ACUTE POLIOMYELiTlS

 

DRAPER

ACUTE POLIOMYELITIS

BY

GEORGE DRAPER, M.D.

ASSOCIATE IN MEDICINE COLLEGE OF PHYSICIANS AND SURGEONS, COLUMBIA UNIVERSITY;
ASSOCIATE ATTENDING PHYSICIAN I’RESBYTERIAN HOSPITAL
NEW YORK CITY

WYHIAFOREWORDBY
SIMON FLEXNER

WITH NINETEEN ILLUSTRATIONS

PHILADELPHIA

P. BLAKISTON’S SON & CO.
1012 WALNUT STREET

COPYRIGHT, 1917, BY P. BLAKISION’S SON & Co.

CAT. mg
DUBLIC HEALTH

THE MA.PLE PRESS YORK PA

 

FOREWORD

The epidemic of poliomyelitis which swept over the Eastern
United States during the past summer and autumn achieved
a new record. The number of cases exceeded that of any previous
epidemic reported and the mortality approached the maximum
recorded.

Hence it becomes very desirable to proﬁt by the experience
gained in the daily study at the hospital and in the home, at the
bedside and in the laboratory, under the exceptional conditions
of the epidemic, in order that we may be prepared to meet the
future with greater knowledge and confidence. '

Dr. Draper’s book is a timely contribution to this purpose;
but it is much more than that. He brought to his task a con—
siderable previous experience in the clinical and experimental
study of poliomyelitis. During the two years in which cases of
the disease were taken into the Rockefeller Hospital, he was one
of the small group in charge of that special service. The results
of the clinical and laboratory studies carried out there have been
assembled into a monograph issued by the Rockefeller Institute
for Medical Research. Of this monograph, Dr. Draper is
part author.

This particular experience is reﬂected in the book which he
has now written, for in it he has combined clinical and experi—
mental data in a way peculiarly illuminating and valuable at
the present time. But in treating the subject in this inclusive
manner, the objective clinical character of the book has not
been lost. Indeed, it may be taken as a practical guide to the
diagnosis, care, and speciﬁc treatment of epidemic poliomyelitis.

The appearance of the book is opportune. Just what the
coming summer and autumn may have in store cannot be
predicted, but it is altogether too much to hope that the epi-

V

181

vi FOREWORD

demic will not prevail in some degree in this country. A great
need has been felt in the past for an experiential book that is up
to date. This need is happily now supplied.

- SIMON FLEXNER.
ROCKEFELLER INSTITUTE FOR '

MEDICAL RESEARCH

PREFACE

The problem of poliomyelitis with which this book attempts to
deal is not a new one and has been much discussed in the litera-
ture of many lands. Until 1907 this country had felt but little
the terror aroused by visitations of acute epidemic poliomyelitis,
and consequently the public and the medical profession at large
have been unaware of the serious menace that the disease
presents.

The reports from other countries bearing on the subject have
not reached the rank and ﬁle of the medical profession so as to
develop in their minds a conception of this protean and remark-
able disease as a clinical entity. This has been largely due to
the facts that what has been written about poliomyelitis has ap-
peared in a variety of languages and also in fragmentary man—
ner. From one author has come remarks on the pathology,
from another description of the clinical course, and from others
discussion of epidemiological and experimental studies. F urther-
more these various contributions have not appeared in any par-
ticular relationship to one another. This is especially true of
experimental and clinical studies. Even the various mono-
graphs which have been published during the past ﬁve or six
years deal with one phase of the problem or another rather more
especially than with the subject as a whole. '-

A further obstacle to the earlier full appreciation of the nature
of the disease has been its two incorrect and unfortunate names:
“Poliomyelitis” (from 7ro Més, gray, and ,uveMs, marrow) has
served to focus the attention of observers upon those symptoms
which were naturally associated with disturbances of the gray
matter of the spinal cord, namely the paralysis. The second
name “infantile paralysis” is a dual misnomer, for the disease
is no more limited to infants than it is to paralytic symptoms.

, It is curious, too, that notwithstanding the gradual realization,

resulting from many severe epidemics, that the malady was of
\‘ii

viii PREFACE

infectious nature, clinicians and the public have been loath to
give up the ﬁxed conception that paralysis is the beginning and
end of the story.

The purpose of the book therefore is to present as completely
as possible, within reasonable space, the more recent conception
of this remarkable disease by correlating as far as possible all the
facts at present available.

It is designed to develop the idea that acute poliomyelitis is a
general infectious disease, in the course of which paralysis is but
an accidental and incidental occurrence.

The observations upon which much of this book is based are
drawn from the epidemic of last summer. For certain parts of
the statistical material I am indebted to the Commissioners of
the New York City Health Department, and of the New York
State Department of Health.

There has been no attempt made to give a complete bibliog-
raphy nor to refer by name to all the individual contributors to
the subject.

1The Monograph and other publications of the Rockefeller
Institute have been drawn on liberally for facts and statistics
and in some instances actual passages of the text have been in-
corporated in the present work.

The author desires to express his sincere appreciation of the
advice and encouragement given by Dr. Simon Flexner and
Dr. H. L. Amoss.

1Reference is made so frequently to the Monograph of the Rockefeller In-
stitute that throughout the book, for convenience, it will be spoken of simply
as the Monograph.

CONTENTS

CHAPTER I
HISTORY
PAGE
First mentions—Early and subsequent epidemics—Development of
clinical knowledge—Development of experimental knowledge. . . I
CHAPTER II
ETIOLOGYH ...................... 6
CHAPTER III
EPIDEMIOLOGY
Concentric or radial method of spread—Isolated cases—Contact
groups—Immunity of areas previously involved—Insects and
lower animals ............................................. r3 .
CHAPTER IV
EXPERIMENTAL DISEASE
The virus—Technique of transmission to monkeys—Bacteriology—
Immunity—Neutralization reaction ........................ 23
CHAPTER V
PATHOLOGY
General visceral lesions—Ganglia—Nervous tissue lesions—Menin-
geal invasion—Perivascular inﬁltration—Neurophages.. . . i . . . . 30
CHAPTER VI
TYPES
Classiﬁcation by paralysis—Classiﬁcation by general symptoms. . . . 38

CHAPTER VII

SYMPTOMS

Prodromata—Onset—Course—Pain—Spine sign—Reﬂexes—Psychic,
Mucous membranes, Digestive tract .......................... 62
ix

X CONTENTS

CHAPTER VIII

SYMPTOMS
PAGE
Clinical pathology—Blood—Spinal ﬂuid .......................... 70
CHAPTER IX
SYMPTOMS
Paralysis—Time of appearance—Degrees—Respiratory-FDelayed
form ..................................................... 7 5
CHAPTER X
PROGNOSIS
As to paralysis—As to life—As to recovery from existing paralysis. . . . 81
CHAPTER XI
TREATMENT
Early hours—After Paralysis—Prophylaxis ........................ 85

INDEX ..................................................... I 47

ACUTE POLIOMYELITIS

CHAPTER I

HISTORY

The story of the development of our knowledge of polio—
myelitis does not follow a single path continuously from the
earliest beginnings to the present time, but rather represents
the converging of several lines of study. Three distinct ave-
nues of investigation present themselves, the clinical, the
pathological, and the experimental. Each of these has a very
deﬁnite history and the contributions to each path have been
made by various observers quite distinct from those working in
other paths. The ﬁrst observation of the clinical phase of the
disease was probably made by Underwood1 in 1774. His
description is very meager and only suggests that he recognized
the fact that children might suddenly become paralyzed after
a brief illness. The next mention of the disease in the litera-
ture is that made by the English physician Badham2 in 1835.
His description is much more deﬁnite and has to do with a small
group of children in a circumscribed neighborhood. There can
be very little doubt that Badham described acute poliomyelitis.
But the ﬁrst systematic study of the clinical picture of this
malady was made by Jacob Von Heine3 in 1840 in the village
of Kolmar in Germany. Heine was an orthopedic surgeon
and saw a great many cases of paralysis in children, and be-
came interested in the subject. His' investigations led him to
investigate the stage of the disease not usually seen by the
orthopedic surgeon and he was the ﬁrst to realize that this
peculiar paralytic visitation was always preceded by an acute
febrile period. Heine’s description of this phase of the disease
demonstrates that he appreciated that there was a febrile reac-
tion which might be so mild as not to arouse any anxiety in

‘the. minds of the parents and pointed out indeed the great
I

2 ACUTE POLIOMYELITIS

contrast between their feelings during the acute stage and later
when they suddenly discovered the paralyzed leg on the morn-
ing following the acute symptoms. To Heine undoubtedly be-
longs the credit for ﬁrst having drawn attention to this disease
as being a clinical entity and also for having given the ﬁrst
complete description of it.

Following Heine’s work, the literature is barren of any dis-
cussion of the disease until 1884 when Strumpell“ in Vienna
described an encephalitic type which he believed to be similar
to the true poliomyelitis anterior of children as described by
Heine. He also drew attention to the fact that there were
certain forms of acute neuritis in children which belonged also
in this same group; thus, he brought together the neuritic type,
the poliomyelitic type and the encephalitic type and supposed
that they were all one and the same disease. He also threw
out the suggestion which was the ﬁrst of its kind, that the dis-
ease was probably of an infectious nature.

The next important step in the clinical study was that of
Medin5 who published in 1889 a description of the large epi-
demic in Sweden. In Medin’s work appears for the ﬁrst time
an excellent description of the acute stage of the disease,.and
we are ﬁrst given the impression that we have to do here not
alone with the paralytic aﬂiiction but also with an acute general
infection.

Then again there follows a long period of silence on the sub-
ject until Wickman6 in 1905, studying the vast epidemic in
Sweden, developed what may well be considered the modern
conception of the disease. His pathological, clinical and epi-
demiological studies form a classical contribution to the growth
of our knowledge of acute poliomyelitis, and established the
disease ﬁnally as a clinical entity. Wickman was the ﬁrst to
point out the so-called abortive type, a name which is unde-
sirable, and which has remained attached to those cases which
never develop paralysis. His epidemiological studies also gave
strong support to the View that the disease was transmitted by
contact.

Since Wickman there have been numerous contributions to
the clinical study of the disease from various countries. Among

HISTORY 3

others, extensive contributions have been made by Muller,7
Zappert,8 and from the Hospital of the Rockefeller Institute.

The history of the development of knowledge of the pathology
‘ of this disease probably begins with the description by the
French in 186 5. At that time Provost and Vulpian9 found an
atrophy of the anterior horns and ganglion cells in old cases of
poliomyelitis dying from other causes. This ﬁnding was cor-
roborated in 1870 by Charcot and Joffroy10 who also went
further and developed the hypothesis that the cells of the ante-
rior horn were the trophic centers of nerve and muscle, and that
they were the point of origin of the pathological process in
poliomyelitis. In 1871 Roger and Damesceno11 went still
further and described in the pathological process of much
earlier cases than had been seen by previous observers, the
interstitial and perivascular lesions. This observation seems
to be the very earliest indication of the more modern conception
of the pathological process in infantile paralysis. After the
work of Roger and Damesceno the next expression on the sub—
ject of the pathology was made by Rissler12 in 1888. He held
out for the theory that the initial damage was directly upon the
ganglion cells of the anterior horns. His pathological material
was largely from more acute cases than had previously been
examined. Nothing further then appeared until the work of
Wickman13 in 1905 when he published his extensive pathological
studies from the acute material of the large Swedish epidemic.
He demonstrated by the most painstaking and extensive
investigation the inﬁltration processes suggested by Rogers
and Damesceno and also showed very clearly the intimate
association of the blood vessels with the whole process.

In 1907 Strauss” pointed out that cases examined shortly
after death in the acute stage of the disease revealed general
swelling of the lymphatic apparatus throughout the body.
Similar observations were mentioned in the same year by
Harbitz and Scheel,l5 and again by Wickman in 1911.16

In 1912 Flexner, Peabody and Draper‘s“ noted that, aside
from the lesions in the central nervous system, there were
generally distributed lesions through the parenchymatous
organs and lymphatic structure of the body. This observation

4 ACUTE POLIOMYE LITIS

agreed well with the growing belief that the diseasewas not
limited to the central nervous system but was a general systemic
infection.

The third path in the growing knowledge of the disease is
that of experimentation. The whole history of this phase of
the investigation is of most recent date. It may be said practi-
cally to begin with the transmission of the disease to monkeys.
Previous to this there had been some attempt to work out a
bacteriology, but without success.

The ﬁrst successful transfer of this disease to monkeys was
accomplished by Landsteiner and Popper‘7 in Vienna in 1909.
But these observers failed to advance the study of the experi-
mental disease further by reason of their inability to propagate
the infection through a series of monkeys. They had used only
the intraperitoneal route of injection. Within a few months,
however, Flexner and Lewis18 succeeded by means of intra-
cerebral inoculations, in carrying on the disease indeﬁnitely
from monkey to monkey. In rapid succession came conﬁrma—
tion of this method by Landsteiner and Levaditi,19 Leiner and
v. Wiesner20 and others. By this means it became possible to
keep the Virus of poliomyelitis growing indeﬁnitely and so to
study its nature, and its behavior toward various physical and
chemical agents. Since then, contributions to the literature
of experimental poliomyelitis have been numerous, and there
have been developments in all branches of the laboratory study
of the disease. In 1909, independently of each other, Land-
steiner and Levaditi,21 and Flexner and Lewis22 showed the virus
to be ﬁlterable.

Finally, in 1914, Flexner and Noguchi23 published the report
of experiments on the cultivation and isolation of an organism
which seemed to be associated always with the disease. Up to
the present time this has neither been controverted nor broadly
conﬁrmed. The most recent observations, however, tend to
conﬁrm the observation that the organism of Flexner and
Noguchi is the cause of poliomyelitis.

A review of the history of this disease is interesting because
it shows that while the paralysis had always been the central
thought about which all discussion centered, nevertheless in

HISTORY 5

almost every description of the disease from the time of Badham
in 1835, there appeared also remarks which indicated that
the observer had recognized the presence of certain symptoms
characteristic of acute infections. From the very ﬁrst all
have agreed that there was an acute stage in poliomyelitis.
Usually this stage was looked upon as representing the prodro-
mal period which, with varying severity, ushered in the paralytic
attack. The demonstration by Wickman of the “abortive”
or non-paralyzed forms went far to break down this View and to
initiate our present conception of an acute systemic infectious
disease in which paralysis may or may not occur.

CHAPTER II
ETIOLOGY

The discussion of the etiology of poliomyelitis will be-
considered here under two main heads, first that of suscepti-
bility and, second that of the active forces of the disease.

Susceptibility.—During the last few years there have been
many observations in the literature of infectious diseases
suggesting the possibility that certain types of individuals
possess special susceptibility toward certain diseases. These
various suggestions are rather vague, but they all indicate that
by a careful study of the type of individual, both physiologically
and anatomically, there may be some things which we have
not heretofore recognized that determine the greater or less
susceptibility of an individual for one or another disease.
Everyone who has worked in poliomyelitis wards has been
impressed with the great number of large, healthy, well—nour-
ished children aﬂlicted with the disease. Any layman who
enters such wards remarks invariably upon the strong and
healthy appearance of the patients. In other words, it is com-
mon experience that poliomyelitis patients are large for their age,
well nourished, plump, and with faces of rounded form. With
the same idea in view of determining types which are sus-
ceptible, many observations have been recorded during the
past year on the question of whether brunettes or blonds are
more susceptible, whether boys or girls are more susceptible,
and whether there is a difference in the susceptibility of various
races. None of these series of observations has yielded results
of convincing nature. Statistics show in the recent cases in
New York that boys were 55.8 per cent., girls 43.7 per cent.
These ﬁgures agree fairly well with those reported from other
epidemics. Thus in Massachusetts“ in r911 the statistics
showed that males were 56 per cent. and females 44 per cent.
of the total. Caverly reports25 males 57—60 per cent. and

females 43—40 per cent.
6

ETIOLOGY 7

TABLE I.——-FR0M REPORT 01‘ MAYOR’S SPECIAL COMMITTEEI

 

City
Native (born in U. S. A.) ......................... 3825
Italian .......................................... I 348
Russian ......................................... 1 287
Irish ............................................ 644
Austrian ........................................ 47 9
German ......................................... 47 9
Polish .......................................... 2 24
Norwegian ...................................... I o I
English ......................................... I 8 I
Hungarian ...................................... 103 ,
'Roumanian ...................................... 5 9
Scotch .......................................... 46
Swedish ......................................... 7 5
Lithuanian ...................................... I 4
West Indian ..................................... 20
French .......................................... I 7
Danish ......................................... I 4
Canadian ....................................... 2o
Bohemian ....................................... I 8
Finn ............................................ 2 6
Syrian .......................................... 9
Greek .......................................... I 7
Swiss ........................................... I 4
Spanish ......................................... I 2
Dutch .......................................... 5
Turkish ......................................... I 0
Cuban .......................................... 6
Slavonian ....................................... 2
Belgian ......................................... 2
Porto Rican ..................................... I
Portuguese ...................................... I
Mexican' ........................................ I
African ......................................... I
South American .................................. I
Indian .......................................... I
Armenian ....................................... 2
Ukarainian ...................................... I
Japanese ........................................ 2
9°05

1Supplied by the kindness of the Commissioner of Health, New York
City.

8 ACUTE POLIOMYELITIS

Racial groups in the City showed various susceptibility. The
foregoing table taken from the report of the Mayor’s Special
Committee26 indicates the distribution of cases among many
nationalities. The negroes seemed to be less affected than the
whites, but the difference in number stricken per capita of the ‘
blacks and whites is not great enough to base absolute statement
of relative immunity upon them. Besides there enters the
factor of less active social intercourse between the two races so
that an epidemic disease starting among the Whites might well
not invade the black race extensively. This same group pro-
tection might be a reason for the apparent immunity of those
peoples whose language made intercourse with Americans
difficult.

‘The type of child which seems to be most susceptible to the
disease is the large, well-grown, plump individual who has
certain deﬁnite characteristics of face and jaws, is broad
browed, and broad and round of face. The teeth are particu-
larly interesting. It was noted that in 50 to 60 per cent. of all
the cases in the hospital at Locust Valley, the central incisor
teeth of the upper jaw were separated by a cleft of varying
width. The wide sp'aced dentition has been a striking fea—
ture and frequently involves all the single teeth of both jaws,
so that each tooth stands entirely free.

For many years the close association of this disease with
the process of difficult dentition was thought to have some
etiological signiﬁcance. While no positive proof can be ad-
vanced that there is a relationship here, yet it is worthy of note
that so many children with poliomyelitis present abnormal
dentition. .

Among the adolescents and young adults who acquired polio-
myelitis and in whom the disease seemed always to be most
severe and indeed usually fatal, the type differed from that
just described. Instead of the very large, well—nourished
individuals with widely spaced teeth, there appeared a more
delicately made type. Of the six or eight fatal cases in young
adults seen by the writer, the similarity of appearance of the
individuals was so striking that all might have been of one
family. All were brunettes, with very delicate dark skins and

ETIOLOGY 9

high coloring of cheeks and lips. Often small deeply pigmented
moles were present on face or neck. There was in every case 3.

Age Chart
(Rheinisch -Westﬁilische Epidemic 1909.)

1—6 1-11'1 2 3 4—7 8—1011— 1—
Age Months

Years

190
180

 

FIG. I.

deﬁnite though ﬁnely chisled maxillary prognathism and
instead of dental separations a tendency to crowding of the

IO ACUTE POLIOMYELITIS

teeth. This type was so deﬁnitely and so frequently associated
with the severe form of the disease that. we have come to attach
grave prognostic signiﬁcance to it. In this connection, it is
interesting to note that a surprising number of the fathers
of children ill with poliomyelitis presented striking anthropolog-
ical markings. Thus one was a deﬁnite acromegalic, while two
others were clearly F roelich types, dark haired, fat faces and
bodies, narrow shoulders, broad hips, and knock knees. In
three others maxillary prognathism was marked and although
the body stature was small the hands were very large and
broad, and there was great physical strength. A seventh
father had widely separated upper incisor teeth and was a tall,
big boned individual. Four of the mothers in this group had
moderate or marked exophthalmos and were high strung, in-
tensely nervous women. In another instance, the mother of
two desperately ill cases had an unusual degree of maxillary
prognathism.

Whether or not these facts have a bearing on the ques—
tion of susceptibility is still problematical. The cited ex-
amples, however, are merely a few of the very many similar
observations made throughout the summer by the diagnosticians
of the New York State Department of Health on Long Island.
It is interesting too, to record the numerous instances of two,
three, four and ﬁve cases in families with such parental types,
suggesting possibly a true family susceptibility.

The ages chieﬂy affected by the disease can best be shown
on a chart. It is obvious that the second year is the most con-
stantly affected.

The number of cases reported in adults was considerable.
Thus the report of the Special Committe indicates that out of
5496 cases the following were above IO years:

Ages No. of cases
IO to 15 ................................ 94
15 to 20 ................................ 3.2
20 to 30 ................................ 4o
30 to 40 ................................ 25
40 to so ................................ 7

Occupation seems to have had no bearing at all upon the sus-

ETIOLOGY ‘ I I

ceptibility. As regards environment, there seems to be little
to mention. In the crowded tenement quarters the disease
raged, and also in the sparsely settled country districts. Further-
more, there seems to be no relationship to the degree of social
evolution of the people involved. Cases appeared in the
humblest and most squalid dwellings, as well as in the most
elaborate mansions.

The recent demonstration by Amoss and Taylor27 of neutral-
izing substances in the nasal secretions of certain human beings
is of great interest. Apparently several facts have been es-
tablished by their work. In the ﬁrst place. although the
'number of individuals observed is not great, it appears that
the nasal secretions of children may possess the neutralizing
substances less regularly than adults. These authors showed
that nasal secretions from a child on the fourth day of an attack
of poliomyelitis had no neutralizing powers. But on the four-
teenth day afterward, neutralizing bodies made their appear-
ance. This seems to be a direct relationship to the development
of neutralizing bodies in the blood which have been shown to
be present on the sixth day. It was further demonstrated in
their investigations that an adult whose nasal secretions con—
tained the neutralizing substance in health lost them during
an attack of choryza. They returned again at the conclusion
of the acute rhinitis.

These observations indicate the possibility, therefore, that
some individuals may be susceptible to acute poliomyelitis
because of failure of these neutralizing bodies in the nasal
secretions. The failure as it were of a ﬁrst line of defense.

Various bacteria have been described in association with
cases of poliomyelitis, but none of theibacteriological ﬁndings
have been satisfactorily conﬁrmed. Since the demonstration,
however, of the virus of poliomyelitis in the emulsions of
spinal cords of children dead with the disease in 1909 by
Landsteiner and Popper, the advance in knowledge of the in-
fectious agent has been steady and rapid. The natural history
of the virus has been worked out very fully in the laboratory.
Finally, the organism itself, or an organism, which appears to
be constantly associated with the disease and able to reproduce

I 2 ACUTE POLIOMYELITIS

it in animals fulﬁlling iKoch’s laws, was isolated by Flexner
and N oguchi in 1914. Up to the present time this organism has
been conﬁrmed by several laboratories and there has been no
complete disproof of its speciﬁcity. Whether or not the poly—
morphous organism described by Mathers,28 Rosenow,29 and
others and having afﬁnities with the streptococcus is the same
biological entity as that of Flexner and N oguchi is a question
which the accumulative weight of scientiﬁc observation and
experiment will determine. At the present writing adequate
proof of a relationship has not been brought.

