A STUDY OF CEREBRAL 
PALSIES OF EARLY 
LIFE, BASED UPON AN 
ANALYSIS OF ONE 
HUNDRED AND FORTY 
CASES. 
BY 
B. SACHS, M. D., 
AND 
F. PETERSON, M. D. 
REPRINTED FROM 
The Journal of Nervous and Mental Disease, 
May, 1890. 
M. J. Rooney & Co., Printers, 
Comer Broadway and 35th Street. 
NEW YORK. A STUDY OF CEREBRAL PALSIES OF EARLY 
LIFE, BASED UPON AN ANALYSIS OF ONE 
HUNDRED AND FORTY CASES* 
By B. SACHS, M.D., 
Professor of Nervous and Mental Diseases at the New York Polyclinic, 
AND 
By F. PETERSON, M.D., 
Lecturer in the Department of Nervous and Menial Diseases at the New York Polyclinic. 
FEW diseases are better known or more thoroughly 
understood than infantile spinal paralysis. Its clin- 
ical symptoms and its pathology have been definitely 
determined, so that poliomyelitis anterior acuta scarcely 
needs further study. The very opposite is true of infantile 
cerebral palsy. While there is but a single form of disease 
included under the term infantile spinal paralysis, we are 
forced to admit that there are several different forms of 
cerebral palsy. The attempt to fix upon certain cases of 
cerebral paralysis in children and to label them infantile 
cerebral palsy as a direct analogy of the better known spinal 
disease has led to great confusion, although we shall see 
that there is some justice in drawing this analogy. Nor is 
it entirely correct to speak of cerebral spastic palsies as 
distinguished from atrophic paralysis, for we shall report at 
least two cases in which the element of spasticity was 
entirely wanting, although the cases were undoubtedly of 
cerebral origin, the proof of which was furnished by the 
post-mortem examination in one of these two cases. 
The large majority of the cases with which we are here 
concerned represent spastic forms of paralysis and as re- 
gards the distribution of the palsy may very properly be 
* Read at the stated meeting of the New York Academy of Medicine, April 
3, 1890. 2 
B. SACHS AND F. PETERSON. 
divided into cases of spastic hemiplegia, of double spastic 
hemiplegia or diplegia, and of spastic paraplegia. Since the 
clinical subdivisions are so easily made, it would seem to 
be a curious fact that these cases have been so poorly 
understood and so little studied. There were many rea- 
sons for this : first and foremost, the great difficulties in 
obtaining autopsies, the majority of these cases either living 
on to a very advanced age, or else dying in almshouses, 
where no interest was taken in them ; then again, the con- 
dition was so frequently associated with idiocy; or the 
individuals were regarded as hopeless cripples that did not 
possesss sufficient interest to repay careful study. And 
lastly, the term infantile cerebral palsy proved to be a 
stumbling-block. A number of cases and some few 
autopsies were reported, disclosing a variety of lesions ; 
there seemed to be little hope of bringing order out of 
chaos. The truth of the matter, that we had a number of 
different forms of disease and a variety of pathological 
processes to consider, was a long time forthcoming. We 
hope to show by this paper that much of the confusion that 
has surrounded this subject will be removed if we consider 
that a variety of morbid symptoms may give rise to any of 
the three forms of paralysis, and that the character of the 
paralysis will depend upon the site and extent of the morbid 
lesion. But for the difference in the areas of the brain 
affected and the degree of irritation or destruction of brain 
substance, the symptoms in all these cases would be very 
much the same. 
The subject which we present has a live interest at this 
present time, and yet it is nearly fifty years ago since the 
first work in this field was done. In 1842, Prof. Henoch 
wrote his inaugural dissertation, “ De Atrophia Cerebri,” 
and gave an excellent account of infantile cerebral paraly- 
sis.1 Heine2 referred to these cases in a monograph on 
spinal paralysis of children, published in i860. Little ’ was 
well acquainted with them. In 1868, Benedikt,4 the neuro- 
logist, described them. The French schools soon took up 
the subject, and Cotard/’ Wuillaumier,0 Bourneville,7 wrote 
important papers on spasmodic infantile paralysis, some of CEREBRAL PALSIES OE EARL Y LIRE. 
3 
them referring to the anatomical features of these diseases. 
As recently as 1883, several English authors (among them 
Hadden8 and Ross9) published the clinical details of a small 
number of cases and the accounts of a few autopsies. 
Two publications have stirred up the recent discussion 
on this question. The first was Kundrat’s10 monograph on 
porencephalus, in which this one morbid state was care- 
fully studied. The second was Strumpell’s11 paper in 1884, 
in which he suggested that infantile cerebral hemiplegia 
was due to a polioencephalitis acuta. This single state- 
ment which was decidedly original, but had no post-mortem 
proof, has raised a great hue and cry which have not yet 
subsided. Whatever other good it may have accomplished, 
Striimpell’s theory has at least imbued an old subject with 
new life. His article was quickly followed by a number of 
valuable contributions, among which those of Ranke,12 Bern- 
hardt,’‘Wallenberg.14 Kast,15 Jendrassik and Marie,18 Gowers17 
and Hoven18 are by far the most important of the European 
contributions. In America, able articles have been written 
by Dr. Sarah McNutt,19 Drs. Sinkler,20 J. Lewis Smith,21 
Knapp,22 Lovett23 and Gibney.24 Chief and foremost of all 
is an exhaustive monograph by Prof. Osier,25 in wEich 151 
new cases were analyzed with a skill which characterizes 
all of Prof. Osier’s work. 
There would seem to be some need of an apology after 
this for the study of another series of cases. Our first 
reason for doing this is, that the work preparatory to this 
paper was begun several years ago, before the publication 
of Prof. Osier’s monograph. Secondly, we had some views 
of our own to advance ; and, lastly, the unusual number of 
cases at our disposal called for special elaboration. 
The cases here reported upon were, with very few ex- 
ceptions, examined by the authors of this paper. We 
are greatly indebted to Dr. Gibney and Dr, Townsend for 
referring the greater number of these cases to us from the 
Hospital for the Ruptured and Crippled. Dr. Gray was 
kind enough to allow us to use the notes on cases seen in 
his department. Ten of the cases were seen in private 
practice. 4 
B. SACHS AND F. PETERSON. 
The physician is no longer content, or at least should 
not be, to make the diagnosis of apoplexy; of hemiplegia, 
or of paraplegia, in the adult. It is his aim to determine 
whether the special form of paralysis be due to hemorrhage, 
thrombosis, embolism, tumor, abscess, or what not. In 
short, he studies the symptoms of each case with special 
reference to pathology of the disease. And so with infantile 
palsies: it is not enough to recognize spastic hemiplegia, 
diplegia or paraplegia, but the attempt should be made to 
determine the special morbid condition underlying each 
form. The large number of cases made it imperative upon 
us to make a distinct effort in this direction. 
In view of the small number of autopsies recorded in 
literature this effort may seem hazardous ; but a single 
autopsy in a well-observed case is a guide in the study of 
dozens of others ; and with the advances made in a knowl- 
edge of cerebral lesions, the neurologist is fortunate in 
being able to reason with a great degree of certainty from 
clinical symptoms to the morbid lesion which they indi- 
cate. 
A thorough knowledge of the clinical symptoms is, 
however, the starting point of this study. In order not to 
weary you with the details of these cases, we give you the 
conclusions to be drawn from our entire series with refer- 
ence to each point at issue. And we shall give but a few 
histories in extenso that you may recognize the chief types 
of which we treat. Before proceeding to these cases, we 
submit a table showing that of the 140 cases* there were 87 
males and 53 females; there were 105 hemiplegias, 24 
diplegias, and 11 paraplegias. 
TABLE I. — Showing the sex and form of paralysis in 140 cases of infantile 
cerebral palsy. 
Form of Paralysis. 
Males. 
Females. 
Total. 
Right Hemiplegia 
15 
52 | inr 
Left Hemiplegia 
27 
53 j10j 
Diplegia 
9 
24 
Paraplegia 
2 
11 
Total 
53 
140 
° Since the above was written we have seen at least fifteen additional cases, 
but we have concluded not to alter the tables in the body of this paper. CEREBRAL PALSIES IN EARLY LIFE. 
5 
HEMIPLEGIAS. 
Case I. (No, 48.) A. F., set. four and a half years, 
male, first child, difficult labor and instrumental delivery. 
From very first day right hemiplegia. Slight athetosis and 
associated movements. Contracture at elbow, formerly 
pes equino-varus, improved by operation. All reflexes of 
right side lively. Mental condition fair. 
Fig. 1.—Case IV., No. 138. Right hemiplegia with contracture and retarded 
growth of arm. 
Case II.—(No. 58.) L. B., female, aet. nine years. Con- 
genital left hemiplegia. Labor normal; fourteenth child ; 
movements of child ceased a few days before birth ; ex- 
pected to be still-born ; weighed four pounds at birth. 
