stances sharp pains in the breast were among the first
symptoms of onset noted. It may very well be the case
that the nerves supplying the respiratory muscles, which
later develop a fatal paralysis, exhibit an early neuritis.
second possible explanation is involvement of cardiac
nerve-filaments; the alarming rise in the pulse rate, which
is a very constant factor of the onset, indicates that there
150 INFANTILE PARALYSIS.
is marked cardiac involvement. The following cases of
endocarditis in previously healthy children occurring
svnchronously with acute poliomyelitis were personally
communicated to the writer by Dr. Ben]. Ayres, of
ENDOCARDITIS AND ACUTE POLIOMYELITIS, WITH
Case i. F. \Y., female. 11 years. Onset July 8. 1912. Gradual.
Paralysis appearing July i2th. Maximum paralysis in right arm and
leg. Residual paralysis slight, February 15, 1913. Atrophy im-
proving under massage and electricity ; history of exposure, un-
known ; insect bites, none.
Heart findings: endocarditis from onset, improved after three
months' treatment. Murmur and slightly accelerated, irregular
action at present.
Case 2. G. B., female, 9 years. Onset March I, 1912; sudden
in character; paralysis date after onset. 8 days; maximum extent,
left leg and arm, muscles of neck, and cervical region; paralysis
residual, none after six months ; atrophy slight. History of ex-
Heart findings : endocarditis, onset on eighth day. Murmur
and accelerated, irregular pulse still persist. (Ayres.)
III. THE ACUTE ASCENDING OR RAPIDLY PROGRESSIVE
Those cases of acute poliomyelitis in which there is
progressive involvement of the cord present characteristic
symptoms which align them clinically in a separate group-
ing. The progression of the paralysis is usually from the
lower extremities upward, and death ensues, when both
diaphragm and intercostal muscles are involved, from
paralysis of respiration. The cases usually succumb during
the first week, and some cases are incredibly swift in termi-
nation. Of 3 fatal cases of the acute respiratory type seen
by the writer, a girl 5 years of age, whose onset occurred
SPECIAL TYPES OF ACLTE POLIOMYELITIS. 151
after some well-marked prodromes, at breakfast, died be-
tween 5 and 6 o'clock of the same day ; 2 brothers, aged 2
and / years, taken ill on Tuesday and Thursday, died of
respiratory failure the following Sunday afternonn.
A classical picture of this form of poliomyelitis is given
by Draper, Peabody and Dochez in their recent mono-
graph, a part of which is abstracted:
"The typical clinical picture i> that of one with a clear, alert
sensorium, righting for every breath until he is literally suffocated.
In fatal cases there is usually a pause after the acute onset of the
paralysis. There may be one or two days without any definite
increase in paralysis, but it is noticeable that the children are not
doing so well as those that will eventually recover. Often the
respiration is more rapid and a trifle more difficult than the degree
of paralysis warrants. They are frequently unusually excitable and
irritable. Then the paralysis may begin to increase. A laryngeal
disturbance with hoarseness, aphonia, or difficulty in swallowing
may be the first evidence of the spreading lesion. If the inter-
i'i >-tals are still active the movement of the chest becomes less
marked. If the diaphragm has hitherto been intact, its movement.
as represented by the abdominal wall, becomes weaker, or there is
an asymmetric movement suggesting a paralysis of one side of the
diaphragm. The ala? nasi dilate with inspiration, and the accessory
muscles of respiration of the neck come into play. As the diaphragm
weakens, the neck muscles become more and more prominent until
it seems as if the whole work of breathing depended on them. The
head is thrown back, and with every breath the lower jaw is pushed
downward and forward in an attempt to get air. Meanwhile the
lungs may have remained perfectly clear until the very end, or a
few hours before death coarse, moist rales may accumulate, an
edema suggesting vasomotor paralysis. Heart sounds have been
audible for as much as five minutes after breathing stopped.
