ; Attend-
       ing Physician to the Philadelphia Hospital, and to the
                  Children's Hospital.
/
/1 ../a,  ./
{Extracted from the Medical Times',of June 15 and July 1.)
      PHII.AD E I, I» II I A :

J.  P.. LIPPINCOTT  & CO.

            187 1.
 
NAIL





 1671
f'tji*. ■»£>> 11 2-3 f,  /«*« / 
 

\>
 

               CLINICAL LECTURE

O.V A CASE  OF PROGRESSIVE MUSCULAR  SCLEROSIS
 (PSEUDOHYPERTROPHIC MUSCULAR PARALYSIS OF
                      DUCHENNE).
                   Delivered May 13, 1871,

             BY WILLIAM PEPPER, M.D.,
Lecturer on Clinical Medicine in the University of Pennsylvania ; Attend-
  ing Physician to  the Philadelphia  Hospital, and to the Children's
  Hospital.

        E., set.  20, was  admitted to  the Philadelphia  Hos-
       .  pital, April 19, 1871.  He was born in Virginia, and
has resided there or in  the District  of Columbia until the
present time.   His parents are  both  dead,—his  father from
cholera,  his  mother  from some unknown  cause.   He  had
two sisters and  a brother, all of whom are  dead,—two from
unknown causes;  but one  sister had paralysis  (apparently
hemiplegia),  and was unable to walk for some time before her
death.  The  patient himself was a delicate and weakly child
so far back as he can recollect.  He never suffered either from
malaria or rheumatism.  He was engaged in the country on
a farm, and his strength was overtasked by heavy  lifting.  He
never, however, met with any injury.  Six years ago he began
to notice  gradually increasing loss of strength in the legs,
which progressed so slowly that for eighteen months he was
still able to run about, though not  so actively as  other boys.
He was not  obliged to use a cane until two years ago, and
since then only in walking considerable  distances.   This
gradually increasing debility was attended with no pain, formi-
cation, or subjective  sense  of change of temperature in the
legs.   There were  also  no contractions or  cramps of the
muscles.   The progressive  debility had not continued long
before he noticed that it was necessary, when he was standing
or walking, to  throw his  shoulders  back  and protrude his
w 
2
abdomen and lower part of the thorax, thus showing that the
muscles of the back were affected at a very early date. During
this early period he could walk quite naturally, but in running
he threw his shoulders far back and stretched his legs widely
apart; he assumed the same position also in going up an eleva-
tion. Two years later the muscles of the arms became affected in
the same way as those of the legs and back.   During the first
three years he merely noticed  that the legs did  not  grow as
they should do, but afterwards atrophy began, first in the  mus-
cles of the calves, shortly after in  those of the thighs and of
the back, and soon afterwards in those of the shoulders and
arms.   About two years ago, after the atrophy of the muscles
of the calves  had become very marked, he  noticed that they
began to increase in size, and this growth has continued  until
they have acquired a size much greater  than they ever had
previously.  This process of renewed growth next appeared,
about one year ago, in  the muscles of the forearm, and has
continued at a slow rate.  During  all this time his weakness
has steadily increased; he has, however, never been kept  in
bed by it, but has been able to get about feebly by the aid of a
cane.   He has  never had  a sense of constriction about any
part of the body.  His appetite throughout has been good, his
digestion fair, and bowels regular.  His urine has  always  been
passed with ease, and has merely been noted to be  occasionally
yellow.  About one year ago he was seized, without  any apparent
cause, with a severe epileptic convulsion, and since that  time
he has had similar attacks at intervals of from fifteen to thirty
days.   He has usually been unable  to tell when these fits  were
coming  on, but occasionally he has had a strange  feeling  in
the head, and has thought of foolish things, before the attacks.
The fits have been attended with entire unconsciousness, sud-
den falling to the ground, and muscular convulsion.  He has
usually been half a day in entirely recovering from them.   He
has never had more than two convulsions on the same day.
  Present condition.—His expression is natural,  mind active,
and special senses unaffected.  The muscles of  the face are
not involved, and their action is perfect.  His tongue is clean
and moist, appetite fair, digestion  easy, and bowels  regular.
There is no enlargement of the abdominal viscera.  The urine
is normal and secreted  in normal  quantity.  His respirations
are easy,  twelve in  the minute,  chiefly  diaphragmatic: the
vesicular murmur is soft and healthy.   The cardiac sounds are
normal.  The pulse is 75, in the recumbent position.
  Muscular system.—The muscles  of the  neck (sterno-cleido- 
3
mastoids and extensors of the head) are of fair size, and their
movements are strong and free.  The trapezii are feeble, and
he retracts the shoulders with difficulty and feebly.   The pec-
toral muscles are moderately wasted and feeble.   The scapu-
lar group of muscles are less wasted, and the scapulae do not
project markedly from the thorax, so that the serrati magni
are probably not much wasted  and enfeebled.   The deltoids
are extremely wasted, and he  is unable to raise either arm
within thirty degrees of the horizontal plane; when the arm is
raised, there is a marked depression below the acromion pro-
cess.   The biceps muscles are also extremely wasted, and he
is able to flex  the forearm only a little beyond a right angle.
The triceps muscles are also very feeble, and the long head of
each is greatly wasted, while  the external and short  heads
appear as quite prominent fleshy masses.
  The forearms seem unduly large in comparison with the
atrophied arms, and are in reality larger than they have ever
previously been. They have, moreover, a peculiar blunt and
swollen appearance, owing to the sudden enlargement of the
muscles above the wrists.  The atrophy of the forearms seems
never to have reached the degree attained elsewhere, so that
the degree of consecutive hypertrophy has not been so marked
as in the calves.  The grasp of the hands is decidedly weaker
than would be  expected from the size of the forearms, that of
the right  being much weaker than that of the left  hand.
There  has been no atrophy of the muscles of the hands.
  When he sits up in bed, he is only able to hold the shoulders
back with effort; there is increased bowing forward of the ver-
tebral column, with absence of the lumbar depression.  There
is decided wasting of the erector spinas muscles on either side.
When  lying in bed, the lumbar  spine is raised, so  that the
obliquity of the pelvis and hypogastric region is  increased.
The muscles of the abdomen and thorax  are not wasted, and
preserve good strength.
  When he is lying down, the feet are strongly extended and
adducted (equino-varus), so that the toes  point towards each
other, while the soles rest  on the bed.   There is great promi-
nence of the tarsus.  The muscles of the thighs are all much
wasted, as are those of the buttocks.  It is with difficulty that,
when lying  down, he can draw up the legs by the  action of
the flexor muscles.   He has much more  power of extending
them by the quadriceps extensors.  The rotators, abductors,
and adductors of the thighs are much less affected.   He can
move in bed only by a wriggling motion. 
4
<
i
  The calves appear as large as those of a vigorous man, con-
trasting very strangely with  the  wasted thighs.   They feel
quite  firm, even when relaxed, and when he contracts the
muscles they stand out well, and  are hard and elastic.  The
heads of the gastrocnemii especially become prominent, stand-
ing out like firm subcutaneous tumors.   He has considerable
power of flexing, adducting, and abducting the feet, but the
extensors are very feeble.  The muscles of the right thigh and
leg are decidedly stronger than the corresponding ones of the
left side.
  In rising from the recumbent position into a sitting one, he
is obliged to make a very strong effort.   When about to stand
up, he throws  his body  forward till  it almost rests  on his
thighs, and then, placing  his hands on his knees and rising  a
little from his seat, he slowly raises his body by sliding his
hands up his thighs;  and when he  has raised himself as far
as  possible in this way, he places one hand  after the other
on  a chair-back or edge of a table, and leans forward.   He
then, by jerks of the  alternate  sides of the body, draws his
legs forward, thus assuming more and more  nearly an erect
position.  So soon as  he approaches this, the  legs  are  widely
separated, the shoulders thrown quickly back, and the abdo-
men protruded, and, after  tottering a  few times,  he secures
his  equilibrium in this peculiar position.  It is very tiresome
for him to stand without some support, and when  he does so
he bears with his whole weight on the right foot, the  sole of
which  rests flat on  the ground, while the  left leg  is thrown
forward in advance, and  the heel elevated from the ground.
When  a support is afforded him, he places both hands on it,
and leans forward, rising on the balls of the feet, so that the heels
are raised one-half inch from the ground. (See figure.)  In this
position he stands for half an hour or more at a time.  The
muscles of the calves are contracted and thrown into prominent
relief.
  In walking, as in standing, the shoulders are thrown very
far  back, and the lumbar depression is rendered very deep;
the arms hang  down  by  the sides, coming decidedly behind
the line of the buttocks.  The legs  are kept quite widely apart.
He advances each one by resting his weight on the opposite
foot, and then swinging forward the whole side, the foot de-
scribing a slight arc.  At the moment of thus swinging forward
either leg, he rises slightly on the opposite foot.  While stand-
ing on the  right foot, the  whole sole  rests  on the ground,
though the heel merely touches it lightly;  but  when  his 
5
weight is thrown entirely on the left leg, the left heel still does
not touch the ground.  The
effort of advancing each leg
is evidently great;  the mus-
cles of the thighs  tremble
and quiver, but those of the
calves contract forcibly and
are thrown, into bold relief.
Walking  is  very tiresome,
and gives him pain and sore-
ness in the back. No fibrillar
contractions are seen in any
of the muscles.
  Electric   examination,
April 23,  1871.—The  mus-
cles of the forearm (tested
on  the  right  side)  contract
well under a faradaic current
of rather unusual strength ;
they  also  respond  well  to
faradization of  the  brachial
plexus.    Electro-muscular
sensibility  is   not  acute,
though  this may be a  mere
individual peculiarity.  The
muscles of the  arm, the pec-
toralis  major,  and  the  tra-
pezius all contract on faradi-
zation,  whether  direct  or
applied to their motor points.
It requires rather too power-
ful  a current to produce these
effects.   A still  more power-
ful  current is required to in-
duce contraction of the thigh-
muscles,  but  they  all re-
spond,  though  feebly :  the
sensibility to  the  current  is
impaired.  The contractions
of the flexors of the leg  on
the thigh are the most feeble,
and are  obtained   only  by
very strong currents.  The muscles of the leg  respond more
actively than the muscles of  the thigh, whether the electrode
 
