INFANTILE SPINAL PARALYSIS. 
A CLINICAL LECTURE, 
DELIVERED AT THE COLLEGE OF PHYSICIAN'S AND 
SURGEONS, 1873. 
BY 
E. C. SEGUIN, M. D. 
REPORTED BY 
Dr. FRANK P. KINNICUTT. 
[REPRINTED FROM THE NEW YORK MEDICAL RECORD, JAN. 15,1874.] 
NEW YORK: 
D. APPLETON AND COMPANY. 
549 & 551 BROADWAY. 
1875. INFANTILE SPINAL PARALYSIS. 
A LECTURE DELIVERED AT THE COLLEGE OF PHYSICIANS AND 
SURGEONS, NEW YORK.1 
By E. C. SEGUIN, M. D. 
Gentlemen : I think that yon may obtain a clearer idea 
of the importance of infantile spinal paralysis if we study it 
not separately, as I had at first purposed we should, but as 
one of the forms of paralysis to which infants are liable. At 
a subsequent meeting we can briefly inquire into the other 
varieties of infantile palsy, and you will then obtain a knowl- 
edge of a great part of the nervous pathology of infancy, and 
be better prepared to diagnose the most important of these af- 
fections-infantile spinal paralysis. The period of life termed 
infancy is that which includes the first dentition to the begin- 
ning of the seventh year. The pathology of this stage of ex- 
istence is treated of separately by authors, in part because of 
the peculiar difficulties in diagnosis presented by children of 
this age, and in part because of numerous peculiarities they 
exhibit, such as susceptibility to the action of causes of disease, 
of medicines, and the exaggeration of certain groups of symp- 
toms, such as the spasmodic element in the sphere of the 
nervous system. There is no essential difference, please re- 
member, between infants and adults in the nature, course, 
and treatment of disease. 
The following synopsis represents the principal forms of 
paralysis which are likely to occur in infancy, together with 
their leading pathogenetic factors : 
(Eeported by Fbank P. Kinnicutt, M. D.) 
1 On November 8, 1873. 4 
PARALYSIS IN INFANCY. 
1. Hemiplegia (clot, injury, embolism, tumor in brain). 
2. Paraplegia (injury, clot, inflammation of cord). 
3. Peripheral paralysis (compression, etc., of nerve trunk). 
4. Inhibitory paralysis (peripheral irritation). 
5. Infantile spinal paralysis (atrophy of motor nerve cells). 
The last of these is the disease we shall study to-day, and 
several examples of it are before you, affecting subjects of 
different ages. The term which I have adopted is one of 
numerous synonyms by which the disease has been knowm. 
The first systematic writer upon the subject, Heine, used a 
corresponding German name, spinale Kinderlahmung, in his 
second edition of 1860. French writers upon the diseases of 
infancy, who studied the subject very thoroughly in its clin- 
ical aspects, Rilliet and Barthez,1 denominated the disease 
paralysis essentlelle de Venfance. Bouchut, entertaining a 
very singular notion of the pathology of the affection, gives 
it the name of parody sie myogenique. Niemeyer retains the 
term essential paralysis, considering it as a safe one to adopt 
during the present unsettled state of opinion upon the ques- 
tion of pathology. The word essential is used by these au- 
thors as equivalent to functional or sine materia. The title 
infantile paralysis is one employed by such authors as C. B. 
Radcliffe and Adams. Duchenne, in the last edition of his 
work on electrization, calls the disease paralysle atrophique 
de Venfance, instead of paralysis atrophique graisseuse de 
Venfance, as in his edition of 1860. Hammond, in his trea- 
tise upon " Diseases of the Nervous System," speaks of or- 
ganic infantile paralysis. 
Symptoms and Course of the Disease.-In brief, infantile 
spinal paralysis may be defined as an acute febrile affection, 
resulting in generalized paralysis, which shortly disappears 
from all but a limited part of the body, wdiere the akinesis 
persists indefinitely without impairment of sensibility, is ac- 
1 Rilliet et Barthez, Maladies des enfants, tome ii., p. 545, et seq. Paris, 
1861. 5 
companied within a few weeks by atrophy of the palsied mus- 
cles, and is followed later by various deformities-the result 
of altered balance of power at certain joints. The anatomical 
lesion of the disease consists in primary (?) atrophy of the 
nerve cells of the anterior horns of the spinal cord (motor 
tract), and in secondary (?), complicating (?) myelitis. 