CHAPTER III

EPIDEMIOLOGY

Wickman ﬁrst made a careful epidemiological study of
poliomyelitis. As a result of his work he concluded that the
disease was transmitted by contact of human cases with healthy
people. In a series of painstaking observations he showed the
undoubted relationship of the village school to the dissemination
of the disease. Before this observation attention had been
drawn to the tendency of the disease to appear along the main
routes of communication. But the immediate methods of
transmission were not suggested; At that time the disease was
looked upon as “infectious but not contagious.” In 1907
Wickman showed that infantile paralysis was spread by trans-
mission from person to person and that the so-called “abortive ”
forms played a highly important part in its dissemination.
Wickman pointed out among other things, that although polio-
‘ myelitis occurred largely in the late summer and early fall
nevertheless epidemics had occurred more than once in the
winter. This is a matter of considerable importance and will
be referred to again in the discussion of the question of in—
sect transmission. .

By studying in detail small circumscribed settlements
Wickman was able to demonstrate that from the village school
as a center the disease spread in a radial or concentric manner.
Furthermore, he demonstrated satisfactorily that the indi-
viduals with the non-paralytic form of the disease were able to
transmit it to others who in turn developed paralysis. Finally,
Wickman recognized that in some instances a healthy inter-
mediary (possibly carrier) might be the medium of transmission.

These original fundamental concepts of Wickman concern-
ing the epidemiology of poliomyelitis have been supported by
observations from every carefully studied epidemic which has
occurred since his classical study.

13

I4 ACUTE POLIOMYELITIS

A second series of groups indicating human contact trans-
ference of poliomyelitis is that also ﬁrst pointed out by Wickman
dealing especially with more isolated cases not connected with
schools. Some excellent examples of this type of group infec-
tion have been published by Sheppard.30 The following two
groups from his series illustrate deﬁnite instances of direct and
indirect contacts:

   

uite’rerk
Greek 1:23,"

  

Wholesale
Warehouse

FIG. 2.—(Reproduced from N. Y. Stale loam. of ﬁled.)

Five cases occurred in this group. Case 1 occurred on the 4th of June;
Case 2 on the 12th of June. The father of Cases 1 and 2 is a Greek fruiterer
who traveled extensively over the city with his fruit team and most of the
time prior to their illness was accompanied by Cases r and 2.

Case 3 occurred on the 26th day of June in a family where the father of
Cases I and 2 delivered fruit, etc., and came into intimate contact with
the Greek fruiterer and his children, Cases I and 2.

Case 4,—An abortive attack occurred on the 30th of June. This case
was also exposed to the Greek fruiterer and his children, and to Case 3
intimately.

EPIDEMIOLOGY I 5

Case 5 occurred on July 19th, an adult which terminated fatally. The
Greek fruiterer (father of Cases 1 and 2) bought his fruit, etc., at the whole-
sale warehouse where Case 5 frequently spent much of her time in the
ofﬁce with her husband (the proprietor of the warehouse). The Greek
traded exclusively with the proprietor and hence the contact was frequent
and intimate and much paper money passed between them. The line of
contact for Case 5 was indirect as far as we know.

 

FIG. 3.—(Reproduced from N. Y. State Journ. of Med.)

Five cases in this group. Case No. I occurred on July 12th and was
unrecognized by the attending physician.

Case No. 2 occurred on July 15th and was previously in intimate con—
tact with Case No. I. This case was also unrecognized at the time. Both,

however, were reported to the local authorities as positive cases a month
or so after their attacks.

Case No. 3 occurred on July 23d in the family of a letter carrier who
delivered mail at the homes of Cases Nos. I and 2.

Case No. 4 occurred on July 21st and was in intimate contact, playing
with Case No. 3 and visiting at the home.

16 ACUTE POLIOMYELITIS

Case No. 5 occurred on August I8th in a young adult who gave a history
of visiting in the house next door to Case No. 2, in which house Case No.

SON
FA THEL/ - SERVANT
nomm/ \
. Iva/war
M, ,_ MOTHER SERVANT 91—, .
C] D ' ‘
/ \ MONKEY
O O —> 0
NJ
Demonstrating’ Healthy Carrier:
4y Mucasal Washing’s
_ [ﬂing t. Peta-Jun.
I Srck Human . Sick Monkey
D Healthy Human 0 Healthy Monkey

Fro. 4.

2 had free access. This young adult came in contact with Case No. 2 in
this neighboring house.

Ernst/1’. Julius
Father -- Nils Gustav
M
I .9
.ﬁ . Franz Oscar .
”other H H. b (h [:1
an/ 12a 9
D - I: \1‘!
0/ \ H
» 0
Healthy Carriers Shown by
Hucosal Washings
- Sick Human 0 Sick Monkey
D Healthy Human 0 Healthy Monkey
FIG. 5.

Such examples as these lend strong support to the hypothesis
that the disease is spread by human contacts. That such
dangerous contacts, however, are not limited necessarily to

EPIDEMIOLOGY I 7

active cases, but may be produced by healthy intermediaries,
is indicated by the example cited. It is worthy of note too, in
this connection, that the virus has been demonstrated in the
mouth and nose washings of individuals who have been in
intimate contact with known cases of poliomyelitis. F lexner,
Clark and Frazier32 report ﬁnding the active virus in the nasal
and pharyngeal secretions of the parents of a child stricken with
the disease. The proof of this observation is complete in the
clinical and anatomical ﬁndings on the monkeys injected with
the parental washings. Both symptoms and pathological
changes were typical of acute poliomyelitis. Kling, Pettersson
and Wernstedt33 carried out extensive investigations of this
point and the main results of their studies are shown in the
following two charts constructed from their protocols.

In the ﬁrst group (Fig. 4) of the four healthy individuals
surrounding the patient, three harbored the virus; in the second
group (Fig. 5) three out of ﬁve carried the infectious agent.
Some doubt still exists as to satisfactoriness of the proof offered
by these experiments, for the pathological changes that these
authors describe in their monkeys are not altogether typical
of acute poliomyelitis. They offer to explain these discrepan—
cies on the ground that in carriers the virus is less virulent.

As there is no convenient way of recognizing these healthy
“ carriers” their number must remain an uncertain quantity and
their control impossible. But there is another large group of
cases which undoubtedly play.a very important part in the
spread of the disease. With the growth of our clinical knowl-
edge of poliomyelitis has come the realization that the majority
of cases never display any evidence of central nervous system
damage. The great difﬁculty of recognizing these unparalyzed
cases and consequent failure to prevent their free circulation in
the community seriously handicaps the accurate study of the
links of an epidemic chain.

One of the prominent epidemiological features of poliomye«
litis is its seasonal occurrence. Fig. 6 shows clearly that the
disease occurs most intensely during the months of July,
August and September. This warm weather relationship has
been one of the strongest reasons for believing that insects are

2

I 8 ACUTE POLIOMYELITIS

responsible for the spread of the malady. But it must be
remembered that winter epidemics have been reported from
Sweden and Norway. Furthermore, during the past winter,

INCIDENCE 0F
INFANTILE PARALYSIS
m

MASSACHUSETTS

BY MONTHS
FOR THE YEARS

I907
I908
l909
IOIO

 

FIG. 6.

in the month of February, a good-sized epidemic occurred in

the mountains of West Virginia.
According to the still unpublished report of the Department

EPIDEMIOLOGY I 9

of Health of West Virginia,* the ﬁrst case in this epidemic started
at Elkins on August 29th; the second case appeared September
9th and the third case October 10th. The disease took epi-
demic proportions about December 10th.

The total number of cases reported was 39 paralyzed and
3 5 non-paralyzed. The epidemic in the neighborhood of
Grafton covered a period between December 10th and Feb. 12th.
In this there were 22 paralyzed, 6 non-paralyzed and 6 deaths.
The ﬁrst case in F airmont was on January 6th; the total para-
lytic cases were I 5 and 3 deaths.

Apparently the deﬁnite effect upon the spread of the epi-
demic was accomplished by preventing gatherings of children
and interstate travel of children under 16 which was rigorously
carried out. Thorough investigations were made of the insects
and small animals in the neighborhood as well as studies of the
food supply and milk; but nothing of importance was discovered.

It is interesting to know that the mean temperature during
the period of December and January was 32°F. Besides
this deﬁnite epidemic there have been occasional scattered
cases in and about New York. One case appearing at
Northport, Long Island, in the beginning of March, and which
had a fatal termination, was particularly interesting because
of the fact that the week before the patient began to be sick
he had been in a rough and tumble ﬁght with a child who had
had the disease during the epidemic of the summer before.
Washings of the nose and throat of this recovered case were
injected into a monkey in the hope of demonstrating that it
was a carrier, but the monkey failed to develop the disease.
This, of course, is not a convincing experiment, because of the
wellknown difﬁculty of producing disease in the monkeys with
nasal washings, in any case.

Attention may also be drawn again here to the experiments
of Amoss and Taylor on nasal secretion already :referred
to. They indicate the possibility that carriers may be those
individuals whose secretions lack the usual neutralizing bodies.

At the present time the most convincing evidence points
strongly to human contact as the means of spread. For in

* This preliminary report is available through the courtesy of Dr. Carrol G. Bull.

20 ACUTE POLIOMYELITIS

addition to the epidemiological studies of Wickman, Sheppard,
Kling and Pettersson, Flexner and Frazier, cited above, there
remain those extraordinary instances of group immunity during
the past epidemic reported by the New York City Department
of Health. One of these, the instance of the 30,000 institu-
tional children in New York among whom no case occurred is
interesting because of the great numbers involved. All the
institutions harboring this large group were under rigid admis-
sion and visit quarantine regulations. Each new child was
detained two weeks in an observation ward before admission
to the general ward, and visitors were excluded altogether from
the Ist of July.

The other instance of group immunity was that of Barren
Island, which lies in Jamaica Bay between Rockaway Point
and the Flatlands, the city dumping ground. About 800 people
live there who rarely visit the main land. Although all the
refuse, rags and dead animals are sent there from the city, no
case of poliomyelitis occurred.

In regard to the insect question, it may be said brieﬂy, that
as yet there is no well-established experimental evidence to
show that insects play a regular part in the dissemination of the
disease. The same negative result is true of investigations
directed to demonstrate an association between human polio-
myelitis and pet animals, rodents, and barn yard fowl. As a
rule, localities which have been visited one year by an epidemic
of poliomyelitis have fewer or no cases the next year. This fact
is well shown in the studies of Kling and Wernstedt, which
indicate that the converse of the proposition may be true. For
it appears that places which are in the neighborhood of an
epidemic area and escape infection very often are severely
attacked the following year (Fig. 7).

A still unexplained phenomenon is the reappearance of the
disease after several years in a place which had once been in-
fected but which had been free during the interval. Such
reappearances have usually been ascribed to the fresh importation
of virus from an outside source. The recently published experi-
ments of Flexner and Amoss,35 however, showing the Viability
of virus preserved in glycerine for 4 to 6 years suggest another

EPIDEMIOLOGY 2 I

possibility. If the virus is able to persist under adverse condi—
tions for so long a period it may be that such reappearances as

XIX s3?

     
   

    

.-.' “:14?” ’3».

IX.

: ”a

  

7779 great ep/Uem/ca/ Fan of /905 “a“..-
The great ep/Hem/ta/ foc/ and some of

the small ones of/9/l —
77w boundary of the counties

FIG. 7.

those just referred to may depend on the reawakening of the
original virus quite as well as upon a fresh importation.

2 2 ACUTE POLIOMYELITIS

The reports of the New York City and State Department of
Health indicate very deﬁnitely that neither milk nor water
supply was found to be associated with outbreaks of poliomye-
litis in any locality. No evidence was to be had, moreover,
that foodstuffs were responsible for the spread of the disease.

CHAPTER IV
EXPERIMENTAL POLIOMYELITIS

With the establishment of an almost constantly successful
method of producing poliomyelitis in monkeys came the pos-
sibility of studying the nature of the virus, its mode of entrance
into and exit from the body, its distribution in the various
tissues of the body and its immunizing powers. A great number
and variety of experiments have been made during the past
few years but space does not permit a discussion of them all.
The more important observations, however, and especially
those which bear directly upon the interpretation of the human
disease will be mentioned.

In the ﬁrst place it was found that if a small quantity I c.c. to
3 c.c. of a 5 per cent. emulsion of the spinal cord of a child dead
from poliomyelitis was injected into the brain of a monkey,
the animal developed 7 to IO days later signs of irritability and
excitement followed by paralysis and death. It was then found
that if such a cord emulsion were passed through the pores
of a Berkefeldt ﬁlter that the clear ﬁltrate possessed the power
of setting up the disease as did the original emulsion, but with
less regularity. When once the disease became established
in the monkey it was a simple matter to transmit it through
an indeﬁnite succession of monkeys by means of intracerebral
injections of the spinal cord emulsion from each last dead
animal. Having obtained thus a virus capable of causing
the disease regularly, it was possible to study its character-
istics. The result of these investigations showed that the
virus was capable of withstanding freezing for months, but,
when dried within the substance of the spinal cord, it survived
only for several weeks. It was destroyed or lost virulence
rapidly if dried in an aqueous solution free from protein. To
heat the virus is not at all resistant, being destroyed by 50°C.
in a few minutes. “Hence,” Flexner states, “it would

23

24 ACUTE POLIOMYELITIS

appear that while the infectious agent can survive in ex-
ternal nature, yet it is incapable of multiplying there, and
needs to be protected by such substances as organic secretions,
etc., that would prevent rapid and complete drying.”

A rather unusual resistance is displayed by the virus to
carbolic acid, which it withstands in solution of 0.5 per cent.
strength. It is readily killed, however, by mercury bichloride.

There are various methods of inoculation which are success-
ful in monkeys, but they are not all attended with the same
regularity of success. The virus may be introduced sub-
cutaneously, intraperitoneally, into the sheath of one of the
large nerve trunks, or directly into the substance of the brain.
The last method is more regularly successful than any of the
others, especially with strains of virus which are fresh from
a human case and have not yet become adapted by passage
through monkeys. When the virus has become adapted to the
monkey it is much easier to produce the disease with it. Indeed
it is even possible by simply painting the nasal mucosa with a
highly adapted virus to produce experimental poliomyelitis.

This experiment naturally lent strong support to the hy-
pothesis formulated by Flexner and his co-workers that the
main route of entry for the virus to the central nervous system
was through the nasal mucosa and thence by way of the sheaths
of the olfactory nerve ﬁlaments through the cribriform plate.
Once arrived in the subarachnoid space the virus was dissem-
inated rapidly by way of the cerebrospinal ﬂuid. With the
ﬂuid it followed the invaginations of the arachnoid along the
perivascular spaces of the anterior spinal vessels into the
interior of the cord. This path of the virus can be followed by
the advancing columns of cells which are thrown out in reaction
all along the course of the vessels to their terminations about
the anterior horn cells.

Further experiments determined the fact that the virus was
present in the nasal mucosa and secretions of a monkey which
had been given the disease by the intracerebral route. In
other words, the nasal mucosa serve not only as a portal of
entry but also as an exit for the virus.

By the same method of Berkefeldt ﬁltration and intracerebral

EXPERIMENTAL POLIOMYELITIS 2 5'

injection of the ﬁltrate of suspected material such as nasal
and buccal secretions, and intestinal content, it was possible
to demonstrate the presence of the virus in the latter situation.

Distribution in the Tissues.—Since the virus could not
be detected by optical methods, inoculation experiments
offered the only means of demonstrating its presence in any sus-
pected material or tissue; but it has been possible in this way to
determine in what tissue of the body, other than the central
nervous system, the virus may exist. It was shown by
Flexner and his co-workers to be present in a mesenteric
lymph node and in the tonsils and pharyngeal mucosa; but it
has never been detected in the spinal ﬂuid or blood of human
cases of the disease. This negative ﬁnding cannot be wholly
explained now. It may depend upon the fact that no instance
of the human disease has been studied sufﬁciently early in its
course, or be due to the dilution of the virus in the ﬂuid, be-
sides which, it must be recalled that being taken directly
from human beings the virus possesses low infective power
for monkeys. The experiments of Clark, Frazier and Amoss
show that after intravenous inoculation in monkeys, the virus
of poliomyelitis disappears from the blood within 72 hours;
and other observations have shown that it is only after
enormous intravenous doses of the Virus that the monkey
develops the disease. Smaller doses intravenously fail to
produce any disturbance.

In this connection, must be mentioned a series of experi-
ments by Flexner and Amoss36 upon the distribution of the
virus in the body. These observers found that if a monkey be
injected intravenously with 50 cc of an active virus n0 symp—
toms developed. If injected with 250 to 500 cc. of the virus
by a similar route the animal succumbed to the disease. ,By
sacriﬁcing animals so injected at various periods following
inoculation they found that the virus was withdrawn from the
blood, ﬁrst, by spleen and bone marrow, next, by the posterior
spinal ganglia, which are extradural and have a blood supply
quite separate from that of the intradural portions of the
central nervous system, and, ﬁnally, by the central nerve tissue
itself. It was noted, however, that before the virus reached

2 6 ACUTE POLIOMYELITIS

the spinal cord the choroid plexus showed signs of injury.
Experiments were then carried out which showed that, if a
monkey were given an intraspinal injection of normal horse
serum thereby setting up a sterile inﬂammatory reaction in the
cerebrospinal space, subsequent intravenous inoculation with
50 c.c. or less of Virus suﬂiced to produce the disease. If, how-
ever, immune monkey serum was injected intraspinally after
the intravenous inoculation paralysis was prevented.

The foregoing experiments have recently been conﬁrmed and
their signiﬁcance ampliﬁed by the experiments of Flexner and
Amossi"7 upon the relation of meninges and choroid plexus to
poliomyelitic infection.

From these latter observations has come an appreciation of
the extreme delicacy of the mechanism for protection which
these structures possess. For example, it was shown, as before,
that an irritative meningitis set up by the intraspinal injection
of horse or homologous monkey serum promoted infection by
the intravenous route. Then followed experiments showing
that when far less irritative ﬂuids were injected intraspinally
the meningochoroid defense was abolished. Thus, for example,
injections of such physiologically accurate ﬂuids as Ringer’s or
Lock’s solution served to reduce the choroid defense so that
infection followed intravenous inoculation of 50 c.c. of the virus.
Indeed removal of spinal ﬂuid and injection of the same ﬂuid
from another monkey sufﬁced in some instances to break down
the defensive mechanism.

Nor was this promotion of infection through meningo—
choroidal injury limited to the results of intravenous inocula-
tion. For it was found that infected intranasal cotton plugs,
which failed to produce infection after two-hour contact in
unprepared animals, did cause the disease if the animal had
previously been given an intraspinal injection of horse serum.

Thus, by disturbing the delicately balanced protective
mechanism of the meningochoroid apparatus infection of the
cerebrospinal tract is promoted whether the virus enter by
the intranasal or intravenous route.

In this connection must also be mentioned the fact
demonstrated by Flexner and Amoss37 that not only does

EXPERIMENTAL POLIOMYELITIS 2 7

meningeal irritation promote the passage of blood borne virus
into the cerebrospinal spaces, but also the passage of neu-
tralizing substances or antibodies which are circulating in
the blood.

This last point is of especial signiﬁcance in connection with
the problem of the serum therapy of the disease. For, if
intraspinal injection of serum renders the passage of blood
borne antibodies to the spinal ﬂuid easy, then intravenous
and subcutaneous injections of immune serum for therapeutic
purposes as well as intraspinal injection are strongly indicated.
As will be seen in the chapter on Treatment, this principle has
been made use of by Amoss and Chesney in treating a series of
human cases.

It is further signiﬁcant that if the meningeal irritation be
slight, caused perhaps by a nearly non—irritant ﬂuid such as
Locke’s solution or spinal ﬂuid, one intraspinal dose of immune
serum serves to protect a monkey inoculated with the virus
intravenously. On the other hand, several doses are needed
when the meningeal damage is more severe. There seems to be
therefore some quantitative relationship between the severity
of meningo—choroidal injury and the amount of immune serum
necessary to prevent paralysis.

This observation may be signiﬁcant in view of the growing
clinical experience that very mild cases, with only a small cell
increase (below 100) in the spinal ﬂuid, often escape paralysis
when untreated. ‘

The conclusions from these experiments are that the virus
cannot pass from the blood to the cerebrospinal ﬂuid and ner-
vous tissues until there has been injury to the choroid plexus
and meningeal blood vessels and lymphatics; and that the virus,
which is in transit in the spinal ﬂuid from the blood to the cen-
tral nervous organs, can be neutralized by an immune serum
which reached the subarachnoid space either directly or indi-
rectly by subcutaneous or intravenous injection with subsequent
passage through the choroid damaged by intraspinal injection.
Finally, it has been shown that monkeys can be infected by
intraspinous injections of properly virulent virus. Virus intro-
duced thus into the cerebrospinal space diffuses with the ﬂuid

28 ACUTE POLIOMYELITIS

along the membranes; in part it becomes ﬁxed to the central
nervous tissue and in part passes out with the spinal ﬂuid into
the blood by the regular channels. In the blood it is presum-
ably lost. Virus which is injected into the spinal canal cannot
be found in the spinal ﬂuid later than 48 hours afterward. This
helps explain the fact that the virus has not yet been demon—
strated in the spinal ﬂuid of monkeys or humans at the time of
appearance of paralysis.

Immunity.—It is a well established fact both clinically in
human beings and experimentally in monkeys that with perhaps
an occasional exception one attack of poliomyelitis confers
complete immunity; but eﬂorts to develop an active immunity
in monkeys without producing the disease have been attended
with only partial success. For attempts to immunize by re-
peated injections of small or attenuated doses have occasion-
ally resulted in the production of the disease, but it has been
possible in some instances to develop an immunity by this
method. Passive immunization has never been accomplished.
The protection afforded by an attack of poliomyelitis in man
was conﬁrmed also for the experimental disease by Flexner
and Lewis;39 following which Romer and Joseph,‘13 Landsteiner
and Levaditi,44 Flexner and Lewis,45 Anderson and Frost,49
demonstrated in the blood of recovered persons and mon-
keys substances capable of neutralizing the virus of
poliomyelitis. These observations were followed by the
therapeutic experiments of Flexner and Lewis”, in which it
was shown that the intraspinal injection of immune (convales—
cent.) serum of monkeys and human beings protected monkeys
from the otherwise fatal. effects of an intravenous inoculation
of the virus. It was upon this work that Netter“1 in I912
based'his report on the therapeutic employment of immune
serum gathered from recovered cases. It is true that the
blood serum of some persons who have not been paralyzed
nor indeed even ever suspected that they have been victims
of the malady may show neutralizing powers. But N etter has
demonstrated that the serum of known non—paralyzed (so-
called abortive) cases contains the neutralizing bodies. It is
possible that these two last-mentioned facts may lend support

EXPERIMENTAL POLIOMYELITIS 2 9

to the opinion expressed by some that many people may
have poliomyelitis and never know it.