From age of two years epileptic attacks every two to four 
weeks. Fine associated movements of both sides. Arm, 
leg, and face of left side involved. Very great retardation 
of growth of arm and leg ; some contractures of flexors of 
arm and wrist; imbecile; microcephalic, 6 
B. SACHS AND F. PETERSON. 
Case III.—(No. 44.) L. E., female, aet. eight years ; 
acquired hemiplegia ; onset at age of five years ; convul- 
sions for nine hours and coma ; could not move, talk or 
walk for three months. Face and leg have recovered con- 
siderably ; very great retardation of growth of arm. Marked 
associated movements. Contracture of right arm ; reflexes 
of right side exaggerated. 
Case IV.—(No. 138.) J. K., male, aet. seventeen years. 
Right hemiplegia at eight years of age following typho- 
malarial fever ; was delirious and unconscious during nine- 
teen days ; no convulsions. After recovering from coma, 
right arm, face, and leg were found paralyzed. Complete 
aphasia and entire loss of memory of everything occurring 
before typhoid. Had to be re-educated, Athetoid and 
associated movements. Reflexes exaggerated right side. 
Enormous contracture of flexors of right hand and fingers 
and great retardation of growth of right upper extremity. 
Right leg somewhat smaller than left; right talipes valgus ; 
asymmetry of face. Electrical reactions and sensation 
entirely normal. Has recovered speech fully and is bright, 
but several years behind others in education. Fig. /. 
DIPLEGIAS. 
Case V.—(No. 141.)* J. O., female, aet. sixteen. Con- 
genital diplegia ; mother kicked in abdomen by horse two 
months before birth of child and made unconscious thereby. 
Three other children, all healthy. Tedious labor, no instru- 
ments used, no fits or convulsions. Did not attempt to 
creep or walk ; teeth at usual age. Patient has menstru- 
ated since tenth year and was weak in back, arms and leg 
from earliest childhood. Extreme spastic contracture of 
adductors and flexors of thighs ; double talipes varus, equi- 
nus on right side. Left arm worse than right. Athetoid 
movements of left hand. Has frog walk. Intelligence 
good. Fig. II. 
Case VI.—(No. 31.) M. L., male, aet. three years, Con- 
genital diplegia. Asphyxiated during labor. Mother had 
pneumonia, and died five days post partum. Rigidity of 
arms, legs and back. Hands did not unclinch for two years. 
Frequent convulsive seizures alternately of right and left 
* This case, although under observation for a long time, was omitted from our 
list by mere accident. The history is sufficiently characteristic to deserve spec al 
mention. CEREBRAL PALSIES IN EARLY LIFE. 
7 
side, including face. Cannot talk, walk or stand. Feeble 
minded; cross-legged position and all reflexes exag- 
gerated. 
Fig. II.— Case V., No. 141. Diplegia; double talipes equinc-varus, athetosis 
of left hand. 
Case VII.—(No. 50.)* C. F., male, mt. one year. Con- 
genital paraplegia. First child, labor hard and dry for 
forty-eight hours. Asphyxiated. From first day up to age 
of six and a half months child had a rapid succession of 
tonic and clonic spasms affecting all the muscles of the 
body, causing rigidity of all extremities, opisthotones with 
extreme arching of back, enormous exaggeration of all 
reflexes, ankle and quadriceps clonus on slightest excita- 
PARAPLEGIA. 
* While this article was passing through the press, this child died. An autopsy 
was obtained by Dr. L. E. Holt. A carelul study of the pathological findings 
will be made and published in due time. But one other autopsy on infantile 
paraplegia has hitherto been published. 8 
B. SACHS AND F. PETERSON. 
tion. Convergent strabismus ; crying continually, Mental 
condition probably imbecile. Epileptic spasms controlled 
slightly by bromide treatment. Fig. III. 
Fig. III.—Case VII., No. 50. Paraplegia. Photographed in epileptiform 
convulsion. 
CHIEFLY MONOPLEGIA. 
Case VIII.—(No. 47.) H. K., male, set. twenty-two 
months. Acquired right hemiplegia ; onset at six months 
following convulsions during pertussis and pneumonia. 
Trace of weakness in right arm ; distinct spastic paralysis 
of right leg ; knee-jerk exaggerated ; feeble minded. This 
case made at first the impression of a monoplegia. 
Case IX.—(No. 61.) M., female, aet. two years at time 
of death. First-born of healthy parents. During the fifth 
month of pregnancy mother was thrown from a carriage 
without sustaining any serious injuries. The child born at 
full term apparently normal in all respects. At age of two 
to three months a general listlessness and nystagmus were 
observed. During its entire life child was unable volunta- 
rily to move any muscle of its body. All muscles extremely 
flaccid, but all reacted perfectly to electrical currents. There 
was not the first symptom of any mental awakening. Dur- 
ing the first year of its life child noticed light, but later on 
absolute blindness set in. There was a developmental 
defect of the optic nerves, which was reported upon by Dr. 
Knapp, a similar condition of the nerves having been 
observed in only two other cases. Hearing seemed to be 
acute. There was unusual hyperexcitability of auditory 
and tactile impressions The child never had convulsions, 
not even during dentition ; no rigidities. All reflexes lively. 
FLACCID PARALYSIS. CEREBRAL PALSIES IN EARLY LIFE. 
9 
Speech was, of course, entirely wanting. The child died 
of pneumonia following bronchitis. The autopsy will be 
referred to later on. This case was made the subject of a 
special paper by one of us26 (S.), and entitled “On Arrested 
Cerebral Development, with Special Reference to Cortical 
Pathology.” This paper was a study of some of the cor- 
tical changes giving rise to idiocy, but we have since come 
to learn that the report of the case and the autopsy have a 
wider significance than was attributed to them at the time. 
Case X.—(No. 80.) H. M., male, set. eleven and three- 
quarter years. The second of three children ; an uncle said 
to have been similarly affected. Asphyxiated at birth; 
instrumental delivery. Began to teethe late; teeth have 
rotted away. Made imperfect attempts to walk at fourteen 
months ; crept around on his buttocks ; both feet turned 
inward, right more than left; learned to talk, but mind has 
always been very feeble. Has had frequent epileptic attacks, 
grand and petit mal. Both upper extremities excessively 
weak, but no rigidities. Lower extremities poorly devel- 
oped. All muscles respond to faradic current, but some of 
them so feebly that very strong currents are needed. Knee- 
jerks weak but present; boy’s father is a teacher who has 
done much with his defective mind. 
From the records herewith presented to you, you will 
infer that much as the cases differ from one another, they 
also have much in common ; they yield a distinct composite 
portrait. The child is either born with, or in its early life 
develops some form of paralysis ; a hemiplegia, a diplegia, 
or a paraplegia. In the congenital cases there has been 
some disturbance during pregnancy,or labor has been tedi- 
ous and difficult or definite cause cannot be given. In the 
acquired cases we have seen that the onset of paralysis may 
occur after acute infectious diseases, during convulsions, or 
from causes that cannot be fathomed. In the majority of 
cases there is marked spasticity and extreme contractures ; 
in two cases there is a flaccid form of paralysis ; in the last 
case reported, the knee-jerks and other reflexes were weak ; 
in all other cases the reflexes were exaggerated, at least on 
the side or sides paralyzed, Some show peculiar associated 
athetoid or other post-hemiplegic movements ; in all, there 
was more or less retardation of growth, and all stages of 
mental impairment were found from weak-mindedness to  B. SACHS AND F. PETERSON. 
complete idiocy ; a few, however, are of good mental devel- 
opment. No changes in sensibility were observed, and the 
electrical reactions were never markedly altered. 
Fig. IV.—Right hemiplegia, from age of 9 months, in a woman 36 years. 
Contracture and retarded development of paralyzed side. 
These cases and some of the symptoms they exhibit are 
referred to by the poet, historian, and the painter. The 
Duchess of Gloucester, according to Sir Thomas Moore, 
had much ado in her travail. Her son, “Richard III., came 
into this world feet foremost. Shakespeare makes “Richard ” 
say of himself: 
“Deformed, unfinished, sent before my time 
Into this breathing world, scarce half made up, 
And that so lamely and unfashionable 
That dogs bark at me as I halt by them.” 
In Raphael’s Transfiguration, the demoniac boy has 
characteristic athetoid position of one hand. CEREBRAL PALSIES IN EARLY LIFE. 
11 
It is now in order to see whether our cases shed any 
new light on the understanding of these palsies, and what 
relation the facts hold to the commonly received classifica- 
tion into three distinct subdivisions. 
TABLE II.—Showing the age at onset. 
Age at Onset. 
Hemiplegia. 
Diplegia. 
Paraplegia. 
Total. 