A. Febrile Stage.-A child, and usually a healthy or 
even a robust child, has an indisposition, with febrile move- 
ment, evidenced by restlessness or drowsiness, hot skin and 
frequent pulse. The mother's attention is often called to a 
coexisting local affection, such as indigestion, intestinal ca- 
tarrh, or morbid dentition. The last is the usual condition 
referred to, because the age when infantile spinal paraly- 
sis is most apt to occur (six to twenty-four months) includes 
nearly the whole period of dentition, and because mothers as 
well as many practitioners are only too willing to hold the 
teeth responsible for any disease which may arise during their 
evolution. The fever has not, to my knowledge, been studied 
with the thermometer. Fevei' has been observed in nearly 
all cases1 (forty out of fifty). When parents assert that no 
fever was present at the outset, it must be borne in mind that 
a certain degree of intelligence is required to enable a person 
to recognize fever; that in some cases only skilled observa- 
tions (thermometrical measurement) will reveal its existence; 
and that it may have been present for a few hours only. Be- 
sides these phenomena, there are several nervous symptoms 
present in a certain proportion of cases, convulsions usually 
not involving the facial muscles, and delirium. Hyperaesthe- 
sia is also present; but whether this is a true hypersesthesia, 
or an evidence of that morbid sensitiveness which is part of 
the febrile state, remains uncertain. 
B. Stage of Paralysis.-As the fever subsides, the mother, 
upon handling the child, discovers that voluntary motion has 
been lost in nearly the entire body. The exact period when 
the akinesis appears, and whether it develops slowly or sud- 
1 Laborde, De la paralysie (dite essentielle) de 1'enfance. Paris, 1864, 
p. 3. 6 
denly, are points not yet investigated. The paralysis is at 
first generalized, often involving all the limbs, very rarely 
the face. At the same time no impairment of sensibility is to 
be noted. In a short time, a few hours, the paralysis recedes 
from some parts and persists in others; it being very rare 
that more than one-half of the body remains palsied. This 
retrocession of the paralysis, its disappearance from some 
limbs, and fixation upon one or two, or upon unsymmetrical 
distant muscles, is highly characteristic of the disease-I might 
almost say pathognomonic. This fixation is usually upon 
parts of the lower limbs, more seldom upon the upper, and 
rarely upon parts of the trunk. In only one case has a mus- 
cle of the head been found definitely paralyzed-the tem- 
poral. The muscular group which is most often affected is 
the anterior tibial and peroneal. Owing to the immunity of 
the abdominal muscles, the bladder and rectum perform their 
functions. 
C. Third Stage.-Inseparably connected with the defini- 
tive akinesis is the muscular atrophy, with loss of electro- 
muscular contractility, and with deformities. The loss of 
irritability in the palsied muscles, as tested by the electrical 
current (faradic), occurs very early-at a period varying from 
one to six weeks. In one case atrophy and loss of electro- 
muscular contractility were well marked on the fourth day 
(Laborde) *. A very few years ago three observers indepen- 
dently made the very valuable observation that these atrophied 
muscles could be made to contract by the application of the 
galvanic current. Mr. Harry Lobb,' Dr. William A. Ham- 
mond,3 and Mr. J. Netten Radcliffe 4 (from 1863 to 1865), 
are each entitled to the merit of making this observation in 
infantile palsy. The application of this reaction to the gal- 
vanic current to prognosis will be stated farther on. 
1 Laborde, op. cit., p. 19. 
3 In a letter to the London Medical Times and Gazette, 1863, vol. ii., 
p. 682. 
3 New York Medical Journal, December, 1865. 
4 Reference by C. B. Radcliife, in Reynolds's System of Medicine, vol. 
ii., article on "Infantile Paralysis," p. 665. London, 1868. 7 
The atrophy of the muscles is both relative and positive, 
and is accompanied by certain histological changes, which 
will be detailed when we study the morbid anatomy of the 
disease. In the case now before you, a young man, seventeen 
years old, in whom infantile palsy set in at the age of twenty 
months, the bones of the legs, themselves much reduced in 
size, seem covered only by skin, and a little adipose tissue. 
