Contributions to the Pathology 
of Infantile Cerebral 
Palsies. 
\ BY 
13. SACHS, M.D., 
Professor of Nervous Diseases in the 
New York Polyclinic. 
REPRINTED PROM 
€TJ)t Neb) ¥orfe ffiebfcal Journal 
for May 2, 1891. Reprinted from the New York Medical Journal 
for May 2, 1891. 
CONTRIBUTIONS TO THE PATHOLOGY OF 
INFANTILE CEREBRAL PALSIES* 
By B. SACHS, M. D., 
professor of mental and nervohiTBiseases IN THE NEW YORK POLYCLINIC. 
About a year ago I had the privilege of reading before 
the Academy of Medicine a paper prepared in conjunction 
with Dr. Peterson, and entitled A Study of Cerebral Palsies 
of Early Life, based upon an Analysis of 140 Cases. If an 
apology is needed for reverting to the same subject, I offer 
simply this: that in the former paper we discussed at some 
length the clinical features of these palsies, and in this arti- 
cle I wish to treat of some of the pathological lesions to be 
found in these early infantile affections. 
It has been my good fortune during the past year to 
see at least sixty-five additional cases, bringing the total 
number up to two hundred and five. For this unusual op- 
portunity of studying so many examples of diseases hith- 
erto but poorly understood, I am specially indebted to Dr. 
Gibney and Dr. Townsend, by whose courtesy the vast 
* Read before the New York Neurological Society, April fJ, 1891. 
For illustrations, see Plates I, II, and III. 
Copyright, 1891, by D. Appleton and Company, 2 
CONTRIBUTIONS TO THE PATHOLOGY OF 
material of the Hospital for the Ruptured and Crippled 
has been in part directed to my department at the Poly- 
clinic. 
The forms of disease here to be discussed are, after all, 
somewhat rare, and although peculiar circumstances have 
enabled me to see more of these cerebral palsies than of 
anterior poliomyelitis during the past few years, I still be- 
lieve that the spinal affection is the more frequent; but the 
large number of cerebral palsies I have seen will give some 
idea of the relative frequency of these troubles. 
In private practice I have seen as many cases of cerebral 
as of spinal infantile palsies; this, too, may be either acci- 
dental or easily accounted for; but I feel certain that the 
number of these cases seen by others will increase very con- 
siderably as soon as the leading symptoms of these affec- 
tions are generally recognized. Many of the cases are seen 
twenty and more years after the onset of the disease ; in 
some, an epilepsy, with very slight hemiparesis; in others, 
hemiparesis, slight contractures, posthemiplegic movements, 
and exaggeration of the reflexes are the only symptoms that 
point to a cerebral affection of old standing. I have seen 
at least six cases of epilepsy which have passed through able 
hands and have been pronounced cases of typical epilepsy, 
but which on closer examination have been found to be in- 
stances of epilepsy associated with early spastic cerebral 
palsy, both conditions being due to one and the same 
lesion. 
Large orthopaedic institutions, pauper asylums, and 
homes for idiots are full of these patients. In an able sta- 
tistical paper on club-foot, published in the Transactions of 
the Medical Society of the State of New York for 1890, Dr. 
Townsend collected seven hundred and twenty cases due to 
spinal lesion, and seventy-seven spastic cases (say one to ten), 
mostly due to cerebral lesions; but Dr. Townsend has been INFANTILE CEREBRAL PALSIES. 
kind enough td tabulate for me the cases seen at the Hos- 
pital for the Ruptured and Crippled during the last year, 
and, with the full knowledge of the subject now at his com- 
mand, he finds the relative frequency of cerebral cases far 
greater than any one would have expected it to he. 
The records of the hospital show for the past year one 
hundred and forty-two spinal cases, with deformities of all 
sorts, and ninety-one of cerebral origin. Doubtful cases 
were omitted from the list. These figures, which are larger 
than any other institution could show, prove that, of the 
cases seen during one year, 61 per cent, were of spinal ori- 
gin and 39 per cent, of cerebral; the proportion is not three 
to one. Dr. Townsend, in a letter to me, expresses his great 
surprise. I should not be surprised if the proportion should 
be found to be still greater in favor of cerebral palsies. 
The clinical features of these cerebral palsies were so 
fully given in the paper* alluded to that I have to-day but 
to add that the symptomatology as established by the 
former studies has been fully borne out by an analysis of 
cases seen since the publication of that paper. 
Let me simply remind you of a few of the points which 
we sought specially to fix upon. First, that the mere form 
of the palsy, while pointing to a different location and a 
varying extent of the lesions in question, should not con- 
stitute a sufficient reason for the creation of special types, 
and that a hemiplegia, a diplegia, or a paraplegia may be 
due to the same morbid processes. Secondly, that although 
the majority of the cases are of the distinctly spastic type, 
flaccid paralyses do sometimes occur which are unquestion- 
ably of cerebral origin ; and, again, that there are a few 
atrophic palsies due to lesions in the brain and not to lesions 
in the spinal cord or the peripheral nerves. These features, 
taken in conjunction with the occurrence of dementia or 
* Jour, of Nerv. and Ment. Dis., 1890. 4 
CONTRIBUTIONS TO THE PATHOLOGY OF 
epilepsy and with the typical contractures and exaggerated 
reflexes, make the diagnosis a very positive one, and I can 
safely say that of the two hundred and five cases we have 
seen, doubt as to the spinal or cerebral origin was enter- 
tained in but a single instance.* 
Accepting these clinical features, we are ready to pass 
on to a consideration of the pathological lesions underlying 
them. The most important conclusion of former studies on 
this point was that the largest majority of these cerebral 
palsies of childhood w7ere due to haemorrhage, thrombosis, 
and embolism. This has been borne out, not only by the 
publications of others, but by my own recent studies. I have 
found a confirmation of my views in post-mortem examina- 
tions, and, much to my gratification, in a recent operative 
case with Dr. Wyeth, in which the diagnosis of epilepsy 
and hemiparesis due to meningeal haemorrhage thirty years 
ago was corroborated as soon as the motor arm center in 
the right hemisphere was exposed. 