                            6

is placed over the nerve in the  thigh, or on  the motor point
of the muscle, or directly over its body.
   When tested with a galvanic current, the muscles of the calves
of the legs contract with each interruption  and renewal of a
current of rather unusual strength (twenty cells, Stohrer), and
electro-muscular sensibility is acute. The muscles of the thighs
also respond, but with more difficulty, to the galvanic current.

   The following measurements were taken :

Right arm, greatest circumference..........................................  7 inches.
  "  forearm, circumference one inch above wrist..................  6  "
                        at middle..................................  8^ "
                        three inches below elbow, point
                         of greatest thickness................  8^ "
  "  thigh, circumference hand's breadth above knee............ io^ "
                     at middle....................................... u% "
                     close to perineum........................... 12% "
  "  calf,             at thickest part.............................. i2ji "

Left arm, corresponding point
  " forearm,   "       "
  " thigh,

  " calf,

  The general sensibility is everywhere normal, and there are
no  subjective disturbances of sensation.  The circulation of
the extremities is somewhat  feeble, and both hands and feet
readily become bluish on exposure  to cold.   The color of the
surface is, however, everywhere normal, without any mottling.
  April 30.—He had to-day an epileptic attack, with frothing
at the mouth, general muscular spasms, and unconsciousness,
lasting for eight minutes. There was deep stupor and sleep for
four hours  subsequently, and he did not entirely recover until
the following morning.  The fit was  preceded  for about  a
minute by the foolish fancies he has frequently had before.
  Ordered  Syr. Phosphat. Comp.,  f^ij, t. d.
            Faradization of arms and legs on alternate days.