These legs also exhibit two accompaniments of the atrophy 
of infantile paralysis, viz., imperfect circulation and dimin- 
ished temperature. The atrophied parts are very purple, and 
are quite cold to the touch. The diminution of temperature 
has been measured by Heine,1 and found very great; the 
atrophied region in one case having a surface temperature of 
only 14° Reaumur (63°.5 Fahr.). This is in striking contrast 
to the temperature of limbs palsied by a cerebral lesion. 
In consequence of this akinesis, indefinitely prolonged, 
accompanied by wasting of the muscular tissue, there are 
formed a number of deformities. Some of these consist mere- 
ly in arrested development, as indicated by the shortening 
of the affected limb-there occurs a relative atrophy. This 
shortening of a limb, a lower limb more especially, gives rise 
to secondary deviations in form, such as twisting of the pelvis 
and lateral curvature of the spine. These secondary devia- 
tions, which are the result of attempts to restore disturbed 
equilibrium, are called compensatory. It is important to 
distinguish these compensatory deformities from the primary, 
or truly paralytic ones, because the treatment of either 
kind differs radically. The positive deformities are caused, 
as stated in the definition, by impairment in the balance of 
muscular power about any articulation. For example, in 
the feet of one of the patients before you, you see an 
example of deformity which constitutes the talipes equino- 
varus of surgeons; toes point downward and inward. The 
anterior and posterior muscles of the legs are palsied and 
atrophied, and consequently the feet obey the laws of grav- 
ity, dropping into their position because the ankle-joint is 
1 Heine, S| inale Kinderlahmung. Stuttgart, 1860, p. 16. 8 
well back upon the posterior third of the foot. Xhere is no 
resistance to passive movement in all directions. In other 
cases only one set of tibial muscles is paralyzed, and the de- 
formities are produced by the unchecked (unantagonized) 
action of the healthy muscles. In the feet we may thus have 
talipes equinus (" the most common and important variety," 
Erichsen), or talipes equino-varus, or any of the varieties 
which you wdll find fully described in surgical text-books. 
In a case of talipes equinus of this sort we find great resist- 
ance to any attempt at overcoming the deformity ; thetendo- 
Achillis is very tense. The muscles governing the move- 
ments of the knee-joints may be paralyzed, and in conse- 
quence we obtain analogous deviations at that joint. About 
the upper extremities the deformities are less striking, but 
are produced by the same double mechanism, obedience of 
parts to gravity, and unchecked action of certain muscles. 
The spinal deformities are nearly always of the compensatory 
sort: for instance, a shortened leg necessitates the inclination 
of the pelvis to the side on which the shortening is; and, in 
order to preserve the equilibrium of the body, the lumbar 
vertebrae bend so as to form a concavity on the opposite side, 
and higher up there occurs a secondary spinal curve to the 
side of the shortened limb. The lateral curvature is known 
technically as scoliosis. This is rarely due to palsy of spinal 
muscles, though I have now under treatment a case of this 
primary paralytic scoliosis. A variety of muscular dis- 
orders may cause scoliosis in individuals not affected with 
infantile paralysis. (Consult the various works on deformi- 
ties.) Other spinal deformities, more often primary, are the 
bending forward of the spinal column, non-angular, called 
kyphosis; and the bending backward, termed lordosis. The 
bending forward is shown in a minor degree (quasi-pathologi- 
cal) in what is termed stooping-a supposed sign of studious 
habits. Lordosis, as first clearly pointed out by Duchenne, 
may be due to palsy of the abdominal muscles, or to bilateral 
palsy of the lower spinal extensors; in both cases the upper 
part of the body is thrown unnaturally backward to preserve 9 
equilibrium. The two forms may be recognized without a 
minute examination of the seat of palsy, by using a plumb-line. 