Not wishing to weary you with the details of these 
pathological studies, I have prepared a table in which I 
make the attempt to give the morbid lesions and the symp- 
toms which most frequently accompany them. Like every 
such attempt, this one will be imperfect; but I trust that 
additions and corrections to be made hereafter, by others 
if not by myself, will make good whatever defects there 
may be in the classification submitted to you. In this table 
I have divided the cases into those of truly congenital ori- 
gin, those occurring during birth, and those that may be 
properly called acute or acquired cerebral palsies. 
* Since the foregoing was written, I have seen one case, and the 
only one, in which there was evidence of a spinal and a cerebral lesion. INFANTILE CEREBRAL PALSIES. 
5 
Morbid lesion. 
Form of 
palsy.* 
Distinguishing symptoms 
and conditions. 
Large cerebral de- 
Diplegia, 
Birth normal, possibly 
fects. 
hemiplegia, 
premature; convulsions 
paraplegia. 
often absent; mental 
condition sometimes 
Prenatal. 
Agenesis corticalis 
Diplegia, 
good, often deficient. 
Birth normal; paralysis 
and minor lesions. 
hemiplegia, 
may be flaccid; great 
(Highest nerve ele- 
paraplegia. 
mental defect; convul- 
ments involved.) 
sions present or absent. 
Meningeal hsemor- 
Hemiplegia, 
Protracted labor, chiefly in 
rhage, rarely intra- 
diplegia, 
primiparte; instrumental 
cere bral ha.1 mo rrh age 
paraplegia. 
delivery; asphyxia at 
Birth 
(later conditions: 
birth. Convulsions soon 
Palsies. 
meningo - encephali- 
after birth and oft-re- 
tis chronica, sclero- 
peated; .early develop- 
sis, and cysts). 
ment of contractures. 
Idiocy frequent. 
[hemorrhage (menin- 
Hemiplegia, 
Sudden onset, generally 
with convulsions ; re- 
peated convulsions; slight 
geal and rarely intra- 
diplegia, 
cerebral), thrombo- 
paraplegia. 
sis (sometimes due 
or no fever; recovery of 
to syphilitic endar- 
leg or arm very frequent; 
teritis). Embolism. 
post - hemiplegic move- 
Later conditions : 
ments. Mental develop- 
atrophy, cysts, scle- 
ment rarely interfered 
rosis, and softening. 
with; after or during 
acute infectious diseases. 
Meningitis chronica. 
Hemiplegia, 
History of onset after at- 
Acute 
diplegia ? 
tack of meningitis. Bas- 
(acquired) 
ilar symptoms with spas- 
Palsies. 
tic paralysis ; basilar 
symptoms sometimes 
wanting. 
Hydrocephalus (rare 
Paraplegia, 
Increasing size of head; 
as sole cause of 
diplegia, 
onset of paralysis grad- 
palsy). 
hemiplegia. 
ual; progressive deteri- 
oration of mind; exclu- 
sion of other lesions. 
Primary encephalitis ? 
Hemiplegia, 
Onset with fever and con- 
(Striimpell.) 
diplegia. 
vulsions, independently 
of or after acute infec- 
tious diseases. 
* The form of palsy is given in the probable order of frequency, 6 
CONTRIBUTIONS TO THE PATHOLOGY OF 
I feel compelled to explain a few points. First, that 
haemorrhage, thrombosis, and embolism were positively 
proved to be the most frequent lesions in the acute cere- 
bral cases; that other conditions so often cited were ter- 
minal and not initial morbid states. It may be surprising, 
too, to many, that primary encephalitis is put at the very 
end of the table, and with a question-mark at that. Strum- 
pell’s now famous theory has taken a wonderful hold upon 
tbe medical mind, and yet I must repeat what I said last 
year—that there is remarkably little proof of the existence 
of this condition. The reasons for this statement must be 
given before proceeding to a discussion of the true morbid 
lesions. Reasoning by analogy, Striimpell concluded that a 
certain number of casesof acute infantile cerebral palsies were 
similar in every respect to cases of poliomyelitis anterior, 
except that the symptoms pointed distinctly to a cerebral 
and not a spinal trouble. It was natural, therefore, for kirn 
to maintain that the gray matter of the cortex was subject 
to the same changes that affect the gray matter of the spinal 
cord ; hence, if we know of a condition of poliomyelitis an- 
terior, why should there not be a condition of polio-enceph- 
alitis? There is no inherent reason why not; but proof is 
wanting. Striimpell himself has abandoned the idea of a 
polio-encephalitis, and now speaks of primary encephalitis; 
but even this theory must be accepted with some reserve. 
The more fascinating the idea, the more carefully we should 
examine into it. The only proof we have of the probable 
existence of this disease in children is given by two well- 
observed cases of Mobius,* in which one child was affected 
by a poliomyelitis and another child in the same family at 
the same time developed typical acute cerebral palsy (spas- 
tic hemiplegia without aphasia). Furthermore, Striimpell f 
* Schmidt’s Jahrbucher, 1884, cciv, p. 135. 
j- Dtsch. Arch. f. Min. Med., xlvii. INFANTILE CEREBRAL PALSIES. 
has reported within the hast year two cases of adult apo- 
plexy in which he was surprised to find a widespread en- 
cephalitis and not haemorrhage or embolic softening, as 
every one would have been apt to believe. 