The Organism.——In 1914 Flexner and Noguchi succeeded in
isolating an organism from the central nervous tissue of cases of
poliomyelitis. Further study indicated that the organism was
probably constantly present in the central nervous organs
of fatal cases. Furthermore, artiﬁcally grown cultures of the
globoid bodies, as they were called, in the ninth generation
were capable of setting up the disease in monkeys.

Morphologically the organism appears as a very small
globoid body measuring 0.015 to 0.03 of a micron in diameter.
It occurs usually in pairs, small groups or short chains. The
extremely small size of the microbe places it almost at the
limits of visibility even with the strongest powers of the micro-
scope. It stains best by Giemsa stain, and by Gram. It can
be readily seen in the dark ﬁeld microscope.

Culturally, it differs from the larger forms of known disease
producing bacteria. Strictly anaerobic conditions are essential
for its growth as well as certain special nutritive media.
Human ascitic ﬂuid in deep tubes with a bit of sterile
kidney or brain tissue in the bottom forms the best medium.
The whole is overlaid with paraﬂin oil. Growth is slow under
the most favorable conditions.

Injection of culture of the globoid bodies into monkeys is
capable of setting up poliomyelitis, typical both in symptoms
and pathology. The globoid bodies, furthermore, may be
detected by microscopic examination directly in the nerve
tissue of human beings and monkeys dead of the disease. So far
the organism may be said in general to have fulﬁlled Koch’s
law of causation.

CHAPTER V
PATHOLOGY

It is a striking fact that just as the attention of the medical
profession was directed to the clinical picture of the disease of
poliomyelitis by the chronic deformities of children, so our
present knowledge of the extensive pathological changes began
with the studies by Charcot and others upon the atrophic
anterior horns of the gray matter. Our knowledge of the
pathological and clinical features of the disease has developed
rapidly and more or less equally in the past IO years, with the
result that in both ﬁelds have appeared indications that the
lesions of acute poliomyelitis are not limited to the central
nervous sytem. While several observers, Rissler, Harbitz
and Scheel, Wickman, and Strauss. recognized the presence
of changes outside the nervous system, they have not laid
particular stress upon the systemic lesions. The visceral
tissue changes, however, are sufﬁciently deﬁnite to form
properly a part of the pathology of the disease.

In the experimental disease in monkeys the pathological
changes are very uniform and characteristic. The several
lesions may be considered as they affect ﬁrst the meninges,
second the spinal cord, third the medulla and pons, fourth the
cerebrum, and ﬁfth the ganglia.

The meninges of the cord and medulla show, as a rule,
mononuclear cellular inﬁltration most pronounced adjacent
to, or surrounding, the blood vessels which enter the ﬁssures
of the cord and are present in the ﬂoor of the fourth ventricle.
The generalinﬁltration of the pia-arachnoid is interstitial and
as a rule, not heavy, while the invasion about the vessels within
the perivascular lymphatics is usually heavy, and sometimes
nodular. The spinal cord presents lesions most pronounced
in the anterior gray matter, less marked in the posterior gray
matter, and least present in the white matter. They are peri-

3O

PATHOLOGY 3 I

c

vascular, interstitial, and parenchymatous. The vascular
lesions, which are often pronounced, extend inward from the
meninges (Figs. 8 and 9); the interstitial ones are associated with
the presence of mononuclear, to a less extent of polynuclear cells,
of red corpuscles, and commonly of serum. Actual necro-
sis of the ground substance arises, but is uncommon on a large
scale. The anterior gray matter is rarely wholly destroyed at
certain levels. The interstitial lesions can, in some instances,
be traced outward, directly from affected vessels. The
lesions of the parenchyma consist of degeneration and necrosis
of ganglion cells, occurring chieﬂy but not exclusively in the
anterior gray matter. The necrotic cells are commonly in-

 

 

 

 

F IG. 8.—(Reproduced from the Monograph.)

vaded by phagocytes, the so—called neurophages. It is not
usual for deﬁnite relation to be obvious between the altered
blood vessels and the affected interstitial substance or paren-
chyma. The lesions of the medulla resemble those 'of the
spinal cord, except as they are modiﬁed by differences in anatom-
ical structure. The vessels most inﬁltrated are those present im-
mediately beneath the fourth ventricle; the deeper lying vessels
tend to be less aﬂected, and the very small branches through-
out the part are involved inconstantly. The focal interstitial
lesions tend to be smaller than those of the cord. No deﬁnite
relation can, as a rule, be made out between the vascular and
interstitial changes. Because of the smaller size and less
uniform distribution of nerve cells, the parenchymatous

3 2 ACUTE POLIOMYELITIS

lesions are less conspicuous; they are, however, essentially
identical With those of the cord. Lesions similar to those in
the medulla occur in the pons and crura cerebri, but less
frequently. The cerebrum is aﬁected far less constantly than
other parts of the nervous system. When present, the lesions
are perivascular and focal interstitial. The cerebral meninges,
as a rule, escape affection. The choroid plexus of the lateral

 

FIG. 9,—(Reproduced from the Monograph.)

and fourth ventricles has not been studied in all instances.
When the virus has been introduced experimentally into the
brain, cerebrospinal ﬂuid, or nerves, the rule appears to be that the
plexus escaped. However, exceptions to this rule occur, in which
case lesions similar to those described below as occurring after
intravenous injection of the virus may arise. The inter-
vertebral ganglia are invariably affected. The lesions are of
two main kinds, interstitial and parenchymatous, and are

PATHOLOGY 33

always focal. The cellular invasion proceeds from two
sources; the pial investment and the blood vessels. In the
former, direct extension may take place from the spinal men—
inges, or extension may occur by way of the connective tissue

 

Fro. Io.—(Reproduced from foam. Exp. Med.)

of nerve roots. In the latter, extension seems to proceed from
the blood vessels. It remains, however, to state that the
involvement of the blood vessels may not arise through the
general blood, but through inclusion of the vessels in the

inﬁltrative process within the septa 0f the nerve roots. In
3

34 ACUTE POLIOMYELITIS

rare instances the blood vessels present, as compared with
other parts of the ganglia, an unusual degree of surrounding
inﬁltration. The ganglionic nerve cells are destroyed in two
ways: ﬁrst. they are obliterated by focal accretions of mono-

 

FIG. 11.—(Reproduced from Joum. Exp. Med.)

nuclear cells, and second, by necrosis and neurophagocytosis, in
the same manner as in the corresponding condition in the

spinal cord.
In addition to these facts F lexner and Amoss showed that

PATHOLOGY 3 5

the character of the central nervous system lesions varied
somewhat depending upon the method of inoculation. All the
animals, whether injected intracerebrally or intravenously,
showed the usual perivascular inﬁltration. But it appeared in
several instances where large intravenous doses caused the dis-
ease that the blood vessels participated much more extensively
in the lesion than when the inoculation had been by a neural
route. Indeed the smaller vessels and capillaries were seriously
damaged indicating the possibility for direct escape of virus
from the blood into the nerve tissue. Besides these vascular
lesions in the nervous tissue itself there were noted deﬁnite
changes in the minute blood vessels of the choroid plexus.
Damage to the ependymal cells was seen, with marked disturb—
ances of the underlying vessels. So far as has been observed
the type of lesions seen in sections of human cords from cases
of poliomyelitis resembles more closely that seen in monkeys
after the intracerebral mode of inoculation.

On opening the skull of a human case of acute poliomyelitis
the (lura appears congested. The pia arachnoid is also mark-
edly injected and often oedematous. The surface of the brain
looks wet and soft, and of a dark grayish-pink color. The
same congestion and moist condition of dura and pia arachnoid
is seen over the cord, and on cross section the gray matter
usually bulges slightly and is dark pinkish gray in color. Fre—
quently tiny haemorrhagic points can be seen. Microscopically
the earliest change which can be seen is a perivascular inﬁl-
tration of small round cells along the blood vessels of the lepto-
meninges. These perivascular lymph spaces, being prolonga—
tions of the arachnoid spaces are free to the access of cerebro—
spinal ﬂuid. If our conceptions of the pathogenesis of the
disease is correct, it is obvious that the virus, having pene—
trated the injured choroid plexus, is suspended in the spinal
ﬂuid and is conveyed thus along these perivascular lymph spaces.
As it travels it calls forth the characteristic tissue reaction,
a pouring out of small round cells, chieﬂy of mononuclear type.
Recently Blanton46 has shown, by means of the oxydase reaction,
that among the mononuclear cells of the exudate may be many
granulocytes. The whole cellular outpouring is so great as to

36 ACUTE POLIOMYELITIS

choke the spaces and bring pressure to bear upon the surrounded
blood vessel. The process then advances from the parietal
meninges and enters the interior of the cord by the anterior
ﬁssure along the branches of the anterior spinal artery. In
addition to the cellular exudate the pial vessels themselves
are extremely engorged and frequently the damage to the
smaller and more delicate arteriole Walls is so great that localized
haemorrhage occurs. That the lesions are not conﬁned to the
anterior grey matter of the spinal cord, but affect also the
posterior, and even the white matter, has been often observed.
As now viewed pathologically, the older name for the disease,
“anterior poliomyelitis,” is hopelessly mistaken. Besides this
interstitial reaction with its cellular inﬁltration, haemorrhage
and oedema, which exert pressure upon the cells of the anterior
horn there appear deﬁnite changes in the ganglion cells
themselves.

These cells show all stages of degenerative change from the
slightest swelling and loss of Nissl’s bodies to complete destruc—
tion. Particularly interesting are the observations that un-
injured ganglion cellsmay be found side by side with other
ganglion cells exhibiting extreme injury and lying in a region of
advanced cellular inﬁltration. On the other hand, disin—
tegrating cells can be seen in sections which are strikingly free
from inﬁltration. When the degenerative process in the cell
is well under way polynuclear cells wander in and occupy the
degenerated cell—often several in a cell, and form the so—called
neurophages.

Cord lesions, however, are not limited to the vessels and the
ganglion cells. There is besides a diffuse cellular inﬁltration
throughout the gray and white matter. These interstitial
changes may reach extreme grades. So that, in addition to
the lumen narrowing collars of cells which surround the blood
vessels, oedema, hwmorrhage, and cellular inﬁltration increase
the burden under which the anterior horn cells have to labor.

Obviously, then, the injury to the central nervous tissues is
a severe and diversiﬁed one. There is still some question
whether or not the degeneration of the anterior horn cell de-
pends solely upon the effect of pressure from hazmorrhage

PATHOLOGY 3 7

and oedema and the Choking off of blood supply, or whether
there may also be from the virus a direct toxic effect upon
, the cell; but the weight of opinion is in favor of a combined
direct toxic action. The probability is that all the forces are
operative and that the anterior horn cells are both poisoned
and strangled to death.

Attention has been drawn to the general nature of the in-
fectious poliomyelitis process, and in conformity with this
fact, Flexner, Peabody and Draper described wide—spread
visceral lesions, in the lymphatic organs especially. They
consist of hyperplasia of lymphatic glands, of spleen, intesti-
nal lymphatic nodes and interstitial small cell inﬁltration in
the portal spaces of the liver, and general cloudy swelling
of the organs. The focal hepatic neuroses described by
them have not been confirmed by other observers, and may
have been accidental in these cases. The tonsils and pharyn—
geal lymphatic structures likewise share in the hyperplasia.

CHAPTER VI

CLASSIFICATION OF TYPES OF POLIOMYELITIS

Almost all existing classiﬁcations of the disease are based
upon the situation of the lesions in the central nervous system.
The absence of muscle weakness was the criterion for giving a
case the misleading name “abortive.” As our knowledge of
the disease has increased we have come to realize more and more
that the three important terms used in connection with the
malady are bad misnomers. Poliomyelitis, infantile paralysis,
and abortive are not only incorrect terms as regards fact, but
they have produced a habit of thought about the disease which
has done much to retard the growth of a clear understanding of
the pathological and clinical mechanism of the infection. Ever
since Wickman pointed out the clinical fact that there were
cases of poliomyelitis which never developed paralysis it has
become increasingly evident that the extent of this group is
much larger than was at ﬁrst supposed. The exact number of
these non-paralyzed cases doubtless varies in different epidemics
and may perhaps depend upon the relationship of variations
in virulence of the infectious agent and differences in individual
susceptibility. But all observers agree that they represent at
least 50 per cent. of the total incidence of the disease, and some
place the ﬁgure as high as 70 to 80 per cent. Even if the
lower valuation be accepted as correct, any system of classi-
ﬁcation based upon paralysis fails to cover, save by sweeping
exclusion, a full half of the recognized cases. The question
then arises whether or not there are other features of the disease
which appear with sufﬁcient frequency and constancy to form
criteria for classiﬁcation. One of the phenomena which led
Wickman to suspect the presence of non-paralyzed cases was
the appearance, in the family of a paralyzed child, of other
Children presenting acute febrile or gastro—intestinal disturb-
ances similar to those seen in the paralyzed case. In other

38

CLASSIFICATION OF TYPES OF POLIOMYELITIS 39

words, the non-paralyzed and paralyzed cases presented a simi-
lar set of general symptoms. Muller carried this observation
a step further when he pointed out that epidemic centers in
different sections of the country supplied examples of somewhat
different types of the acute systemic stage of the disease. Thus,
in one area gastro-intestinal disturbances predominated while
in another there were chieﬂy found cases with inﬂammation of
pharynx and tonsils. He further notes that the non—paralyzed
cases in a given locality presented the same particular set of
general symptoms, which had preceded the advent of muscle
weakness in the paralyzed cases of that locality.

Obviously then we are dealing with a disease which has two
distinct phases, one of general systemic nature and another of
specialized expression in the form of central nervous system
disorder. Furthermore, there may be a variety of symptom
complexes representing the systemic phase.

With these facts in mind it is apparent that a classiﬁcation
of the disease in terms of the paralyses is quite inadequate and
obsolete and that some new arrangement must be made.

Perhaps the most suggestive phenomenon of the whole .dis-
ease is the similarity between the acute systemic phase of the
paralyzed cases and the whole course of the non-paralyzed ones.
Consequently, the question arises as to what the relationship
is between the general systemic phase and the secondary
localized central nervous system phase of the malady.

In the Monograph there appears a discussion of the prodro-
mata of the disease. Here are considered the various symp-
toms and their arrangement, which precede the advent of
paralysis. Several different forms of prodromal expression are
mentioned, notably a series of digestive tract upsets and fever
which become increasingly severe until paralysis appears.
Attention, however, is also drawn to the occurrence of pro—
dromal phenomena which clear up entirely or almost entirely,
so that for a day or so the child appears to have recovered.
“Nevertheless” runs the text at this point. “one or two
days later, and perhaps without warning, the child becomes
paralyzed.”

It is this curious manifestation of two distinct phases or

40 ACUTE POLIOMYELITIS

periods in the course of the disease which this study attempts
to analyze and explain. Though previously recognized by us,
the full signiﬁcance of the phenomenon was but vaguely appre-
ciated. No attempt was made to correlate the events which,
though apparently separate, both in regard to time and char-
acter, in reality formed the complete expression of the disease.

Because of the opportunity to observe large numbers of cases
almost from the ﬁrst moment of illness during the epidemic
on Long Island, it was possible to classify the cases by their
clinical symptoms in the acute or febrile stage of the disease.

Three distinct groups have been separated. In the ﬁrst
two groups there develops a picture of general systemic infec—
tion from which the child appears to recover completely or in
part, then to receive a second blow directly upon the cerebro-
spinal tract.

Because of the two deﬁnite masses or humps of symptoms,
the' analogy to the arrangement of the ’dromedary’s back was
taken to express the type ﬁguratively. The temperature
curve may show one or two elevations but the ﬁgure refers to
all the signs and symptoms of each group or hump whether
there is an associated rise of temperature or not. The total
duration of the combined phases may vary from a few hours to
many days, while the intensity of either phase, the systemic
or the meningeal, may touch the extreme of violence or such
mildness as to escape detection.

The ﬁrst series called the “dromedary” group, shows clearly
two distinct periods of illness with an interval of well being
(see Cases 1—15). In the second series, called the “straggling”
group, this period of comparative well being is not present, but
there is a sustained course of indisposition of varying intensity
(Cases 16—24). In the third, or sudden onset group, all the
signs point from the start to meningeal and nervous tissue in-
volvement (Cases 25~3I). A striking feature of the whole
series is that the second portion of the ﬁrst two groups is very
similar to the whole course of the sudden onset group.

The ﬁrst hump of the dromedary type and the continued
course of the straggling group is composed of a febrile move-
ment with symptoms falling into three main categories—gastro—

CLASSIFICATION OF TYPES OF POLIOMYELITIS 41

intestinal, tonsillar and upper respiratory passage inﬂammation
and general malaise without localization of symptoms. Pursu-
ant then to a remission of all symptoms in the dromedary group,
or a varying duration of symptoms in the straggling group,
one of two things occurs—the patient promptly gets well or
sudden evidence of meningeal involvement appears from which
may follow recovery or paralysis.

Experiment has shown that the virus gains entrance with difﬁ-
culty to the central nervous system tissues of monkeys subjected
to intravenous inoculation. In human subjects the number of
cases recognized as never giving the slightest indication of
central nervous system invasion is steadily growing with our
experience. There are so frequently found in families where a
frank paralytic case occurs, other Children who present per-
sistently the same symptoms which the paralyzed child has
shown in the preliminary hump, that one is led to suppose that
these may be examples of infection in which no penetration of
the meninges occurred.

In the straggling group the same interpretation applies, the
only difference being that these individuals present a continu—
ous course with a fusion of the symptoms of the two stages.
Sudden onset cases may be looked upon as examples of the
malady in which the systemic stage has been overlooked be—
cause of its triviality. In this group the spectacular and violent
picture of meningeal disease dominates and drives the mem-
ory of the slight preceding indisposition from the mother’s
mind. It is very difﬁcult under these circumstances, to get
from the family any history of the child being unwell during
the preceding days.

We have included in this group of sudden onset, Case 41
(treatment series), where the child was punctured at I A.M. hav—
ing gone to bed well. This case might have been reported as
one where the child awoke with a stiff neck and high fever.
Yet the parents of this child remembered that for two days
previously there had been a slight and unimportant disturbance
of the bowels. In other words, this case with sudden meningeal
onset was an instance of typical dromedary course in which there
was apreliminary hump so mild as almost to escape appreciation.

42 '
The Case

ACUTE POLIOMYELITIS

25 (Diagnostic series), is another instance in which

no history of early indisposition was obtained at the time of

the acute onset.

3/71/9900
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may
uaw JO
na paqeadaJ aq p/noqs ampund

uajsenu/ maﬁa!

‘25;

ploaoqs JO uageapuad aJOJaq ’UQ/JDBJU/ ﬂuauaﬁ JO poi/ad

aq.) .79 JUaﬂban new aseas/p ,Ia uoqeu/
If

sen/now UOHOquUJOD
93193 0? 94004 21- 9

'21 '01:}

But later on, after the excitement of the

01/7; dull fora Few hours - sits arounat Mather
forgets about it after a day.

"Child has slight temperature —9.9." C onstlpa t/bn

Green apples” etc. as cause.
Loo/<5 tired - ma y be irritable.

\ Child deﬁnitely sick. Vomits. Temperature 99°-/0/.°
\ ‘ Irritable, Flus ed. Looks activeju Iii.

\
I
I

/\

 
  
  

Sever acute kgeneral infection - glassy bright eye -
resent/ill loo ,drcwsiness and irritability
alternating. Temperature /02.” Vomiting or not.
Flushed. Na meningismus.

Lumbar puncture fluid clean Pressure sli ht or
greatly increased. Amount increased. e/ls 0'5.
Globulin 0 -3 or +.

90494: \z

959%»

 

u/uau/jo po/Jad

eaﬁ

synou 2/ gsyy u_/ a/qen/en

4m Ill/119; ‘uqlsenui/

W. s/i‘ynt 5p. si 0, headache. Fluid: Pressure w ,
clear. Cells / - loo. Global/n + — ++.
_Usua/ly no paralyses.

l-Slight spine sign, lityperaesthetic, reflexes + + or
irregular. Spinal luid clear; Pressman. Cells

[00 1300. Globu/in H. May develop transient or
Facial.

F Definite spine 57m headache. Reflexes + + . Hyper-
aesthetic. Spine fluid clear or slightly hazy or
flocculent. Cells 200 '700. Pressure moderate.
_Cbance ofparalyses great.

 

'.' [Striking meningismus. Spinal fluid' hazy, pressure
normal to «r. Cells 500-2000. Globulin +++5tupor-
tm‘tchings. Sure paralyses or death.

 

 

affair was over, the mother recalled that the child complained
of headache and malaise a day or two before.

In a few instances lumbar puncture has been made during
what apparently was the ﬁrst hump and the ﬂuid at this stage

CLASSIFICATION OF TYPES OF POLIOMYELITIS 43

has been practically negative. There may be a very slight
suggestion of globulin increase as appeared in two or three cases,
but the pressure and volume of the ﬂuid has in almost all in—
stances, been increased. The second puncture in these cases,
made after the signs of meningeal invasion have appeared, has
shown ﬂuids with cell counts all above normal.

If the observations of Flexner and Amoss upon the effects of
intravenous inoculation of virus in monkeys now be recalled
(see page 25), the clinical course of the disease as just dis-
cussed can possibly be subjected to a more logical interpreta—

Fever Paralysis
/—/\——\ perMolur/Ieurane
Gast Intesl: [7/519 cerebral type
UonsilliRtis (encephali'tlc)
Tame/Efﬁe Rem’55’0’7 Lower Motor Neurone
Bu/bo Spinal

/5ymptoms (usual type)
Profound Stupor:

w
Systemic Phase >— Non- -para/yzed w
ISt-h ”mp (abortive) CMSysl'ern Phase
h—R 20d hump
Dmmedary-stragg/Ing ,%
SuaUen Onset
50- 60%

of the total incidence of
the disease ends here.

FIG. 13.

tion. A suggestive analogy becomes apparent between the
ﬁrst febrile period of the dromedary or straggling types and the
phenomena of lodgment of the virus in the spleen and bone
marrow of monkeys after intravenous inoculation. Likewise
the second hump in the human case, with its central nervous
system involvement, corresponds to the late disclosure of the
virus in the central nervous tissue of the monkey.

The accompanying plan (Fig. 12) shows a schematic form
of the foregoing interpretation of the disease.

A possible classiﬁcation therefore of the disease as a whole
on the basis ﬁrst discussed is indicated in Fig. 13.