  Remarks.—l have  been led,  gentlemen, to detail  at
unusual length the symptoms present in this case, not
only  on account  of  its  great interest and  rarity,' but
because it is the first  case  of  this disease that has been
7
6
8/8 
7
carefully studied and described in this country.*  In
commenting  upon these  symptoms, I will ask  your
attention- especially  to  those points which are  most
highly characteristic.
  The mode of invasion of the disease presented a dis-
tinct peculiarity.  It was marked merely by a progress-
ive loss of power in  the muscles of the legs, buttocks,
and spinal region, which was so gradual in its develop-
ment that the patient continued  able to run about for
eighteen months.   In the present case the loss of power
involved the muscles of the buttocks and spinal region
sooner than  usual, since there was a very early devel-
opment of the next two symptoms characteristic of pro-
gressive muscular sclerosis,—peculiarity in the position
and gait of the patient, and marked anterior curvature
of the lumbar spine.  Patients affected with this disease
stand and walk with their legs  widely separated, as
though  to enlarge  their  base of  support  and  thus
increase  the security of their equilibrium.   Duchenne
is  inclined to think that this position cannot be exclu-
sively due to the weakness  of the legs, since  in other
forms of partial paralysis  of the legs the same position
is  not  assumed to an equal degree.   It appears to me
that the  separation  of  the  legs  may  also  be partly
accounted for by the extreme obliquity of the pelvis
caused by the lordosis of the lumbar vertebrae ; and a
further cause of this separation of the legs will be found
in the mode of walking.
  The weakness of the legs  and of the  gluteal muscles
gives to  the patient  a peculiar gait, which  I  have at-
tempted to describe. This peculiarity consists essentially
in the fact that the patient, in taking a step forward, for
instance, with the right foot, throws his  entire weight
on the left leg, leaning over to that side,  and then, by
a jerk of the right side of the body, the right leg is
thrown or drawn  forward, the foot describing  a small
  * In the Boston Medical and Surgical Journal, November 17, 1870,
there is an interesting paper on this subject by Drs. Ingalls and Webber.
Unfortunately and unavoidably, the report of the case, which serves as the
introduction to the paper, is very meagre. The article contains,however,
a valuable tabulated summary of all the cases of this disease on record up
to that date. There is also a complete bibliography appended. 
8
 arc, and the toe pointing downwards.  It is evident that
 this mode of walking must be an additional cause of the
 separation of the  legs, since, when the weight of the
 body is  thrown on  one leg and the other is swung
 around, the step can  be made more readily and much
 longer when the feet are wide apart.
   While the weight of the body rests  on either foot, it
 will be noticed that the heel is raised  slightly from the
 ground, or at most touches it very lightly.  It is evident
 that in such a mode of walking as this the muscles of the
 leg upon which the whole weight of the body is thrown,
 and which serves as a fulcrum, must be subjected  to a
 severe strain  and be thrown into a state  of powerful
 contraction.
   It is curious to observe in our  patient that, while the
 wasted thigh-muscles tremble and contract feebly, the
 muscles  of the calves  appear to contract very power-
 fully, and stand  out,in  bold relief.   I  shall return to
 this point, but will now merely call attention to  the
 further proof of the greater power of these calf-muscles,
 shown by the elevation  of the heel from  the  ground
 at the very moment that the whole weight  of the body
 is resting on the same leg.   This elevation of the heel
 is not a voluntary act, intended to give greater height,
 so that the sweep of the other leg may be more readily
 effected, but is the unavoidable result of the marked
 superiority in power of the extensors of the foot over the
 flexors.
   The next striking peculiarities about patients with
 this  disease  are the mode of rising from the sitting to
 the standing position,  and the posture  assumed while
 standing.  Nothing could more strikingly demonstrate
 the great weakness of the extensors of  the back  than
 the manner in which our patient  gradually raises  him-
 self into  the  erect posture by the power of his arms.
 The weakness of the same muscles compels him, when
 standing, to  counteract the tendency to fall forward by
throwing the shoulders  far back, while the lumbar spine
 projects forward,  thus  deepening greatly  the  lumbar
 depression,  and producing  the   deformity known as
 " ensellure," or " saddle-back."   Duchenne calls atten-
tion to a peculiarity of the spinal lordosis in this disease, 
9
as distinctive from that seen  in atrophy or paralysis of
the muscles of the  abdominal walls, in the fact that a
vertical line dropped from the most  prominent spinous
process falls behind  the plane of the sacrum.   This
peculiarity is very clearly shown  in  the accompanying
wood-cut, which illustrates the position my patient as-
sumes when standing and leaning on a support.
  I have already alluded to the disproportionate strength
of the muscles of the  calves; and this is also clearly
seen in the existence of double equino-varus.  It is im-
possible  to ascertain  the  precise  period when  this
deformity began, but  it is  probable that,  as is usually
the case in this  affection,  we may class  it as one of
the later symptoms.  At  all times, but especially when
the patient walks, the  tendo-Achillis on each side ap-
pears unusually tense, prominent, and large ; but there
can.be no doubt that the tendency to club-foot is due
solely to the superior strength of the muscles of the calf
(the  extensors of the foot) as compared with that of the
flexors. Thus, on directing the patient to make various
movements with his feet, it is readily perceived that the
movements of flexion of  the foot are very feeble, while
those of extension and adduction are quite vigorous.
  Finally, it remains, in  studying the  symptomatology
of this case, to examine carefully the relation which the
atrophy and  hypertrophy of the  muscles  bear to  each
other.   I desire to call more particular attention to this
point,  since,  in  the cases  of this disease hitherto re-
corded, muscular atrophy has either not  been present,
or has not attracted the careful study it merits, at  least
from a theoretical point of view.   The changes in the
muscles  have  invariably been  preceded, as in the
present case, by a stage of  progressive debility of vary-
ing duration, after which the first alteration observed
in the  muscles has been, in a majority of cases,  a
gradual increase in their  bulk.  In a few cases, atrophy
of certain groups of muscles has coincided with enlarge-
ment of others.  In the present case, however, the pro-
cesses have  been  differently related.   In all  of the
muscles affected, including those of the extremities, of
the buttocks, lumbo-spinal region, and shoulders, the
first  change  noticed  has  been  a slowly developing 
10
atrophy, which  has advanced in  the  case  of certain