Several times a characteristic arrhythmia has set in for the last
few hours of life. It is interesting that in one case, in association
with the institution of artificial respiration and a lessening of
cyanosis, the irregularity of heart action completely disappeared.
"\Yith the onset of respiratory difficulty, it seems as if the
children were suddenly awakened and made to realize the struggle
152 1. \FAXTILE PARALYSIS.
before them. One sees a sleepy baby become all at once wide awake,
high strung, alert to the matter in hand, and this is, breathing. The
whole mind and body appeared to be concentrated on respiration.
The child gives the impression of one who has a fight on his hands
and knows perfectly well how to manage it. Instinctively he
husbands his strength, refuses food, and speaks when necessary
with few words. One little child, aged 4, unable to move, but with
a mind that seemed to take in the whole situation, said abruptly to
the nurse, between her hard-taken breaths, 'Turn me over.' 'Scratch
my nostril;' and then, to the doctor, 'Let me alone, doctor.' 'Don't
touch my chest.'
"Pressure on the chest, tight neck-bands, anything that ob-
structs easy respiration is immediately resented. The child is
nervous, fearful, and dreads being left alone. He often shows an
instinctive appreciation for the specially efficient nurse. The mouth
becomes filled with frothy saliva which the child is unable to swallow,
so he collects it between his lips and waits for the nurse to wipe it
away. The pallor is distinctive, the lips blue, cyanosis absent, and
sweating profuse. The mind becomes dull, unconsciousness follows,
and an hour or more later respiration cease-.'
As a typical case may be considered the following:
\\erner A., 14 years. For three days, fever and severe con-
stipation. On third day, paralysis of both legs, next day ascending
to abdominal and thoracic muscles. On the fifth day, death from
respiratory failure. (Kelly, Seattle.)
Case of Ascending TY/V, wth Death on Fortieth Day. E. F..
male, 18 months. Onset, May 26, 1908. Fever, restlessness, de-
lirium; pain on moving limbs; temperature when first seen (after
paralysis began) 100.5 F., late, thirty-eighth day, 108.5 to IIO F.,
per rectum. Rash : bright first two days. Paralysis of both lower
extremities followed by partial paralysis of both arms ; inability t< >
lift head; left facial paralysis and convergent strabismus of left
eye. Patellar reflexes abolished; Babiaski's sign present; twelfth
day, motion returned to arms; fourteenth day, motion returned to
limbs; fifteenth day, paralysis of rectus subsided; eighteenth day,
involvement of hypoglossal; twenty-fourth day. twitching of arms
and legs; twenty-sixth day, spastic contraction of hands; thirty-
seventh day, crowing spasms of larynx ; thirty-eighth day, tempera-
SPECIAL TYPES OF ACUTE POLIOMYELITIS.
ture 108.2 F., per rectum; respiration rapid and irregular, be-
coming Cheyne-Stokes in type ; fortieth day, moist rales over lower
lobes of lungs, and dullness over same area. Death occurred on
fortieth day, at 5.30 P.M., the temperature (rectal) one hour previous
being 110 F. and pulse 154. Dr. Fellman's diagnosis was "infantile
paralysis of cerebral origin." (Dr. G. H. Fellman, Milwaukee,
Fig. 47. Same as Fig. 46.
Fig. 46. Spinal type. Paralysis of
serrati, latissimus dorsi, and erectors
of spine; atrophy; scoliosis. Ante-
rior surface. (N. Y. Hospital for
Deformities and Joint Diseases.)
The paralysis in this case was of the ascending type;
we are indebted to a careful observer for this first record
of great disturbance of the heat center as shown by a rectal
temperature of 108 to 110 F. It probably occurs and is
overlooked in many cases of poliomyelitis. The steady
progression of the paralysis, which in this case was much
154 INFANTILE PARALYSIS.
prolonged, is shown by the late involvement of the cortex
(spastic contractions twenty-sixth day) and final involve-
ment of centers of respiration and heat.
Case of Deseendiiif/ Type with Death on the Fourth Day.