44 ACUTE POLIOMYELITIS

DIAGNOSTIC SERIES
DROMEDARY GROUP

Case 1.—S. L. Boy. Age 9 years. Northport, L. I.

September 8, 1916. Child complained of headache and fever. Lasted
24 hours. He was then all right until 2 days ago.

September 17, 1916. Headache and fever returned (8—day interval).
Was constipated for following 2 days.

September 19, 1916. Vomited several times during the last 18 hours.
His temperature was Ioo.4°. Muscle tenderness in the thighs and calves.
Suggestion of left facial weakness. No spine sign.

Lumbar puncture at 48 hours. Fluid clear, pressure normal, cells 40.
Globulin negative. No further paralysis developed.

Discussion—This case illustrates the common phenomenon met in this
disease of two distinct febrile periods with a free interval. Here the ﬁrst
period lasted 24 hours, the interval 8 days (rather longer than usual), and
the second period 18 to 24 hours. In the last period the facial weakness
developed.

This we have called the “dromedary” type of case because of the two
“humps” in the temperature curve.

Case 2.—H. C. G. Boy. Age 5 years 6 months. Port Washington, L. I.

August 15, 1916. Vomiting several times and complaining of pains in
stomach. Temperature at this time ranging around 101°. This con-
tinued for 24 hours when the temperature dropped, the patient ceased to
vomit and felt as well as usual.

August 18, 1916. This morning, 8 hours ago, patient began to com-
plain of pain in left leg. Father stated that during sleep boy had muscular
twitching conﬁned chieﬂy to the arms and legs. Attending physician
states on seeing him this morning could not detect any deﬁnite paralysis,
but thought the left leg was weak, as he was not able to contract the thigh
as he should.

Physical examination showed the patient in a comatose state and when
awakened or aroused the eyes are staring and glassy in appearance. No
ocular weakness, no facial weakness, throat negative. Neck markedly
rigid. Abdomen distended. Extremities, aside from slight movements in
toes and external rotator of thigh, both legs paralyzed. Left completely.
Paralysis of erector spinze.

Reﬂexes.—Knee jerks absent on both sides. Puncture not done.

Discussion—In this instance the ﬁrst hump is deﬁnitely associated with
gastrointestinal symptoms, and the second with central nervous system
symptoms. The free interval is clean cut and of about 48 hours’ duration.

CLASSIFICATION OF TYPES OF POLIOMYELITIS 45

Case 3.—M. L. Age 3 years. Patchogue, L. I.

August 23, 1916. Temperature 104°. Wanted to lie down.

August 24, 1916. Temperature 99.5°. No signs. Well until

August 28, 1916. “Feverish” last night. Examination was negative
except for a slight left facial paralysis. No puncture was made.

August 31, 1916. Reported by Dr. Overton to have died from sudden
respiratory failure yesterday A.M. after removal to the hospital.

Discussion.—This case is rather unusual in the development of respira—
tory failure 3 days after the establishment of a facial paralysis without
other muscles involved. It is a well—marked dromcdary type. No
puncture was made.

Case 4.—M. T. Boy. Age 8 years. Oyster Bay, L. I.

August 13, 1916. Child began to complain. A little drowsy, slight
headache. Was taken to the family physician who found the temperature
102°. Was given a cathartic and the condition apparently cleared up.

August 18, 1916. The child began to feel drowsy again and had no
appetite, refused breakfast, and complained of slight headache. A doctor
was called in who suspected the case to be one of poliomyelitis. Tempera-
ture registered 102°.

Physical examination showed the eyes “glassy.” Mouth and nostrils
negative. Very slight rigidity of the neck. Extremities show no paralysis
or muscular weakness.

Rcﬂexcs.—Knee jerks inconstant, but when obtained are active. No
Kernig.

Lumbar puncture at 12 hours. Fluid clear under moderate pressure,
about 8 c.c. obtained. Cell count 40. Noguchi plus. Albumin plus.

August 21, 1916. In Locust Valley Hospital, doing well, no paralysis.

Case 5.-—L. C. Girl. Age 3 years. Port Washington, L. I.

August 26, 1916. Child had a chill followed by fever. This occurred
again 2 days later. The mother thought this might be malaria, and
gave the child quinine. Appetite was poor for 3 days and the child
was restless and irritable.

September 1, 1916. Mother noticed that the child was unable to walk.
She crawled about on her knees. She had always been well until last
winter when she had measles and pertussis.

September 2, 1916. Physical examination showed a robust, well—
nourished child with large tightly ﬁtting teeth. Legs were drawn up in
ﬂexed position and it is extremely difﬁcult to straighten them out. They.
are quite tender. Kernig is very positive. Neck is stiff and child is
tender along the spine. Child feels feverish and is hyperaesthetic.

Reﬂexes.—The knee jerks were not obtained.

Child has not vomited. Bowels are constipated.

Sizinal puncture at 48 hours. Pressure was 16 mm., reduced to 6 after
withdrawing about 15 c.c. of ﬂuid. Cell count 40. Globulin ++.

46 ACUTE POLIOMYELITIS

September 3, 1916. Child much better to-day. Legs have straightened
out. No temperature. No paralysis.

Discussion.—In this instance the remission of symptoms is not com-
plete. The appetite was poor and the child irritable for a period of 3
days. The ﬁrst hump is unusual in having an irregular or divided curve
resembling malaria. The second'hump is not strongly marked and the
meningeal invasion appears to advance slowly during 2 days (September
151; and September 2150. The cell count is low. No paralysis de-
veloped but there was a slight weakness of the lower extremities for a.
time.

Case 6.—R. S. Girl. Age 12 years. Babylon, L. I.
August 14, 1916. Child taken sick with chill and fever. No diar-
rhoea.

August 15, 1916. Vomited after taking castor oil the night before.

August 16, 1916. Patient feels much better and does not seem to
have any fever according to the mother.

August 17, 1916. Patient complained of pain in her eyes, head,
back of neck when attempting to ﬂex it. No cough, slight drowsiness.
Temperature 103.2°.

August 18, 1916. Temperature 103.2°. Physical examination showed
the eyes negative, neck extremely rigid, pain being caused on attempt
to ﬂex the neck or spine. Cervical and inguinal glands palpable. Throat
Very red with small white patch conﬁned to the left tonsil. Lungs nega-
tive. Slight systolic murmur, heart loudest over the apex and trans-
mitted to the axilla.

Reﬂexes.—All reﬂexes normal.

Slight ataxia. Abdomen negative.

Lumbar Puncture—Fluid clear under slightly increased pressure. Cell
count 690. Pandy, Noguchi and Ross Jones +.

September 22, 1916. Diagnosis. Acute anterior poliomyelitis.

September 2 3, 1916. Temperature normal. Patient has recovered
with spastic action of both feet when walking.

Discussion—The intermission in this case is of short duration. Note
localization of symptoms in the head and neck with onset of second hump.
Again the very high cell count presaged damage to the central nervous sys-
tem tissue. In this instance, however, ﬂaccid paralysis did not occur, but
a marked spasticity persisted.

Case 7.—T. R. D. Boy. Age 3% years. Babylon, L. I.

August 5, 1916. Bilious. Vomiting and headache, then well for 3 to
4 days.

August 11, 1916. Has had pain in the stomach for 2 days. Tempera-
ture normal. Child restless, irrational.

August 12, 1916. Temperature 10°. 5°. No paralysis.

CLASSIFICATION OF TYPES OF POLIOMYELITIS 47

Spinal puncture at 24 hours. Slight turbid, blood. No increased
pressure. 980 lymphocytes. Red blood corpuscles present.

September 3, 1916. .Complete recovery. No paralysis.

Discussion—Again a marked free interval. Note especially the very
high cell count, 980. Even though red blood cells appeared in the ﬂuid
there were not enough to explain the great number of lymphocytes. That
this case should have recovered without paralysis is unusual in View of the
high count at such an early hour.

Case 8.—V. C. Boy. Age 6 months. Hempstead, L. I.

August 15, 1916. Child began to be sick. Vomiting and diarrhoea
followed eating ice cream. Temperature 100°. This dropped to normal
and the child was better for an interval of about 36 hours. The tempera-
ture then rose.

August 18, 1916. Neck rigid and reﬂexes normal. Right arm shows
loss of power, not complete.

Knee jerks. Right negative; left pOSitive; also weakness of the right
thigh. No Kernig. Anterior neck muscles weak.

Spinal ﬂuid at 18 hours. Clear. Pressure ++. Cells 250.

Case 9.——D. S. Girl. Age 414 years. Bayshore, L. I.

August 9, 1916. The child vomited and had a sore throat on this and
the following day. She was then apparently well for 4 days.

August 15, 1916. Headache. Temperature 103+°. Stiff neck.

August 16, 1916. Temperature 101° (axilla). Lungs negative. Ex-
amination otherwise negative except for drowsiness.

Spinal puncture at 48 hours. No increased pressure, 188 cells, 50 per
cent. mononuclears.

September 1, 1916. Child well. Never developed paralysis.

Discussion.—The differential count showing 50 per cent. mononuclears
indicates that the meningeal process is no longer very early and agrees with
the time of puncture as estimated from the symptoms.

Case 10.—H. P. Girl. Age 20 months. Oyster Bay, L. I.

July 15, 1916. Child began to be sick. Fever and vomiting lasting 1
day. The next day she appeared to be well. Temperature 98°.

July 17, 1916. Temperature 102°. Knee jerks absent. Walked nor-
mally. Badly constipated.

Spinal puncture at 24 hours. Fluid clear. Pressure +. Few ﬂocculi.
Cells 40.

Physical examination showed no spinal tenderness or rigidity.

Knee jerks were absent. Patient otherwise normal. No paralysis
developed. The child made an early recovery.

Discussion.—Mild case. The ﬁrst febrile period was about 24 hours
long; free interval 36 hours and the ﬁnal febrile period about the same
length. Lumbar puncture performed 24 hours after the second hump
showed 40 cells.

48 ACUTE POLIOMYELITIS

Case 11.——O. R. Girl. Age 7 years. Patchogue, L. I.

August 18, 1916. Temperature 101°. Feels poorly. Next day well
again. Temperature normal for two days.

August 21, 1916. Rise of temperature to Ior.5°. Twitching of the
arms. Does not seem very ill.

Spinal puncture at 24 hours. Pressure +. Cell count 1180, 60 per
cent. mononuclears.

August 23, 1916. Died of respiratory paralysis.

Discussion.—This is an example of the dromedary type of case with a
2—day interval. In the meningeal stage of the disease there is some
discrepancy between the mild clinical picture which the child presented
and the very high cell count.

Case 12.—H. P. Boy. Age 8 years. Garden City, L. I.

August 5, 1916. Sudden onset of illness. Fever rising to 102°. Slight
sore throat.

Physical examination otherwise negative.

August 7, 1916. Temperature 100°. Examination at this time showed
red throat; tender slightly enlarged upper left anterior cervical node.
Otherwise negative. There was no change in the neck, spine, nerve
reﬂexes or muscles. The diagnosis was called negative.

August 10, 1916. Temperature rose rapidly to 102°. Child was
drowsy, vomiting twice; had headache and seemed prostrated. During
the next 6 hours he became progressively worse, showing a temperature
of 102°, ﬂushed face, widely dilated pupils. Stiff, retracted hand and
neck; stiff unbending spine. There was no paralysis or changes in the
reﬂexes except the Kernig sign which was markedly positive. Typical
projectile vomiting. Consciousness was clouded, with short periods of
delirium.

Diagnosis.——Poliomyelitis and encephalitis. At request of family
physician puncture was not made at this time. The following day at
48 hours spinal puncture showed a clear ﬂuid under slight pressure, with
a cell count of 260. The clinical course was rapidly and progressively
worse, with accentuations of all the ﬁndings, and ﬁnally death. N0
muscular paralysis could be made out.

Discussion.—This is a case of overwhelming severity. The free interval
is well marked. The diagnosis at the time of the ﬁrst hump was negative
owing to the entire absence of signs pointing to the central nervous system
involvement. The delay in puncturing was unfortunate.

Case 13.—F. M. Age 18 months. Glen Cove, L. I.

August 10, 1916. Child ill with fever and slight diarrhoea consisting of
several watery movements a day. This lasted 2 days when the child
began to be petulant and peevish. The fever after the ﬁrst 2 days of
illness remained normal.

August 16, 1916. For the past 24 hours the child has cried when

l

CLASSIFICATION OF TYPES OF POLIOMYELITIS 49

touched. The neck has been stiff and retracted and the back stiff and
tender. The temperature is 984°. The temperature has been repeated
and is correct. The neck is tender and retracted. Spine is arched and
tender. The knee jerks are normal. There are no paralyses. Physical
examination is otherwise negative.

Spinalﬂuid at 24 hours. Clear under pressure. 200 cells. No paraly-
sis developed.

Discussion.—This case presents a free interval of 4 days. The most
unusual point about the second hump is the absence of elevated tempera-
ture. Signs of meningeal irritation are present, however, both by physical
sign and laboratory evidence.

Case 14.—\'. L. Girl. Age 3% years. Lynbrook, L. I.

July 3, 1916. Patient returned from a motor trip feeling cold and chilly.
That evening had slight fever and felt indisposed. The fever continued
for three days when a physician was called.

July 6, 1916. Temperature 100°. No pain. No stiffness. Bowels
regular. Cathartic was given on the night when the fever ﬁrst appeared.
For four days following this the child felt well and played out of doors in
the yard. ,

July 11, 1916. The child vomited during the night and had fever.

July 12, 1916. Child slightly listless and more than uncommonly
quiet. Temperature 100.16+°.

July 15, 1916. Temperature 101.11+°. The child has remained up
and about the house. Appetite is indifferent. The child asks for sweets
and cake. Physical examination at this time shows a very well-nourished
child, quiet but not appearing sick. Eyes normal. Throat normal.
Knee jerks are present; other reﬂexes are normal. No motor disturbances.

Lumbar pummre at 72 to 96 hours. Fluid came in drops with possibly
increased pressure. Clear. Cell count 140. Mononuclear cells predom-
inating. Globulin +.

Discussion.—A mild case showing well-marked dromedary form. The
free interval is about 4 days.

Puncture performed on the fourth day following the second hump.
There were still 140 cells per c.c. The puncture was made late in the
second hump, after the child had begun to be better again.

STRAGGLING GROUP

Case 15.—D. M. Girl. Age 4 months. Hicksville, L. I.
August 24, 1916. Child was noticed to be feverish.
August 25, 1916. Physician was called and found a temperature of
103°. Patient seemed sick but without any apparent reason.
August 26, 1916. Seen again, temperature 102°, still constipated but
no other signs of illness.
4

50 ACUTE POLIOMYELITIS

August 29, 1916. At noon temperature 101.8°, still constipated, much
more drowsy and sick looking; shows no paralysis. Yesterday, though
not seen by physician, mother noted that the head was held stiff and the
baby cried whenever it was moved. To—day the patient appears sick,
sweating and drowsy. Has a slight spine sign, no Kernig and [no
paralysis.

Lumbar puncture after 24 hours. Fluid under slightly increased pres-
sure, clear, cell count 337. Knee jerks ++. Noguchi ++++.

Case 16.—L. W. Girl. Age 4% years. Great Neck, L. I.

August 6, 1916. Child developed a temperature of 1016", pulse 100 to
110.

August 11, 1916. Since onset has been apathetic and at times very
irritable. Bowels constipated. Complained of sharp shooting pains in
the abdomen. No vomiting.

Physical examination shows marked hyperaesthesia, particularly along
spine. Marked rigidity of the neck. Marked Kernig on both sides.
Knee jerks, left not obtained, right very active. Abdomen negative.

Lumbar puncture at 24 hours. Fluid clear under moderate pressure.
370 cells. Noguchi +. Albumin +. '

This case never developed paralysis.

Case 17.—-M. A. Boy. Age 4%, years. Port Washington, L. I.

August 17, 1916. Child has been drowsy and very irritable for several
days.

August 18, 1916. This morning had fever. Headache and pain in the
back of the neck last night, about 12 hours ago. Was constipated for
several days previous to this and was given numerous cathartics without
success. Mother states that last night she gave the child castor oil but
he vomited it. The family physician saw the child about an hour ago
and found his temperature 103°.

Physical examination shows the boy lying in bed and apathetic. Eyes
staring and glassy in appearance. Tonsils and pharynx considerably
congested, but without exudate. Heart and lungs negative. Abdomen
normal. Extremities: No' paralysis or muscular weakness. Knee jerks
markedly exaggerated, ++++. Most marked on the left side. Kernig
marked on both sides, most on the left. Skin reﬂexes are active. Slight
rigidity of the neck, hyperwsthesia.

Spinal puncture at 12 hours. Fluid clear under pressure. About 12
c.c. obtained. Cell count 250.

September 2. 1916. Patient seemed to be completely well 24. hours
after puncture and has had no subsequent paralysis or complications.

Discussion.—This is an example of the unimportant impression that
the early days and hours of the disease make upon the mother. Yet the
suggestion is clearly of an indeﬁnite period of “out of sorts” preceding
the headache of August 18th.

CLASSIFICATION OF TYPES OF POLIOMYELITIS SI

Case 18.—D. S. Girl. Age 4 years. Hicksville, L. I.

August 13, 1916. Mother noticed that the child had a fever of 103°.

August 14, 1916. Child vomited.

August 15, 1916. Child was given calomel, had two movements and
temperature 102°.

August 16, 1916. Temperature 101°.

August 17, 1916. Temperature normal. Yesterday morning she was
given castoria, last night and this morning castor oil, but no result. She
vomited again on this day. Very drowsy, somewhat irritable when dis-
turbed, and has complained of headache.

Physical examination shoiavs weakness in the back when sitting up.
Some rigidity of neck. Arm and abdomen reﬂexes present. Station wide.
Marked ataxia. Eyes and throat normal.

Lumbar puncture at 108 hours. 10 c.c. ﬂuid, clear, under no increased
pressure. Cell count 220. Noguchi +. Pandy +. Ross-Jones +.
Knee jerks absent. Slight weakness of right quadriceps. Plantar re—
ﬂexes present. Child was quarantined at home.

August 18, 1916. Died of respiratory paralysis at 5 RM.

Case 19.——E. H. Girl. Age - —. Mineola, L. I.

August 19, 1916. Child began to complain of headache and feeling
warm. Temperature 103°. No vomiting or diarrhea. Child drowsy,
slept at short intervals throughout the day.

August 20, 1916. Child seen by Dr. Tibbets. Temperature 102°.

August 22, 1916. Pain in the back and back of neck, temperature
100.4°.

August 23, 1916. Not seen by physician.

August 14, 1916. Physical examination showed a well-developed child,
up and around the house walking; eyes normal; throat slightly congested.
Palpable cervical and inguinal glands; heart and lungs negative. Ab—
domen: Liver slightly enlarged one ﬁnger below the costal margin. Ex—
tremities: slight muscular weakness of the left leg. Child walked with
limp, no pain. Knee jerks both present, less on the left side. Other
reﬂexes normal. N o Kernig.

Lumbar puncture at 48 hours. Fluid under tension, clear, about 6 c.c.
obtained, cell count 50. Globulin + —.

Discussion—Cases 15 to 19 illustrate a straggling course in which the
invasion of the meninges is rather more sharply marked than in many.

In Case 15 the mother had noticed that the head was held stiff and that
the child was hyperaesthetic. Cases 17 and 19 illustrate what an unim-
portant impression the ﬁrst part of the disease makes on the family.
These cases hold out more hope of early recognition at the onset of men-
ingeal stage than on those which follow.

Case 20.—J. M. Boy. Age 3 years. Port Washington, L. II.
August 16, 1916. Illness began with a cough and fever during the night

5 2 ACUTE POLIOMYELITIS

which continued for 3 days. Vomited several times in the beginning
and complained of pain in the stomach.

August 19, 1916. This morning on getting out of bed fell on the ﬂoor
and after some diﬂiculty succeeded in getting to his feet, but walked with
difficulty, dragging his right leg. Physician was called in and temperature
found to be 103°.

Physical examination showed eyes normal, mouth and teeth in good
condition, tonsils and pharynx slightly congested. Lungs: marked bron-
chitis, many sonorous rales heard throughout the chest. Heart: no mur-
murs. Rate 100. Abdomen: normal. Extremities: marked weakness
on rotating leg outward of right side and extension of thigh upon hip. No
rigidity of neck. No Kernig. Reﬂexes: knee jerks, left leg is absent,
right active and constant.

Lumbar puncture after 72 hours, ﬂuid clear, under no tension, about 4 c.c.
obtained. Cell count 240.

Note.—In this instance, one of the few seen in the Long Island epidemic,
respiratory tract symptoms predominated.

Case 21.—M. E. A. Girl. Age 4 years. Wheatly Hills, Old Westbury,
L. I.

August 8, 1916. Child began to be ill with slight headache and was
very irritable, running a temperature of 101° and 102°. No gastric dis-
turbances. Bowels constipated.

August 11, 1916. Physical examination showed the patient somewhat
languid. Eyes are normal. Abdomen normal. Extremities: no mus-
cular weakness or paralysis. Knee jerks are present and equal. No
Kernig.

Lumbar puncture at 72 hours, ﬂuid clear, under moderate tension, about
8 c.c. obtained. Cell count 200. There were no signs of central nervous
system involvement.

Note.—Patient’s brother James, aged )7, was sick from July 2d to 4th,
vomiting and fever, which was thought to be a simple gastric enteritis
and was treated for such.

August 12, 1916. Child removed to Roslyn Hospital.

August 19, 1916. Child has developed a distinct weakness of the left
tibialis.

Discussion.—There is no clear indication in this case when the menin-
geal invasion began. The very mild character of the infection and espe-
cially the lack of symptoms of meningeal irritation are interesting in view
of the rather high cell count. The delayed appearance of weakness is
unusual.

Case 22.——R. B. Girl. Age 3 years. Sea Cliff, L. I.

August 5, 1916. Illness began with vomiting, drowsiness and tempera-
ture of 101°.

August 10, 1916. . Since last note temperature has ranged between 101

CLASSIFICATION OF TYPES OF POLIOMYELITIS 53

and 98.8°. On physical examination the child appears to be prostrated,
generally weak, no paralysis. Kernig on both sides, and reﬂexes present
and equal.

Puncture performed by Dr. Hoch of Rosyln yesterday (August 9, 1916)
at 96 hours. Cell count 220.

Note.—Child has been having convulsions described as epileptic in
character, since 10 months of age. Total number of convulsions about I0.
Patient did not develop paralysis.

August 30, 1916. Slight loss of weight, but up and about and very
active. Showed no weakness or paralysis at any time.

Case 23.—D. B. Girl. Age 9 years. sea Cliff, L. I.

August 6, 1916. Illness began with temperature of 102°, vomiting,
malaise.

August 10, 1916. Vomiting has persisted since onset, temperature
ranged between 986° and 102°. Child has been very drowsy at times
hard to arouse. No weakness or paralysis has been detected.