I can not allow that the occurrence of such a condition 
in the adult is sufficient proof of its occurrence in the 
young; but even granting the analogy, all that we can infer 
is that among the many thousands of cases of adult apo- 
plexy a very small number may be due to an encephalitis, 
and it is possible that an equally small or smaller number 
of these infantile cases may be due to the same condition ; 
but all the evidence we have is entirely against the assump- 
tion that a primary encephalitis is the rule in the acute 
brain palsies of children. I uphold what I said a year ago— 
that polio-encephalitis should be diagnosticated last, not first, 
and I can not understand why this encephalitis should always 
take the form of a hemiplegia, as Strumpell would have it. 
I have seen at least two cases in which, if in any, the symp- 
toms of onset corresponded accurately to the description 
given by Strumpell, but the form of paralysis was a diplegia 
and not a hemiplegia. However much one may be inclined 
to give this theory its due weight, it has undoubtedly been 
a hindrance to the understanding of the pathology of the 
diseases in question. We might as well allege cysticercus 
to be the most frequent form of brain tumor in children as 
to maintain that a primary encephalitis is the most frequent 
cause of spastic palsy in children, and to raise these rare 
and doubtful cases to the dignity of the cerebral palsy is an 
absurdity. 
From the tables which I have submitted it is evident 
that there are many morbid states giving rise to the same 
symptoms. Of the three autopsies which I have had, each 
one represented a condition entirely different from the other 
two. Two of these three autopsies I wish to explain to- 8 
CONTRIBUTIONS TO TIIE PATHOLOGY OF 
night.* The first case is not only interesting as a con- 
tribution to the pathology of this special subject, but 
would be able to stand on its own merits if reported, for 
the tumor developed in the brain shortly before death. 
The history of this first case is as follows : 
J. W., one of the one hundred and forty patients, a healthy- 
looking hoy, eight years of age, was well until six years and a 
half old; then without any known cause was seized with con- 
vulsions and developed right hemiplegia. When brought to 
the Polyclinic, three months later, he presented the symptoms 
of a typical spastic hemiplegia of the right side, including 
the face, and in this permanent involvement of the face pre- 
sented at least one unusual feature. He furthermore gave 
the history of loss of speech following the attack, and of re- 
peated epileptic seizures involving the right hand only. His 
mental development was only a little retarded, while his 
head showed the hydrocephalic condition, and during ob- 
servation the head was noticed to increase in size. No other 
deformities of the skull. It was a mere matter of chance 
that this case sought admission to the Montefiore Home, 
where he continued under my observation. While there he 
was doing extremely well, -was happy, ran around freely, and 
there was every prospect of his remaining an inmate for many 
years. No changes were noted until the end of October, 1890, 
when one day he suddenly fell down and the right hemiparesis 
of old standing had developed into complete hemiplegia. 
There was no loss of consciousness during this occurrence. 
The face was not more paralyzed than before; there was no 
incontinence of urine and fseces. Within a few days after 
this fall the boy developed fever varying between 101° and 
lOSh0 F. During this time a disturbance of vision was de- 
veloped which ended in absolute blindness. Speech became 
more and more difficult; he developed a mild stupor which 
gradually deepened into coma. Two weeks later intermittent 
* For an account of the third case, see Jour, of Nerv. and Ment, 
Dis., Sept, and Oct., 1887. INFANTILE CEREBRAL PALSIES. 
9 
opisthotonos was observed, this condition, too, becoming per- 
manent. After five weeks, with the continuance of all the other 
symptoms, left ptosis and paralysis of the left rectus externus 
and anaesthesia of the right cornea were added; the pupillary 
reflexes were lost, and the contractures of the right side in- 
creased. Dr. Roller, who made an ophthalmoscopic examina- 
tion, reported that the papillae were swollen and whitish gray, 
not distinctly outlined, arteries very small and thread-like, 
veins dilated and tortuous—in short, a retrogressive papillitis. 
From the time of the fall until deep coma had been established 
the slightest touch over the left motor area was extremely 
painful, the contractures became extreme, the reflexes were 
exaggerated throughout, the anaesthesia of the cornea became 
absolute, and for fully thirty-six hours before death the right 
eye ceased winking; respiration became irregular, and the boy 
finally died eight weeks after the onset of this last attack. 
Convulsions were not repeated during the whole of this time. 
The old hemiplegia was ascribed to a cystic formation prob- 
ably due to haemorrhage over the left motor area. For a few 
days after the development of the increased paralysis and dur- 
ing the continuance of the fever the idea of abscess in connec- 
tion with the old cyst was entertained ; but this was soon aban- 
doned, and a tumor growing in the walls of the old cyst was 
the diagnosis made in the presence of the house staff and ad- 
hered to to the end. In no other way could the increase of the 
former hemiplegia, without the addition of further symptoms, 
be explained. 
The tumor was supposed to be a glioma or gliosarcoma, but 
the development of basilar symptoms later on made me hesitate 
and led me to believe that a basilar meningitis had been devel- 
oped, and it was therefore natural to suppose that the original 
tumor, although the boy was in excellent health, was of a tu- 
bercular nature. In this I was mistaken, for the basilar symp- 
toms must be attributed directly or indirectly to the second 
tumor found in the right temporo-sphenoidal lobe. 