Dropping the line from the shoulders, it will clear the sacrum 
in cases of lordosis due to palsy of the erectors of the spine ; 
whereas in palsy of the abdominal muscles it will fall within 
the sacrum. In the latter case there is a deepening of the 
normal lumbar curve without positive backward projection 
of the upper part of the body.* 
One word more concerning the genesis of primary de- 
formities. It is often said that, in club-foot and other de- 
formities, the efficient cause of the deviation is spasm of the 
preponderating muscles. This I believe to be extremely rare, 
and a belief in this erroneous doctrine leads to insufficient 
(merely orthopedic) treatment of the deformities. 
Changes in nutrition in the paralyzed parts ; many of these, 
as observed in the disease, consist in what may be termed 
relative atrophy, i. e., arrested development or retarded growth, 
e. g., diminution in the calibre of the blood-vessels, not only 
of the parts affected, but extending farther into the vessels 
above the atrophied muscles, and even into the main trunks. 
In a certain number' of cases of atrophied lower extremities, 
a marked diminution in calibre has been found to exist in the 
iliacs, and even in the lower portion of the aorta. In the boy 
before you, with extreme atrophy of all the muscles below 
both knees, the whole vascular system of the lower extremi- 
ties is abnormally small. It is necessary to bear in mind that 
no pathological change is discoverable in the walls of these 
vessels; it is an excellent example of simple arrested develop- 
ment. Again, we find the bones of the implicated regions 
diminished in size, the arrested development affecting rather 
their circumferential than their longitudinal growth, only a 
slight shortening being found to exist even in cases of long 
standing.-Let us now devote a few moments to the study of 
the more positive changes in nutrition, as exhibited in the 
1 Duchenne, De 1'electrisation localise, 3me Edition, Paris, 1872, p. 498. 
2 Cases by Charcot and Joffroy, Archives de physiologic normale et 
pathologique, 1870. 10 
muscles. The morbid anatomy of the muscular system in in- 
fantile spinal paralysis has been the subject of laborious and 
careful investigation, and the results of the latest researches 
tend to convince us of the existence of the different kinds of 
muscular degeneration, though by no means of equally frequent 
occurrence, in this disease. By far the most common form is : 
(«.) The simple atrophy, a form which almost always affects 
such muscles as are kept in forced repose for a long period ; 
it manifests itself in a shrinking of the individual muscular 
fibres ; a transverse section reveals the separation of the con- 
tractile substance proper from the sarcolemma ; moreover, as 
a rule, we find a fatty infiltration of the cells of the connective 
tissue. (6.) A granular degeneration is described as succeed- 
ing in order of frequency. In this form proteinaceous gran- 
ules (bodies unaffected by ether, dissolved by acetic acid) are 
found in the fibre itself; the striation disappears gradually, 
more slowly than in the simple atrophy ; as in the latter form, 
a fatty infiltration of the interstitial tissue also exists, (c.) A 
true fatty degeneration is believed to be comparatively rare. 
The earlier belief, that it constituted the peculiar muscular 
lesion in infantile paralysis, aside from its occasional occur- 
rence, may have arisen from the almost unexceptional co- 
existence of the interstitial fatty changes with the forms 
above described. 
Pathological Anatomy.-We have now to consider the 
morbid anatomy of the disease itself. By the earlier writers 
it was' believed to be essentially -functional in its character. 
The first step toward giving us a clearer conception of the 
true nature of the affection was made by Heine, who pub- 
lished the results of his observations in 1840; discarding the 
functional theory, he expressed his belief that the disease was 
due to a violent congestion, with perhaps a subsequent in- 
flammation of the nervous centres. Later, cases were pub- 
lished by Laborde and Cornil, in which a sclerosis of the 
antero-lateral columns was described. In an autopsy by 
Echeverria, sclerosis and amyloid degeneration of the antero- 
lateral columns, sclerosis of the anterior nerve roots, and 11 
brown pigment in the nerve cells, were found. In a case 
of von Recklinghausen's, tubercular deposit was discovered 
in the substance of the cord. II. Roger and Duchenne, Jr., 
reported two cases in which autopsy revealed atrophy of the 
anterior and antero-lateral columns, diminution in size of the 
nerve fibres, increase of the interstitial connective tissue, and 
the presence of numerous amyloid bodies. In an unrecog- 
nized case of infantile paralysis, Mr. J. Lockhart Clarke, of 
London, described an atrophy, a degeneration of the cells of 
the anterior horns. 