Congenital 
22 
A) 
7 
49 
During 1 st year 
27 
1 
2 
30 
‘ 2d “ 
17 
1 
— 
18 
“ 3d “ 
2 
1 
19 
“ 4th “ 
4 
— 
— 
4 
“ 5th “ 
4 
— 
— 
4 
“ 6th “ 
2 
— 
— 
2 
“ 7th “ 
1 
— 
— 
1 
“ 8th “ 
5 
— 
— 
5 
“ 9th “ 
— 
— 
— 
— 
*• 10th “ 
— 
— 
— 
Under 15 years 
4 
— 
— 
4 
Unascertained 
3 
— 
1 
4 
Total 
105 
24 
11 
140 
From the above table we learn that of 105 cases of 
hemiplegia 22 are congenital; of 24 cases of diplegia 20 are 
congenital, and so are 7 or possibly 8 of the 11 cases of 
paraplegia. Diplegias and paraplegias are more likely to 
be of congenital origin, hemiplegias are more apt to be 
acquired in the first three or four years after birth ; but it is 
well worth noting that there are 22 congenital cases of 
hemiplegia (over 20 per cent, of all cases of hemiplegia); 
some of the cases noted as occurring in the first year may 
be congenital, and this would help to swell the percentage 
of congenital hemiplegias. It will not do, therefore, to 
make the broad distinction so frequently made on the basis 
of the acquired or congenital character of these palsies. 
Our table is in happy agreement with the one given by 
Osier as regards hemiplegias (15 of 120 were congenital). 
Sixty of our hemiplegic cases were developed before the 
close of the third year of life ; then there is a distinct fall- 
ing off up to the age of ten ; between ten and fifteen we 
have a few more ; in three cases the age could not be 
ascertained. Will you also note that some of the acquired 12 
B. SACHS A AD F. PETERSON. 
cases of paraplegia or diplegia have occurred after the age 
of three years, and one or the other of these cases may 
have been congenital. 
TABLE HI.- -Showing age at examination. 
Age. 
Hemiplegia. 
Diplegia. 
Paraplegia. 
Total. 
Under 4 years 
40 
16 
8 
64 
Between 4 and 10 years 
6 
2 
34 
“ 10 and 20 - 
11 
2 
1 
17 
“ 20 and 30 “ .... 
18 
— 
— 
18 
Under 40 years 
7 
— 
— 
7 
Total 
105 
24 
11 
140 
This table records the ages at examination, from which 
it is apparent that diplegia and paraplegia are compara- 
tively short-lived while hemiplegias often attain a very 
considerable age. Statistics of the exact ages at death 
would be more accurate; but inasmuch as our material 
includes cases from every kind of institution, even from 
pauper asylums, the inferences to be made are tolerably 
correct. 
TABLE IV. - Showing causes given in 91 cases of acquired cerebral palsy. 
Causes Given. 
Hemiplegia. 
Diplegia. 
Paraplegia. 
Total. 
Convulsions 
20 
1 
21 
Pneumonia 
6 
— 
6 
Trauma to Head 
G 
— 
6 
Pertussis 
4 
— 
4 
Measles 
2 
2 
4 
Scarlatina 
3 
3 
Onset with fever 
2 
— 
1 
3 
Hereditary Syphilis.... 
2 
— 
— 
2 
Cerebro-spinal Meningitis 
Onset with fever and convulsions 
2 
1 
— 
3 
only 
2 
— 
— 
2 
Frignt 
2 
— 
— 
2 
Hyprocephalus 
— 
— 
2 
2 
\accinia ' 
1 
— 
— 
1 
Typho-malarial Fever 
1 
— 
1 
Small-pox 
1 
— 
— 
1 
Tonsillitis 
1 
— 
1 
Epileptic Seizure 
1 
— 
— 
1 
Gastro-enteritis 
1 
— 
1 
Unascertained 
2G 
=— 
1 
27 
Total 
83 
4 
4 
91 CEREBRAL PALSIES IN EARL Y LIFE. 
TABLE Y.—Showing ascertainable causes in 49 cases of congenital cerebral 
palsy. 
13 
Causes. 
Hemiplegia. Diplegia. Paraplegia. 
Total. 
Instrumental delivery, tedious labor.. 
4 
1 1 
6 
Ante-partum trauma to mother 
2 
3 — 
5 
Premature birth 
1 
2 1 
4 
Asphyxia at birth ... 
— 
O 
3 
Asphyxia in twin birth 
— 
1 1 
2 
Tedious labor, breech presentation. . 
2 
— — 
2 
Primipara, dry birth, tedious labor . 
— 
— 1 
1 
7 mos. child, dry birth (48 hours) 
• 
1 — 
1 
Primipara (set. 45), tedious labor 
— 
1 
1 
Maternal fright (ante-partum) 
1 
— — 
1 
Uraemia of mother 
Pneumonia of mother (died 5 days post- 
1 
1 
partum), child asphyxiated 
Convulsions of mother during preg- 
— 
1 
1 
nancy, difficult la or . . . 
Mother in fever for 10 weeks, ante- 
— 
1 
1 
partum . .. 
1 
— — 
1 
Unascertained 
10 
6 3 
19 
Total... 
22 
20 7 
49 
In these tables we have analyzed, as far as possible, the 
causes in 91 acquired cases and 49 congenital cases of cere- 
bral palsies. 
Among the acquired hemiplegias the acute infectious 
diseases, including pertussis and pneumonia, play a very 
important role ; a strikingly large number have come on 
during convulsions ; in these cases the convulsions are not 
the initial convulsions of acute infectious diseases; the 
latter are considered separately in Table VI. The cases 
that have come on with fever and convulsions are noted in 
addition; but not wishing statistics to prove more than 
TABLE YI.—Showing the relation of convulsions to the onset of the palsies. 
Cases in which convulsions apparently preceded or were associated with 
the palsies occurring in — 
Pertussis 3 
Pneumonia 2 
Scarlatina 1 
Dentition 1 
Vaccinia 1 
Baptism 1 
Fright 1 
With beginning of menstruation 1 
Fall on head 1 
Gastro-enteritis 1 
Total ; : 13 
Apparently immediate symptom of a focal lesion—in 2 cases. 
Idiopathic and apparently only cause of palsy—in 20 cases. 
Palsy occurring in ordinary epileptic seizure—in 1 case. 14 
B. SACHS AND F PETTERSON. 
they should, it is but fair to add that in many of these cases 
fever may have been present, and that from among these 
20 cases we may allow that several, if not all, show the 
onset Strumpell claims for his cases of polioencephalitis. 
We ask you also to note that in 6 cases of hemiplegia there 
was a distinct history of traumatism, that 2 hemiplegias and 
i diplegia were the result of cerebro-spinal meningitis ; 2 
cases of diplegia came on after measles, a fact of some 
importance. In 26 cases of hemiplegia we were not satis- 
fied with the statements elicited, and have therefore marked 
them as “causes unascertained.” The table of causes in 
the congenital cases points a moral. In 16 cases of the 49, 
say in 33.3 per cent., there was some difficulty in labor, 
simple delay or instrumental delivery. The older writers, 
Little, Gaudard,27 and others refer to this cause, but have 
tolerably favorable statistics, Little mentioning but 4 cases ; 
Wallenberg gives 6 of 160 cases, and Osier 9 of 97 cases. 
The authors mentioned referred to hemiplegia only, and 
speak of forceps delivery as the element of danger. Our 
percentage is higher, because we include all forms of cere- 
bral paralysis, and tedious labor as well as instrumental 
delivery. The moral is, that the forceps should be applied, 
if necessary, or delivery hastened by other means if pro- 
tracted labor can be averted. A child’s brain and skull 
have a wonderful power of resistance, but do not credit 
them with greater virtue in this respect than they really 
possess. The mother’s life is by far the more important, 
but it is well to reflect that other things being equal she 
prefers a child that is neither paralyzed or idiotic. 
As regards the mode of onset, of the congenital cases, 
it would appear paradoxical to say anything ; but in several 
cases which were distinctly congenital, attention was first 
drawn to the disease by the appearance of convulsions at 
an early day. In these cases the convulsions are due to the 
same lesion or process which is responsible for the palsy. 
In the acquired cases convulsions preceded the onset of the 
other symptoms' in 36 of 83 cases of hemiplegia, and in one 
case of acquired diplegia ; loss of consciousness generally 
accompanies the convulsions ; in 6 cases there was a dis- CEREBRAL PALSIES IN EARL V LIFE. 
15 
tinct onset without loss of consciousness or convulsions ; 
this occurred in 4 cases of left hemiplegia and in 2 of right 
hemiplegia; 2 of these left hemiplegias were distinctly 
syphilitic. 
TABLE VII.—Analysis of six cases iD which there was onset without loss of 
consciousness or convulsions. 
Hemiplegia. 
Age. 
Cause. 
Right with aphasia 
Right 
Left 
Syphilis. 
Left. . : 
8 “ 
Unknown. 
Left 
“ 
Left 
m “ 
Fall on head. 
Striimpell has made the onset with convulsions and 
fever a distinctive feature of his cases. The 6 cases referred 
to in our list answer to his description of infantile cerebral 
palsy as regards the hemiplegic form of paralysis. It is 
more natural to infer that they are not cases of polio- 
encephalitis than that they are anomalous cases of that 
class. 