V. H., female, 3 years and 9 months. August 2/th, vomited
pear; 28, vomited everything given her, including water; played
about, was sleepy; 8 P.M., physician called; temperature 102 F. ;
knee-jerk present, pupils reacted ; Kernig absent. Gave calomel and
ordered baths and ice to suck; 29th, temperature 100.3 F- 5 vomited
everything given her; slightly jerky; no other symptoms. 3.30 P.M.,
all attempts to drink choked her and liquids came out through the
nostrils; with some ejection of frothy substance from mouth; 8
P.M., throat filled with saliva and air-bubbles, regurgitated one-half
teaspoonful of water; 9.30 P.M., temperature 10x3.5 F. ; pulse good;
child looked well except for paralysis of deglutition. August 3Oth,
2 A.M., child dying; no convulsions; no other paralysis; died at
4.30 A.M. (Armstrong and Cowern, 17 cases of poliomyelitis at
St. Paul, Minn., in 1909.)
The separation of the acute ascending (or descending)
paralysis from the spinal type is wholly arbitrary, and ac-
cording to Wickmann such cases belong to the spinal type
unless there is a fatal involvement of the muscles of
The paralysis in these cases makes steady progress, up-
ward or downward from the area first involved, until
paralysis of respiration closes the scene.
IV. ACUTE BULBAR-PONTINE TYPE OF POLIOMYELITIS.
Case of Bulbar Type zvith Moderate Coitical Involvement.
The patient, a child of 2^/2 years, could not protrude the tongue ;
not only was the left side of the face paralyzed, but there wa>
oculomotor paralysis and motor paralysis of the fifth nerve, with
the consequent strabismus and ptosis, and inability to close the
jaws. This was later associated with a spastic paralysis of the
right arm and leg, showing a spread of the lesion and the involve-
ment of the upper motor neurons to the limbs of the opposite side
SPECIAL TYPES OF ACUTE POLIOMYELITIS. 155
of the body. The child eventually made a good recovery. (Or.
Colin K. Russel, Montreal, 38 recent cases; a study of poliomyelitis i
Case of Bnlbar Type i^itJi Cranial-ncrrc Inrolremcnt Only.
\\'. C, male, 6 years ; fever, headache, stiff neck, constipation ;
unconscious for several days; difficult breathing; inability to
swallow; loss of hearing and speech for eight days; eighth day.
right facial paralysis; difficult mastication. Facial and hypoglossal
paralysis lasted for six weeks. Complete recovery. (Dr. Kelly.
Bulletin \Yashington State Board of Health, i
In the bulbar-pontine form there is paralysis of the
muscles supplied by nerves which take their origin in the
medulla or pons ; the cranial nerves most often involved are
the facial, hypoglossal, and ocular. There may be involve-
ment of the throat and larynx. Cases of the bulbar-pontine
type may be associated with a spastic paralysis due to cor-
tical involvement, as in the first case above given, with a
lower segment paralysis; with acute respiratory paralysis
and death due to invasion of the vital centers which are
disposed along the floor of the fourth ventricle; or to
tremor and ataxia due to interruption of the conducting
fibers from the cerebellum.
Facial paralysis is the most frequent manifestation of
this type; it is usually unilateral, but may be bilateral. It
is frequently the only manifestation of the acute disease,
and in sporadic form occurs not infrequently among adults.
A considerable number of cases among adults are con-
stantly in attendance at the clinic of the New York Hos-
pital for Deformities and Joint Diseases.
Five per cent, of the cases in the Massachusetts epi-
demic of 1909 had facial paralysis.
Ocular disturbances are common. There may be a
transient nystagmus or diplopia. Internal squint, due to
involvement of the external rectus, and divergent squint
with ptosis, from paralysis of the oculomotor, are often
seen. There may be fixation from paralysis of all the
156 INFANTILE PARALYSIS.
muscles. There may be transient blindness; or optic
atrophy with permanent blindness.