The autopsy was performed within twenty-four hours after 
death. The skull and the spinal canal were the only parts 
opened. The skull was large and thin, with enormous occipital 10 
CONTRIBUTIONS TO TIIF, PATHOLOGY OF 
bulging. The fontanelles were closed. The calvaria was easily 
removed, there being no adhesion between the dura and the 
skull. The unusual size of the brain was at once made evident, 
the posterior portion having been enormously expanded by the 
accumulation of fluid within the ventricles, and' the hemi- 
spheres being so thin that the fluctuating mass beneath could 
be distinctly felt and all trace of normal fissuration was en- 
tirely lost. The conditions are best explained by reference to 
Plate I, Plate II, and Fig. 1 in Plate III.* While the brain was 
still in situ, the cyst occupying the left motor area and the tumor 
in its walls could be distinctly observed. After the brain had 
been removed, further changes were observed at the base; first 
of all a large cystic formation f at the apex of the left temporo- 
sphenoidal lobe, pressing in upon and almost covering the left 
crus. The optic nerves were evidently atrophied, and the left 
abducens was extremely thin. There was no thickening of the 
meninges in the interpeduncular space nor over any part of the 
base. Pushing the basilar cyst aside, the degenerated condition 
of the left crus was extremely marked. Next in order we came 
upon the large and hard tumor in the right temporo-sphenoidal 
lobe. Upon puncturing the anterior cyst, large quantities of 
fluid escaped—surely mot e than a pint—and with it the posterior 
bulging diminished, showing that this anterior cyst had com- 
municated with the ventricle. A small portion of the tumor in 
the right temporo-sphenoidal lobe wras at once removed for ex- 
amination, but with this exception the brain was submerged in 
toto in Muller’s fluid, in which it was allowed to harden for a 
few weeks before any further examination was made. The 
spinal cord was removed and suspended in Milller’s fluid. The 
brain and spinal cord have been made the subject of careful ex- 
amination, which has yielded the following facts: 
The unusual weight of the brain was caused by the accumu- 
lation of fluid in the ventricles, and the twro tumors. The right 
* Special acknowledgment should be made to Dr. Macdonald for 
the beauty of his drawings and his careful study of the specimens sub- 
mitted to him. 
f The cyst, in reality, formed part of the apex of the temporo- 
sphenoidal lobe. INFANTILE CEREBRAL FALSIES. 
11 
hemisphere was slightly cedematous, very much flattened in its 
occipital portion, but otherwise normal; the pia could be re- 
moved freely from every part of its surface. The left hemi- 
sphere appeared larger than the right, in consequence of the 
greater amount of fluid in the left ventricle. All the blood- 
vessels were of normal appearance. The pia could easily be re- 
moved, except over the cyst; here no pia could be made out; 
it was evidently an integral part of the roof of this cyst. 
The old cyst (Plate II) occupied an area bounded anteriorly 
by the post-central convolution, posteriorly by the anterior 
portion of the interparietal fissure, while it extended upward 
within an inch of the chief longitudinal fissure, and down- 
ward as far as the upper end of the fissure of Sylvius. It had 
thus involved a portion of the posterior central convolution, 
the superior and inferior parietal lobules, and the gyrus supra- 
marginalis. The roof of the cyst was formed by a thickened, 
somewhat transparent, membrane. On cutting through this 
membrane, it was evident that there was a very large amount 
of detritus in the cavity of the cyst, while in the lower anterior 
end of this cavity a hard, small, round tumor is felt. Under the 
surface the destruction has evidently exceeded these limits, and 
the whole of the posterior central convolution was undermined 
and softened. The posterior portion of the left hemisphere in 
the hardened specimen, though now very much contracted, of- 
fers far less resistance to pressure than the portion frontad of 
the sulcus Rolando does. 
The actual size of the “ small round tumor” in the cyst was 
not suspected until vertical sections were made through the brain 
many weeks after it had hardened in a bichromate solution. 
You will all grant that the term “ small round tumor’’does not 
do justice to the facts (Plate II, Fig. 2). The part protruding in 
the cyst was a minimal portion of this huge tumor. As you 
see, it extends to the ventricles from the outer margin of the 
cortex, pushing everything aside, and leaving only here and 
there some normal cortical tissue. It begins, furthermore, at 
the anterior end of the Sylvian fissure and extends well back to 
the beginning of the occipital lobe; it has entirely displaced 
the ventricle, which would be difficult to recognize were it not 12 
CONTRIBUTIONS TO THE PATHOLOGY OF 
for the great thickness of its ependyma. Sections of this tu- 
mor, stained in carmin, picrocarmin, and hsematoxj’lin, prove 
it to be a small-celled sarcoma in which there are also some 
spindle-shaped cells surrounded by a large amount of fibrous 
tissue. 
The base presents a larger number of pathological changes. 
In the hardened specimen we are struck first of all by the col- 
lapsed condition of that portion of the left hemisphere lying 
caudad of the fissure of Sylvius. Next we observe the peculiar 
cystic condition of the inner part of the temporo-sphenoidal lobe 
which pressed seriously upon the left crus. In the right temporo- 
sphenoidal lobe, about two inches below its apex, a large tumor 
was found extending from the outer surface as far inward and 
downward as the ventricle, and this tumor has all the character- 
istics of the tumor in the old cyst, is uniformly hard to the touch, 
and, as the microscopical examination has shown, is also a small- 
celled sarcoma. Both olfactory nerves are extremely thin; the 
optic chiasm and optic tracts had been pushed aside and are dis- 
torted in consequence of the growth of the cyst of the left side 
(Plate III, Fig. 1). The left optic tract is very much smaller than 
the right. The left crus shows such marked atrophy of the 
middle portion that the internal and external portions almost 
fall upon themselves. The right crus is broad and normal. The 
left third nerve is very much compressed ; the right third ap- 
pears normal. In the fourth and fifth nerves no changes are to 
be observed, nor in the macroscopical appearances of any of the 
other cranial nerves. The pons shows an inequality in favor 
of the right side, while in the medulla this is not so distinct.* 
The microscopical examination of the brain and cord showed 
changes which were in part visible in the fresh specimen, namely, 
very marked secondary degenerations in the left pyramidal tract 
of crus, pons, and medulla, and throughout the entire lateral col- 
umns of the right side of the cord. There is also a slight degen- 
erated area in the left lateral column. Changes in the anterior 
columns are not very distinct. 