On this subject of initial convulsions and loss of con- 
sciousness a word should be added, even at the risk of 
anticipating some inferences regarding the pathology of 
these palsies. Initial convulsions and loss of consciousness 
are distinctly cortical symptoms. They indicate very con- 
siderable cortical disturbance either by direct injury or by 
severe or sudden injury to any part of the brain, which 
would also imply disturbance of the cortex as of every 
other part of the brain. Relatively small injuries to the 
cortex, hemorrhages or cortical encephalitis, will bring 
about loss of consciousness and convulsions; relatively 
large injuries to the interior need not exhibit these symp- 
toms. The exception is in cases of embolism or sudden 
hemorrhages in which the suddenness of the shock disturbs 
the entire brain. This argument was urged by one of us28 
(S.) in a paper published some years ago in which a typical 
case of capsular hemorrhage was diagnosticated mainly on 
the line of argument just referred to ; and in examining 
statistics of Wallenberg and others with reference to this 
point, we find that convulsions occurred only in cases of 16 
B SACHS A AD F. PETERSON. 
embolism anywhere, and in all cortical affections, however 
slight these may have proved to be. If all cases of infantile 
hemiplegia were cases of polioencephalitis corticalis, con- 
vulsions would invariably be present, but such is not the 
case. 
The form of paralysis has been frequently referred to. 
Hemiplegia, double hemiplegia or diplegia, and paraplegia 
speak for themselves. Table I. gives the relative number 
of cases of each form in our list. Monoplegias are n’ot 
included, although other writers had reported some such 
cases. We have seen but one case in which we were 
tempted to make a diagnosis of monoplegia, and this case 
gave distinct evidence on closer examination that the arm 
as well as the leg had been involved in the earlier course 
of the disease. The march of the disease resembles adult 
hemiplegia in this that the leg recovers very much more 
quickly than the arm for reasons that need not be given 
here. Under the heading of diplegia we have classed all 
cases in which both upper and lower halves of the body 
were involved ; in some of these one leg or one arm had so 
far recovered that the cases might have been interpreted as 
hemiplegia with an additional involvement of the other arm 
or leg ; but here again on closer scrutiny we became con- 
vinced that at one time all four extremities had been 
affected. 
The involvement of the face is a matter of some doubt. 
The majority of the cases were seen at a time long after the 
recovery of the face. We can vouch, however, for the fol- 
lowing statements. The face was affected in 11 cases of 
right hemiplegia, in 9 of left hemiplegia, and in 2 cases of 
diplegia. In 2 cases (1 of right and 1 of left hemiplegia) 
the leg was worse than the arm ; in all other hemiplegics 
the arm was the part more affected. In all diplegics the 
legs were more affected than the arms. Trunk and neck 
muscles were distinctly involved in two cases of diplegia. 
Strabismus occurred in one of right hemiplegia, in four of 
left hemiplegia, and in three cases of diplegia. 
It has been doubted whether aphasia followed the same 
laws in the infantile hemiplegia as in the adult form, and CEREBRAL PALSIES IN EARL V LIFE. 
Bernhardt13 has seen fit to write at length on this special 
subject. Aphasia can only be said to be present if the 
hemiplegia comes on in an individual who had already 
acquired articulate speech, hence the 49 cases of hemiplegia 
and the 21 of diplegia which occurred before the age of two 
years are excluded from this consideration and of the 
remaining 56 cases of hemiplegia the fewest dispensary 
patients or their parents could give satisfactory statements. 
We have records of 17 cases of hemiplegia with undoubted 
aphasia. Of these 17, 10 were cases of right hemiplegia 
and 7 cases of left hemiplegia. Eight of these 17 cases were 
observed by one of us (S.) in private practice. Of these 8, 
5 had been distinctly aphasic, and three of the 5 were cases 
of left hemiplegia. This relatively large proportion of 
aphasia in cases of left hemiplegia is rather striking by 
contrast with the adult cases. As we grow older we appear 
to become more and more left-brained. In earlier years 
both hemispheres are equally entrusted, soqt seems, with 
this highest faculty of speech. Bernhardt also comes to the 
conclusion that aphasia in children accompanies right as 
well as left hemiplegia. Prof. Osier notes aphasia in 13 out 
of 120 cases of hemiplegia and only one of these with left 
hemiplegia. Wallenberg’s statistics give 45 cases in 94 
right hemiplegics and 17 in 66 left hemiplegics, but he 
includes all sorts of speech disturbances, and the statistics 
cannot well be utilized with regard to true aphasia. Defec- 
tive speech was noted three times in our cases of right 
hemiplegia, twice in diplegia, and in most of our 80 cases 
of idiocy. 
The reflexes are either lively or exaggerated in the 
large majority of cases. The exceptions are noted in 
Table VIII. 
17 
TABLE VIII. — Showing tlie condition of the deep reflexes (knee-, elbow- and 
wrist-jerks) in 11 cases in which they were not exaggerated. 
Form. 
Normal. Diminished. Absent. 
Total. 
Hemiplegia 
4 1 3 
8 
Diplegia 
1 1 1 
3 
Total 
5 2 4 
11 
In all other cases the de 
ep reflexes were exaggerated. 18 
B. SACHS AND F PETERSON. 
The points to be noted are these: The exaggeration of 
reflexes occurs in the parts paralyzed or paretic. The great 
excitability of the reflex is often the best proof to be had 
of the former involvement of the leg or arm, although 
bilateral exaggeration 'of the reflexes in cases of unilateral 
paralysis must be taken into account ; owing to the extreme 
contractures of the opposing sets of muscles, the reflexes 
can frequently not be obtained. This is true particularly 
of the ankle clonus and triceps reflexes. We must note, 
however, that in several cases the knee-jerks and other 
reflexes were subnormal and in some cases absent. In 
one case (No. 50) the quadriceps clonus could be obtained. 
Disturbances of motion, such as choreiform, athetoid 
associated movements are observed with unusual frequency 
after hemiplegia, and as we have learned also after diple: 
gias in children. 
In 105 cases of hemiplegia, choreiform movements occurred in 6 
“ “ “ athetoid “ “ 21 
“ “ “ associated “ “ 15 
“ “ “ rhythmical “ “ 1 
“ •* “ ataxia “ 1 
“ “ “ tetanoid contractions “ 1 
In24 cases of diplegia, choreiform movements occurred in 1 
“ “ “ ataxia “ 1 
“ “ “ athetoid movements “ 1 
“ “ “ nystagmus “ 2 
These disturbances of motion after single and double 
hemiplegias have an unusual interest; they all point to 
some interference with the proper transmission of motor 
impulses either of the voluntary or of the inhibitory kind. 
The changes in the pyramidal tract are no doubt largely 
responsible for these peculiar movements, and that dis- 
turbances anywhere in the motor tract may bring about 
such aberrant movements is probable from the fact that 
these movements occur from the most diverse lesions, from 
lesions in the cortex as well as from lesions of the crus, as 
shown in an unpublished case of our own. Of associated 
movements we have seen a number of happy examples. In 
one instance the movements of the paretic arm and hand CEREBRAL PALSIES IN EARLY LIFE. 
19 
A and B—Movements of the normal hand. 
a and b—Movements of paretic hand. 
following the movement of the opposite side were so con- 
siderable that we were able to take tracings exemplifying 
this fact. Westphal28 has offered the theory that in health 
there is a tendency for both upper extremities to act con- 20 
B. SACHS A AD F. PETERSON. 
jointly, but that inhibitory impulses permit unilateral and 
single action. In disease this inhibition is removed, and 
therefore the effort to move one arm or hand results in the 
movement of both sides. The irradiation of impulses, there- 
fore, enters primarily into this question, but it seems to us 
to be open to doubt whether this irradiation occurs in the 
brain or in the spinal centres. In every case we must call 
in cortical inhibition to explain the separation of these 
irradiating nerve currents during normal life. Greidenberg has 
gone very fully into this special topic. (Arch. f. Psych, vol. 17). 
Rigidity with contracture is one of the cardinal features 
of all these palsies, and the deformity resulting therefrom, 
as a rule, leads the patients or their relatives to seek medi- 
cal advice. With the exception of the flaccid cases before 
noted, a very considerable number go on to marked con- 
tracture of one or several groups of muscles. Table IX. 
TABLE IX.—Showing the forms of contracture in the various cerebral palsies. 
Form of Contracture. 
Hemiplegia. 
Diplegia. Paraplegia. 
Total. 
Flexors of elbow 
29 
29 
“ “ both elbows 
— 
3 — 
3 
“ “ carpus and fingers 
23 
1 — 
24 
“ “ knee 
5 
5 
“ “ both knees 
— 
2 
2 
Ext nsors of knee 
1 
— — 
1 
Adductors of thighs (cross-legged 
position) :. 