muscles [e.g. the biceps flexors of the arms and the calf-
muscles) to an  extreme  degree.   Thus,  wherever en-
largement of the muscles is  noted, it has been devel-
oped as a secondary change consequent upon a primary
process of atrophy, a fact which appears to  me highly
important as bearing on the affinities of the  disease we
are considering.
  The modes of distribution of these two conditions are,
however, quite  dissimilar.  Thus,  in the case of the
atrophic change, it has advanced from the feet upwards,
successively involving the muscles  of the calves, thighs,
buttocks, lumbo-spinal  region,  shoulders,  arms,  and
forearms. On the other hand, the  process of consecu-
tive  enlargement, having  also appeared first in the
muscles of the calves, has affected in addition only the
muscles of the  forearms  and two  of the heads of the
triceps muscles.  This irregularity in  the distribution
of the excessive muscular  growth has been noted in
other cases, in some of which  it has remained limited to
the legs, or has  involved in addition the arms and even
the face.  The usual rule is, however, for it to affect the
legs first, and thence to extend to the truncal muscles.
  The statement is made by several observers that the
weakness of the muscles increases with the increase in
their bulk;  and in certain cases this would appear to
have been the case.  More usually, however, no direct
relation  exists  between  the  loss  of  power and  the
apparent enlargement of the muscles; and it may even
happen, as  in the present case, that those very muscles
are by far  the  strongest which have undergone most
marked secondary enlargement.  This is clearly seen
in the production of double equino-varus by the over-
action of the extensors of the feet, and is no less true of
the muscles of the forearms.  It is important to note
carefully this fact,  since  it  shows conclusively  that,
whatever may be the nature of the change in the muscle
w.hich leads to its enlargement, its first  and direct effect
is not to weaken the contractile power.
  The affected  muscles in this  disease give different
results when tested with faradaic and with galvanic cur-
rents ; the results also vary at different  stages of the 
II
same case.  In the present instance, the results accord
with those obtained in a number of cases, especially in
those studied by German  observers ; that is to say, the
muscular contractility, as  tested by faradization, is  im-
paired in all the affected muscles, those which are hyper-
trophied, however, contracting more actively than those
which are atrophied.   The galvano-contractility is also
slightly impaired.  The  electro-muscular  contractility
has been found unimpaired in  the earlier stages of the
disease ;  but later it diminishes, the muscles continuing,
however, to respond actively to galvanism after they have
partly lost their power of responding to faradization.
  Electro-muscular sensibility has been found normal
or impaired in different cases : in my patient it is dimin-
ished to  faradization, but  remains acute to galvanism.
The temperature of the affected parts  remains normal
in some  cases, while in others it is lower than that of
the trunk, and the skin has then been observed, in a
few cases, to be marbled or mottled.
  There  is an entire want of disturbance of the general
health in this singular disease.  The appetite remains
good until  a late period, digestion is well performed,
and the  action of the bowels  is regular.  Neither the
rectum nor the urinary bladder becomes paralyzed. The
disease is not  attended by  any pain  or  alteration of
general  sensibility.
  It is a  singular fact that in a notable proportion of the
cases progressive muscular  sclerosis has  occurred in
children of feeble intelligence or in idiots.  There is,
however, no necessary connection between it  and  any
kind of  cerebral disturbance, since in  some cases the
disease has existed in a  well-developed form in con-
junction with a normal condition of the mental functions.
The complication of  epileptiform convulsions, which is
presented in the case before us, is a hitherto unobserved
one.  It is,  however,  associated with such perfect reten-
tion of memory, such activity and clearness  of  mind,
and such integrity of all the special senses, that  I can-
not regard it as any evidence of an organic affection of
the brain. I shall, however, return to this point hereafter.
  I have thus dwelt upon the various symptoms of this
disease,  which we have seen to  be characterized by a 
12
period of gradually increasing  debility, soon followed
by peculiarities  in the mode of standing and walking,
by lordosis of the lumbar  spine, and by equino-varus ;
while later  still the enfeebled muscles either undergo
atrophy, with a subsequent remarkable enlargement of
a greater or smaller number of them, or they pass into
this  state of enlargement without undergoing any pre-
vious diminution in size.   The subsequent course of
such cases, so far as known, maybe told in a few words.
In all instances where the disease has reached the stage
in which the symptoms are fully developed, a fatal result
has  followed.  The disease is  a slow  one, and  may
occupy several years in reaching the period of its full
development; it then remains  stationary  for several
years longer; but finally a stage ensues in which the loss
of power rapidly increases and extends, with or without
accompanying atrophy,  to muscles  previously unaf-
fected.  The sufferer is soon confined to bed, and death
occurs in one or two years, either from sheer prostration
or from some intercurrent disease.
  When we come now to ask ourselves what relation
this disease bears to the various forms of paralysis or of
muscular atrophy, we are met by the difficulty that, until
the present time, but one careful  post-mortem examina-
tion has been made of the body of a patient dying from
this malady. In this instance the nervous centres were
examined  by Cohnheim, but  with entirely  negative
results.   But although,  therefore, there is still great
need of further  examinations of the internal organs,
nerve-centres, and ganglia of the sympathetic nerve,
much light can be  thrown upon the question  by the
careful examination of the tissue of the affected muscles.
This is secured by the use of a little instrument, devised
by Duchenne,  and termed an  " emporte-piece,"* by
which  fragments can be obtained from the substance
  *This useful little instrument is shaped like a trochar.  The blade is,
however, a hollow cylinder, composed of two parts, one of which, bearing
the point, is fixed, while the other can be withdrawn a little by sliding a
movable button on the handle. The trochar is introduced closed into the
substance of the muscle, the button withdrawn, so as to open the cylinder
and allow a fragment of muscle to project into it; the button is then pushed
forward, cutting off and securing the little morsel of tissue. 
•3
of any superficial muscle and  subjected to microscopic
examination.
   I  have thus  obtained a  fragment from  each of the
gastrocnemii and from the  left deltoid  muscles,  and
have  found the  following appearances,  after  careful
microscopical examination of each piece.           ^  j^f  ,„jt*0