Stephenson, of London, has observed a group of cases
in children the chief characteristic of which is the sudden
onset of strabismus at an age when ordinary squint is not
altogether common. The child, often apparently in usual
health, is put to bed, and on awakening next morning is
found to present squint. Stephenson's observations lead
him to conclude that the oculomotor symptoms in these
cases depend on an acute focal encephalitis, quite analo-
gous with the better-known forms of that disease. He has
seen 28 such cases, all the patients being under 6 years of
age, and half of the number under i year. Although the
paralysis may affect any of the extrinsic muscles of the
eyeball, yet in three-fourths of the cases the external rectus
muscle alone is involved. The extrinsic musculature of
the eye is seldom attacked. Stephenson says that the com-
mon form of encephalic strabismus is very apt to be con-
fused with ordinary concomitant convergent strabismus.
Transient aphasias and transient deafness are not
rarely seen in this type of poliomyelitis. Dysphagia, with
salivation and regurgitation of all liquids through the
nares, is frequent. Dyspnea and the Cheyne-Stokes syn-
drome, when there is no paralysis of the chest muscles,
point to alarming involvement of the pneumogastric
V. ENCEPHALIC TYPE.
Cases of spastic hemiplegia with resultant contrac-
tions, but no atrophy, are frequently seen in close associa-
tion with cases of the flaccid paralytic type. The associa-
tion may occur in two members of the same family, and
this association is not infrequently seen in one individual
who presents, after the acute attack, both spastic and
SPECIAL TYPES OF ACUTE POLIOMYELITIS.
Fig. 48. Atrophy and lordosis with Fig. 49. Same as Fig. 48. Pos-
rotation following upper segment terior view.
paralysis, with paralysis of serrati,
latissimus dorsi, and erector spinse.
Anterior view. (X. Y. Hospital for
Deformities and Joint Diseases.)
Spastic lesions arise from injury to the motor cortex
of the cerebrum, or destructive invasion of its paths of
A spastic paralysis, however, is but one of the results
of an encephalitis produced by the virus of poliomyelitis.
There may be associated with the spastic paralysis : tremor,
an acute ataxia, athetosis, and clouded mentality.
The association of a flaccid paralysis of the extensors
of one or both legs, with a spastic condition of the great
Fig. 50. Oculomotor type. Strabismus. (N. Y. Hospital for
Deformities and Joint Diseases.)
toe or toes, or of the fingers of the hand of the opposite
side, is seen so frequently in the clinic of the New York-
Hospital for Deformities as not to arouse comment.
Three cases, the first and third of which were seen at
this clinic, are given :
SPECIAL TYPES OF ACUTE POLIOMYELITIS.
Hospital for Deformities, Examining Room, May, 1911. M. K.,
4-year-old girl, of Irish- American parentage; well developed; con-
scious; carried in by mother. Onset ten days previous, with fever
and vomiting. Child spastic and rigid from head to heels; spas-
ticity increased on handling; when placed on feet on examining
table child was rigid as a bottle and could be passed back and forth
between the hands as a bottle might be if tapped lightly on the neck ;
Fig. 51. Oculomotor type. Strabismus. (X. Y. Hospital for
Deformities and Joint Diseases.)
this action increased the spasticity until the child was standing
rigidly and involuntarily on tiptoes.
Armstrong and Cowern, of St. Paul, reported 17 cases
of poliomyelitis, in 1909.
C. T.. aged 6 years, female; Sept. 3d, malaise and headache;
Sept. 4th. feverish, drowsy, constipated ; Sept. 5th, 5 P.M., first seen
by physician, who considered it a case of indigestion, gave calomel,
160 IXFAXT1LE PARALYSIS.
and ordered citrate of potassium, which was vomited. Vomited
several times; told her mother her left hand hurt her and "wanted
to stay shut." Sept. 6th. paralysis of hand; could not extend
fingers. Child was up and appeared well save for a "wobbly" gait.