13 
2 
15 
Talipes equino-varus 
17 
— — 
17 
Double talipes equino-varus 
— 
5 
2 
7 
Talipes equino-valgus 
3 
— — 
3 
Talipes equinus 
2 
— — 
2 
will give the main points, which need no further explana- 
tion except this, that attention should be drawn to the fact 
that cross-legged position of the legs occurs in diplegias 
and not exclusively in paraplegias, as is generally stated. 
Furthermore, that the contractures may be so extreme that 
the individual has a frog gait, as in the case of J. O., and 
that in three cases of hemiplegia there was distinct talipes 
equino-valgus, while in all other conditions there was 
either simple varus or equino-varus position. 
Why flexor and not extensor muscles are the seat of 
contracture, adductors and not abductors, is a puzzling 
question. It is probably due to the mechanical principles 
involved in the construction of joints. CEREBRAL PALSIES IN EARL V LIFE. 
A word in passing with regard to trophic disturbances. 
In many of these cases the circulation in the skin of the 
paralyzed limbs is as poor as in infantile spinal paralysis. 
There is often the same livid hue of the palsied limb. In 
all cases occurring early in life, and particularly in those of 
congenital origin, there is apt to be a very marked retarda- 
tion of growth. This was most distinct in nine cases of 
hemiplegia, three of diplegia, and three of paraplegia. 
Atrophy of the thenar eminence was observed in one case 
of diplegia, coming on after a cerebro-spinal meningitis. 
The association of epilepsy with infantile cerebral pal- 
sies is perhaps the gravest feature of these diseases. In 
our experience it is the one danger to be feared, and should 
be considered most carefully in any case of cerebral palsy 
in a child. In our list, 62 out 140 cases were afflicted with 
epilepsy, or 44.3 per cent, of all cases. There were among 
the hemiplegic cases 41 cases of general epilepsy, 9 of the 
Jacksonian type, and one case of petit mal (in all about 50 
per cent.). In 24 cases of diplegia 7 had general epilepsy 
(29 per cent.), one had Jacksonian epilepsy. In 11 cases of 
paraplegia 4 had general epilepsy (about|36 per cent.). 
The percentage of epilepsy in our own list differs but'slightly 
from that given by Gaudard, Wallenberg, and Osier. In 
view of the high percentages conceded on all sides, there 
can be but little doubt that taking all cases of ordinary 
epilepsy, a very fair proportion developed in connection with 
infantile palsies. Every sign of early palsy may have dis- 
appeared, while the epileptic taint remains. A case seen 
in private practice brings this out very forcibly : 
21 
E. B. (No. 81), girl seventeen years of age ; menstruated 
at age of eleven ; third of four children. All others died of 
acute infectious diseases. Father was fifty-six years of age 
at time of birth of child. Mother was thirty years younger. 
The child has had epileptic attacks every three to four 
months for some years. No convulsions during childhood. 
Had been treated for ordinary epilepsy by many physi- 
cians ; brominized for years. Closer inquiry revealed the 
fact that about four years ago the girl had an apoplectic 
attack, and on examination we found distinct evidence of 
left hemiplegia. Very marked weakness of left side ; greatly 22 
increased reflexes ; slight mental enfeeblement and marked 
anaemia. Bromides were discontinued, the patient put on 
tonics, and is doing well, at least as well as under bromides, 
which had evidently deepened the mental apathy. 
B. SACHS AND F. PETERSON. 
It will be seen that the percentage of epilepsy was 
greatest in hemiplegia, but that it was a distinctive feature 
of all forms of paralysis here considered. 
Taking into account the cortical o.igin of a large num- 
ber of these cases of epilepsy, it was natural to expect a 
higher percentage of Jacksonian epilepsies, but in most of 
these cases the original focal lesion has disappeared, and a 
general atrophy and sclerosis have been established. Gen- 
eral and not localized epilepsy is the natural result of this 
change. 
Together with the occurrence of epilepsy we should 
note the large number of cases exhibiting some form of 
mental enfeeblement. The conclusions on this point are 
presented in Tables X and XI, where we have attempted 
TABLE X. — Showing the relation of mental defect to the age of onset alsy. 
Age of Onset of Paralysis. 
Feeble- 
mindedness. Imbecility. Idiocy 
Total. 
Congenital 
6 15 14 
55 
Under 3 years 
10 18 6 
34 
3-5 years 
5-10 “ 
2 3 - 
5 
2 3 
5 
Over 10 years 
1 — 
1 
Total 
21 39 20 
80 
TABLE XI.—Showing, the relation of mental defect to the form of palsy. 
Form of Mental Defect. 
Hemiplegia. 
Diplegia. 
Paraplegia. 
Total. 
Feeble-mindedness 
16 
2 
3 
21 
Imbecility 
31 
7 
1 
39 
Idiocy 
7 
8 
5 
20 
Insanity (epileptic) 
1 
— 
— 
1 
Total 
55 
17 
9 
81 
to distinguish between feblee-mindedness and imbecility 
and idiocy. Eighty of 140 cases exhibited some form of 
mental impairment ; 69 were either in congenital cases or 
in those acquired in the first three years of life ; 52 per cent, 
of the hemiplegic patients, 71 per cent, of the diplegic, and 
about 82 per cent, of the paraplegics were thus afflicted. CEREBRAL PALSIES IN EARLY LIFE. 
23 
The worst form (idiocy) was most marked in the para- 
plegias (45 per cent.), and least marked in hemiplegia, 
being found in only 6.75 per cent, of all cases. Here again 
mental impairment can be said to be in proper relation to 
the extent of the cerebral lesion which is presumably less 
extensive in cases of hemiplegia than in the other forms of 
cerebral palsies; though we must allow that the later 
development of many of the hemiplegias may have some- 
thing to do with these results. 
As a point of special interest we wish to add that Little 
in 19 cases of paraplegias in which there was some impair- 
ment of mental condition found 13 feeble-minded or idiotic 
(68 per cent.) and 6 (32 per cent.) of good intelligence. 
TABLE XII.—Analysis of stigmata degenerationis (exclusive of contractures) 
present in 57 cases of cerebral palsy in children. 
Microcephalus 
Hemiplegia. 
21 
Diplegia. Paraplegia. 
4 2 
Total. 
27 
Leptocephalus ... 
19 
1 — 
20 
ivlacrocephalirs 
4 
— 1 
5 
Marked cranial asymmetry. 
25 
— 2 
27 
Marked facial asymmetry 
19 
— — 
19 
Cranium proganaeum 
“ Gothic ” palate 
. . 5 
2 — 
7 
9 
1 — 
10 
Imperfectly developed teeth.... 
10 
1 1 
12 
Supernumerary teeth 
1 
1 
Hirsuteness 
1 — 
1 
Neuropathic ear 
1 
1 
2 
Strabismus 
3 
8 
As for cranial defects,29 the table appended will give all 
the information we have, though it is well to note that in 
most cases of hemiplegia there is a flattening of the skull 
on the side of the lesion, and in almost all cases of cerebral 
palsy most of the cranial diameters are below the normal 
averages. 
In this review of clinical symptoms we have shown that 
excepting the fact of paralysis, there are no symptoms 
peculiar to infantile hemiplegia that are not also found in 
diplegia and paraplegia. While the symptoms vary some- 
what in degree in these different forms, all forms have all 
symptoms in common, excepting those of the onset. It is 
a difference of degree, not of kind. It remains for us to 
prove whether or not a study of pathological conditions 24 
compels us to draw a distinction between these three forms, 
and whether or not hemiplegia, diplegia, and paraplegia 
respectively represent distinct morbid entities. We shall 
see that a variety of morbid lesions is to be found under- 
lying these conditions, and that the same lesion or condi- 
tion may in the one case be responsible for a hemiplegia, 
in the other for a diplegia, and so on. And furthermore, if 
definite forms of disease are to be diagnosticated, the diag- 
nosis must rest upon other symptoms rather than the mere 
form of the paralysis. This branch of our inquiry is beset 
with great difficulties. In the scarcity of autopsies we have 
shared the fate of other writers. In spite of our very large 
clinical experience, we have but two autopsies of our own.* 
But we claim this one advantage that in both these cases 
the post-mortem findings were of very recent date—a 
great advantage, if we reflect that in most of the cases 
recorded in literature the conditions found were the final 
result of pathological processes which had continued for 
years, and which shed no light whatever upon the initial 
morbid lesion, and yet this is the salient point of the entire 
controversy. With the information gained by our macro- 
scopical and microscopical studies we have analyzed the 
records of 105 autopsies including our own. This list could 
have been enlarged if we had had access to the publications 
of Richardiere30 and some others. Our list, however, in- 
B. SACHS AND F. PETERSON. 
TABLE XIII.—Analysis of pathological findings in hemiplegia, diplegia and 
paraplegia, based upon the most recent autopsies, including Wallenberg’s 
and Osier’s cases, but not those of Richardiere or Audry. 
Lesions. 
Hemiplegia. 