  The  fragment  removed from the left  deltoid was  of a
slightly pale reddish color.  When examined microscopically,
a large majority of the  fibrils showed distinct, though  often
fine  and  delicate, transverse  striation.   In a  few  instances,
striation was entirely absent, the fibrils looking homogeneous
and  much like ground-glass cylinders.   In a very few fibrils,
also, distinct longitudinal striation was visible, and in others
there was multiplication  of the nuclei in the sarcolemma.  In
not  a single fibril was there any trace  of fatty degeneration.
The fibrils varied in size from  ^'f to ^", or even, in a
few  cases, y^".  The striation was particularly faint,  or at
times even absent, in the largest fibrils.  There was  a  large
amount of  interstitial white  fibrous tissue, with  abundant
granular  matter  containing many oval nuclei.  In places
there were small  collections of minute fat globules or refract-
ing  granules.
  The fragments removed from the  gastrocnemii presented
closely analogous conditions.   The muscular tissue was merely
rather paler red  than normal.  The muscular fibrils varied
greatly in appearance and  in  size.   The transverse striation
was  in  some fibrils perfectly healthy,  but in  a majority  it
was  altered, though in various ways.  Thus, in some it was
very faint and difficult to distinguish ; in others, it was wholly
absent, the fibrils presenting the appearance of fine  ground
glass.   In other  fibrils there  was  a marked appearance of
longitudinal  striation, due to delicate fibres or very fine  fusi-
form cells arranged in the long axis of the muscular fibril.  In
many fibrils there was distinct excess of the  nuclei of the sar-
colemma,  which appeared as large oval  nuclei with a  puncti-
form nucleus.  A few fibrils presented streaks of minute fatty
granules along their centres,  and a very small number were
decidedly fatty.   The muscular  fibrils varied greatly  in size
also.  Many were about j]./' to  3£ff" in  diameter; but  a
number were ¥£ff" to  ¥^?T>/, while others were as much as
jW>jW> so/' in width.  There was  a large excess of
interstitial tissue, in places taking the form of  long, narrow,
wavy bands  of pure white fibrous tissue; in others, appearing 
M
as abundant granular stroma, thickly strewn with oval nuclei.
There was also some curly, elastic fibrous tissue.  There was
a considerable amount of interstitial fat, existing as scattered
globules, or arranged in patches of large, closely aggregated
fat-globules.  In places isolated muscular fibrils lay imbedded
in this fibroid tissue so as to be scarcely visible; but in other
places a number of fibrils lay directly in contact with each
other, forming a little bundle, around which the excessive
growth of interstitial tissue had occurred.  The arterioles and
capillaries appeared healthy.   No nerve-fibrils were detected.
  Similar examinations have,  as  before stated, been
made in a number of the cases of this disease, and have
yielded results agreeing  in all essentials with those I
have found in the muscles of this patient.  The points
which  I  desire to dwell upon as of capital importance
in their bearing on the  pathology of the disease are, in
the first place, that the primary fundamental change in
the affected  muscles is an excessive growth or hyper-
plasia of the interstitial connective tissue. This is found
to have taken  place even in those muscles which have
not undergone any increase in bulk, or which are even
reduced in size (for instance, the left deltoid in this case).
In the latter case it is evident that the process cannot
have advanced far, and  it also appears probable  that
there is a certain amount of simple atrophy of the mus-
cular fibrils developed simultaneously. . This, however,
does not appear to be the only change in the muscular
fibrils, which are also found to begin to lose their trans-
verse striation, and to present increase in the nuclei of
their sarcolemma, or distinct longitudinal striation.  Ob-
serve, however, that there is  not the slightest tendency
to a primary fatty degeneration of the muscular fibril. It
may happen that this interstitial growth never reaches
such an extent as to cause apparent enlargement of the
muscle,  so that only certain muscles may thus enlarge.
Thus,  as a rule,  the  muscles of the calves are the first
to undergo this  subsequent  change, and they may be
the only ones  in which it appears, although numerous
other muscles may present the first stage of the process.
  In those muscles which do undergo this subsequent
enlargement, the hyperplasia of interstitial  connective
tissue is found to have reached an extreme  degree.  The 
rS
appearances presented indicate that the entire process
has been one of sclerosis, in which there has been rapid
growth of nucleated fibro-cellular tissue, with the devel-
opment of bands of wavy fibrous tissue, and even some
curly elastic fibres.  It is easy to recognize, therefore,
the identity of this process with the other sclerotic  in-
flammations, as of the  connective tissue of the nervous
centres (sclerosis of brain and spinal cord), of the lungs,
liver, and kidney (cirrhosis), and  of the  subcutaneous
tissue  (scleroderma).   There is, however, one point in
which this  affection  of the  muscles appears to differ
from the other sclerotic conditions mentioned.   In the
latter,  we constantly observe that, with the progress of
the change, a tendency to  organization  and contrac-
tion of the newly-formed fibrous tissue soon manifests
itself, while the essential elements of  the part (nerve-
tubules, liver-cells, or  uriniferous  tubules)  are com-
pressed and undergo  atrophic degeneration.   In the
disease we are now considering  however, there is a
simultaneous change in the muscular fibrils, even in the
early stage ; but this does not appear to depend wholly
on the hypertrophy of  the interstitial connective tissue,
nor does  it maintain any definite  or constant relation
with this latter change throughout the course of the
disease.*  Indeed, as is seen in this patient, those verv
muscles which present the greatest degree of sclerotic
enlargement may be the strongest of  the whole  series
which  are implicated in the disease. It is true that the
muscular fibrils of such muscles present a further stage
of the change begun in the  first period of the disease.
Their transverse striation is still more delicate and faint,
or is  even, in  a number of  fibrils, entirely lost.  But
they do  not  seem  to have  undergone  any further
atrophy;  indeed, the measurements I  have made, and
the increased strength in the muscles of the  patient's
calves,  would  point  to the  belief  that  the  muscular
fibrils may temporarily share the exaggerated  nutrition
  * It may be that in some cases where there is marked loss of power,
with general preservation of the size and striation of the muscular fibrils,
the sclerotic change in the connective tissue compresses th,e branches of
the motor nerves as they traverse the muscular tissue. 
i6
of the surrounding connective tissue, and undergo a
delusive increase in size and power.* Thus, I find that
the fibrils in the gastrocnemii muscles of this patient
are fully one-third wider than  those  in his left deltoid,
and that some of the former  have acquired the enor-
mous size of j^j// in transverse diameter.
  Whether this transitory stage usually exists or not, the
sclerotic change does not depart from its inevitable law
of development.  Already in this second stage we have
seen patches of fat-globules  appearing in the interfibril-
lar spaces, and as the disease passes into the final stage,
this  fatty  degeneration of the muscle advances with
varying rapidity, even leading  in  some cases to such
an accumulation of fat as to  be visible  to the unaided