To Prevost (a pupil of Charcot's), therefore, is due the 
credit of first recognizing this cell degeneration as the true 
lesion in this disease. In 1866 he published the report of 
the autopsy in which this lesion was discovered. Since that 
date a number of cases have been reported by Charcot and 
his pupils, in which a similar cell degeneration has been found. 
Studied with the microscope, we find that it consists in an 
increase of the normal pigment of the nerve cells ; the latter 
are observed to become densely packed with pigment gran- 
ules, and, finally, to wholly lose their cell character. In their 
place a simple granular mass, which gradually undergoes a 
marked diminution in size, is seen. In a certain number of 
cases no granular change is discoverable, the cells seeminglv 
being subjected to a simple wasting process. 
Other morbid changes, indicating a myelitis, have been 
described as among the lesions of infantile paralysis, e. g., a 
sclerosis, an increase of the interfibrillar connective substance 
of the medullary columns, with a marked increase in the 
nuclei of that substance; the formation of cavities in the 
gray matter, apparently through a process of liquefaction ; 
small clots in the same substance ; corpora amylacea in both 
the gray 1 and white matter; and, finally, what can only be 
described as condensed patches of tissue in the former. 
The question is yet disputed whether the granular cell 
1 The theory now gaining ground in regard to the character of these 
bodies is, that they are due to an amyloid degeneration of the round cells 
of the neuroglia. 12 
No. 
Q 
03 
P 
Author. ' 
1 Age at 
Onset. 
Age at 
Autopsy. 
Mode of Onset. 
Parts paralyzed. 
Lesions of the Nervous System. 
Lesions of Muscles. 
Bibliography. 
1 
1825 
Hutin.; 
7 
49 
Convulsions. 
Both legs. 
Atrophy of lower end of cord, and 
Not stated. 
Cited by Heine, Spinale 
1842 
of its nerve roots. 
Kinderlahmung, p. 151, 
1860. 
2 
Longet. 
8 
Not stated. 
Right leg. 
Atrophy of roots of right sciatic 
Idem. 
Longet, Anat. et Phys. 
1849 
Fliess. 
nerve. 
du Systeme Nerveux, 
L, p. 358. Paris, 1842. 
Ci tea by Laborde, Para- 
3 
Upperextremities 
Congestion of meninges over cer- 
Idem. 
1850 
Rilliet et Barthez. 
vical enlargement of cord. 
lysie de i'enfance, p. 
113. Paris, 1864. 
4 
• 
One arm. 
None. (Microscope not used.) 
Idem. 
Gazette Med. de Paris, 
1850 
1850, p. 681. 
5 
Idem. 
Both legs. 
Idem. (Idem.) 
Idem. 
Idem. 
6 
1855 
Behrend. 
1 
• 
Right lower ex- 
Chronic spinal meningitis. 
Fibres small; not fatty 
Cited by Heine, op. (At.. 
1863 
Von Recklinghausen. 
tremity. 
p. 150. 
7 
* 
Both legs. 
Tubercles in cord. 
Deutsche Klinik, 31 jan. 
1863. 
Gazette Med. de Paris, 
8 
1863 
Cornil. 
2 
49 
Unknown. 
Idem. 
Amyloid degeneration and atro- 
Fibres fatty. 
Bouvier. 
phy of white columns of cord. 
Sclerosis ofantero-lateral columns 
1864, p. 290. 
9 
1863 
1 
2 
Idem. 
All limbs. 
Fibres very small and 
Cited by Duchenne fils 
ofcord. 
granular; not fatty. 
in Archives Gen. 1864, 
ii., p. 205-9. 
Idem. 
10 
1863 
Henri Roger. 
Idem. 
Not stated. 
Idem. 
Not stated. 
11 
1864 
Laborde. 
8mo 
2 
Febrile. 
Both legs. 
Sclerosis of antero - lateral col- 
Fibres small; not de- 
Laborde, op. tit.. p. 104. 
umns of cord • cells normal. 
generated. 
Fibres small and gran- 
12 
1864 
Laborde et Cornil. 