Diplegia. Paraplegia. 
Atrophy, sclerosis and cysts 
40 
19 
Porenc phalus 
2 
4 
Hemorrhage 
23 
— — 
Embolism 
7 
Thrombosis 
5 
— — 
Agenesis 
1 
'1 
Tubercle 
1 
General cortical sclerosis 
— 
— 1 
Total 
79 
24 1 
Not including 64 cases of hemiplegia with porencephalus, and 32 cases of 
bilateral porencephalus collected by Audry. 
°A third autopsy has been added since the above was written (cf. note p. 301). CEREBRAL PALSIES IN EARL V LIFE. 
eludes all the recent 'Cases,* and the report of these will 
atone for the omission of those described by the older 
writers. 
The first and the most conspicuous feature of this table 
is the prominence given to atrophy, sclerosis, and cysts. 
All these are terminal conditions and are almost useless 
for the determination of the initial lesion. Cysts are no 
doubt frequently due to hemorrhages, and if this could be 
statistically shown, the number of cases due to hemorrhage 
would have been materially increased. Zacher has noted 
one case in which cystic formations occurred together with 
an osteoma, but the patient died thirty-three years after 
onset of lesion. Wallenberg has recorded an interesting 
case of cyst in the left peduncle. 
Porencephalus is a secondary condition, and although 
much has been written on this subject, we know little of its 
origin. In some cases it is probably the result of arrested 
development, due to interference with foetal circulation 
(Kundrat) ; in others it may have been the result of early 
encephalitis-or even intra-uterine cerebral hemorrhage. A 
number of different lesions may bring about a condition of 
porencephalus; moreover, the term has proved to be exceed- 
ingly elastic, and what one author has termed atrophy, 
another has called porencephalus. Audry,37 for instance, 
has collected 64 cases of this condition, some of which in 
the other lists are lab.eled atrophy or atrophy and sclerosis. 
We are forced, therefore, to rely upon cases in which the 
initial lesion has not disappeared ; and here the first fact 
that is brought out with great distinctness is that hemor- 
rhage, thrombosis, and embolism, the conditions which give 
rise to adult apoplexy, are also found to be a frequent cause 
of the cerebral palsies of early life. There is mention in 
the table of a case of tubercle reported by Seeligmiiller.38 
It is hardly fair to include such a case, for it was one of 
general tuberculosis in the course of which a hemiplegia 
appeared. While no other similar cases have been pub- 
lished, it is evidence of faulty logic that Seeligmiiller should 
* Two cases of Kast, one by Hoven, Wallenberg, Salgo,31 Langenbeck,32 
Furbnnger,34Zacher,35 Hirt,36 Peterson [cf. page 323 of this article], and Sachs.26 26 
B. SACHS AND F. PETERSON. 
have inferred from this one case that latent tuberculosis is 
almost the sole cause of infantile hemiplegia. His case 
simply shows that hemiplegia may appear together with 
other symptoms, but there can generally be little doubt as 
to the nature of the process. It is for this reason that we 
have excluded from our list a case of our own in which the 
autopsy revealed a tubercle of the quadrigeminal region 
which had given rise to a hemiplegia in the course of the 
disease. 
It may be surprising to find that polioencephalitis of 
Striimpell is not referred to. It is time that we should 
define our position with regard to this question. First of 
all, in order to distinguish this from two other lesions which 
have been termed polioencephalitis inferior (progressive 
bulbar paralysis) and polioencephalitis superior (nuclear 
ophthalmoplegia), let us speak of this as polioencephalitis 
corticalis. What proof have we that there is such a condi- 
tion ? Anatomical proof, none ; we are willing to concede, 
however, that some of the many cases of atrophy and 
sclerosis may have been due to this polioencephalitis, but 
it is unfortunate for StriimpeH’s theory that all of the au- 
topsies made soon after the onset of the disease have shown 
other conditions, and not a polioencephalitis. But let us 
be charitable or just, and say that even these autopsies were 
not made in cases sufficiently recent. We must add, how- 
ever, that cases which correspond very closely to the cases 
which Striimpell considered typical of polioencephalitis 
corticalis showed hemorrhage, embolism, etc., of recent 
origin. Striimpell says, however, that not all cases of 
infantile hemiplegia need be due to this cause, and that all 
authors have misinterpreted his views. Is there no proba- 
bility, then, that a few or any of the cases of infantile 
hemiplegia are cases of polioencephalitis corticalis? There 
is some circumstantial evidence showing that there is a 
brain-lesion which would seem to be analogous to spinal 
palsy of children (poliomyelitis anterior). MobiusS9 gives 
the history of two children of one family, aged one and one- 
half and three years respectively, who were stricken down 
with fever, loss of appetite, and somnolence. One developed CEREBRAL PA LSIES IN EA RL V LIRE. 
27 
a typical poliomyelitis of the upper extremity; the other, 
spasmodic hemiplegia without aphasia. This is striking 
clinical evidence, though some might claim it to have been 
merely a coincidence. Another proof: Striimpell has but 
very recently reported two cases of adult apoplexy in which 
every one would have made the diagnosis—and indeed he 
made it—of embolic softening, but the post-mortem exami- 
nation revealed a condition of encephalitis haemorrhagica 
of the gray as well as of the white matter. Marie,16 who is 
inclined to support Striimpell, expressed the opinion in 1885 
that the encephalitis would attack the white as well as the 
gray matter, and thinks that this would not destroy the 
analogy with poliomyelitis, for in that condition the white 
fibres are sometimes involved. Jendrassik and Marie favor 
the perivascular (inflammatory) origin of the condition of 
lobar sclerosis, which they have carefully described. In 
view of all this, we venture the opinion that polioenceph- 
alitis corticalis may be the cause of some of the cases of 
infantile palsies ; but, we add, not of the hemiplegia alone, 
for we have seen several cases, including one seen by the 
courtesy of Dr. Holt, in which all the symptoms were those 
of Striimpell’s disease, but there was a diplegic and not a 
hemiplegic form of palsy. In these cases the cerebral char- 
acter of the symptoms was so distinct that a confusion with 
poliomyelitis was out of the question. 
We insist that, until further pathological proof shall be 
forthcoming, polioencephalitis corticalis shall be diagnosti- 
cated last, not first. In a short paper, published some years 
ago in the Journal of Nervous and Mental Disease, 
one of us insisted that there was strong reason to think, by 
analogy with adult apoplexy, that the lesion might be the 
same in the infantile form. A short abstract of that history 
will show the analogy : 
M. M. (Case No. 75), boy, two and one-half years old ; 
one and one-half years previously pneumonia; tonsillitis 
with fever up to 102°. Four days after this, typical right 
hemiplegia and aphasia, positively without coma or convul- 
sions. The onset was as typical as in the ordinary mild 
hemorrhage into the internal capsule in the adult, and the 28 
B. SACHS AND F. PETERSON. 
progress of the disease and the mode of recovery (which be- 
came complete) were quite like what we see in adult cases. 
In 1887 the evidence on this point was not so strong as 
it is now, and this leads again to the subject of thrombosis, 
hemorrhage, and embolism. These vascular troubles were 
generally, considered to be peculiar to advanced age, with 
the exception of embolism, which every one is ready to 
concede may occur at any age in which heart-disease occurs. 
Thrombosis was thought frequent enough, from the occur- 
rence of syphilitic endarteritis in children. Hemorrhage 
in adults is attributed to the existence of miliary aneurisms. 
In the child, miliary aneurisms have been found, and Prof. 
Osier2r,li has described a large aneurism of the anterior cere- 
bral artery occurring in a boy six years of age. If ather- 
amotous degeneration of the arteries be less frequent than 
in adults, another condition is found to which Reckling- 
hausen refers in his book on the “ Pathology of Circulation 
and Nutrition,” page 84. This is a fatty degeneration in 
the wall of the cerebral blood-vessels. Little notice has 
been taken of this, as indeed of all else that pertains to the 
vascular pathology of children. 
Meningeal and cortical hemorrhages are shown to be 
more frequent in children, while all other cerebral hemor- 
rhages are more frequent in adults. This will explain the 
more serious character of the symptoms in the young, and 
the more frequent occurrence of epilepsy and mental impair- 
ment in children. As the prognosis would be materially 
affected according to the cortical or cerebral character of 
the lesion, we have sought for the point of differential 
diagnosis between lesions so situated. To this end the 
occurrence of convulsions is specially to be considered. In 
the paper referred to it was stated : “ Loss of consciousness 
is an extremely variable symptom; it seems to depend 
rather upon the quantity of blood effused than upon the 
area involved. Not so with convulsions. A convulsion, if 
it is anything, is a cortical affair, the result of cortical irri- 
tation.” To which should be added that the irritation may 
be direct or indirect; the sudden shock imparted to the CEREBRAL PALSIES IN EARLY LIFE. 