eye  as yellowish streaks.   This extreme condition is,
however,  very rare,  and much more frequently the
accumulation of fat  is  moderate.  Even  when very
great, however, it is found  to be  far more due to  in-
crease of the interstitial fat than to a true fatty degen-
eration of the  muscular fibrils.  Their  nutrition must
be, however, very gravely  impaired, so that they un-
dergo atrophy, and in many places entirely disappear,
leaving their sheaths empty.   This change  coincides
with the rapid extension of paralysis which character-
izes the final stage of the disease.
   This detailed account of the muscular lesion naturally
leads to  the question of the  pathology of this curious
affection.   It cannot be held that the disease depends
upon or is essentially connected with any cerebral lesion.
It is true that in a number of cases the patients have been
idiotic, or at least exhibited marked impairment in intel-
lectual development: in the present case, also, epileptic
convulsions are present as a complication. It must, how-
ever, be remembered that cerebral disturbances of any
kind whatsoever are not uniformly present,  that  dis-
orders of special sense are rare,  and that some cases of
the disease  have been observed associated with a nor-
mal state  of the intellectual faculties ; and, finally, that
in the one case where the nervous  centres have been
 * This enlargement of the size of the fibrils of the gastrocnemii has also
been observed by Leyden (loc. cit.). 
i7
 examined, the brain was found healthy.  The  peculiar
 character of the muscular lesion and  its symmetrical
 distribution are additional proof, if more were wanting,
 of the absence of all connection between the disease we
 are discussing and any cerebral lesion.
   Nor is the argument more strong in favor of a spinal
 lesion as the cause of this affection.  It is true that the
 first idea which will arise, on learning from a patient that
 his malady began with gradual loss of power of both legs,
 is that there is some disease of the anterior columns of
 the spinal cord. When, however, as  in the present case,
 we further find that there has been no alteration of sen-
 sibility, no loss of co-ordination of muscular movements,
 no subjective sensations, such as of formication or of
 constriction, no implication of either bladder or rectum ;
 when also we learn on careful examination that the loss
 of power was not in  reality the primary symptom, but
 was preceded by and existed only in proportion  to
 certain muscular changes,—we must conclude  that the-
 disease is not dependent upon any affection of the spinal
 cord.  The most important fact to be clearly appre-
 hended here is that in reality there is no paraplegia, in
 the strict and only correct significance  of  the  word,
 present in the disease we are  studying.   It is of course
 true that a paralyzed muscle will often undergo atrophy
 or fatty degeneration, but these changes are then depend-
 ent upon loss of function and of innervation, and  are
 essentially secondary to the interruption  of  the  trans-
 mission of motor power.  WTidely different, however, is
 the relation  which here exists between the loss of power
 and the alterations in the muscles.  There is through-
 out the course of the disease no real loss  of motor nerve-
 power, nor  any interference with its transmission, but
 merely an interference with its manifestation, owing to
 a progressive sclerotic change in  certain muscles. This
 change has been slowly advancing for some time before
 the loss of power is so marked as to attract  the notice
 of the patient;  and just in proportion as it progresses,
 do the muscles become more and  more weak,  until,
 when the final stage  of the sclerosis is attained, their
contractile power is so completely lost that the patient
is bedridden and almost motionless. It is on account 
i8
of the radical difference between this process and any
form of paraplegia that I object to the name "pseudo-
hypertrophic paralysis," applied by Duchenne to this
disease,  and  greatly  prefer  "progressive  muscular
sclerosis,"  as expressing accurately the  pathological
condition present.
  Having, then, excluded the possibility of either a cere-
bral or spinal origin for this disease, I can  only offer
the somewhat unsatisfactory view of its  pathology, that
it consists  essentially  in a  perverted nutrition of  the
muscles  affected, probably dependent upon a lesion of
the branches  of the sympathetic nerve which are dis-
tributed to the tissues involved.  This opinion that the
sympathetic nerve is primarily affected, does not, it is
true, rest on any positive or convincing evidence.   In a
certain number of cases, however, especially in those ob-
served in Germany, there have been symptoms noticed,
such as reddish or bluish discoloration of the skin of the
affected parts and variations in their temperature, which
would certainly indicate some marked  disturbance in
the vaso-motor  supply of the  cutaneous  vessels, and
have accordingly led many of the observers of this dis-
ease to adopt this view of its pathology.  It must be con-
fessed, however, that such symptoms are not constant,
or at least  are not present at all stages of every  case:
thus, in the present instance, the most careful examina-
tion fails to determine them.  Still, for  the  present, in
fault of  any exact knowledge or of any more  satis-
factory explanation, this view of the pathology of pro-
gressive muscular sclerosis may be accepted.
  I may add that no additional light is to be derived
from a study of its causes.   It is eminently a disease of
infancy and childhood, making its  appearance in  the
vast majority of cases between the  ages of five and
thirteen years.  It has, however, been observed to  begin
in one case at the age of fourteen years ; in the present
case it was first noticed at the age of fifteen years; and in
two cases observed by Benedikt (loc. cit.), and in one by
Laycock (loc. cit.), the  disease seems to have originated
in adult life.  The disease is much more common in the
male than in the female sex; and, finally, it frequently
affords  evidence of a hereditary tendency, two or even 
19
four cases having been more than once observed in  a
single  family.  It usually appears spontaneously, not
appearing  to depend upon  any  particular external
causes.  In single instances it has been attributed to
such causes as the  influence of cold  and damp, or an
attack  of some eruptive fever.  In my own case, the
cause assigned by the  patient, protracted over-exertion
in doing work too heavy for his years, is far more likely
to have really influenced the development of the  dis-
ease.  It must be conceded, however, that in  its eti-
ology,  as well as in its pathology,  this curious affection
still presents an unsolved problem.
  Let me now invite your attention to the relation which
this  disease bears to other  affections.   I  shall not oc-
cupy your  time by any lengthy discussion of the diag-
nosis between progressive sclerosis of the muscles and
atrophic infantile paralysis.   The suddenness of attack
in this latter affection, frequently associated with fever
or with some cerebral disturbance, as convulsions, the
occurrence of  complete  and more or  less extensive
paralysis, the gradual disappearance of the paralysis in
some parts, while in  others it remains permanent, the
diminution and ultimate loss of electro-muscular con-
tractility, the occurrence at a later period of fatty degen-
eration and atrophy of the affected muscles, with arrest
in the  development of the bones and marked deformi-
ties, and the entire absence of any secondary enlarge-
ment of the parts involved, constitute a  series of dis-
tinctive features so clear and decisive  as to render the