Physical examination shows the eyes normal. There is a slight weak-
ness of the facial muscles. Mouth: teeth in poor condition, many carious,
and gums infected. Tonsils slightly congested. Heart: soft blowing
systolic murmur at apex. Lungs: negative. Abdomen: negative. Ex-
tremities: no apparent weakness or paralysis. Knee jerks present,
normal. Temperature 99.8°, pulse 96. Kernig sign on both sides. Child
appears prostrated. ‘

Puncture at 96 hours. Fluid clear, under slight pressure, 8 c.c. obtained.
Cell count 140. Noguchi +, albumin +.

Note.—Patient’s sister, aged 3 years, punctures yesterday (August 9,
1916). 220 cells, no paralysis.

Case 24.—W. E. Boy. Age 1 year 6 months. Smithtown, L. I.

August 10, 1916. Child taken sick, running a temperature of 101° to
102°.

August 17, 1916. Since the above date the child has been running a
constant temperature of 101° to 102°, and has slept the greater part of this
time. Vomited several times and complains of pain in epigastrium.

Physical examination showed temperature 102°, pulse 100. Eyes are
equal. Mouth: teeth and tonsils in good condition. Heart and lungs
negative. Abdomen: normal. Extremities: no weakness or paralysis.
Knee jerks very active and equal. N o Kernig sign. '

Puncture.— Fluid under moderate pressure. Cells 320.

Discussion—Cases 20 to 24 inclusive illustrate the most diﬂicult of all
types to recognize. The signs of central nervous system disease, are
absent practically throughout and often when the lumbar puncture
ﬂuid shows a high cell count. Cases 21, 22 and 24, frequently the
ﬁrst indication of central nervous system disease is the paralysis
occurring surprisingly in the course of a mild febrile upset. The

54 ACUTE POLIOMYELITIS

mechanism of the straggling type of case is probably similar to that of
the dromedary.

SUDDEN ONSET GROUP

Case 25.——E. E. L. Girl. Age 3 years IO months. Oyster Bay, L. I.

August 21, 1916. Suddenly at ten this morning seized with pain in
back of neck. Continued to play until 12 o’clock, then gave in and began
to be feverish. Became worse. 3 RM. temperature 102.6°. 7.15
temperature 102.4°.

Physical examination. showed a well—nourished child, yellow hair,
brown eyes, incisor teeth separated. Patient presents acute febrile
picture, with deﬁnite ﬁne ataxic tremor on motion. Knee jerks are
absent. Patient is apprehensive and nervous. There are no weaknesses.

Spinal ﬂuid hazy, pressure normal, cells 2430. Given 15 c.c. of serum.

August 22, 1916. Attending physician thinks the patient slightly
improved. Has had a fair night with 6 hours sleep. Bowels have not
moved and no food has been taken since last Visit. Physical examination
shows stiffness and tenderness of the neck and spine, and a positive Kernig
in each leg. There are no paralyses or weaknesses made out. Tempera-
ture is 102.2°.

Lumbar puncture—20 c.c. of cloudy ﬂuid under normal pressure. cell
count 2220 leukocytes, and no red cells. The globulin reaction is very
marked. F ehling reaction positive.

August 22, 1916. At 9.30 P.M. attending physician reports that
patient has rather suddenly assumed an opisthotonos position. Tempera-
ture 103°. Face quite ﬂushed, breathing somewhat rapid. 15 c.c. of
serum together with 1% c.c. of adrenalin chloride were given intraspinally.
Cell count was not made.

August 24, 1916. Temperature is about 1° lower than on the pre-
vious day, but is still higher than it should be. Opisthotonos continues
and paralysis of the right arm with weakness of the left. Cyanosis of the
lips and face and evidence that the accessory respiratory muscles are
involved.

Spinal puncture performed and 15 c.c. of serum together with 1% c.c.
of adrenalin chloride were given. Cell count 250.

August 25, 1916. At 10 AM. condition is very poor. Temperature
high, pulse rapid, appearance cyanotic. 2 c.c. of adrenalin chloride was
given intraspinally. Died 11.30 AM. of respiratory paralysis.

Discussion—Here is an example of overwhelming cerebrospinal infec-
tion. At the time the patient was ﬁrst seen no history could be obtained
of symptoms pointing to any general infection preceding the attack on the
meninges. Some months later, however, after the excitement and anguish
of the moment had passed, the mother remembered that on the previous
day the child had complained of feeling badly.

CLASSIFICATION OF TYPES OF POLIOMYELITIS 55

Case 26.—D. S. Girl. Age 14 years. Babylon, L. I.

August 21, 1916. Gone feeling in stomach.

August 22, 1916. Pain in her neck and right shoulder. Temperature
102°, pulse 130.

August 23, 1916. Slight pain in shoulder. Examination showed no
paralysis. Left knee jerk less than right; right knee jerk present; irri-
table and slight stiffness in the neck. Catamenia, usually no symptoms.

Puncture at 48 hours. No increase in pressure, 504 cells. '

September 3, 1916. Complete recovery. No paralysis.

Discussion.—It is a question whether the ﬁrst complaint of “gone
feeling in the stomach” represents the beginning of the disease or the
beginning of central nervous system involvement. The early appearance
of pain in the neck and shoulder suggests the latter. Consequently the
case is grouped among those with “sudden onset.” The high cell count
at-such an early stage would have made a paralysis not unexpected.
None developed.

Case 27.—R. W. Boy. Age 1 year 2 months. Hempstead, L. I.

August 18, 1916. Parent states that nothing wrong .was noticed with
the child until several hours ago, when he felt unusually hot and somewhat
irritable, crying a great deal, and suspected his neck being somewhat sore
as he cried'on movement of head. Attending physician, one hour ago, '
could not detect any physical abnormalities, aside from temperature of
103°, and slight rigidity of the neck.

Physical examination shows child lying in bed, drowsy and very hot to
the touch. Cries on movement of the head or extension of the thighs.
Mouth, tonsils and pharynx are negative. Heart 130, no murmurs.
Lungs are normal. Abdomen is normal. Extremities: no muscular
weakness, or paralysis detected. Temperature 103°. Reﬂexes: knee
jerks are both present, equal and markedly exaggerated. Kernig mod-
erate on both sides.

Puncture at six hours. Fluid clear under great pressure. About 20 c.c.
obtained (ﬂowed for a few seconds a constant stream). Cells 2 30.

August 31, 1916. No signs of paralysis noted. Temperature normal.
Child up and about.

Discussion.—The ﬁrst complaint of the child directed attention to the
stiffness and tenderness of the neck and caused the parents to notice that
he was feverish. Lumbar puncture within a few hours showed a. marked
meningeal involvement.

Case 28.—M. N. Girl. Age 3 years. Islip, L. I.
August 14, 1916. Child drowsy, twitched in sleep and vomited.
August 15, 1916. Knees and back hurt. Temperature 103.8°.
Physical examination was negative.
Puncture at 36 hours. Pressure moderately increased, 330 cells, 60
perLcent. mononuclears. I i

56 ACUTE POLIOMYELITIS

September I, 1916. Child now well. Never developed paralysis.

Discussion—Child went to bed well but during the night vomited and
twitched. The next day there were 330 cells in the spinal ﬂuid. No
history was obtained of previous indisposition.

Case 29.—-W. H. Boy. Age 22 months. Huntington, L. I.

August 23, 1916. Taken sick at 1 P.M. No vomiting, no pain:
Bowels loose, four movements. Markedly drowsy, apathetic, appetite
gone. Temperature 103.5°. Positive Kernig on the left. Patellar re—
ﬂexes slightly diminished on both sides.

Spinal ﬂuid at 36 hours, shows slight increased pressure, cell count 70.
No paralysis developed.

Discussion—The looseness of the bowels at the time of the meningeal
reaction is rather unusual. The drowsiness and positive Kernig point to
central nervous system invasion, and the cell count conﬁrms it.

Case 30.—L. F. Male. Age 23 years. Oyster Bay, L. I.

August 17, 1916. Complained of pain in the abdomen radiating to
middle of back. In the evening it was in the middle of the back and in
back of the neck.

August 18, 1916. Does not have pain in the abdomen. Has severe
headache. After taking medicine prescribed by the doctor felt nausea
and ﬁnally vomited. Patient constipated.

Physical examination showed the patient sitting up. Answers questions
quickly. Neck stiff and painful. Knee jerks, both sides, present, slightly
exaggerated. No evidence of paralysis.

Lumbar puncture at 36 hours. 15 c.c. of clear ﬂuid under slight pressure.
15 c.c. of serum drawn off and serum given. Cell count 13 2. Globulin:

Pandy + + + +. Noguchi + + + +. Ross—Jones + + + + .

Discussion—The patient was punctured about 36 hours after the onset
of symptoms. A well—marked meningeal involvement was already pres-
ent. The localized pain in the abdomen is a phenomenon which occurred
several times in cases with no general systemic symptoms. It is some—
what hard to decide whether this symptom belongs to central nervous
system involvement or to the digestive disturbance of a systemic phase
of short duration.

Case 31.——K. McL. Boy. . Age 18 months. Northport, L. I.

August 19, 1916. Sister has had the disease. Child in bed sleeping,
with no history of disease other than slight diarrhea for two days. Con-
stitutionally he has seemed well and is awakened from sleep for the pur—
pose of examination and temperature. This child was well on going to
bed after playing all day. At I AM. the temperature is 105°F.

Physical examination shows normal eyes, ears, nose and throat, heart,
lungs and abdomen. Neck and spine stiff and tender. The head will
not ﬂex upon the chest. Suspension by the head and buttocks causes

CLASSIFICATION OF TYPES OF POLIOMYELITIS 57

arching of the back and pain. Kernig is positive in both legs and no
paralysis is made out in any part of the body. Reﬂexes normal.

Spinal puncture shows clear ﬂuid under normal pressure with a moderate
globulin test and 320 cells.

This patient was given serum and his further history is related in con-
nection with that group of cases.

Discussion—In this instance the mother objected to having the child
awakened at one o’clock in the morning to have his temperature taken.
The diagnostician of the Health Department insisted on the ground of
the slight intestinal disturbance of the previous day and the fact that
the sister was ill with frank poliomyelitis. This course was justiﬁed by
the ﬁnding of the high temperature and high cell count. If this case had
not been observed at this time, but the ﬁrst observation had been made
the following morning and the child found with high fever and meningeal
irritation it would have been considered a typical example of what the
English call “paralysis of the morning,” having gone to bed well and wak-
ing up ill and would have been reported as a case of sudden onset, but
fortunately the parents remembered the very slight intestinal upset of
the previous two days which had not been sufﬁcient to make the child
stop playing. The meningeal invasion must have taken place at some
time between six or seven in the evening and one o’clock in the morning.

MULTIPLE PUNCTURE GROUP

Case 32.—A. L. Male. Age 32 years. Oyster Bay, L. I.

August 21, 1916. Patient felt poorly.

August 22, 1916. He felt all right.

August 23, 1916. Felt feverish and somewhat “dopey.”

August 24, 1916. Complains of headache, feverishness and slight stiff—
ness of the neck. Temperature 102°. Patient is a large acromegalic
type. Pharynx is congested and he has a slight cough. Heart and lungs
are negative and there is no other explanation of the temperature. Knee
jerks are present. Neck is slightly rigid. S [ﬁnal ﬂuid is clear and shows
no cells. Globulin +, and pressure 3 mm. of mercury. No history of
vomiting or constipation.

August 25, 1916. Temperature 101°. Still has cough and complains
of headache. Feels weak. Spinal puncture reveals no increase of
pressure, ﬂuid clear with no cells. Neck is distinctly stiff but not mark-
edly so.

August 26, 1916. Temperature Ioo.4°. Neck more rigid. Did not
sleep well last night, feels restless. There is considerable tremor of both
hands, especially of the right side. No Kernig or clonus. Knee jerks
still present. Spinal ﬂuid is still clear, but shows so cells. Globulin
again positive. 15 c.c. of serum given with 1% c.c. of adrenalin chloride
intraspinally. Taken to Locust Valley Hospital.

58 ACUTE POLiOMYELITIS

August 27, 1916. Running a slight temperature. 15 c.c. of serum
administered. .

August 29, 1916. Temperature normal. Patient feels well and would
like to get up, but there is a slight though deﬁnite weakness of the left
thigh and leg.

Discussion—The patient was the father of two children who had the
disease, in the same week, one of which was fatal. The case is interesting
because it shows a dromedary type and the series of lumbar puncture
demonstrate the very slow reaction of the meninges to the invasion of the
disease. It is worth while noting that the ﬁrst and second specimen of
ﬂuid had no cells but the globulin was increased.

Case 33.—]. M. Boy. Age 3 years. Glen Cove, L. I.

August 18, 1916. Slightly ill, continued so for two days. Apparently
no temperature. Took his food and slept well. Had two loose move-
ments and did not seem his usual self.

August 22, 1916. Showed rather an abrupt change with a rapid onset
of fever and three or four attacks of vomiting. Temperature remained
high; child seemed peevish and restless, but no appetite and bowels were
constipated. At times he complained of pain on swallowing. There
has been no cough, pain in chest or abdomen.

Physical examination shows a well-nourished, splendidly developed child.
Eyes and ears normal, Throat shows large tonsils but no evidence of
inﬂammation. The cervical glands are not enlarged or tender. The
heart, lungs and abdomen are normal. There are no paralyses. Knee
jerks cannot be done. Kernig sign is negative. The neck is stiff and
tender, and back the same. Supporting child by head and buttocks
causes arching of the spine and pain.

Lumbar puncture at 48 hours—Shows IO c.c. of clear ﬂuid under normal
pressure. Cell count 40. The globulin test shows a moderate reaction.
Fehling’s test is negative.

August 24, 1916. Patient distinctly better to-day. Temperature is
going down but drowsiness still continues. There is no Kernig. Knee
jerks are present and only slight stiffness of the neck. The child cries.
There is left facial palsy observed for the ﬁrst time. Cell count 190 at
the bedside. Although this is a slight increase over the original count
yet because of the facial paralysis which has developed and the low tem-
perature it was deemed wise not to give him any serum.

August 25, 1916. Temperature is coming down. Child is brighter but
still keeps very quiet. No further paralyses.

'August 26, 1916. Temperature is still descending. No additional
paralyses.

I. August 29, 1916. Temperature normal. Child sitting up and playing.

Discussion.—~This case presents two days of general mild illness preced-
ingja sharp aggravation of symptoms accompanied by stiff neck and tender

CLASSIFICATION OF TYPES OF POLIOMYELITIS 59

back. Spinal ﬂuid withdrawn 48 hours after the onset of severe symptoms
showed 40 cells; 48 hours later with the appearance of facial palsy a second
puncture showed 190 cells.

Case 34.—L. G. Girl. Age IO years. Oyster Bay, L. I.

August 18, 1916. Complained of sore throat, which is red. Tempera-
ture 99.4°.

August 19, 1916. Temperature 100° to 100.4°. Throat still red.
Cervical lymph nodes enlarged. No vomiting. Appetite good. Bowels
moved under catharsis. No spinal sign. Knee jerks absent. They were
present yesterday. Spinal flu-id at 24 hours is clear, pressure slightly
increased, no cells. Globulin +.

August 20. 1916. Temperature normal. Patient apparently well.
Temperature rose during the day to Ioo.4°.

August 21, 1916. Temperature normal. Later 992°. Headache
began. No spinal sign. Knee jerks still absent. Spinal ﬂuid at 48
hours. Fluid clear, pressure normal, cells 16. Globulin +.

August 30, 1916. Child quite normal, having no paralysis at any time
and shows no loss of weight. Both knee jerks and ankle clonus have
returned.

Discussion—This is a very mild case of dromedary type in which the
ﬁrst puncture was done during the ﬁrst hump. Note the positive globulin.
Then followed a period of normal temperature, succeeded in turn by a
second temperature rise accompanied by headache. At this time the
spinal ﬂuid showed small cell increase and positive globulin.

Case 35.—W. Z. Boy. Age 2 years. Great Neck, L. I.

August 1 2, 1916. Patient well until afternoon when he was feverish and
listless. No vomiting.

Spinal Puncture.——Pressure normal, ﬂuid clear and increased in amount.
No cells. Globulin negative.

August 13, 1916. Same symptoms as yesterday. Spinal puncture at
30 hours. Fluid under moderate pressure, cell count 90. Child sent to
Hospital at Roslyn.

August 31, 1916. Temperature 998°. Weakness of lumbar muscles
with lateral curvature in the thoracic region to left. Slight spinal
tenderness.

Discussion.—This is an instance of short course. Puncture was made a
few hours after the onset of the symptoms, and showed a negative cell
count and no globulin. Twenty-four hours after with the development
of slight spinal signs the spinal ﬂuid showed 90 cells. In this case there
was rapid improvement and it was not until several weeks after the acute
disease that slight weakness of the lumbar muscles was discovered. In
this case the period of invasion of the meninges was indicated by the con-
secutive lumbar punctures.

60 ACUTE POLIOMYELITIS

Case 36.—G. L. Boy. Age 7 years. Hempstead, L. I.

August 15, 1916. Large, well-nourished boy. Teeth slightly wide.
Began this A.M. Headache and temperature. Patient ﬂushed and
bright eyed, quiet, neck slightly stiff. Knee jerks ++.

Spinal ﬂuid at 8% hours. Clear, pressure normal, cells 3.7. Globulin
++.

August 16, 1916. Temperature 988°. Neck and back very slightly
stiff and tender on stretch. Muscles and reﬂexes normal. Child looks
well. Does not seem ill. Kernig negative.

Lumbar puncture at 32 hours shows 35 cells with clear ﬂuid under no
pressure. In view of the marked general involvement and low cell count
it was decided that serum be not injected.

August 18, 1916. Patient much better, neck still a bit stiff. Knee
jerks ++.

September 1, 1916. At Garden City Hospital. Temperature 98°.
Up and about. No weakness or paralysis. No spinal tenderness.

Discussion—This case was a very short dromedary type. The ﬁrst
puncture done within several hours of the onset of symptoms showed 3.7
cells and a strongly positive globulin and indication of a beginning dis-
turbance of the meninges. Twenty—four hours later there was a deﬁnite
cellular reaction in the spinal ﬂuid. In the meantime the patient became
much better but the spinal tenderness was more marked. The patient
cleared up rapidly without any paralysis. In this case the second spinal
puncture was probably made in the period of the second phase although
clinically this stage of the disease was unimportant.

Case 37.—T. W. Girl. Age 15 months. North Hempstead, L. I.

August 19, 1916. Pale, sick appearing, fretful girl. Temperature 102°
to 104°.

August 20, 1916. Spinal fluid at 48 hours. Clear, under increased
pressure. Withdrew about 10 c.c. Cells 70. Onset the day before was
noticed about 7.30 A.M. when the patient became drowsy and refused
the bottle and later vomited. Vomited four times during the day. Has
not vomited to—day. Bowels all right. Knee jerks present. Neck not
stiff. No paralyses. Weakness in the knees.

August 21, 1916. Temperature 100°. Spinal puncture at 72 hours.
Cell count 80. Appetite has returned. Bowels move normally. Slept
well last night, and is quite cheerful and bright. Slight stiffness of neck
still present.

August 23, 1916. Doctor reports that patient is sitting up with normal
temperature. N o paralysis.

August 25, 1916. Doctor reports that patient is sitting up and seems
perfectly well.

Discussion—In this instance it is diﬂicult to determine whether the
rather sudden onset represents systemic invasion or meningeal invasion.

CLASSIFICATION OF TYPES OF POLIOMYELITIS 61

The ﬁrst lumbar puncture was done 48 hours after the original onset of
the symptoms. The second puncture following the ﬁrst after 24 hours
showed only very slight increase in cells. There was no continuance of
the temperature and the stiff neck. This was a mild infection through-
out. The advance in the cerebrospinal space was never very great.

‘7

CHAPTER VII

SYMPTOMS

In its early hours the clinical course of acute poliomyelitis
resembles in general that of all the acute infectious diseases
of childhood. Fever is almost invariably present with its
attendant restlessness and dry-mouthed discomfort. The
picture in the individual case is colored by symptoms depending
on which particular set of organs is chieﬂy involved. Perhaps
the most usual form is disturbance of the gastrointestinal
tract simulating a simple “summer diarrhoea”; vomiting is
likewise a very frequent symptom. But tonsillar and pha-
ryngeal inﬂammation or upper respiratory tract symptoms
are not uncommon. Still, even in the midst of an epidemic, it is
hard at ﬁrst to realize that the ﬂushed, hot, restless patient
is already in the grip of the insidious disease that may cripple
for life if it does not kill. Yet those symptoms do not rep—
resent a prodromal stage, they are the expression of the fully
developed infection. It is impossible to determine at this
period of the disease whether the subsequent course will be
dromedary or straggling in type, or whether it will terminate
at the end of the systemic phase.

Notwithstanding the foregoing remarks, however, there
seems to be little doubt in the minds of those who have seen
much of the earliest hours of the disease that a very deﬁnite
and characteristic clinical picture presents itself. But it is
diﬂicult by descriptive method to transfer an adequate impres-
sion of the subtile and striking difference between the onset
hours of infantile paralysis and those of any other of the acute
infectious diseases of childhood. To say that the temperature
is elevated, often as high as 103° or 104°, and that the child is
ﬂushed and miserable; that vomiting often occurs and that
drowsiness supervenes, does not offer sufﬁciently distinguish—

ing evidence of the special type of infection. Nevertheless,
62

SYMPTOMS 6 3

in acute poliomyelitis, this common symptom complex is
shot through with delicate manifestations that are unmistak-
ably speciﬁc, but which must still be viewed as clinical impres—
sions—those helpful though indeﬁnite aids in diagnosis.

Now when'infantile paralysis becomes epidemic in a locality
which has been previously free from its presence, the physicians
in that territory soon appreciate this difference fromJthe usual
illnesses of children. Without exception, all speak of the
peculiar expression about the eyes. For, besides a glazed
porcelain quality of the sclera and cornea, and the not infre-
quent puﬂiness of the circumorbital tissues, there is a look of
mingled apprehension and resentfulness, quite unlike the alert,
bright and shining eye of other fevers. The psychic change

 

 

 

 

FIG. r4.—(Reproduccd from the Monograph.)

NOTE—Separation of upper central incisor teeth.

responsible for this look ﬁnds further expression in a character-
istically annoyed shrugging of the shoulder which occurs when
the child is touched or simply spoken to. Indeed there is fre-
quently a snarling whine of resentment which is synchronous
with this gesture of discontent.