29 
cortex by the occurrence of embolism anywhere in the 
brain is apt to cause convulsions, and a lesion in any part 
of the gray matter of the central nervous system may excite 
convulsions; but hemorrhage over the cortex, even if 
slight, is apt to be accompanied by convulsions. Hemor- 
rhage into the interior of the brain, unless very large, and 
the condition of thrombosis—slow occlusion of a cerebral 
vessel—are more apt to be marked by absence of convul- 
sions and possibly also by preservation of consciousness. 
In other words, if you can exclude embolism and sudden 
and very large hemorrhage, and lesion of the lower gray 
centres, the absence of convulsions at the onset of an apo- 
plectic attack is in favor of a lesion in the interior of the 
brain rather than in or upon the cortex. Of this I am more 
certain still, that whatever may be the symptoms accom- 
panying the onset of an apoplectic attack, if the convulsions 
reappear after the initial symptoms, the lesion is cortical, 
or else an additional insult has occurred, A possible ex- 
ception might be made in favor of thalamus lesion. These 
statements are corroborated by the results of recent au- 
topsies, though only a small number of cases refer to all the 
facts needed. A case observed and examined post-mortem 
by one of us (P.) is in point : 
A. W., male, aged fifteen, bright at school, expert swim- 
mer, at age of eight or nine years was in the habit of diving 
a distance of twenty to thirty feet from a railroad-bridge. 
Shortly after this began to suffer from intense headaches, 
which gradually grew worse, until he was twelve years old, 
when mental changes began to be apparent. Gradually 
loss of memory, confusion of mind, and steady progress 
toward dementia. At the same time moroseness, melan- 
cholia, morbid fear, and coprolalia. One month after 
admission into the Poughkeepsie Asylum had a severe 
epileptic fit. Two days later right hemiplegia with constant 
right-sided hemi-epilepsy ; became comatose. The clonic 
spasms of the right side continued at intervals of several 
days, but gradually became limited to the right leg alone. 
Four days later, death. Autopsy showed the outer dural 
surface to be normal; on the right side the subdural space 
presented a limited pachymeningitis hmmorrhagica interna, 
but merely a thin organized detachable stratum of long 30 
B. SACHS AND F. PETERSON. 
Fig. VI.—Showing extent of pachymeningitis hmmorrhagica over superior 
surfaces of hemispheres. 
Fig. VII,—Showing extent of process on inferior surfaces of left hemisphere. CEREBRAL PALSIES IN EARL Y LIRE. 
31 
standing. Over the left side, however, the pachymeningitis 
was exceedingly widespread, extending over the whole 
surface of the hemisphere, both above and below, except 
in the anterior fossa of the skull. Over the convexity of 
the hemisphere the haematoma was very thick, consisting 
of strata of various ages, some of them undoubtedly dating 
from the beginning of his symptoms. Between two and 
three ounces of fresh coagula were spread on the convexity, 
especially in the Rolandic region. The extent of the pachy- 
meningitis and hemorrhage is shown in the accompanying 
illustration. The left hemisphere was greatly compressed ; 
the brain-substance itself seemed normal. The brain 
weighed ounces. The ventricles were widened and 
distended with clear serum. There was no disease of or 
injury to the cranial bones. There was no lesion of any 
kind in substance of hemispheres, ganglia,pons, or medulla. 
Figs. VI. and VII. 
Thrombosis occurs in a comparatively small number of 
cases. It is due either to the fatty change in the walls of 
the blood-vessels, or to syphilitic endarteritis, of which we 
have seen several cases, and Seibert40 has described one, 
and is probably found in marantic cases. Gowers lays par- 
ticular stress upon the thrombosis and occlusion of smaller 
cerebral veins, and thinks this the most important factor in 
the causation of infantile hemiplegia. All that we can say 
is that he must prove this to be true ; the autopsies analyzed 
give no evidence whatever of this condition. 
Thus far we have had reference chiefly to the pathologi- 
cal lesions of infantile hemiplegia. In diplegia nothing is 
said in our table of hemorrhage, thrombosis, and embolism, 
though it is more than likely that some of the cysts referred 
to were originally due to clots, and the occurrence of menin- 
geal hemorrhages over both hemispheres giving rise to 
diplegias is well known. But these cases either die early 
before the form of paralysis is well established, or if they 
live for many years the initial hemorrhage has disappeared 
and the secondary conditions only remain. You will please 
observe, however, that what is properly termed agenesis 
corticalis occurs in a case of hemiplegia reported by Kast, 
and in the case of diplegia reported by one of us (S.) The 32 
B. SACHS AND F. PETERSON. 
microscopical changes appear to have been very similar in 
both cases—in the one case unilateral, in the other bilateral, 
which accounts for the hemiplegia in the one case, for 
diplegia in the other.* 
Fig. VIII.—Outer aspect of surface of left hemisphere, showing exposure of 
the island of Reil. (X) Region from which first block of tissue had been le- 
moved. (Cf. this journal, vol. x-14). 
In the cases of Kast and Sachs there was no evidence of 
the agenesis having been due to early intra-uterine inflam- 
mation ; in both cases there was a mere arrest of develop- 
ment and nothing more. The changes found in the case 
reported by one of us were limited to the large cells, in the 
cortex of which there was not a normal specimen to be 
found throughout the entire brain. There was no evidence 
of perivascular inflammation and only very slight thicken- 
ing of neuroglia-tissue, with considerable retardation of 
development of the white fibres entering the gray matter of 
the cortex. The changes in the cells and the atrophies of 
the surface will be seen on inspection of the two accom- 
panying figures. Figs. VIII and IX. 
* A similar condition has been found by Jensen41 in a case of idiocy. CEREBRAL FALSIES IN EARLY LIFE. 
33 
The pathology of paraplegia has not been determined. 
We have but one case with autopsy, that of Foerster,42 in 
which case Birch-Hirschfeld found a general cortical scle- 
rosis with probable descending degeneration.* Ross was 
induced to state, only a few years ago, that he thought the 
Fig. IX.—Section of first temporal convolution. Distortion of pyramidal cells. 
Smaller cells and neuroglia cells distinctly nucleated. 
X 500 diameters. 
changes of the spinal lateral columns due to traction at 
birth might be responsible for spastic paraplegia. This is a 
bare possibility; but the occurrence of idiocy and mental 
enfeeblement in 9 out of 11 cases of our own and in most of 
the reported cases, and the frequent occurrence of convul- 
sions, make a cerebral origin much more probable. 
The question arises whether it is possible to determine 
the morbid lesion in any given case, and we submit the 
* See note page 301. 34 
B. SACHS AND F. PETERSON. 
following as the result of our clinical and pathological 
studies : 
The form of paralysis is not the most important factor in 
diagnosis. 
Acquired cases of hemiplegia and diplegia, but particu- 
larly the former, are apt to be due to the same causes that 
prevail in adult apoplexies ; namely, hemorrhage, throm- 
bosis, or embolism. Meningeal and cortical lesions are 
more frequent. Absence of convulsions at onset probably 
points to an intra-cerebral lesion. Occurrence of convul- 
sions at onset points generally to cortical lesions or to 
embolism anywhere in the brain. In a few cases affections 
of gray matter lower down in the central nervous system 
may also be attended by convulsions. 
Frequently repeated convulsions after onset point with 
great certainty to cortical lesion. 
Cases coming on after acute infectious diseases have been 
proved to be due to vascular derangement, particularly to 
hemorrhage and embolism, but some cases may be due to a 
polioencephalitis corticalis ; the onset with very high fever 
and convulsions makes the latter more probable. 
Traumatism is an important factor in the causation of 
meningeal hemorrhage during early life and particularly 
during the act of labor. 
Congenital cases of diplegia and hemiplegia may be due 
to early meningeal hemorrhage and possibly to an early 
encephalitis. 
In acquired and congenital cases of hemiplegia and 
diplegia we may have either a condition of porencephalus 
or simple arrest of development. If acquired, there would 
seem to be the history of slow development of the symp- 
toms without predisposing cause. If congenital, there may 
be a history of traumatism to mother. 
In later life hemiplegia or diplegia associated with large 
amount of mental impairment and with contractures point 
to general atrophy, sclerosis, with secondary degenerations, 
or to a condition of porencephalus, the origin of which it is 
often difficult to determine. CEREBRAL PALSIES IN EARLY LIRE. 
35 
In conclusion, a word regarding treatment. So far as 
prophylactic measures are concerned,, we wish to repeat our 
warning to the obstetrician : Hasten protracted labor, for 
the skillful use of forceps and careful manipulation are less 
apt to do injury than the prolonged compression of skull 
and brain in the pelvic canal. In the acute cases the same 
principles which obtain in the treatment of adult cases 
should be applied. 
Medical advice is generally sought for the relief of the 
secondary conditions—epilepsy, idiocy, and contractures. 