differential diagnosis easy and certain.
  A disease from which  it is much more important to
carefully distinguish progressive sclerosis of the muscles
is progressive muscular atrophy occurring in childhood.
The especial importance of the relations of these two
diseases depends on the fact that both  are alike diseases
of nutrition of the  muscles, thus constituting a group
quite distinct from all  the forms of true paralysis.   In
both the disease begins—usually without any apparent
cause—insidiously, and progresses  slowly but surely.  In
both the loss of motor power is secondary to the changes
in the  muscular tissue ; in both the muscular degenera-
tion  and consequent loss of power almost  invariably 
20
 progress steadily to a fatal result.   In progressive mus-
 cular sclerosis  the  positive anatomical  proof is  still
 wanting, but analogy, theory, and  some special symp-
 toms lead us to believe in the existence of a lesion of
 the sympathetic nerve system.  In progressive muscu-
 lar atrophy, careful post-mortem  examination has re-
 peatedly demonstrated the actual  presence of such a
 lesion. These two diseases, then, stand related to each
 other as being alike caused by disturbance of the  tro-
 phic  nervous system, but they are at the same time
 most positively separated from each other by marked
 differences in their course and symptoms.
   Thus, in  progressive muscular atrophy, the disease
 nearly always  begins in  the upper extremities, and
 invades subsequently the trunk and lower extremities.
 Indeed, Duchenne has pointed out that when this dis-
 ease appears in childhood, which is quite rare, it begins
 in the face, where it produces atrophy of the orbicularis
 oris and the zygomatici, and does not  extend to  the
 trunk and extremities until after a period varying from
 two to three years. It then follows the same descend-
 ing course  seen in cases occurring in  adults.   The
 atrophy usually affects the muscles irregularly, so that
 various deformities and  vicious positions of the parts
 involved  are  developed.   Microscopic  examination
 shows a progressive fatty degeneration and atrophy of
 the muscular fibrils, and  in proportion as this increases
 there  is loss of power and of electro-muscular con-
 tractility.   One further  symptom  of high diagnostic
 value is the  frequent occurrence of fibrillar contractions
 in the affected muscles. Finally, the muscles which have
 progressively atrophied never undergo any secondary
 enlargement, nor does microscopic  examination reveal
 any lesion of the interfibrillar connective tissue.  In all
 of these particulars, then, progressive muscular atrophy
 differs widely from progressive muscular sclerosis, which
 is almost exclusively a disease of childhood, beginning
 in the muscles of the lower extremities and advancing
 upwards, producing a peculiar mode of  standing  and
 walking, and in  which the affected muscles, with or
without a stage of atrophy,  undergo remarkable en-
largement, without fibrillar contractions, and with pre- 
21
servation of electro-muscular contractility till a com-
paratively  late period  of the disease.   Microscopic
examination also  shows, even in the early stages of the
disease, a marked hypertrophy of the interstitial  con-
nective tissue  in the affected muscles, together  with
peculiar  changes of  the  muscular fibrils,  not at all
resembling fatty degeneration ; while later, this sclerotic
process terminates in fatty degeneration of the interstitial
tissue, and increasing degeneration and atrophy of the
muscular fibrils.  There is also a want of constant  rela-
tion between the  degrees of sclerosis,  of the changes in
the muscular fibrils, and of the impairment in muscular
power.  This hasty summary of the  main distinctions
between  these two affections will show  how readily a
differential diagnosis  can  be established.
  In  regard  to the prognosis of progressive muscular
sclerosis, the disease may be pronounced incurable,
unless treatment  is instituted during  the earlier stages,
before the affected muscles have become markedly en-
larged.  Even when, however, it has progressed to an
advanced stage in certain muscles, its progress in other
portions  of the body may probably be arrested.  The
duration of the disease is rarely less than six years, and
may extend to upwards of fifteen  or twenty.  Thus, in
the present case,  the disease has been in positive exist-
ence  for five years, and  yet has  only passed  into the
second stage, and would probably, even were no treat-
ment adopted, require several more years to run its
course.  When a fatal result is produced, it is either by
the extreme  prostration  and lowered vitality of the
patient,  by  weakening  of  the  respiratory  muscles,
favoring pulmonary engorgement, or  by some intercur-
rent disease.
  Fortunately, however, it may be safely asserted that
treatment, when instituted early and faithfully pursued,
exercises a powerful  control over the progress of the
disease.  Unless  there  are special concomitant symp-
toms, such as anaemia, epileptiform convulsions, digest-
ive derangement, or the like, there is no clear indica-
tion for internal  medication, nor has the use of any
drugs been followed by decided benefit.   Those which
may be given most rationally, as tending to modify the
nutrition of the nervous system, are the alterative nerve 
2$
tonics, of which I should  be disposed  to  especially
recommend the nitrate of silver.   Of course, in addi-
tion, care must  be taken to improve  the state of the
blood, if it be anaemic, and to correct  any disturbance
of digestion.   If  the  case  is complicated  with epi-
leptiform convulsions,  as in my patient, a  course ot
bromide of potassium may be directed with advantage,
The remedy, however,  from which most good is to  be
expected, is electricity.  This has  been used with very
great  benefit, in the form of faradization by Duchenne,
and in that of galvanization by Benedikt and  others.  I
have pointed out to you that the electro-muscular con-
tractility is usually preserved until  late in the disease,
though very different results are obtained in some cases
by  the  use  of the different  varieties  of  current,—the
muscles sometimes contracting most powerfully under
the application of a faradaic, and at others under that of
a galvanic, current.  I should recommend the employ-
ment  of whichever form  is  found  to  secure  the  most
active muscular contractions.  If the  faradaic current
be used, it should be  applied  directly to the affected
muscles, or one electrode may be applied  over the
motor point  of  the muscle (i.e. over  the trunk of the
motor nerve  before it enters the muscle)  and  the other
over its  body. If the galvanic current be indicated, one
electrode (the copper pole) should  be applied over the
carotid  fossae, along the anterior  border of the  sterno-
cleido-mastoid muscles, since in this region the cervical
portion  of the sympathetic nerve is most readily access-
ible;  and the other electrode (the zinc  pole) may be
applied along the lumbar spine, or over the motor point
of the affected muscles.   In  some cases it may also be
advantageous to combine the galvanization of the cer-
vical  sympathetic with faradization  of  the  affected
muscles.  In the  present case,  I  have  directed the
muscles to be thoroughly  faradized every other day.  I
have told you that the muscles responded quite actively
to the stimulus  of this  current; and already there is a
positive improvement  in  the power of his legs and in
his ability to walk. I am therefore encouraged to per-
severe in this treatment, in the hope that by its pro-
longed use the progress of the disease may be ultimately
arrested. 
2j
                         BIBLIOGRAPHY.