* In Plate III, Fig. 1, after the hardened specimen, some of these 
points are not so distinct as they were in the fresh specimen. INFANTILE CEREBRAL PALSIES. 
13 
In spite of the manifold lesions found in the brain of 
this child, there is no difficulty in explaining the relations 
between these lesions and the symptoms during life, nor in 
determining the sequence in which these various pathologi- 
cal conditions became established. That the old hemi- 
plegia was due to the cyst in the left hemisphere there can 
be no doubt. Some doubt there may be, however, as to 
the origin of this cyst, but, in view of the peculiar detritus, 
of the very irregular margin of the cyst, we need have no 
hesitation in assuming the haemorrhagic origin of this for- 
mation. Moreover, the area involved in the cyst does not 
correspond to the territories supplied by the main branches 
of the middle cerebral artery ; there is no reason, therefore, 
to think of an initial embolic softening, and, more than that, 
the blood-vessels were found normal. The existence of 
the hydrocephalus probably antedated the cyst in the left 
hemisphere. It was specially noted in our records that the 
head was increasing, and I have no doubt that the smaller 
cystic formation near the apex of the temporo-sphenoidal 
lobe was of very recent development. The other changes 
at the base were the result of compression or of the sec- 
ondary degeneration following upon the destruction of a 
large portion of the left motor area. 
We have learned in the course of our studies not to at- 
tach too great an importance to the hydrocephalic condi- 
tion pure and simple. There are very few cases in which 
the hydrocephalus was the cause of the infantile cerebral 
palsy. In an analysis of one hundred and four cases with 
autopsies, not a single case could be attributed to this con- 
dition, although other lesions were often found associated 
with a hydrocephalus. Inasmuch, too, as our little patient 
was bright and well until eight weeks before his death, we 
can assume with perfect safety that, however much the 
hydrocephalus may complicate the anatomical appear- 14 
CONTRIBUTIONS TO THE PATHOLOGY OF 
ance of the brain, it was not responsible for any of the 
symptoms. 
It is not a little surprising to find that the cortex will 
tolerate great hydrocephalic pressure and yet not suffer in 
its functions. I have no doubt that the occipital cortex in 
this case performed all its functions normally until a few 
weeks before death. The tumor unquestionably increased 
the hydrocephalic condition, but the head was noted to be 
large and increasing long before the symptoms of tumor 
appeared. And remember that in this, as in so many other 
cases, the general intelligence remained good. I was curi- 
ous to compare the cortical structure of the occipital region 
with those of other regions less affected by the hydro- 
cephalus; pieces of cortex were therefore excised from the 
right and left occipital regions and from the left frontal 
region. 
The examination of these specimens showed, first of all, 
the marked diminution of gray matter in the parts much 
compressed. In the three specimens which I present,* you 
will observe that in the one representing the extreme hy- 
drocephalic condition there is scarcely a normal pyramidal 
cell to be detected ; the blood-vessels are small, and some of 
them show a slight cellular proliferation of the vessel walls ; 
in the other specimens these conditions are less marked, 
and in the frontal section, where the hydrocephalus exerted 
the least influence, you find a tolerably normal condition of 
the cells, but a surprising dilatation of the veins, and many 
of these veins are completely filled with blood. But in all 
these sections there is no evidence of sclerosis. 
I was so firmly convinced of the existence of a haemor- 
rhagic cyst in this case of acute cerebral palsy that I was 
at once ready to explain the lesion which could give rise to 
an increase of the old symptoms. Some new process, I 
* The demonstrations were made at the meeting. INFANTILE CEREBRAL PALSIES. 
15 
argued, must have started up in the old lesion, and the walls 
of the cyst seemed to me to offer the very best opportunity 
for the incursion of a growth. The diagnosis of such a 
tumor was made easy by the rapid development of double 
optic neuritis, of blindness, and, above all, by extreme pain- 
fulness over the left motor area. Considering the well- 
known fact that tumors are most apt to develop in atrophic 
or mal-developed tissues, and considering, furthermore, the 
relative frequency of these cases of cysts in the brain, it is 
surprising that so few instances of tumor development in 
old cysts have been reported. I have carefully examined 
the writings of Bernhardt,* of Nothnagel, f of Mills, J and of 
Starr# bearing upon this subject, and have not found the 
records of a single case exactly like my own. Cysts of all 
dimensions are frequent enough, and in three cases only— 
those of Jackson,|| Moines,A and EscribanoQ—is there any 
note of the joint occurrence of cyst and tumor; but in 
none of these cases, even, was there any good reason to be- 
lieve that the cyst was developed in childhood, or that it 
antedated by any considerable length of time the develop- 
ment of the tumor. Microscopic examination has shown 
that the two tumors in this case are of exactly the same 
character, although the one at the base is much smaller than 
the one in the left hemisphere. There is every reason to 
believe that it was developed later than the one which 
caused the hemiplegia. The tumor at the base, however, 
is evidently responsible for the symptoms which were de- 
veloped toward the end of life, which pointed to an in- 
* Hirngeschwiilste, Berlin, 1881. 
f Topisch. Diagnost., etc., 1879. 
% Pepper’s System of Med., v. 
# Keating’s Cyclop, of Bis. of Children, iv. 
|| Med. Times and Gaz., Nov., Dec., 1872. 
A Arch. f. path. Anat. u. Phys. u. f Min. Med., lxx, 1877. 
Schmidt’s Jahrbiicher, 1867, i. 16 
CONTRIBUTIONS TO THE PATHOLOGY OF 
volvement of many of the cranial nerves, and which led me 
on this very account to suspect that there was a basilar 
meningitis. 