There is, besides, another smaller number of cases that
present certain perfectly deﬁnite signs of early disturbance of
the central nervous system. These are the cases of overwhelm-
ing infection, where for example, after 6 or 8 hours of illness the
spinal ﬂuid shows 1500 to 2500 cells per c.mm. Again the
temperature is high and the usual picture of a sick feverish
child appears. But, in addition, there are other striking phe-
nomena. The child is restless, breathes rapidly and seems to

64 ACUTE POLIOMYELITIS

be busily and actively resisting some incomprehensible dis-
turbance of its usual comfort. In these instances, the irri-
tability and resentful manner are not marked, but the whole
organism seems to be composed of tensely drawn wires—a
universal overstimulation. This pressor state of the nervous
system is so marked that a sort of impulsive ataxic tremor is
present in every motion, especially when that motion has intent.
Probably of similar nature to these irritative signs are the
muscular twitchings described in the Monograph and recently
emphasized by Dollivar. The ataxic tremor may be present in
the less fulminating cases, after the invasion of the central
nervous system has taken place. It is interesting to recall at
this point that the very earliest symptoms in the monkey sub—
ject of experimental poliomyelitis are not at all unlike those
just described, for the animal becomes highly excitable and
seems to develop the same state of intense excitability of the
entire nervous system. Usually a few cases are met with
whose profound stupor masks all other signs and symptoms so
that no speciﬁc clinical impression is produced.

One physical sign of great importance, however, must
be mentioned especially at this time. It depends upon the
fact that in acute poliomyelitis any manipulation which brings
about anterior bending of the spine causes pain and, there-
fore. is resisted by the patient. The resulting stiffening of
the body has generally been loosely described as “stiff neck”
or “ Kernig’s sign,” but there is an essential difference between
these reﬂex phenomena of meningeal irritation and the volun-
tary protection rigidity assumed by the patient with poliomye—
litis to prevent anterior ﬂexion of the spine. This conscious
effort is often carried to a moderate degree of opisthotonos,
and is the cause of the unwillingness of children with this dis- '
ease to be picked up and handled even by the mother. Atten-
tion was called to this sign in the Monograph and we refer to
it here as the “spine sign.” This phenomenon may be present
before any invasion of the meninges has occurred as shown by
negative spinal ﬁndings. We have suggested as an explanation
for the sign that in ﬂexing the spine anteriorly the intervertebral
spinal ganglia are pulled upon. If it be recalled that the virus

SYMPTOMS 65

has been found experimentally in the posterior spinal ganglia
(see p. 25) before meningeal invasion this suggestion for the
mechanism of the spine sign receives some support. It is con-
ceivable that the ganglia being the seat of inﬂammatory re—
action may be unduly sensitive.

If the disease be in the earliest hours a child is found lying
upon the sofa or curled up in a chair. Its usual spirited activity
has gone, and, quietly without complaining of any special dis-
tress, it simply ceases to move about or play as before. It
prefers to lie down and keep silent. At this time the tempera-
ture may be elevated to a moderate degree—loo or 101.
Not infrequently there is a deﬁnite pufﬁness about the eyes.
Physical examination reveals nothing abnormal or at the most
a slight redness of the throat, and coated tongue. In a few
cases at this period slight tenderness may be found on bending
the neck forward, or by forcing the Kernig manipulation
to the limit, for both these procedures cause anterior spinal
ﬂexion. But the signiﬁcant thing about the clinical picture
at this stage is the absence of any sign of central nervous
system involvement.

Obviously it is important to detect when the invasion of
the meninges takes place or, in other words, when the systemic
phase passes over into the meningeal. Sudden and deﬁnite in-
crease in the spine sign may indicate that this extension has
occurred. Rapidly developing intense headache, or distur-
bances of tendon reﬂexes may also mark it. But evidence has
been gathered by spinal ﬂuid examination to show that menin-
geal reaction to the disease may be actively under way when
there is no sign or symptom to indicate it. (See Cases II, I4,
and 21.) This phenomenon calls to mind those instances of
cerebrospinal syphilis, in which an apparently healthy man
may have pathological changes in his spinal ﬂuid as extreme
as those seen in tabes or fully developed paresis.

Heretofore it has been the habit of physicians to wait for
a conﬁrmatory paralysis to establish the diagnosis of polio-
myelitis. Such delay, of course, is not now permissible,
since the hopeful possibilities offered by serum therapy have

arisen. Consequently it is necessary to recognize the disease
5 .

66 ACUTE POLIOMYELITIS

at the earliest possible moment, preferably while it is still
in the general systemic phase. Clinical observation, especially
in epidemic time, can go far toward making the diagnosis, but
with an isolated case it is not by any means secure. Ex-
amination of the spinal ﬂuid, however, offers a criterion of
great value. In several instances where lumbar punctures were
made in the early hours of the systemic phase and repeated at
6- to 10- or 12—hour intervals, it was possible to observe
the reaction of the meninges to the invasion of the virus cases.
This will be discussed more fully in the chapter on blood and
spinal ﬂuid.

These considerations clearly bring up the question as to the
propriety of making repeated punctures. Now during the early
and middle part of the epidemic last summer, it was believed
that serum of recovered cases was only valuable if injected
intraspinally. It was essential, furthermore, to introduce the
serum as soon as possible after meningeal invasion took place.
This requirement became at once the justiﬁcation for making
multiple punctures, because the spinal ﬂuid alone presented,
absolute evidence that this event had occurred It is possible
though that in not a few cases the appearance or intensi-
ﬁcation of the spine sign may prove almost as delicate and reli-
able a test of meningeal involvement as a pathological spinal
ﬂuid.

Anticipating a point of treatment just here it might be stated
that since the immune serum possesses speciﬁc neutralizing
power over the Virus, its administration during the stage of
systemic infection is indicated, not by way of meninges alone,
but by way of the blood. This view is not wholly theoretical but
has received deﬁnite support from the recent work of Amoss and
Chesney,‘15 which indicates that, besides the intraspinal use of
serum, intravenous or subcutaneous injection has additional
therapuetic value.

Under this new condition of effective administration the
earlier in the disease the serum is given the better. Hence,
the necessity is no longer that of waiting for the moment of
meningeal invasion but becomes that of recognizing the systemic
phase of the disease as promptly as may be.

SYMPTOMS 67

It may be well to state in this connection that at this period,
in mild cases, differentiation from trivial digestive disorders,
or light infection of upper respiratory tract is impossible. In
epidemic times, every such case should be viewed with suspicion
and watched closely

When the disease is more intense, the child develops the
glazed eye expression described elsewhere, and looks much
more ill. It is quite common to see patients at this time so
severely intoxicated as to present almost the picture of a very
severe case of pneumonia, and yet have no trace of meningitis
or other central nervous system involvement

Such a child may be found lying on its back, with thighs
slightly ﬂexed and everted in a frog— like manner, and the head
usually rotated to one side The eyes are partly or wholly
closed and there is a peculiar, tired, wilted expression Not
infrequently, the chin is pointed upward a little, indicating a
small degree of retraction. From this drowsy or almost sleep—
ing condition, the patient can be roused suddenly often by
the gentlest touch or manipulation of an extremity. Very
frequently when the leg is lifted only a few inches from the bed,
an expression of annoyance, rather than distress, crosses the
face, and if the leg be the paralyzed one, the child often tries
to free it from the examiner’s hands by twisting the trunk and
shoulders. This procedure is a surprisingly common one and
is usually accompanied by a pettish, fretful, rather bored look
and whine. But when the examiner stands back from the bed,
the patient lapses almost at once into the drowsy state. In
contrast to these cases are those of a more sthenic nature with
evidently greater meningeal irritation. These children are
almost always found lying on their sides with their heads drawn
well back and their knees and thighs ﬂexed, a typical menin-
gitis posture. Occasionally a true opisthotonos appears.
One such patient could not be made to lie on his back, evi-
dently because the ﬂat line of the mattress prevented the slight
degree of opisthothonos which made him comfortable; but when
a pillow was doubled up under the lower dorsal and lumbar
region so that an opisthotonos was induced by gravity acting
on hips and shoulders, the child promptly went to sleep in the

68 ACUTE POLIOMYELITIS

dorsal position. Such cases also are apt to have the drowsy,
wilted look. Much more rarely, the child is Wide-eyed and has
an anxious, apprehensive, rather frightened expression. Many
times these patients do not wait to be touched before objecting,
but cry out even when the nurse or doctor approaches the bed;
and it is surprising how keenly the little patients seem to deter—
mine whether or not an approaching person is coming to per—
form some service which necessitates manipulation. In these
cases one is amazed at the ingenuity and activity with which
the child, using what muscles he has, braces and turns and twists
to escape painful positions. Indeed, in two instances where
both legs, both arms, back, anterior and posterior neck muscles
were paralyzed, the hopeless attempt at defense was limited
to wagging the head from side to side and feebly whining.

From this point several developments in the course of the
disease are possible. The condition may clear up rapidly and
permanently in 12 to 24 hours or the curious “ dromedary” type
may eventuate. There may be a continuous course of increas-
ing intensity ushering in meningeal and nervous invasion.

There are certain more general signs and symptoms which are
common to such large numbers of cases that they may well be
mentioned separately. Pain is a very frequent symptom, often
spontaneous in the form of headache or aching bones and
muscles. Great tenderness of muscles may appear and be so
intense as to dominate the picture for several weeks. Indeed
this muscle tenderness may be so keen and persistent that it
is the only thing which keeps an otherwise well child ﬂat in bed.

The superﬁcial lymph nodes are always palpable and often
enlarged and the pharynx and tonsils very frequently red and
congested. Many cases show a peculiar weakness of the an—
terior neck muscles, apparently not a true paralysis, which can
be demonstrated by lifting the shoulders of the patient off the
bed. The head then hangs back limply,

The reﬂexes are most irregular in their behavior. There
may be no change whatever, or there may be any degree of
abnormality from absence of tendon reﬂex to the most extreme
exaggeration. ' Not infrequently one knee jerk may be active
and the other diminished or absent. These changes are usually

SYMPTOMS 69

present only after meningeal invasion has taken place. In
many instances loss of a tendon reﬂex is the forerunner of
paralysis. It is a fairly common occurrence to see the knee
jerks or ankle jerks disappear for a day or two and then return
and the patient recover completely without paralysis.

During the ﬁrst or systemic phase, especially if gastro—
intestinal symptoms dominate the picture diarrhoea is very
common. But one of the most striking facts in the whole
disease is the almost universal occurrence of constipation during
the second or nervous system phase.

The temperature curve of the disease is usually of short
duration and falls rapidly through 24 to 48 hours. Not in-
frequently, however, irregular or prolonged curves are met with.

CHAPTER VIII

CLINICAL PATHOLOGY

The Blood.—T he blood in acute poliomyelitis shows a con‘
stant change. While the previously accepted view was that a
leukopenia was the rule, the investigations of LaFetra and those
reported in the Monograph indicate that a leukocytosis is the
more correct ﬁnding. The total white cell count in the pre-
paralytic stage shows a constant and marked elevation of from
15,000 to 25,000. In the differential counts a deﬁnite poly—
nucleosis appeared. The increase of polynuclears averages 10
to 15 per cent. above normal and there is an average diminu-
tion of lymphocytes of 15 to 20 per cent.

The Cerebrospinal Fluid.—In acute poliomyelitis the spinal
ﬂuid presents different conditions depending on the stage of the
disease at which it is examined. If the puncture be made in
the very early hours after a child shows symptoms of illness the
ﬂuid is clear, and the pressure often increased. Furthermore,
the volume of ﬂuid seems to be greater than normal. Micro-
scopic examination, however, fails to reveal the presence of any
cellular elements. There may be a very faint (0— +) reaction
for globulin, but this is not constant. If no further symptoms
develop and the child recovers after a day or two, it is obvious
that such a spinal ﬂuid has been of no diagnostic value. Yet
if such a case be in the family where one or two other members
are stricken with paralysis and have been through a similar
systematic phase as that just referred to, we are led to assume
that we have been dealing with a case of poliomyelitis that has
terminated at the end of the systemic phase or ﬁrst hump of a
dromedary type (abortive). There has been no penetration
of the meninges by the virus under these circumstances and the
spinal ﬂuid shows no pathological changes unless the increased
amount and pressure be looked upon as pathological.

Now when the patient, after the interval of a dromedary

7O

CLINICAL PATHOLOGY 7 I

course, or following the straggling period of the other type
suddenly develops increased stiffness of the neck or very severe
headache with renewed temperature, pathological changes in
the ﬂuid may be expected. A second puncture done at this
time—possibly 12 hours or more after the ﬁrst——pr0videsa
ﬂuid whose pressure may be deﬁnitely less than before and
whose clearness may or may not be impaired, Is it rarely
opalescent or turbid. Here at once is a gross point of dif—
ference from the ﬂuid of epidemic cerebrospinal meningitis.
Zingher has described a “ground glass” appearance of the ﬂuid
due, he says, to the increase of cells. The present author
has not seen that this phenomenon differs from the appearance
always ascribed to an excesive white cell content of spinal ﬂuid.
On microscopial examination the cell content is found to be
increased. Anything over IO cells to the cubic millimeter is
pathological, and the count may run as high as 2500 per c.mm.
At the earliest period of meningeal involvement the cells are
largely of a multilobed type resembling and usually spoken
of as polynuclears. They are not, however, the polymorpho-
nulcear neutrophiles of the blood, but more probably the wander-
ing tissue cells or clasmatocytes of Marchand. Very rapidly
these cells give place to small lymphocyte types so that by the
end of 24 to 36 hours, these latter cells represent over 90 per cent.
of the total. The globulin content now begins to rise and is
easily demonstrable by the methods of Noguchi, Pandy or
Ross Jones. The Wassermann reaction is regularly negative
but the colloidal gold test of Lange shows almost constantly a
weak luetic type of curve. During the following days there is a
gradual descent in the number of cells in the ﬂuid and a slight
rise in the globulin content.

Generally speaking, the highest cell counts appeared in those
cases in which the spine sign was most intense. Undoubtedly
in some of these instances there was a combination of factors
in the production of the extreme stiffness of the neck. On the
one hand, the voluntary effort, as already discussed, played a
part, and on the other, the element of true reﬂex spasm oc-
casioned by the extreme meningeal irritation was added. Ex-
amples of this type are cases E. E.L. No. 25 and R. N. No. 32.

7 2 ACUTE POLIOMYELITIS

The former presenting extreme neck stiffness 7 hours after
her ﬁrst complaint of feeling badly had 2430 cells per c.mm.;
the latter having gone to bed apparently well, had been restless
in the night and had awakened in the morning with marked
rigidity of the neck and 2000 cells per c.mm. Both these chil-
dren were treated promptly and repeatedly intraspinally with
serum. Case 28 died, and Case 32 survived with very exten-
sive paralyses which at the present writing, 7 months after the
attack, are improving remarkably well.

With very few exceptions the intensity of the spine sign
and the cell count in the spinal ﬂuid bore a fairly close relation-
ship so that we came to feel that it was possible roughly to
prognosticate the number of cells that would be found in a
given case after testing the cervical stiffness. Nevertheless,
there were some examples of quite opposite character, those
with high cell counts and no signs of spinal irritation and others
presenting the reverse condition.

There is no doubt as was pointed out in the monograph, that
ﬂuid drawn later than 24 to 36 hours after the period of menin—
geal invasion provides only diagnostic criteria. It is possible,
however, that spinal ﬂuid taken in the ﬁrst 12 to 18 hours
following meningeal involvement may have some prognostic
signiﬁcance depending upon the number of cells per c.mm.
Whatever indications may be suggested by differences in cell
counts lie at the extremes, rather than within the more average
ranges. Thus cases with cell counts below 100 rarely developed
paralysis while cases with counts of 500 or over frequently
did. Practically every fatal case showed more than 600 or 1000
cells per c.mm. These ﬁgures apply to ﬂuids taken within a
few hours after the occurrence of meningeal invasion as deter-
mined by the history and clinical observation.

There is one group of cases to which, in this connection,
especial attention should be called. Patients of this group
presented a clinical picture of varying severity. Some were
profoundly toxic, drowsy or indeed comatose. Spinal ﬂuid
examinations in this group always showed a surprisingly low cell
count, usually below 100 per cimm. The subsequent course
in all of them was striking because of its mildness. An isolated

CLINICAL PATHOLOGY 73

facial paralysis usually transient was almost the rule in this
series (Case 33, Diagnostic Series).

To sum up, it may be said then that spinal ﬂuid taken during
the ﬁrst hump of the dromedary type, or the early part of the
straggling course, shows no cellular increase and little or no
globulin. The pressure and quantity, however, may be notice—
ably greater than normal. After meningeal invasion has

 

 

FIG. 15.—Facial paralysis in case with profound stupor. (Reproduced from
the Monograph.)

occurred, the pressure is deﬁnitely lower and cellular elements
appear. In general cases with cell counts below 100 per cubic
millimeter Within the ﬁrst 12 to 18 hours are less apt to develop
a paralysis than are cases with counts of 500 or more. The
exception to the ﬁrst group are those cases which have an iso-
lated facial weakness. By making multiple punctures (at 10
to 12-hour intervals), it is possible to detect the time of men-

74 ACUTE POLIOMYELITIS

ingeal invasion. The puncture is most conveniently done
when the child is lying on the right side with knees drawn up
and head down so that the spine is ﬂexed well forward. With
young children cocaine is not necessary but the patient must be
ﬁrmly held to prevent sudden twistings of the body While the
needle is in place. A microscope and counting chamber should
be in readiness at the bedside so that a count may be made While
the needle is left in the spinal canal. During the count the
obturator of the needle should be reinserted to check the ﬂow
of the spinal ﬂuid. In the early hours of the disease the patient
experiences much greater physical discomfort from the anterior
ﬂexion of the spine necessary to separate the spinous processes
than from the introduction of the needle itself.

CHAPTER IX

THE PARALYSES

It is not proﬁtable to discuss here in detail the relative
frequency with which various muscles are paralyzed. The
pathological process may involve any part of the central
nerve tissues so that the neurological manifestations are mul-
tiform. The degree of nervous disturbance may vary from the
mildest meningeal inﬂammation, giving signs of irritability,
spine sign, and increased cells in the ﬂuid, to a widespread
destruction of the gray matter of the cord, causing rapidly ad-
vancing paralysis and death from failure of the anterior horn
cells governing the muscles of respiration. Between these two
extremes a great variety of conditions appear. The clinical
signs of muscle weakness depend upon the pathological process
but they do not represent with any accuracy the extent of the
lesions. For at autopsy there is often found much more exten-
sive disease of the cord than was indicated in life by weakened
musculature. Frequently there is a slight weakness of the legs
so that the child seems to prefer to crawl about instead of
walk. This may last for a few hours and then disappear.
There may be, on the other hand, deﬁnite transient paralysis
of an arm or leg lasting from a few minutes to half a day or
‘ more. Or there may be a complete ﬂaccid paralysis of one or
more extremities, neck or back, which persists for a time and
disappears or remains as a permanent disability. Much more
rare are the hemiplegic and spastic forms of paralysis, due
to upper motor neurone involvement. These are the true
“encephalitic” types described by Strumpell. In comparing
this and the more usual form of the malady he says “in both
diseases the chief seat of the lesion is in the gray matter,
in one case in the gray matter of the anterior horns, and in
the other in the corresponding portion of the cerebrum, the
cortex.” Besides these paralytic manifestations there are

75

76 ACUTE POLIOMYELITIS

met certain other forms of the disease. Among these may be
mentioned the rather rare multiple-neuritic in which a
continuance of pain along the course of the peripheral nerves
is intense. Occasionally also one sees patients who have a
marked ataxia and stagger like cases with cerebellar disease
of other origin. Psychic disturbances of various sorts are
seen frequently. Convulsions may occur, or profound stupor
often resembling some types of tuberculous meningitis. In
this type of case now and then a faint twitching 0r tremor
passes over an extremity or the whole side. Yet, despite the
coma-like condition. the patient can be rather easily roused
by handling or prodding. There is almost immediate response
and objection in the manner which has been so often seen in
the other cases of this extraordinary disease, a displeased,
irritated whine, and a vexed shrugging movement of the shoulder
forward and upward, conveying quite distinctly the child’s
wish to be let alone. Other cases of this kind may show a more
stuporous condition with partly closed eyelids beneath which
moves a slowly rolling eyeball. These individuals may or may
not have retraction of the head, and lie prostrated and somno—
lent. Still other patients behave as though heavily drugged,
and carry out sharp commands by slow, lazy, intensely
apathetic motions.

As a rule, the stupor clears with considerable rapidity. after
a duration of from three to six days. In one instance. the
patient after four days awoke as though from sleep. looked
about in a bewildered fashion and then said she wanted to go
home. Other cases regain normal mental condition more slowly,
but the process occupies only a few hours. Occasionally pro-
longed clouding of the sensorium is seen as in case J. L, No.
29 (Treatment Series), where the patient remained comatose
or stuporous for many days. Frequently children who recover
present a highly excitable and nervous condition for weeks after
the acute attack is passed and they are again up and about ap-
parently as well as ever. Emotional instability shown by
purposeless and alternate weeping and giggling is also not
infrequently seen.

The accompanying chart shows the days upon which paraly-

THE PARALYSES 77

sis appears. Obviously the second day is that on which most
of the cases become paralyzed.

One of the most impressive things about the paralysis is
its insidious and unexpected advent. A child goes to bed
well with strong and active limbs to waken with a paralyzed
member. In many cases there is no warning of the approaching
weakness and the patient seems unaware that power has gone.

31

 

I , 6 I0 II I2
FIG. 16.——(Reproduced from the Monograph.)

Such a child lies quietly in bed, often not acutely ill for the
fever may be passing, and when asked to move an arm or leg
fails to respond, silently, without remark of astonishment. At
other times there may be some premonitory indication of ap—
proaching paralysis. Slight muscular weakness or involuntary
twitchings, or the loss of a tendon reﬂex often precede the ﬁnal
crippling. As a rule, however, the paralytic stroke is sudden
and complete, the initial paralysis being ﬁnal in its extent. A

78 ACUTE POLIOMYELITIS

certain number of cases show a progressive involvement of
muscles. Thus the weakness may begin in part of one or
another extremity, extend then to the whole of that limb
and then on to another arm or leg. Practically all cases which
go on to fatal termination belong to this progressive group.

It is not always easy, especially in very young children, to
recognize the presence of a paralyzed muscle or group of
muscles. Of course, complete ﬂaccid paralysis of a Whole
extremity is obvious. But an isolated deltoid weakness, for
example, or failure of the outward or inward rotators of the
thigh may often escape detection. One most important and
frequent oversight on the physicians’s part is failure to recog—
nize weakness or paralysis of the intrinsic muscles of the back.

Children are very quick to circumvent a muscular incapacity
of one group of muscles by substituting makeshift motions to
attain a desired end through the use of other groups of muscles
not usually called upon for the particular purpose in view. Thus
if the biceps and supinator longus are out of commission and the
child wishes to ﬂex the forearm upon the arm, he will accomplish
the desired motion by swinging the whole extremity forward
and upward so that the forearm is ﬂung up into the ﬂexed
position. Then he will hold it there with his other hand.
Or the same motion may be more slowly carried out by crawling
with the ﬁngers up over the front of the body and clinging
with them to the bedclothes.