1 
2 
Idem. 
Idem. 
Cortical sclerosis of cord ; sciatic 
Idem, p. 109. 
Prevost. 
neuritis; cells normal. 
ular; not fatty. 
13 
1865 
78 
Unknown (infan- 
Left lower ex- 
Atrophy of cells of left anterior 
Fibres fatty. 
C.-R. Soc. de Biologic, 
tile ?). 
tremity. 
horn ot cord; atrophy of left 
antero-lateral column. 
1865, p. 215. 
14 
1866 
Echeverria. 
3 
10 
Febrile. 
Right limbs. 
Cells of anterior horns filled with 
Fibres granular; not Echeverria, On Reflex 
granular pigment; diffused my- 
fatty. 
Paralysis, p. 29. New 
1866 
elitis. 
York, 1866. 
15 
Idem. 
2 
2J 
Febrile diarrhoea. 
Both legs. 
Nerve cells granular; diffused 
Fibres fatty. 
Idem, p. 33. 
myelitis; nenes shrunken. 
CASES OF INFANTILE SPINAL PARALYSIS. 13 
16 
17 
18 
19 
20 
21 
22 
23 
24 
25 
1867 
1868 
1870 
1870 
1870 
1871 
1871 
1871 
1873 
Win. A. Hammond. 
Lockhart Clarke. 
Charcot et Joffroy. 
Parrot et Joffroy. 
Vulpian. 
Roger et Damaschino. 
Idem. 
Idem. 
Lancereaux et Pierret. 
Roth. 
H? 
2 
2 
2 
1 
32 
40 
3 
69 
2 
2j 
3 
18 
2 
Palsy of 4 years' 
standing. 
After cow-pox in- 
oculation. 
Sudden, non - fe- 
brile. 
Unknown. 
Idem. 
After dysentery. 
After variola. 
Febrile. 
Febrile. 
Left lower ex- 
tremity. 
Upper extremities 
All limbs. 
Left lower ex- 
tremity. 
Right lower ex- 
tremity. 
Left upper ex- 
tremity. 
Both legs. 
Both legs and left 
side of back. 
Left arm. 
Both legs. 
Small clot in cord. 
Atrophy of nerve cells of anterior 
horns of cervical enlargement; 
central myelitis. 
Atrophy of cells of anterior horns ; 
atrophy of antero - lateral col- 
umns ; slight myelitis. 
Atrophy of cells of left anterior 
horn; atrophy of left antero- 
lateral column and nerve roots. 
Atrophy of cells of right anterior 
horn; some sclerosis of white 
columns. 
Atrophy of cells of left anterior 
horn ; sclerosis of antero-lateral 
columns; central myelitis and 
softening: left anterior nerve 
roots small. 
Atrophy of nerve cells of anterior 
horns; myelitis evidenced by 
sclerosis of antero-lateral col- 
umns and central spots of soft- 
ening. 
Atrophy of cells of anterior horns; 
patches of softening in gray 
matter ; sclerosis of antero-lat- 
eral columns. 
Atrophy of cells of left anterior 
horn; atrophy and sclerosis of 
left half of cord. 
Atrophy of cells of anterior horns 
of lumbar enlargement, and cen- 
tral myelitis ; atrophy of ante- 
rior nerve roots. 
Not stated. 
Idem. 
Fibres small, but not 
degenerated. 
Idem. 
Fibres small; striated; 
finely granular (fat- 
ty?)- 
Fibres small, with fat- 
ty granules and nu- 
merous sarcolemma 
nuclei. 
Fibres small; in part 
striated; with much 
granulo-fatty depos- 
it. 
Idem. 
Not stated. 
Not stated. 
Journal of Psychologi- 
cal Med., 1867, p. 51. 
New York. 
Med.-Chir. Trans., vol. 
li., p. 249. London, 
1868. 
Archives de Phys., 1870, 
p. 135. Paris. 
Idem, p. 310. 
Idem, p. 316. 
Gazette Med., 1871, p. 
480. 
Idem, p. 505. 
Idem, p. 541. 
Cited by Petitflls, Atro- 
phie aigue des cellules 
motrices,p. 33. Paris, 
1873. 