In view of the unusual size of the tumor, I wish to allay 
any doubts as to its relation to the old hemiplegia. If the 
tumor was the cause of the old hemiplegia, what were the 
s\mptoms of the cyst? Surely not the increase in the 
hemiplegia, for the complete disintegration of the contents 
of the cyst proved thetn'to be far older than two or even 
six months. I can not positively assert that the tumor be- 
gan to develop a few months before death; it probably 
began a little earlier, and had evidently attained a respect- 
able size before it produced prominent symptoms; but the 
sudden accession of headaches, double optic neuritis, and 
semi-coma point to a sudden and rapid growth. That there 
were no local convulsions need not surprise us if we re- 
member that the old cyst left very little motor cortex capa- 
ble of “discharging.” The size of the tumor, astonishing 
as it is, is not an indication of great age, for sarcomata are 
known to grow with extreme rapidity in the brain and in 
other organs. I remind you of the sarcomata, many pounds 
in weight, that have developed within a few months in the 
breasts of young women. In this instance we are again 
reminded of the fact that it is quite impossible to foretell 
anything regarding the size of a brain tumor. The tumor 
in this case, though the most striking morbid condition, 
need not detract from the importance of the old cyst, which 
I hold to be the residue of a subpial luemorrhrge three years 
ago, the cause of this acute form of infantile cerebral palsy. 
The second case which I shall take the liberty of re- 
porting is of a very different character from the first—dif- 
ferent in its clinical symptoms and in the pathological find- 
ings. As this case is to be reported in full, together with 
a series of studies by Dr. Holt and myself, I shall give INFANTILE CEREBRAL PALSIES. 
17 
but brief details this evening. The patient’s history was 
giveu in the paper of last year, from which I quote the fol- 
lowing : 
The child was a little boy one year of age. He had con- 
genital spastic paraplegia. The mother, a primipara, was in 
good health, but the labor was hard and dry for forty-eight 
hours. The child was asphyxiated when born. From the first 
day up to the age of six months and a half the child passed 
through a rapid succession of tonic and clonic spasms affecting 
all the muscles of the body, causing rigidity of all extremities, 
opisthotonos with extreme arching of the back, enormous exag- 
geration of all the reflexes, including a patellar clonus on the 
slightest excitation. There was convergent strabismus and 
continual crying. The mental condition, as far as could be 
judged, was deficient but not absolutely idiotic. The epileptic 
spasms were so frequent that we succeeded in obtaining a photo- 
graph of the child during one of these spasms. In the intervals 
between the spasms the child could move its hands and arms, 
but the legs remained in the condition of spastic rigidity. As 
the parents confessed themselves unable properly to care for the 
child, we referred it to Dr. Holt’s Babies’ Hospital, where the 
child remained for a few weeks, passed through an acute eruptive 
disease of doubtful character, and finally died. The autopsy 
was made within twenty-four hours after death by Dr. Holt, 
who has kindly left the brain to me for detailed examination. 
The most noticeable feature of the brain was the absolute ad- 
herence of the pia over both hemispheres: it was impossible 
to remove even the smallest strip from any part of the cortex. 
The brain appeared somewhat firmer to the touch, but, as far as 
the flssuration could be determined through the adherent pia, 
there was no unusual change in this respect. But most striking 
of all was the marked symmetrical atrophy of the frontal halves 
of both hemispheres. The brain and cord have been carefully 
hardened in Muller’s fluid, and the cortex, the ganglia, and the 
whole spinal cord have been made the subject of careful micro- 
scopical examination. The change in the cortex is very evident 
on specimens stained in carmine, picrocarmin, and hema- 
toxylin. 18 
CONTRIBUTIONS TO THE PATHOLOGY OF 
From whatever part of the cortex specimens were ex- 
amined, the same change was shown throughout. We have, 
first of all, a general adhesion of the pia to the cortical 
tissue; the pia is thickened and characterized by a general 
cellular infiltration ; its blood-vessels show marked cellular 
proliferation; the veins in the subpial space are dilated and 
filled with blood, and small branches of the pial sheath 
passing in between the convolutions show the same changes 
that we find in the pia that is stretched over the convex 
surface. In the cortex itself, instead of the normal arrange- 
ment of cells, we find few if any normal pyramidal cells; 
but in the outer layers, and particularly in what would cor- 
respond to Meynert’s third and fourth layer, we find an 
enormous profusion of small glia cells. The blood-vessels 
are in part normal, but many of them show marked small- 
cell proliferation of their wails. There is unquestionably a 
thickening of the neuroglia. The anatomical diagnosis is 
clearly that of a chronic meningo-encephalitis. In the 
drawing (Plate III, Fig. 2) the space a is somewhat arti- 
ficial. The changes in the cells and in the vessel walls are 
distinctly shown; to the right of the pial projection there 
is a structureless area, probably the result of a small haemor- 
rhage. We can not err in attributing this meningo-en- 
cephalitis to a very wide-spread effusion of blood between 
the pia and the cortex at the time of birth. Protracted 
labor and the marked asphyxia are the clinical conditions 
which corroborate that view. The spinal cord, as far as it 
has been examined up to the present time, reveals a most 
distinct degeneration of both lateral columns. That this 
degeneration is secondary to the cortical lesion there is 
every reason to believe, for this degeneration can be recog- 
nized in all parts of both motor tracts and in the pyramidal 
tracts of the pons and medulla, as well as in the lateral INFANTILE CEREBRAL PALSIES. 
19 
columns at every level of the cord. It must be remembered 
that the cortical affection was bilateral. 