Feb. 19, 1910, child carries left hand in right; with effort she can
extend fingers and thumb, and the fingers are in a state of semi-
flexion with distal joint of thumb semiflexed. This was a case of
direct infection from a cousin.
Hospital for Deformities, May, 1911. F. B., male aged 19
months. \Yell-developed boy ; American parents ; walked and talked
at 14 months. Acute onset, April 19, 1911 (a sister also contracted
the disease, but made a good recovery). High fever; head sweating;
strabismus ; opisthotonus ; unconscious nine days. Five weeks later,
paralysis of extensors of both legs ; spastic right and left great toes ;
fingers of both hands spastic, and hands and arms constantly em-
ployed in slow, athetoid movement when awake. Constant slow,
vermicular motion of torso; makes no effort to sit, stand, or talk.
Head hydrocephalic. circumference i8*4 inches; fontanels un-
closed ; mentality clouded, but recognizes parents ; marked irritability.
A case of spastic paralysis in an adult has been reported
by Drs. Anderson and Frost :
Mrs. W., 22, waitress, was taken sick the latter part of June.
1910, with fever and indefinite general symptoms. After several
days she became paralyzed in both lower limbs. She was admitted
to a hospital about one week after onset. She was said to have had.
at that time, a flaccid motor paralysis of both lower extremities,
which, however, became spastic within a few days. When the pa-
tient was seen, the latter part of July, 1910, both legs and tint/Its
were quite spastic. No active motion was possible except of the
toes and slight flexion of the left knee. Passive motion was limited
to partial flexion of the thighs and slight flexion of left knee very
little of the right knee. The patellar reflexes greatly exaggerated on
both sides ; ankle-clonus on right side ; sensation for touch and pain
was normal. Examination was otherwise negative. The patient's
general health was good.
November 25, 1910, the left leg could be moved, but rather
awkwardly. The right leg showed little, if any, improvement.
Patellar reflexes were still exaggerated, more so on the right side.
There was no ankle-clonus and no atrophy.
SPECIAL TYPES OF ACUTE POLIOMYELITIS. 161
"The spasticity of the paralyzed limbs, exaggeration
of reflexes, and absence of atrophy in this case indicated a
lesion in the upper motor segment, either in the motor
cortex of the brain -or in the pyramidal tracts of the cord.
The case was included in our series in order to ascertain
the diagnosis, since it represents a rare clinical type of
poliomyelitis, the diagnosis of which has always been un-
certain, and whose occurrence has been a matter of some
dispute." (Anderson and Frost.)
In Sophian's series of 20 cases seen in a period of
three weeks during the Xew York epidemic of 1911, 12
of the cases w r ere of the encephalic type, that is, 60 per
cent, of a group of cases of poliomyelitis presented a pre-
ponderating cerebral involvement. This is a possible re-
sult of epidemic poliomyelitis that is little known, and of
extreme importance, and Dr. Sophian's brief table of the
20 cases is therefore given:
TWKXTY CASES FROM FALL EPIDEMIC OF 1911.
1 . .Myelitic form 3 cases.
All showed paralysis of both lower extremities.
2. Landry's ascending i case.
All 4 extremities, intercostals, and face.
3. Abortive form (one ataxic) 4 cases.
Slight, temporary quadriceps, paralysis with ataxia, i case.
Temporary paralysis right side of face and arm, i case.
4. I'olioencephalitic, cerebral forms 12 cases.
Ilemiplegia in 5 cases; bulbar involvement in 3.
Ophthalmoplegia (complete), 2 cases, associated with left
facial palsy in i case, and with palsy of the left lower
extremity in the other.
lUilbar involvement, alone, i case.
lUilbar involvement, with paralysis of one upper extremity,
(See 3 cases of bulbar involvement with hemiplegia.)
Isolated paralysis, 2 cases.
Left facial, right facial and right upper extremity, i case.
162 INFANTILE PARALYSIS.
Left upper extremity, left side of face, internal left eye.
XOTE. / case with left facial palsy, and a left-arm paralysis, the
latter possibly myelitic in origin.