In order to detect whether or not a given muscle or group is
paralyzed it is necessary to put the muscle to be tested in such' a
position that it must work against gravity. For by slight
change in position a child will succeed in having the weight of
an extremity accomplish the desired ﬂexion or extension which
the paralyzed muscles can no longer bring about. With younger
children who cannot carry out commands, it is sometimes neces-
sary to prod the skin slightly with a sharp object in order to
make them attempt to move.

Following a rapidly advancing paralysis of arms or legs, signs
of embarrassment of the muscles of respiration begin to make
their appearance. A very small number of cases seem to have
direct involvement of the medullary respiratory center and

THE PARALYSES 79

seem to die from rapid exhaustion of this center although the
muscles of respiration are still operating. In either case the
picture is almost the same and constitutes one of the most dis-
tressing spectacles in the Whole of clinical medicine.

A striking feature of the fatal cases is the condition of the
sensorium. There is a peculiar, vivid alertness of the mental
state of these patients. The frequent condition of drowsiness
seen in the earlier stages of the disease gives place to apprehen-
sion and psychic activity.

With the onset of respiratory difficulty, it seems almost as if
the children were suddenly awakened and made to realize the
struggle before them. Little children seem to age in a few
hours. One sees a heedless, careless, sleepy child become all at
once wide~awake, high-strung, alert to the matter in hand,
and this is, breathing. The whole mind and body appear to
be concentrated on respiration. Respiration becomes an active,
voluntary process, and every breath represents hard work.
The child gives the impression of one who has a fight on his
hands, and who knows perfectly how to manage it. All he
wants is to be left alone, not to be interfered with, to be allowed
to carry out his ﬁght on his own lines. Instinctively he husbands
his strength, refuses food, and speaks, when speech is necessary,
quietly and with few words. One little child of four, so help—
lessly paralyzed that she was unable to move, but with a mind
that seemed to take in the whole situation, said to the nurse
clearly but rather abruptly between her hard—taken breaths, “ My
arm hurts”; “Turn me over”; “Scratch my nostril”; and then
when the doctor approached, “Let me alone, doctor!” “Don’t
touch my chest.” Pressure on the chest, tight neck bands,
anything that obstructs easy respiration is immediately resented.
The child demands constant attention, is irritated unless
everything is done exactly as he wishes it, and often shows an
instinctive appreciation for some especially efﬁcient nurse.
He is nervous, fearful, and dreads being left alone. 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. He likes to have his lips wet with cold
water, but rarely attempts to take it into his mouth, for he

80 ACUTE POLIOMYELITIS

knows he cannot swallow it. During the whole course it is
remarkable that cyanosis is absent. There is a little bluish
tingeing of the lips and tongue, but much more distinctive is
the pallor, which is sometimes striking. Sweating is profuse.
Then, as respiration gets weaker, the mind becomes dull, and
with the occasional return of a lucid interval, he gradually
drifts into unconsciousness. An hour or more later respiration
ceases. This peculiarly alert, keen mental state has been much
less noticeable in smallbabies. They tend to be dull and drowsy
most of the time; but in the older children this alertness has
been such a characteristic feature of the fatal cases, that it
is preferable to ﬁnd a child in a stuporous condition, rather
than with a mind whose nervous acuity seems due to a percep-
tion of impending danger. .

It should be clearly appreciated, however, that many cases
may Show some interference with respiration and still not go
on to a fatal termination. For those anxious hours of suspense
occasioned by these instances there is a gratifying relief in the
return of increasing depth and sufﬁciency of the breathing.
Furthermore, it seems to be true that death in poliomyelitis
is invariably the result of failure of the respiratory mechanism
and not to toxzemia.

CHAPTER X
PROGNOSIS

The problem of prognosis in acute poliomyelitis involves
several considerations: (1) What is the mortality? (2) Will
paralysis appear? (3) Will an initial paralysis advance? (4) Will
the paralysis be permanent?

In regard to the ﬁrst question it may be said that mortality
statistics are somewhat misleading. Until a very short time
ago when the diagnosis of the disease was determined by the
appearance of paralysis, statistics showed that approximately
IO to 15 per cent. of the cases were fatal. If, however, in the
light of our present knowledge mortality be ﬁgured on the
basis of all cases whether paralyzed or not, the percentage
should fall. This would be true because it is only cases which
develop paralysis that die. In the recent New York epidemic
the mortality rate ran as high as 27 per cent. This ﬁgure was
based on all cases accepted by the Department and these include
a very much larger number of non—paralyzed cases than have
been included in such statistics in any previous recorded epi-
demic. Consequently, notwithstanding the introduction of
large numbers of non-paralyzed cases into the total, the death
rate was higher than it has ever been before. There can be no
doubt, therefore, that the exaggerated death rate, and the great
number of paralyzed cases, indicated an extremely high virulence
of the infecting agent in the recent epidemic. But no accurate
ﬁgure for mortality in poliomyelitis can be established until
diagnosis of non-paralyzed cases becomes as deﬁnite as it is
in the smaller paralyzed group. In acute [poliomyelitis there
is a peculiar element of chance not present in other general
infections; namely, the accident of the lesion destroying simul-
taneously the phrenic and intercostal centers, an accident which‘
is invariably fatal. Unfortunately, there is no way of knowing

where the lesion will occur, or if an existing lesion will advance.
6 81

82 ACUTE POLIOMYELITIS

Flaccid legs, arms or facial muscles point only to the cord seg-
ment most seriously injured when the case is ﬁrst observed, and
form no criterion of the extent or subsequent behavior of the
lesion. Anterior horn cells that lie immediately outside the
zone involved by the pathological process may continue to
function properly, so that the proximity of the lesion to the
phrenic and intercostal centers does not necessarily make the
outlook worse. This and the fact that in most cases the initial
lesion in the cord is the ﬁnal one, and rarely advances, is
perhaps the most encouraging knowledge that we command
in attempting to make a prognosis as to life; for, as was
pointed out in the section on paralysis, death in uncomplicated
poliomyelitis invariably results from failure of the muscles of
respiration. In other infectious diseases where death has
been considered to depend upon toxzemia, mortality statistics
represent more nearly an average failure of human resistance,
affected less, perhaps, by the element of chance.

At the bedside of a given case, however, there are certain
phenomena which seem to have some vague prognostic sig-
niﬁcance. Our experience has been that the profoundly
stuporous cases usually get well. Increasing alertness and
apprehension on the part of the child with an existing paralysis
is of graver signiﬁcance. Prognosis for life is markedly less
good in older patients particularly of the type described in
the chapter on Etiology.

When a child becomes acutely ill during an epidemic of
poliomyelitis, so that the diagnosis is practically assured, the
question at once arises whether paralysis .will appear or not.
In the presence of such a problem there is a distinct sense of
obscured vision, because there seems to be no relationship
between the severity of the symptoms in the systemic phase
(ﬁrst hump of dromedary type) and the accident of meningeal
invasion. In some cases it has been possible to recognize al-
most the moment of occurrence of that event by repeating the
lumbar puncture as already described.

If no evidence of meningeal irritation is found criticism
is naturally leveled at the procedure of multiple puncture.
For it is unfortunately still true that, without evidence of

PROGNOSIS 83

central nervous system involvement, either through spinal
ﬂuid changes or paralysis, there is no incontrovertible proof
of the correctness of diagnosis.

The spinal ﬂuid, contrary to the opinion usually held, offers
undoubtedly some prognostic suggestions. There are a suﬂi-
ciently large number of observations to indicate that cases
which show cell counts of less than 100 per c.mm. during the
ﬁrst 12 to 18 hours rarely develop muscular weakness, or at
the most a transient facial paresis. Furthermore, cases
having cell counts of 200 to 500 very frequently develop paraly-
sis of the severer sort. With few exceptions the fatal cases
showed counts of over 700 or a thousand. I

Exceptions to these general statements occur. For example,
a certain number of cases with cell counts of 150 to 300 per
c.mm. escape paralysis. But there are remarkably few ex—
amples of paralysis in cases showing spinal ﬂuid cell counts
below 100 per c.mm. in the ﬁrst 12 to 18 hours. Our ex-
perience last summer fully agreed with that stated in the mono-
graph that after 24 to 36 hours the spinal ﬂuid had no prognostic
value.

Sometimes warning of approaching paralysis may be recog-
nized in certain clinical signs. Occasionally there is increased
pain in the extremity, although subjective indications are
slight and infrequent. Loss of tendon reﬂex is a far commoner
occurrence and often spasmodic muscular twitchings precede
the loss of power. Both these signs, however, may occur with-
out subsequent paralysis. There are no signs which indicate
whether or not an existing paralysis will advance. All that can
be said on this point is that as a rule the initial involvement is
the ﬁnal one. Usually if no additional muscle-weakness appears
within 6 to 12 hours of the ﬁrst paralysis there is small chance
of any further involvement. In a very few instances there has
been a remarkable delay in the initial appearance of paralysis
after onset of meningeal involvement as shown by spinal
ﬂuid examination (Cases 17 and 22 of Treatment Series). These
are numerous enough, however, to make one apprehensive of a
possible paralysis until the seventh or eighth day.

The ﬁnal question in prognosis can be answered rather

84 ACUTE POLIOMYELITIS

more deﬁnitely by statistics than any of the others. With
the advancing knowledge of the disease has come the satis-
factory realization that there is a strong tendency for the weak-
nesses or paralyses to improve. Wickman reports on 530
cases analyzed 1 to 1% years after the acute attack. Of these
56 per cent. were paralyzed and 44 per cent. were cured.
The Massachusetts records show a much lower percentage
(16.7 per cent.) of complete recoveries. It is too early yet
to study the recent epidemic from this point of view. But all
who have worked with the disease have been struck with the
remarkable early return of power in badly paralyzed muscles
and the full recovery of partial cripplings. Even after many
months unlooked-for improvements may cheer the patient
spirits of the convalescent and the family.

CHAPTER XI
TREATMENT

Prophylaxis—If it be accepted that acute poliomyelitis is
spread by human contact, isolation of the patient is the es—
sential point from which to start an effective quarantine.
The disease should be managed like every other acute contagious
infection. There is still some difference of opinion over
the question of proper duration of quarantine, but there can
be none concerning the necessity. Furthermore, a quarantine
which covers only the paralyzed individuals is incomplete.
For when the great number of children who roam about suffering
from the mild form of the disease is considered, the inadequacy
of a quarantine for paralyzed cases alone becomes apparent.
In addition to these, moreover, are the unknown number of car-
riers among healthy individuals and convalescents. In this
relation the recent work of Amoss and Taylor on neutralizing
bodies~ found in the nasal secretion of human beings is of
particular interest. Although their experiments as reported
do not cover a very large series of individuals, nevertheless
the indication from them is that the neutralizing bodies in
this position form a ﬁrst line of defense. This has a bear-
ing on the question of local prophylactic treatment which
has been so much discussed in the past. The problem can,
in the light of this new knowledge, be more intelligently dis—
cussed. The obvious purpose of local prophylactic treat—
ment is to reduce the number of, or perhaps remove entirely
the poliomyelitis organisms from the nasal mucosa. To
accomplish this by mechanical means alone is unprom—
ising. Hence, antiseptic chemicals have been added to the
ﬂuids sprayed or douched into the nose. Now that we
have learned that the nasal secretions are themselves de-

structive to the virus, we should aim to conserve them.
85

86 - ACUTE POLIOMYELITIS

Whether their action is best promoted by no interference, or
by the gentle impetus to increased secretion afforded by
bland saline and alkaline ﬂuids, may be still regarded as an
open question. But it would now appear to be patent that
severe measures are contra-indicated, not only on general
clinical grounds, but also from the standpoint of local pro-
tective action. Arguing from analogy to other acute con—
tagious diseases, it'is highly probable that the case of infantile
paralysis is chieﬂy a menace during the very earliest days of its
course. But there must be a case to start an epidemic. Con—
sequently any recognized case is obviously the potential
center of an epidemic focus and should be promptly isolated.
Indeed it might be a more valuable procedure to quarantine
the entire household for a short period of time, than to iso-
late the case and attendant, for 6 to 8 weeks as now advo-
cated by most Boards of Health. It is difficult to hold
healthy and busy adults so long in a state of captivity. But
it might be easily possible to gain their cooperation for 10
days, so that evasions of the sanitary regulations would not
be attempted.

In addition to the protection of the community by adequate
quarantine regulations much may be done by individuals to
protect themselves. It is only necessary to think how fre—
quently in the course of a day the secretions of nose and
mouth, and even the content of the lower bowel are passed either
directly or indirectly from one individual to another. How
common a sight it is to see someone with a coryza blow his nose
into an already saturated handkerchief and immediately there-
after extend a still moist hand to pat a child on the head and
face or shake hands with a friend. Several instances arose
during the past epidemic which led the writer to enquire what
the custom of certain individuals was in the matter of washing
the hands after using toilet paper. The surprising answer was
that the hands were never washed after that procedure! As a
result of these experiences, the following notice is suggested
for posting in all water-closets, nurseries, kitchens, and
pantries.

TREATMENT 87

I

NOTICE ‘

INFANTILE PARALYSIS, and other diseases, are carried in the secre-

tions of the nose and mouth, and also in the movements from the
bowels.

Think how often your HANDS come in contact with these substances
and then how often those same hands touch other people or objects.
In this way disease is spread.

Therefore after blowing your NOSE, COUGHING or SNEEZING into
your hand, or after using TOILET PAPER, you should wash your
hands thoroughly.

There are CHILDREN in this house. Think of them and often wash
your hands.

Of similar nature is the danger of transferring nasal and mouth
secretions to children by kissing and fondling. It is often diffi-
cult to persuade a mother who has been caressing a sick child
not to kiss her other children when she leaves the patient. But
it would be a wise precaution not to kiss children on the mouth
at any time, and during an epidemic of poliomyelitis not at all.

Undoubtedly the most effective means of isolation of patients
is hospitalization. Arrangements should be made in advance
for the prompt hospitalization of all cases of the disease. Other
children in families from which cases are removed should be
held in quarantine for IO days to see if secondary cases develop.

In the hospitals the technique for doctors and nurses and
attendants should be that of any properly conducted contagious
hospital. Physicians working in the ﬁeld should wear gowns
and masks, wash their hands most carefully or bathe them in
bichloride solution (1—5000) or alcohol after completing the ex—
amination of the case. All excreta should be disinfected before
being sent into the sewage system and all dishes boiled after use.

ORGANIZATION OF FIELD WORK

A good organization for making early diagnosis, giving
treatments, and hospitalizing cases in an epidemic center is
most important. There should be a sufficient number of
doctors with clinical and laboratory experience, working from
a. central office or laboratory, to go out on call ready to do
lumbar punctures and give serum. Each man should carry
with him a microscope and counting chamber so that the cell

88 ‘ ACUTE POLIOMYELITIS

count of the ﬂuid can be made at the bedside. When enough
ﬂuid for the cell count has escaped, the puncture needle with
obturator replaced should be left in the back while the count
is made so that if serum is indicated it may be immediately
injected.

Until late in the epidemic of last summer the use of serum
from recovered cases was limited to intraspinal injection. This
method was based on the experiments and observations of
Flexner and Lewis, who showed that intraspinal injection
of serum derived from recovered monkeys or human beings
would prevent paralysis in monkeys, after intracerebral in—
jections of virus, and the clinical application made by Netter
to human cases. Since then knowledge has advanced and the
mode of serum injections improved.

The method consists in obtaining serum from the blood
of individuals who have suffered an attack of infantile paraly-
sis. According to Netter subjects most favorable as a source
for serum are those whose acute attack lies from 6 months
to perhaps a few years in the past. Amoss and Chesney
urge the use of serum from cases as soon after the acute attack as
possible. The author found that the serum of one case ﬁve
years after the acute attack was especially effective. The
blood should be drawn directly from the vein into a sterile
centrifuge tube or ﬂask which can be slanted. By centrifugal-
ization somewhat more serum can be obtained from a given
amount of blood than by the still clotting method, and also
more rapidly.

The serum is pipetted off and stored in convenient sterile
retainers. Serum which contains red blood cells or much dis-
solved haemoglobin is undesirable because it often gives rise
to severe reactions in the spinal meninges causing headache,
intensiﬁcation of pains, and fever often with chills.

To carry out the intraspinal treatment a lumbar puncture
is made preferably with the patient lying on the side with
thighs ﬂexed and head bent forward so as to throw apart the
spinal processes. After 20 c.c. at least have been removed
and it is desirable to withdraw all the ﬂuid that will come,
10 to 15 c.c. of serum are slowly run in by gravity. For in—

TREATMENT 89

travenous or subcutaneous injection a large syringe of 20 c.c.
capacity may be used.

When the recent experimental work by Flexner and Amoss
is considered, the rationale for combined intraspinal and in-
travenous or subcutaneous use of immune serum becomes ap-
parent. The fact that injury to the meningo-choroidal defen—
sive mechanism permits the entry not only of infectious agents
but also of antibodies from the blood to the subarachnoid
spaces makes obvious the indication for this method of treat-
ment. For if the beneﬁcent action of immune poliornyelitis
serum be the result of its power to neutralize the Virus in the
spinal and lymphatic ﬂuids before it becomes attached to the
central nervous system, then it is desirable to bring as large a
quantity of the serum as feasible into the subarachnoid space.
Now it is unwise to inject more than 15 c.c. of serum directly
into the spinal canal of a patient suffering with infantile paraly—
sis. This quantity is proper both for adults and for children
of two or three years. Below this age the quantity injected
should be diminished to 5 or 10 c.c. An intraspinal injection
of immune serum therefore has double purpose. It acts di-
rectly upon the virus already present in the spinal canal and at
the same time by increasing the permeability of the meningo-
choroid complex permits the entry by that route of those anti-
bodies circulating in the blood which have been introduced by
subcutaneous or intravenous injection.

It is further clear from the experimental work referred to
that immune serum is the only ﬂuid which has a restraining
effect upon the advancing virus in the cerebrospinal space.
Normal horse or monkey serum serves only to destroy the
barrier of the meningo—choroid complex but provides no
neutralizing substances. It is difﬁcult, therefore, to under—
stand why there should be any curative value in other than
speciﬁc immune sera, especially earlier in the disease at the
time when the serum is most needed.

Serum Group—During the course of the summer we have
been frequently impressed with the large number of cases show-
ing low cell counts in the ﬁrst twelve or twenty—four hours after
the meningeal invasion that did not develop paralysis, and

go ACUTE POLIOMYELITlS

likewise that 'many cases with very high counts become par-
alyzed. It was hoped that deﬁnite prognostic assistance might
develop from this observation, but a careful subsequent analy—
sis does not ﬁrmly establish the assumption. Fatal cases in
many instances had. cell counts in the neighborhood of 1000
or more. In the latter part of the epidemic when serum was
plentiful, and the cases less Violent, many patients with low cell
counts were treated, and recovered Without paralysis. The

 

 

 

 

 

 

UNTREATED
23:23:: : Hours after onset of meningeal invasion i

Name ‘ (13:8 C1211; :I—éiG—IZEIZ-ISiI8-24éz4—30‘30-36‘136—42J42—43 Pgiarllﬁls
R.W .............. i27i230l6‘ rrrrrrrrr l ..... 1 ............... i ..... i0
W. H ............. 29 7011 ............................... o
M.A .............. l 17 250-“ 12‘ .............................. lo
M.T .............. 4} 4o 12»: .......... i .................... ‘0
V.C ............... ‘ 81250, ....... ‘18‘ ............... l .......... P
D.M .............. 15 337 .. ......... 24 o
L.W ............. ‘ 167370 ....... i ..... 24‘ ..... ‘ ,,,,, ‘ .......... ‘
L.C ............... 5‘ 40 W‘...‘ ..... 24 o
R. S ............... 6 690 ............ g 24 .................... P Spastic
T. R. D ............ 71980} ....... l ,,,,, 24 i .................... o rbc in

‘ ﬂuid

H. P rot 40W‘ 24‘ ..... i ............... lo
O.R ............... ‘ 11‘1180 ............. 24 .................... PD
F. McQ ............ 13i200 ....... i ..... 24‘ .................... o
W.Z .............. i 35‘ 901‘ 301 ............... ‘0
GL 36. 35 ..............‘ 32 .o
M.N .............. ‘28‘33ol...‘....‘.....‘....41,H..\36......o
D.S ............... 26 504‘ ............ ‘l .......... ........ 48 o
W...E 24 320 ............ l ............... l ..... ?‘o
J.M ............... 20 240‘“ ‘ 72 ‘P
M.E.A ........... 21 200“ 72 P
R.B ............... ‘ 22220“ 96 1o
D.B .............. j 23 I40 ....... ‘ ......................... 96 P
D. S ............... l 18 ‘ 220 l ....... ‘ ..... l .................... ‘108 PD
EH 19‘501481PW
S.L ............... ‘ 1‘ 40““\ 48 ‘PF
D.S ............... 9 188
H.P ............... ‘ 12‘260
V.L ............... i 14‘140
J.McM............ 33 40
J. McM....r..r....1 sglrgo‘
L.C ............... 34‘ 16
T.W .............. 373‘ 70 r ‘
T.W .............. 37 80
o = No paralyses.
P nParalyses
D=Death.
W-Weakness.
Phi—Facial.

TREATMENT 91

deduction as to the therapeutic value. of the serum treatment
in these instances must be very carefully guarded‘ because
of the fact that not a few untreated cases with low cell
counts also escaped paralysis.