I have only to add with reference to this case that it has 
a special significance, inasmuch as it is the second case of 
congenital spastic paraplegia in which an autopsy has been 
made, or at least recorded; and it is of extreme value, it 
seems to me, as proving, beyond the shadow of a doubt, that 
these cases of congenital spastic paraplegia are of cerebral 
origin and not due to spinal-cord lesions. In the only other 
case of infantile spastic paraplegia dating from birth which 
has been recorded with autopsy, Forster* found a general 
sclerosis of the brain ; this may have been a secondary con- 
dition, but the case loses much of its value since no micro- 
scopical examination was made. Only within the last few 
years so eminent an observer as Rossf was inclined to think 
these cases of spinal origin and due to traction at birth. I 
have elsewhere stated that the occurrence of idiocy and 
mental enfeeblement in fully 80 per cent, of the cases of 
congenital spastic paraplegia would of itself seem to point 
to the brain as the source of the disease; and if, as in my 
own case, the lateral columns are affected, the affection is 
secondary to the initial cerebral lesion. The unusual con- 
vulsions in my case must be attributed to the fact that 
there was an active and widespread encephalitic condition ; 
this inflammatory state was not at an end before life termi- 
nated, and the constant occurrence of epileptoid seizures 
is what we might expect in such a condition as the one 1 
have just described. 
The knowledge of the pathological lesions underlying 
these various conditions is not only a matter of scientific 
curiosity, but it has a most distinct bearing upon the 
* Jahrb. f. Kinderheilfc., xv. 
f On the Spasmodic Paralyses of Infancy. Brain, v. 20 
CONTRIBUTIONS TO THE PATHOLOGY OF 
treatment of these diseases. Hitherto the majority of 
cases have either not been treated at all or else they have 
helped to swell the numbers in orthopaedic and other hos- 
pitals, and many of them are the inmates of our pauper in- 
stitutions. The orthopaedic surgeon will have to attend to 
the correction of the physical deformities; in those cases 
in which a persistent palsy, or more especially an extreme 
contracture of one or both of the extremities, is the chief 
residue of the disease, the surgeon will no doubt sooner or 
later be able to give a fair measure of relief. But it is 
more important for us to consider whether we have a right 
to interfere with the cerebral lesion in order that we may 
combat the development of idiocy or epilepsy, or whether 
it be possible—one or the other of these conditions having 
been established—to obtain relief by surgical procedures. 
The question can not be decided unless some such analysis 
of the morbid lesions be attempted as I have given in this 
paper. If we have to deal with a condition of poren- 
cephalus or with a condition of cortical agenesis, it is mani- 
festly impossible to improve this condition by an opera- 
tion ; and if such brains are incased within a microcephalic 
skull, even the recent operation of craniectomy will do no 
earthly good. As for the birth palsies, no surgeon will be 
bold enough to attempt the removal of a subpial or sub- 
dural clot in a child only a few days old; and long before 
the child is strong enough to tolerate any such serious op- 
eration, the mischief is done, an encephalitic or a sclerotic 
condition has been established for which the surgeon’s 
knife can promise no relief. It is only in the cases of ac- 
quired cerebral palsies that one would naturally think of 
the possibility of operative procedure. Should the diag- 
nosis point to thrombosis or embolism, there is no good 
reason for surgical interference. But how about Qases of infantile cerebral palsies. 
21 
haemorrhage ?* Arguing from the analogy with adult cases, 
there would seem to be no good reason to interfere in 
cases of haemorrhage until some time has elapsed after the 
initial apoplexy; for presumably, as in adult apoplexy so 
also in the infantile forms, much of the clot will be ab- 
sorbed ; but if we leave the clot to be absorbed, a very 
short time may suffice for the establishment of secondary 
changes in the brain and spinal cord. In adults the clot is 
generally in or near the ganglia; in children it is most fre- 
quently upon the surface. It is my belief that the greatest 
good will be done if the surgeon will exercise his shill at 
this early period. 
I have no hesitation, therefore, in recommending that, 
if the symptoms point to the formation of a large clot over 
the motor area of a child otherwise healthy and strong 
enough to endure the operation, the attempt be made to 
remove the clot in order at once to release pressure upon 
the given area and to prevent secondary degeneration. It 
is commonly urged that in many cases we can not at the 
start state with any degree of certainty whether the case is 
a spinal or cerebral affection. This I can not concede ex- 
cept in the rarest cases. In several instances-1 have made 
the differential diagnosis at once, and in others within 
twenty four hours after the onset of the trouble, and I 
claim no special diagnostic powers. The excellent recov- 
eries from surgical procedures upon the brain have led up 
to this view, and I firmly believe that recent cases will give 
more satisfactory therapeutic results than the cases of old 
standing. My own experience covers three cases of infan- 
tile spastic palsies of old standing in which the patients 
have recently been operated upon—one by Dr. Gerster and 
two by Dr. Wyeth. The time is too short to speak of the 
ultimate result as regards the persistence of the epilepsy, and, 
* It goes without saying that this diagnosis is sometimes impossible. 22 
CONTRIBUTIONS TO THE PATHOLOGY OF 
of course, we do not expect the surgical operation upon the 
brain to improve an old-timed hemiplegia. In one of the 
three cases, as I intimated at the beginning of this paper, a 
haemorrhagic infiltration and discoloration of the pia, with 
marked thickening of the same, was found as proof of the 
old meningeal haemorrhage. Small vertical incisions were 
made through the pia at this point by Dr. Wyeth to release 
the local pressure. In the other two cases, although the 
dura was opened, no change could be made out. There 
are several possibilities which must be considered : 
First, every trace of the old trouble may have disap- 
peared; and, secondly, in cases of meningo-encephalitis or 
of sclerosis the changes can only be made out by micro- 
scopical examination. Take the case of Frobel, the child 
with spastic paraplegia, and you will readily perceive that 
if its brain had been exposed intra vitam, the changes in it 
might not have been recognized. Next we must consider 
whether, if we have good reason to suspect the existence 
of a cyst or of a scar, it would be wise to make this the 
point of attack. From the fact that a cyst acts somewhat 
like a foreign body in the brain, there could be no harm in 
removing it, or at least in emptying its contents, provided 
drainage of this cyst does not mean withdrawal of a large 
portion of the cerebro-spinal fluid, and many cysts are en- 
tirely independent of other parts and cavities of the brain. 