   This disease was first  recognized and described as a distinct affection
 by Duchenne in 1861  although some few unrecognized cases lfad been put
 on record before that date. Since that time there have been forty-eight cases
 including the present one, published.  This does not  include four cases
 referred  to as published by Meryon {loc.  cit.), but which are somewhat
 doubtful, though  two at least  appear to have been genuine instances of
 this disease.  I he total  number of cases may therefore be estimated at
 about fifty.

   Edward  MERYON.-Med.-Chir. Trans., vol. xxxv., 1852, p. 72- and
 Pract. and Path.  Researches on Paralysis, London, 1864, p. loo et sea
   Duchenne.—Electrisation localisee, 2eme ed., 1861, p. 364 •  Arch Gen
 de Med  t.  1., !868 p. 1; Gazette des Hopitaux, 35 and 36, 1868; and De
 la Paralysie musculaire  pseudo-hypertrophique ou Paralysie myo-scle-
 rosique,  Pans, 1868, 8vo, pp. 132.
   Spielman.—Gaz. Med. de Strasbourg, 1862, No. 5
   Kaulich.—Prager Vierteljahrsschrift, 1862, Bd  73
   H. W. Berend.—Berl. Allg. Med. Centralzeitung, 1863, No  9
   Eulenburg und Cohnheim.—Verhand. der Med. Gesel  vol i   i86q
 pp. 101-205  ; Canstatt's Jahresbericht, 1866,  ii p  261             >    J
   EuLENBURG.-Berl.  Klin.  Wchnsch., ii.  So, 1865;  Schmidt's  Jahrb
 1866, 1. p. 291.                                               J
   Stoffella.— Wien. Ztschr., xxi., i. p. 85, 1865; Schmidt's Jahrb., 186c;
 IV. p. I79.                                               J     J   3
   Griesinger.—Arch. d. Heilk., vi., i. p. 1, 1865;  Schmidt's  Jahrb
 1005, iv. p.  179.                                              J
   HELLER.—Arch. f. Klin. Med., i., vi. p. 616, 1866;  Schmidt's  Jahrb
 i860, 11. p. 286.
   WERNiCH.-Arch. f.  Klin. Med., 2, ii. p. 232, 1866;  Schmidt's  Jahrb
 1506,iv. p. 295.
   Sigmundt.—Arch. f. Klin. Med., i., vi. p. 630, 1866; Schmidt's Jahrb
 1866, 11. p. 285.
   Coste und  Gioja.— Schmidt's  Jahrb., vol. xxiv. and vol. cxxx   1866
 11. p.  285.
   Leyden.—Berl. Klin. Wchnschr., 1866.
 _  Lutz.—Arch. f. Klin. Med., iii. 4, p. 358,1867; Schmidt's Jahrb., 1868
i.  p. 171.
  Seidel—Centralblatt,  1867, p.  666, and Canstatt's Jahresbericht  1867
 2, 1. p. 295.                                                        '
   Bergeron.—Gaz. des  Hop., 1867, p. 249; Schmidt's Jahrb., 1868  i
 p. 171.
   Hoffmax.—U. d. sogen. Muskelhypertrophie, Berlin, 1867; Canstatt's
Jahresbericht, 1867, 2, i. p. 294.
  W.  Adams.—Trans.  Path.  Soc. of London, vol. xix., 1868  p 11
  L. Clarke.—Ibid., pp. 6, 9.
   Hillier.—Diseases of Children, London, 1868, p. 253.
   Benedikt.—Elektrotherapie, Wien, 1868,  p. 186.
  Roquette.—U. d. sogen. Muskelhypertrophie, Berlin, 1868 ■ Canstatt's
Jahresbericht, 1868, 2, i. p. 268.
  M. Clymer.—American Edition of Aitken's Science and Practice of
 Modicine, 1868, vol. ii.  p.  680.
  Ollivier.—Des Atrophies musculaires, Paris, 1869, p. 178.
  B. W. Foster.—London Lancet, May 8, 1869, p. 629.
  J. Russell.—Med. Times and Gaz., May  29, 1869, p. 571.
  Niemeyer.—Text-Book of  Practical Medicine (American  Edition)
1869, vol. ii.  p. 519. 
24
  Meigs and Pepper.—Diseases of Children, 4th ed., Philadelphia, 187CJ,
P- 587.
  Rosenthal.—Diag. u. Ther. d. Nervenkrank., Eriangen, 1870, p. 216.
  Jaccoud.—Traite d. Path. Int., Paris, 1870, vol. i.  p. 364.
  W. B.  Kesteven.—Journal of Mental Science, April, 1870, p. 41.
  L. Down.—Journal of Mental Science, April,  1870, p. 46.
  D. Dyce Brown.—Edin. Med. Journ., June, 1870, p. 1079.
  M. Clymer.—New York Med. Record, July 16, 1870.
  Ingalls and  Webber.—Boston Med. and Surg. Journ., November 17,
1870.
  T. Laycock.—Med. Times and Gaz., January 14, 1871, p.  33.


                          SYNONYMY.

  Duchenne, 1861.—Paralysie hypertrophique congenitale.
       "    1868.—Paralysie  musculaire pseudo-hypertrophique,  or
Paralysie myo-sclerosique.
  Stoffella and Griesinger,  1865.—So-called  Muscular Hypertrophy.
  Heller, 1866.—Lipomatosis luxurians musculorum progressiva.
  Sigmundt, 1866.—Muscular Palsy in Consequence of Hypertrophy of
the Interstitial Fat and Connective Tissue.
  Seidel, 1867.—Atropie musculorum lipomatosa.
  Bergeron  and Lltz, 1867.—Fatty Muscular Hypertrophy.
  Jaccoud and others, 1870.—Sclerose musculaire progressive (Progress-
ive Muscular Sclerosis). 
<»
 
 
 
 
 

»• »>>>
NLH D
D55T122  b

!»
»> ri»> ■ »_;




>> > jj



1 >» ->
^ >5  -
i) ) 2I>3>
> > .»» »> -


 0 3 5*rs>
j*#»
i>



£3
NLM005591226