In the treatment of the epilepsy the usual remedies may be 
employed : above all, the bromides and chloral. But these 
should be administered with the utmost discretion, for in 
many cases the epileptic attacks are so infrequent that they 
do far less harm to the patient than the drugs, which in- 
crease mental stupor and are very apt to cause anaemia and 
malnutrition. The proper use of electricity and massage in 
the early stages will prevent to some extent the formation 
of extreme contractures. If such contractures exist,we place 
our reliance upon the orthopedic surgeon, who finds in these 
cases a very wide field for the exercise of his surgical and 
mechanical skill. In cases in which the hand is so deformed 
as to be of less use than an artificial hand would be, ampu- 
tation would be justified, provided there were no marked 
rigidity at the elbow. This has been thought of in the case 
of J. K., whose portrait has been shown. In one case, in 
this city, with extreme athetosis, the arm was amputated 
and the patient rendered more comfortable. This should 
be done only in the severest forms. 
The question of surgical interference in cases of hemi- 
epilepsy deserves passing notice. In very recent cases, in 
which there is no prospect of spontaneous recovery and in 
which the character and site of the lesion can be accurately 
inferred, the idea of operation might be entertained, but it 
is wholly inadvisable in cases of long standing in which 
secondary conditions have been permanently established. 
The result in two cases of Bullard43 and Mitchell44 has not 
been encouraging. 
Trepannation for the relief of severe headaches and local 
epilepsy may be attempted. 36 
B. SACHS AND F. PETERSON. 
As for the condition of mental enfeeblement, much can 
be done by careful manual and mental training. This 
should be begun at an early day, and the results will be as 
satisfactory as in Bourneville’s department of the Bicetre, 
where the improvement is evident from the change in the 
facial expression of patients on admission and after they 
have been under treatment and instruction for some time. 
In only two cases that we have seen of infantile palsies 
can we conscientiously state that there has been complete 
recovery. 
REFERENCES. 
1 E. Henoch.—Cf. also Lectures on Children’s Diseases. London, 1889. 
New Sydenham Soc. Publication. 
2 J. von Heine.—Spinale Kinderlahmung. Stuttgart, 1860. 
3 Little. —Obstet, Soc. Trans. 1862, vol. iii. 
4 M. Benedikt.—Electrotlierapie. Vienna, 1868. 
5 Cotard.—Etude sur l’atrophie partielle du cerveau. Pans, 1868. 
6 Wuillaumier.—De l’epilepsie dans l’hemiplegie spasmodique infantile. 
These de Paris, 1882. 
7 Bourneville.—Recherches cliniques et therapeutiques sur l’epilepsie, 
l’hysterie et l’idiotie. Paris, 1882. 
8 Hadden.—Brain, vol. vi., 1883-1884, p. 302; also St, Barth. IIosp. Rep., 
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p. 465. 
10 Kundrat.—Die Porencephalie. Vienna, 1882. 
11 Striimpell.—Jahrb. fur Kinderheilk. N. F., 1881, vol. xxii. Of. also 
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1887. 
Ueber primare acute Encephalitis. Deutsche med. Wochenschr., 
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1886. 
13 Bernhardt—Virchow’s Arch., vol. cii., 1885. 
Jahrb. fiir Kinderheilk., 1886, p. 384. 
14 Wallenberg.—Jahrb. fiir Kinderheilk., 1886. 
Arch, fiir Psych., vol. xix., p 297, 1888. 
15 Kast.—Arch, fiir Psych., vol. xviii., 1887 p. 437. 
16 Jendrassik and Marie.—Arch, de Physiologie, vol. i., 1885; also Paul 
Marie, in Progres medicale, No. 36, 1885, p. 167. 
17 Gowers.—Dis. of Nerv. Syst., Am. ed., p. 801, 1888. Cf. also Lancet, 
1888, vol. i. 
Medico Chirurg. Trans., vol. lix., 1876, p. 271. 
18 Hoven.—Arch, fiir Psych., vol. xix., p. 563, 1888. 
19 Sarah McNutt.—Am. Journ. Med. Sciences, Jan., 1885, vol. i. 
Am. Journ. Obstet, 1885. 
Arch, for Pediatrics, Jan , 1885. 
20 W. Sinkler.—Med. News. Phil., 1885, vol. i. 
21 J. L. L. Smith.—Journ. Am. Med. Assn., Feb. 25, 1888. 
22 P. C. Knapp.—Journ. Nerv. and Ment. Dis., 1887, vol. 480. 
Bost. Med. and Surg. Journ., Nov. 22, 1888. 
23 Lovett.—Bost. Med. and Surg. Journ., June 28, 1888. CEREBRAL PALSIES IN EARL Y LIFE. 
37 
24 Gibney.—N. Y. Med. Bee., vol. xxx., p. 393. 
25 Osier.—(a) The Cerebral Palsies of Children. Monograph. Phil., 1889. 
\b) Also Phil. Med. News, July 14 to Aug. 11, 1888. 
(c) Am. Journ. Med. Sciences, 1885. 
(d) Can. Med. and Surg. Journ., 1886. 
(e) Alienist and Neurologist, 1889, p. 16, on Idiocy and Hemi- 
, plegia. 
26 Sachs.—Joum. Nerv. and Mental Dis., Sept, and Oct., 1887. 
Intracerebral Hemorrhage in the Young. Journ. Nerv. and Ment. Dis., 
Aug., 1887. 
27 Gaudard.—Contrib. a l’etude d’hemiplegie cerebrale infantile. Geneva, 
1884. 
28 Westphal. — Arch, fiir Psych., vol. iv., 1873, p. 747. 
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fantile Cerebral Hemiplegia. N. Y.»Med. Journ., April 6, 1889. 
30 Bichardiere.—Etude sur les sclerose encephaliques de 1’enfance. These 
de Paris, 1885. 
31 Salgo.—Centralbl. fiir Nervenheilk., June 15, 1889. 
32 Langenbeck.—Quoted by Banke in Jahrb. fiir Kinderheilk., 1886, 
p. 316. 
34 Fiirbringer.—Deutsche med. Wochenschr., 1889, xv., 67. 
Berl. klin. Wochenschr., p. 16, 1889. 
35 Zacher.—Arch, fiir Psych., 1889, vo'. xxi., p. 38. 
36 Hirt.—Path. und Ther. der Nervenkrankheiten, p. 223. Vienna, 1890. 
37 Audry.—Bevue de Medecine, June and July, 1888. Summary of Au- 
topsies in 103 Cases of Porencephalus. 
v 38 Seeligmiiller.—Jahrb. fiir Kinderheilk., 1879, vol. xiii. 
39 Mobius.—Schmidt’s Jahrb., 1884, vol. cciv., p. 135. 
40 Seibert.—Jahrb. fiir Kinderheilk., No. 22, 1885. 
41 Jensen.—Arch, fiir Psych., vol. xiv., p. 752. 
42 Forster.—Jahrb. fiir Kinderheilk., vol. xv. 
43 Bullard.—Bost. Med. and Surg Journ., Feb. 16, 1888. 
44 Mitchell.—Beferred to by Osier. Monograph, p. 102. 
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Ashby and Wright.—Diseases of Children. London, 1889. 
J. W. Buneberg.—Fall af sa kallad hemiplegia spastica infantilis. Finska 
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Schultze.—Deutsche med. Woclienschr., 1889, p. 287. 
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vol. xiii. 
E. D. Fisher.—Epilepsy and Hemiplegia of Children. Joum. of Nerv. 
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S. Gee.—On Hereditary Infantile Spastic Paraplegia. St. Barth. Hosp. 
Bep., vol. xxv., 1889, p. 81. 38 
B. SACHS AND F. PETERSON. 
A. J. Richardson.—Lancet, Nov. 10, 1888. 
H. Fritsche.—Jahrb. fur Kinderheilk., May 10, 1889. 
A. B. Marfan.—Arch, fur Kinderheilk., 1889, vol. x., p. 384. 
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A. Pilliet.—Contrib. a l’etude des lesions histologiques de la substance 
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A. Weichselbaum.,—Porencephalie und mangelhafte Entwick. der recht. 
ober. Extremitat. Ber. der K. K. Krankenanst. Rudolphstift. Vienna, 
1888, 385. 
Edwards.—Liverpool Med.-Ohir. Journ., July, 1888. 
E. Powell.—Brit. Med. Journal, June 30, 1888. 
E. M. Sympson.—Cong, and Infant. Spastic Palsy. Practitioner, 1889, 
p. 114; also Feb.. 1888. 
G. Anton. —Ein Fall von Mikrocephalie mit schweren Bewegungsstorungen. 
Wien. klin. Wochenschr., 1889 ii. 
Ter Grigoriautz.—Hemiplegic chez les enfants (103 pages). Paris, 1888. 
D. Burgess.—Manchester Med. Chron., 1888-’89, ix., p. 471. 
C. J. Nixon.—Trans. Roy. Acad. Med. Ireland, 1888, vol. vi., p. 21. 
Aime M. Gibotteau.—Notes sur le developpement des fonctions cerebrales 
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Max Wolters. — Angeb. spast. Gliederstarre. etc Bonn, 1888. 
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