But the operation would surely do no good if done as late 
in life as in Dr. William A. Hammond’s case, in which the 
patient, who was twenty years of age, had carried the large 
cyst from the very earliest period of life.* The presence of a 
cyst unquestionably acts as an irritant’ upon the neighboring 
brain area; it is therefore in cases of persistent hemi-epilepsy 
associated with infantile hemiplegia that the attempt to re- 
move the cyst or other morbid lesion might be attempted 
* N~. Y. Med. Jour., 1890. INFANTILE CEREBRAL PALSIES. 
23 
justly enough. Cases of diplegia and paraplegia associated 
with epilepsy do not appear to he the proper cases for op- 
eration, for to do any reasonable amount of good, both 
halves of the brain would have to be operated upon. This 
should not be attempted unless operations upon cases of 
hemiplegia with epilepsy have shown that some good can 
come from such an operation. 
The matter becomes still more difficult in those cases 
in which a general lobar sclerosis or a condition of primary 
encephalitis is suspected. In lobar sclerosis the disease is 
always widespread, and if one area was removed, the re- 
maining ones would be sufficient to continue many of the 
symptoms. Meningo-encephalitis has an acute and a chron- 
ic state. In the acute state we would surely not operate, 
and in the chronic state we can not say exactly how far 
the inflammatory process has progressed, and we could do 
no good unless after removal of an encephalitic area the 
child’s brain was sufficiently young to take upon itself func- 
tions that were lost. And let us reflect that if this could 
occur in a given case, we should have a right to expect that 
the injured brain before operation would assume the func- 
tions of parts that through disease were practically lost 
to it. 
There are two facts, moreover, which are well calculated 
to dampen our surgical ardor : First, a brain that has been 
the subject of epileptic discharges falls into what one may 
justly claim the epileptic habit. Remove the original focus 
of disease, and the habit or other foci of disease may re- 
main. My own experience in the surgical treatment of 
focal epilepsy leads to anything but a roseate view. Sec- 
ondly, granting that the removal of a clot or an old infiltra- 
tion or a scar may inhibit the epilepsy, you may and prob- 
ably will have to face the alternative of a palsied arm or 
leg or both. Considering how useless many of these con-  PATHOLOGY OP INPANTILE CEREBRAL PALSIES. 
tractured, athetoid, and paralyzed extremities are, the choice 
would be an easy one for us; but it is eminently proper 
that the patient, if old enough, should express his prefer- 
ence. 
And yet there is promise enough among this special 
class of cases, and if we are to fix upon the one of a dozen 
cases of infantile palsies in which the surgeon may come 
to the rescue, we must, above all, have a thorough under- 
standing of the morbid lesions. DEAWN FROM THE SPECIMENS BY DR. H. MACDONALD, AND REPRODUCED DIRECT. 
Ventral aspect of brain, showing bilateral hydrocephalus, cysts, and tumor^ 
Plate I. Fig. 1.—Showing position of cyst with portion of tumor. Roof of cyst has been laid open by 
dissection. The hydrocephalic enlargement is omitted to economize space. 
Fig. 2.—Vertical section through cyst and both tumors, showing also distortion of the brain axis 
and displacement of the left ventricle. f7, the cyst. _P, the pons. I , the left ventricle. 
Plate II. Fig. 2.—Drawn from microscopical section through the motor cortex, in a case of spastic 
paraplegia, a, Demarkation between cortex and pia. i, Blood-vessels in transverse 
and longitudinal section, showing infiltration of their walls, c, Altered cells with 
pericellular spaces, p, The pia, thickened and infiltrated, sending projection down- 
ward between two convolutions. 
Fig. 1.—Brain axis, showing atrophy of the left crus and the left half of pons. 
Plate III. REASONS WHY 
Physicians Should 
Subscribe 
FOB 
The New York Medical Journal, 
Edited BY FRANK P. FOSTER, M. D.,1 
Published by D. APPLETON & CO, 1, 3, & 5 Bond Si 
X. BECAUSE : It is the LEADING JOURNAL of America, and 
contains more reading-matter than any other journal of its class. 
2. BECAUSE: It is the exponent of the most advanced scientific 
medical thought. 
3. BECAUSE : Its contributors are among the most learned medical 
men of this country. 
4. BECAUSE: Its “Original Articles” are the results of scientific 
observation and research, and are of infinite practical value to the 
general practitioner. 
5. BECAUSE : The “Reports on the Progress of Medicine,” which 
arc published from time to time, contain the most recent discov- 
eries in the various departments of medicine, and are written by 
practitioners especially qualified for the purpose. 
6. BECAUSE : The column devoted in each number to “Therapeu- 
tical Notes” contains a resume of the practical application of the 
most recent therapeutic novelties. 
7. BECAUSE : The Society Proceedings, of which each number con- 
tains one or more, are reports of the practical experience of 
prominent physicians who thus give to the profession the results 
of certain modes of treatment in given cases. 
8. BECAUSE : The Editorial Columns are controlled only by the 
desire to promote the welfare, honor, and advancement of the sci- 
ence of medicine, as viewed from a standpoint looking to the best 
interests of the profession. 
9. BECAUSE : Nothing is admitted to its columns that has not some 
bearing on medicine, or is not possessed of some practical value. 
XO. BECAUSE: It is published solely in the interests of medicine, 
and for the upholding of the elevated position occupied by the 
profession of America. 
Subscription Price, $5.00 per Annum. 
and July. 
Volumes begin in