Virchow's Archiv, 1873; 
Bd. Iviii., Hf. 2, p. 263. 
Note.-Dr. Allbutt's case (Lancet, 1870, ii., p. 84) I reject because of evident traumatism. 14 
degeneration is to be regarded as the primary lesion. The 
fact that, in one case at least,1 the cell lesion has been ob- 
served without any concomitant myelitis, would seem to sup- 
port Prof. Charcot's view that the cell degeneration is the 
primary and essential lesion. This is further strengthened 
by the recent revelations concerning the state of the nervous 
centres in progressive muscular atrophy ; in that disease the 
cells of the anterior horns being found in part or wholly de- 
stroyed by a similar pigmentary degeneration, without sur- 
rounding myelitis. 
Prof. Charcot was so kind as to give me some sections of 
the cord from the case, now classical, which he published 
under his own name and Joffroy's (his interne) in 1870. I 
will pass around two microscopes armed with half-inch objec- 
tives, one showing a transverse section of a normal spinal 
cord, the other the section from Charcot's case. Both sec- 
tions are from the mid-dorsal region of the cord, a part in 
which the anterior horns are small and the cells few. The 
normal anterior horn exhibits six or eight large well-defined 
multipolar ganglion cells, stained red by carmine, their nuclei 
standing out more deeply tinged than the body of the cell. 
On the other hand, careful examination of the morbid section 
shows nothing but a somewhat condensed gray horn tissue, 
without one distinct ganglion cell. The granulations which 
probably once existed in the place of some of the cells have 
been dissolved by the method (Clarke's) used in preparing 
the section. I would also call your attention to the fact that 
the diseased anterior horn is shrunken and less club-shaped 
than the same part in the healthy section. 
The differential diagnosis of this from other paralytic 
affections of infants I leave until our next meeting, when we 
shall review the whole group briefly. 
The prognosis of infantile spinal paralysis is not good for 
many reasons. The disease is a severe one, accompanied by 
a serious central lesion, and is possibly incurable in a certain 
proportion of cases in spite of every favoring circumstance. 
1 Case by Charcot and Joffroy. 15 
Then usually we are consulted weeks, months, and even 
years after the stage of atrophy and deformity has set in, and 
the cure is then more questionable in proportion to the period 
of time which has thus elapsed. Many of the deformities can 
be remedied, at any age, by proper orthopedic treatment; 
but that is not curing the disease. Until the recent (see supra) 
discovery of the reaction of atrophied muscles we had no 
guide in prognosis beyond time, and the appearance of the 
parts. Now, we know that if any contraction can be obtained 
by means of the galvanic current (interrupted), there is some 
hope of restoring the muscles to activity. One authority 
(Dr. Hammond) 1 says, "If the muscles can be made to con- 
tract with either the induced or the primary currents, the 
cure is merely a matter of time and patience ; " but I am 
afraid that this is rather a sanguine expectation. I should 
give a very guarded prognosis, under these circumstances, in 
all cases having lasted beyond a year. 
I will be very brief about the treatment. The manage- 
ment of the first or febrile stage is a matter of uncertainty ; 
few practitioners see the cases in this stage, and, when they 
do, the diagnosis of simple fever, or of fever symptomatic of 
some teething or intestinal disorder, is usually made. Were 
I to meet with such a case, and have due reason, from occur- 
rence of delirium, convulsions, and the presence of hyperses- 
thesia, to suspect impending spinal palsy, I should leech the 
child's spine, and apply counter-irritants to the extremities. 
Besides, treatment indicated by the state of the mouth or 
bow'els should be carried out. The treatment of the second 
stage is likewise a matter about which no rules based on solid 
experience can be laid down. I should favor irritating the 
spine and the extremities, keeping the child's bowels free, 
and applying electricity, in either of the forms commonly 
employed, to the palsied muscles. 
The management of the third stage may be divided into 
1. The treatment of the central lesion and of the atrophy; 
and 2. The curing of the deformities. 