Ages of cases ranged from 3 weeks to 22 year-, t Sophian.
Xew York. )
Fig. 52. Acute bulbar type. Left facial. (X. Y. Hospital for
Deformities and Joint Diseases.)
Classification of Symptoms of Encephalic Type.
Modified from Reginald Miller.
Polioencephalitis superior. Rolamlic cortex-spastic
hemiplegxas (Strumpell's paralysis).
Frontal area associated with mental defectives and
< )ccipital area blindness with normal eye-grounds and
SPECIAL TYPES OF ACUTE POLIOMYELITIS. 163
Symptoms common to all : Stupor, coma, meningitic
cry, bulging fontanels.
Polioencephalitis inferior (bulbar-pontine type see
above). Paralysis facial, oculomotor auditory one side
only. Tremor (pontine) : bulbar paralysis (vital center of
medulla ) .
Fig. 53. Acute bulbar type. Right facial. (X. Y. Hospital for
Deformities and Joint Diseases.^
Encephalitis cerebelli (predominant ataxia type).
Ataxia well marked or extreme; not demonstrable while
patient is stuporous, evident when patient rallies and makes
voluntary movement; nystagmus; scanning speech. (Clin-
ical diagnosis confirmed twice; post mortem in i recent
case and in i case of thirty years' standing.)
Encephalitis of midbrain and connections: Acute
tremor; hypertonus: excessive emotionalism. Tremor, due
164 INFANTILE PARALYSIS.
to the alternate action of groups of muscles and their an-
tagonists ; a slow, rhythmic movement of the intention type,
at the rate of about five a second. It is of the intention
type, and appears only when an attempt is made to use the
affected limb. Hypertonus, not a true spastic condition,
but sufficient to make the movement of limbs slow, stiff,
Thalamic encephalitis : Spastic paraplegias and hemi-
plegias may have an associated athetosis or chorea due to
lesions in the optic thalami. (See 111, encephalic type,
All types of encephalitis enumerated above may
I. In epidemic form.
II. In sporadic form.
III. As congenital cases from intra-uterine infection.
Congenital spastic paraplegias. Mental deficiencies of all
Polioencephalitis of a pure type, with no paralysis,
spastic or otherwise, may occur. This class of case among
male adults is almost uniformly fatal, and is rarely recog-
nized in its relation to the epidemic disease. Such a case,
confirmed by the post-mortem examination, is here given :
Anatomic Investigation of 19 Cases of ILpidcmic .Icntc Polio-
myelitis. Male, 39 years; fever; headache, stiff neck, vomiting,
some rigidity of limbs, couvulsive seizures, clouded consciousm-^- :
coma, death on twelfth day; no paralysis nor paresis.
Necropsy. Diffuse hyperemia of central nervous system ;
softened encephalitic foci in the right temporal lobe and gyms
fornicatus of both sides. Inflammation extended with lessened in-
tensity to basal ganglia, along aqueduct of Sylvius, through medulla
oblongata and was even demonstrable in upper portions of cord.
(Harbitz and Scheel.)
Gregor and Hopper reported 132 cases of poliomyelitis
in Cornwall and Devon, Kngland, in 1911. One case
SPECIAL TYPES OF ACUTE POLIOMYELITIS. 165
O. N. B., male; onset August 23th, temperature 100 to 101
F. ; vomiting. August 3Oth, very irritable. Kernig present on
both sides ; f undi normal ; paralysis of external recti ; no other
paralysis. September 2cl, semicomatose, gradually deepening to
stupor. September 3d, coma, died.
Frontal-area Involvement, with Resulting Mental De-
feet. Feeble-minded conditions subsequent to and caused
by acute poliomyeloencephalitis have received little con-
sideration as yet by investigators of the recent pandemics
of the disease; the writer considers it probable that a
majority of all morons, idiots, and imbeciles are victims
of this acute infection of the nervous system. Of the few
brief references in the literature there is one of Dr. Mark