1 A Treatise on Diseases of the Nervous System. New York, 1871, 
p. 692. 16 
1. We know no means which will -with certainty remedy 
the central lesion which I have described as existing in this 
disease. Strychnia and nux-vomica were prescribed by Heine 
and by other older authorities, but are now abandoned. The 
hypodermic injection of strychnia about the wasted parts has 
been recommended of late, and is worthy of a trial; from -fa 
to grain may be injected with safety, according to the age 
of the patient. Of course every thing which shall tend to im- 
prove the patient's general condition (hygiene, nutritious food, 
cod-liver oil, exercise) will favor the reconstruction of the 
atrophied nerve cells. 
2. The means of treating the palsy and atrophy con- 
sisted, until a few years ago, in the (nearly always vain) 
application of the faradic current, cold and hot douches, and 
the systematic friction of the atrophied muscles. These last 
are valuable, especially the alternate use of ice (or cold 
water) and hot water to produce hyperaemia. Beyond these 
in value comes the use of the galvanic current, which will in 
many cases produce good contractions in the wasted muscles. 
The number of cells to be used must be determined by trial; 
10-20-30 elements of Stohrer's battery may be required to 
obtain a reaction. The positive electrode should be placed 
upon the nerve trunk supplying the atrophied group of mus- 
cles, and the negative sponge upon various muscles of the 
group; the current being meanwhile interrupted slowly by 
removing and replacing the negative electrode, or (to produce 
maximum irritation) reversed as well as interrupted by a 
mechanical contrivance on the battery or in the hand. I 
would suggest the use of nitrous oxide gas for the purpose of 
avoiding the intense pain produced by a large number of cells. 
Especially is anaesthesia useful in first examinations when you 
want to base a prognosis upon the result. An advantage of- 
fered by the use of this adjunct is, that, the child being still, 
you are able to recognize a small muscular contraction which 
might be overlooked during the struggles of the suffering pa- 
tient. How difficult it is to be sure that contractions occur 
under these circumstances, those of you who have attended in 17 
the electrical room of the college will remember. I am led 
to make a remark which I should have made when speaking 
of the prognosis, to the effect that a sate negative prognosis 
cannot in my opinion be based upon a first or second galvanic 
examination. If you can afford the time, and your patient 
the money, you should ask for a number of trials, at least six, 
before saying that the patient cannot be cured or improved. 
A great difficulty in the way of proper and successful galvan- 
ization consists in the very common stretched state of the 
atrophied muscles. For instance, in a palsied leg with healthy 
posterior tibial muscles, there exists pes equinus, and in con- 
sequence the wasted anterior tibial muscles are stretched 
to a great degree. Now, gentlemen, I believe that this tense 
condition will prevent galvanic reaction for a long time, if not 
indefinitely; and the relief of the tension either by mechanical 
contrivance (shoe), or better still by a tenotomy and a shoe, is 
followed by success in treatment. In illustration I would cite 
a private case of my own, a lady suffering from symptomatic 
muscular atrophy consequent upon cerebro-spinal meningitis, 
in whom the muscles of the legs were in much the same state 
as the muscles in cases of infantile spinal palsy ; the posterior 
tibial muscles having in part recovered. The anterior tibial 
muscles were kept tense by a strong pes equino-varus, and for 
several months careful galvanization (even electro-puncture) 
produced no reaction. At last, as a dernier ressort, I asked 
Dr. H. B. Sands to cut the tendo-Achillis in both legs and to 
put the limbs in plaster of Paris. This was most dexterously 
done, and four days after the tenotomy distinct contractions 
appeared under galvanization in the atrophied muscles. 
The muscles, after improving in size under the above 
means, gradually begin to obey the will, and also respond to 
the faradic current. This stage in recovery should be carefully 
looked for, and the change of current made. 
The indications for tenotomy and for mechanical treatment 
of the deformities are various, and really out of my province. 
Ton would do well to call in the aid of a surgeon skilled in 
the devising of apparatus, and make use of the instrument as 
2 18 
auxiliary means in promising cases. The most important use 
of tenotomy I take to be that referred to above, facilitating 
the galvanic treatment. Incurable cases, and cases in which 
only slight improvement can be hoped for, had better be at 
once sent to an orthopedic surgeon for advice and treatment. 
The foregoing table of autopsies, in cases of infantile spinal 
paralysis, may prove useful. I believe it to be quite full.