 

 

 

 

 

 

 

 

 

TREATED
i Hours after onset of meningeal invasion
N ‘Case ‘ Cell ‘ ‘ ‘ ‘ Paral-
ame . no. 1 count ‘1—61 6—12‘12—18 18—24‘24—30‘30—36‘36—42 42—+ 03:15:31:
4 ‘ 1
L. J .............. e l 80 4 l ..... ‘ ..... j .......... l lllll I ..... i ...... o
A. M .............. 34 80 6 ............................... ’ 96? ‘PD
EL 2842430...11o .............. l .......... ‘ ...... ‘PD
R. L .............. 30 530 ...v 12 .................... l ..... 1 ...... o
R.I\ .............. 32i2000 8 .P
K. McL ........... l 41 ‘ 3201... 7 l .................... 1 ........... o
1.6 ............... 24‘ so 71/2‘PF
E. H ............. 3 l 120 Io .......... v ..................... P
R. J .............. 4 l 120 12 l ............................... PW
W. K ............. s 720 s .................... : ........... 31>
C.L .............. 11 500 12 ‘ ..... ‘ ..... z .......... l ........... [0
K. M ............. 13 I30 10 .......... ‘ .......... 1 ........... o
H. M ............. 14 120 9 .................... 1 ........... ‘o
A. C 19 l 250‘ 10—11 .................... ' ........... o
G.S ............. 39‘ 170 12 o
J.L .............. 29‘ 490 ........ 14 ‘10
B. N ............. 31 420 ........ ‘ I3 ........................... ‘0
W. E ............. 25 1200 ........ ‘ 15 1 ............... i ........... 40
M. N ............. 12 40 ........ l 18 l ..... ‘ ..... ‘ ..... l ........... ‘0
S.M ............. 17 640 ........ 18 ‘P
F. H .............. 21 400 ’ ........ 15 1 ............... ‘ ........... P
G.S .............. 44 270 17 ............... ‘ ........... o
B. G .............. 26 180 .............. 24 ..................... |o
L. G .............. 27 430 ............. 24 ..... ‘ ..... l ........... P
T.D ............. 2 7o 24 ..................... 0
L. J .............. 5 90 ............. 24 .......... ‘ ........... o
L. M ............. 15 I40 24 ‘ ..................... PD
M. S ............. 16 320 24 7 ...................... o
H. McC .......... 37 l 240 ............. 24 ...................... 0
A. S .............. 38 222 ............. 24 ..................... PW
C. W ............. 42 280 .................. 3o ..... ‘ ........... PW
W. C ............. 43 215 .................. 1 26 b ................ P
M. McA .......... 35 485 30 ........... PD
0. N .............. l 22 620 35 ............ P
R. M ............. 23 221 36 ‘5 ........... P
W. R ............. 18 325 ....................... 3o 1 ........... P
H. K ............. 20 950 ....................... 36 ............ PD
M. B ............. 36 240 ....................... 30 l ........... PW
D. D ............. 1 1 1420 l ............. 1 ............... l ..... 1 72 PI)
E. K .............. 7 320 ............................ ‘ ..... 4das o
M.H ............. 9‘ 425 ‘48 P
M. L ............. 10 1 510 ............. l ............... l ..... l 48+ PD
A. H .............. 45 39 ................................. 72 ‘P
R. E ............. l 46 200 l ‘ l 48 o
F. S .............. 40 130 ........ , .......... 1] .......... ‘ ..... 60 P
A. L .............. 33 50‘ 1 { ..,. I 48 PW

 

92 ACUTE POLIOMYELITIS

The tables constructed to show the number of hours elapsing
between the onset of meningeal symptoms and the performance
of lumbar puncture have been prepared with a view to comparing
the results in the untreated and the treated cases. A glance
at these tables will show that while it does not follow absolutely
that cases with a low cell count do not develop paralysis or
that those with a high cell count always do, it is quite obvious
that the tendency of the cases showing the higher cell counts
in the early hours is toward paralysis. It is also indicated
from these charts that after 36 hours the cell count in the
spinal ﬂuid is of little or no prognostic value whatever. This
observation corresponds to that reported in the monograph.
But the cell counts in the ﬁrst 12 or 24 hours furnish
something of prognostic signiﬁcance as mentioned before in
Chapter VIII. Group comparisons are not particularly valu-
able, especially in view of the difference in the severity of the
cases according to the period in the epidemic during which
they occurred. .

The tables by Amoss and Chesney where the result of
combined intraspinal and intravenous or subcutaneous use
Of serum is reported are somewhat more convincing than
those based on intraspinalinjection alone. A study of their
case reports which follow those of the author are also in—
structive. Throughout both groups, however, runs the sug-
gestion that cases with low cell counts in the early hours
have a better chance of escaping paralysis .than those with
high counts at the same period.

Zingher50 reported a large series of gases treated with im-
mune human serum, but gives no clinical records of the pa-
tients. His whole presentation of the case for serum therapy
rests upon an analysis of percentages. It must be admitted
that his ﬁgures are more favorable than any others which have
been so far published. Thus, of 54 cases treated in the pre-
paralytic stage, 44 recovered without ever developing paraly-
sis; 5 were paralyzed, but recovered ultimately, and 5 were
permanently crippled. It would be interesting to know what
types of cases were included in this series, and the time at
which they were treated.

TABLE I.——REPRODUCED FROM AMOSS AND CHESNEY (JOURN. Exp. MED.). SUMMARY OF CASES THAT RECEIVED SERUM

 

 

 

 

TREATMENT
‘ Time ‘ l l
i Spinal ﬂu1d 2:22:53)? 1 Serum adm1nistrat1on Tem- i bgﬁin 1 Total 1
(11?ng Age Climcal cond1t1on 7 7 777 1 disease 7 777 77 77 777777 7 7} Dali??? $383332; 1am821nt Result
No. of Glob- and ' Subdur 1 Subcu- Intra- treat- l temper- :1 serum
; cells ulin treat- a . tane- . venous 1 ment ‘ ature g1ven
1 1 ment 1 ous v 1 1 l 1
' l
Yrs 1 Hrs c c 1 c.c. c c °F. 1 Hrs c c
l 1
1 ‘33 Ascending paralysis of 280 ++l 72 i 10 l ...... ‘ 20 101.2 ........... l 30 Died 10 hrs. after treat-
legs. bladder. and ab- 1 I l 1 ment.
- dominal and thoracic 1 ' 1 ‘
1 muscles. 1 l 1 l 1 l l
2 ‘10 Ascending paralysis of 270 : + + 96 » 20 1 60 ‘ ....... 101.4 24 1 80 Deltoid and diaphragm
legs. bladder. abdom- ‘ 1 functioning 24 hrs. later.
1 inal wall, diaphragm. left l | 1 1 1 . . 1 1 Voided 4 days later.
1 deltoid and right facial . ‘ ‘ l 1
‘; muscles 1 1 1 .
3 1 3 Right facial and degluti— 208 + 72 i 15 4o 1 20 1 104.2 18 ‘ 75 No further progress of par-
! tion muscles paralyzed. ‘ 1 1 l l 1 1 l l alysis. Subsequent im-
1 1 1 1 l ‘ provement marked.
4 133 Weakness of left leg and 50 + 1 54 2o ...... 50 103 .0 60 70 No progress of paralysis.
1 abdominal muscles. 1 1 ‘ 1 1 ‘ j 1 Subsequent 1mprovement
5 1 2 Weakness of stemoclei- 37 1 + 96 5 30 l ....... 98 .2 ........... 35 No essential change.
domastoids both legs. 1 ‘
6 4 and. intercostals. 1 1 1 l
Partial paralysis. 920 + +l 3o 10 1 25 1 ....... 102 .o 60 35 i No increase. Complete
1 ‘ recovery rapid.
7 1 2 Weakness of ﬂexors of 99 1 + 48 1 5 1 30 ....... 101 .4 24 3s No progress of lesion. Sub-
1 right thigh ............. 1 ‘ 1 1 1 1 se uent improvement.
8 ‘1|%2 Weakness of left quad- ........... 48 1 5 1 20 1 ....... 102.0 ‘ 48 1 25 ‘ Sligt increase in weak-
nee 1 1 ‘ ness. _ .
9 3 weakness of left anterior ‘ 115 + 72 I 15 1 4o 1 ....... 100.2 1 Low lever 55 Deﬁnite 1ncrease 1n extent
1 tibialis. _ l l 1 1 1 1 for 2 wks. 1 l of paralysis of left leg.
10 ‘ 1%; Weakness of r1ght deltoid. 30 1 ++ 24 5 ............. 101.0 1 24 5 No increase in weakness.

 

1

INCINLVEIHJ.

£6

TABLE I (Continued)

 

 

 

 

 

 

N

Clinical condition

Weakness of left peroneal

and quadriceps and
slight weakness of in-
tercostals.

Slight right toe- drop

No paralysis. Left knee
jerk diminished.

N 0 paralysis.
N o paralys1s ............

1

 

 

 

 

. . 1 Time i . . .
1 Spinal ﬂu1d between Serum adm1mstrat1on Tem- Time Total
ﬁ_ 1 onset of 1. _ ___,. __ perature1 between amount
1 1 diseaise 1 b before trgatment] of Result
1 an 1 11 cu— _ treat— ‘ an norma serum 1’
231131 Gullﬁ” treat- 1 Subdural . tane- 3:53:15 ment temper- ‘ g1ven 1
1 1 ment 1 1 ous . . 1 ature 1
. 1 1 1
30 j: 1 12 1 10 1 30 11111111 1 101 .o 1 3o 1 4o 1 No increase in paralysis.
1 1 Rapid disappearance of
1 1 weakness noted on admis-
1 1 1 51011.
250 1 ++1 24 1 10 1 4o 1 103.0 1 24 50 No paralysis.
850 + +‘ 48 1 5 1 15 102 .5 00 2o Developed partial paral-
‘ ysis in arms. legs. and ab-
: 1 1 1 1 1 dominal muscles.
120 1 ..... 1 31 1 5 20 ....... ‘ 103 .0 ........... 25 1 D1ed1n 66 hrs
360 . ++1 36 1 10 20 . 103.2 ........... 30 mm in 28 hrs. _-
730 ++ 6 IO 20 102.0 . 96 30 Slight partial aralys1s of

N0 paralysis ............
No paralysis ............

No paralysis ............

No paralysis. 1
No paralysis.
No paralysis. . . .
N0 paralysis. , . .
No paralysis. . .
No paralysis. . . .
N o paralysis ........

 

1Noparalysis..........::1

 

1 1 1 1 1 1 both arms. S11 equent re-
‘ 1 ; 1 1 covery complete

60 i 36 1 6 : 25 ....... 102.0 22 ‘ 31 Subsequent rise to 102°F.
1 Variable temperature for
‘ 5 days. No paralysis.

 

379 + 22% 1 10 1 25 ....... 103.4 32 35 No paralysis.
1 (2 doses.) ’
150 1 ++1 24 1 10 102.4 1 15 35 ' N0 paralysis.
75 + + 18 1 10 101.4 22 35 N0 paralysis.
230 + +1 66 5 102 .4 1 32 45 . N0 paralysis.
88 1 ..... 1 76 20 101.6 36 50 N0 paralysis.
250 1 ..... 1 3o 1 15 101.2 12 55 No paralysxs.
40 + 31 25 103 .0 16 60 N0 paralysis.
260 . + 48 22 103.2 ‘ 22 67 No paralysis.
4o 1 + +1 38 20 101.0 1 48 120 1 No paralysis. Hy paras-

 

thesis disappeared in 48
r

 

176

SILI’IHANOI’IOE HIHDV

TREATMENT 95

Peabody51 has recently reported on 51 serum—treated cases
in Massachusetts during the fall of 19r6. Of these, 51 cases
treated in the paralytic stage, 3 5, or 69 per cent., recovered
without ever developing paralysis; 5 cases, or IO per cent.,
died within 24 hours; and II cases, or 2:: per cent, became
paralyzed, but 6 of these only slightly. The serum used in
Peabody’s cases was all from patients whose acute attack was
ﬁve years or more in the past. It was used only intra-spinally.

TABLE IV.—-REPRODUCED FROM AMOSS & CHESNEY, (JOURN. EXP. MED.) .
RESULTS IN CASES TREATED WITHIN 48 HOURS AFTER ONSET WITH
MORE THAN 30 00. OF SERUM

 

 

 

 

Time between a ar- l
Case No. enttr 808115131: 3313p Toszarluiingivd; 0f i Result
‘ _ Hrs. \ C.(:.

7 48 3 5. —
25 48 . 67 +
26 38 1 20 +
I 7 36 ‘ 3. I +
24 3 I ‘ 60 + .

6 3° ‘ 3 s +
23 30 _ 5 s +
I 9 24 l 3 5 +
I 2 24 50 +
1 8 2 2% : 3 5 +
20 I8 3 5 +
I I ‘ I 2 4o . +

Table IV shows the result of cases which were treated by
Amoss and Chesney early and with large amounts of serum.

The circumstances surrounding the group of fourteen cases,
in which no paralysis was detected at the time serum was ad-
ministered, are more favorable for a conclusion. T wo of the
patients of this group developed respiratory paralysis and died;
and two others developed some degree of weakness or partial
paralysis of certain muscle groups. The ten remaining cases
(71 per cent.) never showed any detectable weakness.

Serum Treatment—Obviously no incontrovertible general
conclusions can be drawn from a study of the tables and the

96 ACUTE POLIOMYELITIS

foregoing serum treated cases, especially those of intraspinous
treatment alone Each instance must be considered separately.

BAJEEE'E Z 3, 4- 5
1916 Septlb 19 -20 7.1

N.
HOURZ 610 4 4812 a

H

H

u.-
0

In]
9;
F
3510
r1]
“2‘
[:1
in

PULSE
RESP. 31 32 3

FIG. I7.—Temperature chart of case 20. Series of Amoss and Chesney.
(Journ. Exp. Med., 1917, xxv, 599).

 

But in the study of these cases several interesting points appear.
In the ﬁrst place other excellent examples of the various types
described in the section on Classiﬁcation are presented, and

TREATMENT 97

certain unusual events, notably the delayed paralysis (Cases
17 and 22), and the pressure symptoms after treatment (Cases

3? 3 4 5 6
1916 5 14 15 1e 17

HOUR N' N'

p.
O
No

y-L

8

“’0

ix]
[2
B
«t
M
m
0.
>1
M
B

LO
' (P

PULSE 7
RESP? 32, 32. 50 7.4- 2.0 26 25

 

FIG. 18,—Temperature chart of case 7. Series of Amoss and Chesney
(Jaurn. Exp. A[(d., 1917, xxv, 508).

12, 29, 32, 42, 43, and 25A). Whether the serum played a part
in delaying the paralysis in those cases or not is still an open

question. Of somewhat similar nature, perhaps, is the obser-
7

98 ACUTE POLIOMYELITIS

vation that in the treated group there are rather more instances
of partial paralysis and transient weakness than in the untreated

B55352: 2, 3
1916 Oct. '7 8
H N.

URE
,.
O
N

r.
3.
cc.Intrd5pindlly

ccSubcuIdne

p
O
O.

l"
4
05
m
D.
2
H
e

co
“’0

PULSE.
RESP. 28

 

' FIG. 19.—Temperature chart of case 25. Series of Amoss and Chesney
(Journ. Exp. Med., 1917, xxv, 601).

group. The matter of pressure effect following intraspinal

injection is most important and should be specially emphasized.

In several cases undesirable symptoms followed‘ treatment

TREATMENT 99

and seemed to be the result of it. Two main types of disturb-
ances appeared; one presenting the aggravation of symptoms of
meningitis common to all therapeutic intraspinal injections and
to which reference has already been made above (Cases 42 and
43 are examples). The other undesirable reaction is much
more alarming and consists of respiratory embarrassment with
general collapse. The breathing becomes rapid and shallow,
and often irregular (Cases 12, 25A, 29, 32, and 36). In most
instances these symptoms rapidly disappear following the release
of spinal ﬂuid by lumbar puncture; and it was later learned that
they could be avoided by using small quantities of serum (5 to 10
c.c.) and slow injection by gravity method after removal of a
larger amount of spinal ﬂuid. It is conceivable that death
may be hastened in cases where serum is given in too large doses
and two rapidly, after the involvement of the centers of the
respiratory muscles has begun. That these occasional instances
of the undesirable effects of intraspinal injection occur in the
treatment of epidemic meningitis also is well known; but in
that disease as in poliomyelitis they are the exception. By
withholding immune human serum from the individual suffering
with poliomyelitis, the patient may be exposed to a greater and
far more frequent danger than that contained in the rather
rare chance disturbances due to increased intracranial pressure.

An analysis of the treated cases shows that in four cases in
which weakness or paralyses was already present when the
ﬁrst serum treatment was given, there was no restraining effect
upon the advancing process (Cases I, 10, 2‘0 and 21).

Another group which seems not to have been inﬂuenced by
the serum consists of those cases with low cell counts (50 to
150 per c.1nm.) and an isolated facial palsy. This is a very
deﬁnite type of case, is always mild, and the facial weakness
almost always clears up whether treated or not.

The remainder of the series is composed of cases which
represent as nearly as possible average examples of this multi-
form disease. There are numerous instances in which serum
was given and paralysis occurred and numerous instances in
which paralysis did not occur. The only thing which clearly
differentiates many of the cases is the clinical impression at the

IOO ACUTE POLIOMYELITIS

time of treatment and this cannot be transmitted adequately
in words.

One thing seems to stand out fairly deﬁnitely——the need for
early introduction of the serum, both intravenously and intra-
spinally. Working from the hypothesis that the serum operates
by neutralizing the virus which is not yet ﬁrmly attached to
the nervous tissues and so restrains its effects, we attempted
to give the serum as soon after penetration of the meninges had
occurred as possible. Amoss and Chesney added the intra-
venous use of serum on the basis already discussed. This
appears to increase the therapeutic value of serum, both by
providing larger amounts of immune serum and therefore pro-
moting penetration of the serum directly into the nerve tissue as
discussed by Mott52 and by Flexner.53 In the dromedary type
of case the moment of meningeal involvement is often marked
with amazing sharpness and, if a child has been under constant
and careful observation during the ﬁrst hump and intermission,
it has been possible in several instances to treat within a few
hours of the onset of the meningeal stage, or second hump.

In cases of the straggling type, unfortunately, the greatest
difﬁculty is often found in recognizing from clinical signs
the moment when the invasion of the meninges occurs. If
the serum is regularly withheld until this event takes place
there may well be loss of valuable time, for in this disease time
is an important factor, after penetration of the meninges
has been completed. Consequently every effort should be
focused on the detection of the meningeal involvement at the
earliest possible moment. In some instances the bafﬂing
phenomena of greatly increased cell count without clinical signs
of meningitis demonstrates the difﬁculty of the problem (Cases
II, 14, 21 and 24). Occasionally in the absence of the spine
sign (painful anterior ﬂexion of the spine) or negative Kernig
a marked onset of drowsiness seems to have been the signal of
meningeal invasion. In a few instances loss of one ankle or knee
jerk has been the only indication of disturbances of the central
nervous system. But these may not mark the beginning. With
this difficulty in view the question arises whether the use of serum
is not perhaps indicated before signs of central nervous sys-

TREATMENT IOI

tem involvement appear. The occurrence of multiple cases in
a family is so common that this indication becomes stronger
for the treatment of a child developing fever in a family where
one member is already stricken. Since the introduction
of the intravenous and subcutaneous method, it is no longer
necessary to wait for the meningeal stage. Therefore. the
earlier the diagnosis can be positively made and serum intro-
duced the better. Now in epidemic areas many cases may be
seen so early that a negative spinal ﬂuid is found at the ﬁrst
puncture. This fact brings up the question of the desirability
of giving an intraspinal injection of immune serum at this
time. It is probably wiser to give a large intravenous or sub—
. cutaneous dose at this stage, and puncture again in IO to 12
hours. If at this second puncture the spinal ﬂuid shows patho—
logical change then the intraspinal serum injection should be
given at once, and also another dose by vein or subcutaneously.

When we consider,the recorded facts and impressions re—
garding the use of immune serum, including a recognition of
the dangers attendant upon all subarachnoid injections, small
though they be, the question arises of the degree and advis-
ability of resorting to the serum at all.. This question must ulti—
mately be decided both upon statistical grounds and Clinical im-
pressions and observations. As regards the former, attention
may be called here to the type of case which presents the pic-
ture of a very profound stupor with the isolated facial paralysis.
As regards the second consideration, it'should be stated that
all the physicians who had opportunity to observe came to feel
that the serum possessed deﬁnite and often striking power to
prevent paralysis, especially when the combined method was
used. But the impression was also gained that the serum was of
beneﬁt, not in all, but especially in those cases in which it
was given within about 30 hours from the time of the appearance
of signs of meningeal invasion. That the serum is of far less
value after the advent of paralysis would appear to be indicated.
Yet even that point is one not easily decided and hence. what
the limit of its value may be can only be determined from a
far larger number of observations.

These observations should also be compared and correlated

102 ‘ ACUTE POLIOMYELITIS

with those of Netter whose views on the value of the serum
are somewhat more positive than ours. He is deﬁnitely of the
opinion that cases treated after paralysis has appeared clear
up with a speed and completeness that does not occur without
the use of serum. Several of his cases belong to the rather
common variety with profound stupor already mentioned as
having a uniformly good prognosis, so that it is somewhat difﬁ-
cult to credit the serum unequivocally in these particular in-
stances. But it may fairly be questioned whether his protocols
really bear out the contention since with him as with us the
statistical proof rather fails to bring conviction though the clinical
impressions obtained form a strong note in his contribution.
The notion which presents itself from studying this series
of cases is that once the meningeal invasion is established,
that is 24 to 36 hours after the onset of clear meningeal signs,
the chances of arresting the progress of the disease in the
central nervous system are already seriously diminished. All
this merely means that the serum, if it be employed (but
here again the fact must not be forgotten that we are at the
beginning stages of the speciﬁc treatment of poliomyelitis
and may have to revise our judgment later), should be used
early, which in turn means prompt diagnosis through careful
watching and the lumbar puncture ﬁndings. The evolution .of
the disease is rapid and its course must be considered in terms
of hours, not of days. Consequently, any child who develops
febrile symptoms without adequate and obvious cause, and then
promptly recovers or straggles along half sick, should be watched
for the ensuing week with greatest care lest the sudden appear-
ance of a meningeal invasion, insidiously striking while the
Child is at play or sleeping, take the family and physician un-
aware and valuable time be lost. But as long as other, surer,
and hence better, methods of treatment are not available it is
doubtful whether in individual instances we are justiﬁed in
withholding the serum even at a later stage of the disease
than here considered as most promising. The problem is one
to be weighed pro and con in the individual case and will
doubtless to some-extent be decided by circumstances and
predilection, and whether serum is readily available or not.

TREATMENT 103

Remembering that it is human serum we are forced to use
at present, the supply must always be limited. There must
be a choice too as regards source, the medical history of the
donor and the length of time since he suffered an attack of
poliomyelitis. While it is true that neutralizing bodies may
still be detected several years after recovery from the acute
disease, yet analogy would suggest the advisability of choosing
persons more recently affected. Netter believes the most
potent serum is found in individuals whose acute attack lies
between three months and four years in the past. It is, of
course, always possible that one specimen of serum is less
active than another; hence, pooling of the supplies should be
practiced when collected, as they should be in advance and in
anticipation of the occurrence of cases of epidemic poliomyelitis.

The Wassermann reaction should of course be done on all
specimens of serum taken with the View to therapeutic use.

After-care of Acute Stage.—As the child passes from the
acute febrile period of the disease it recovers rapidly in general
health and well being. If no paralysis has appeared the patient
is up and about as well as ever at the end of a day or two if the
case be mild, or, at most, a week if severe. In a few cases of very
toxic type the febrile period has been much prolonged (Case
29). If paralysis is present care must be taken to prevent posi—
tions of arms or legs that may promote contractures. If there is
footdrop a right-angle splint should be applied at once, or even
a complete plaster bandage, to hold the foot at right angles.
When the deltoid is paralyzed the shoulder should be held up
by an axillary pad and the arm placed in such a position that no
V pull comes upon the injured muscle. For further detail in
managing the early hours of paralysis and subsequent muscle
training the reader is referred to the book by Dr. R. W. Lovett
on the After Care of Poliomyelitis.

TREATMENT SERIES

Case 1.—D. D. Female. 22 years. Northport, L. I.

September 14, 1916. Patient’s brother Thomas has been in the hos-
pital since last night. Patient awoke this morning with paralysis of both
legs. For past three days she has had headache, feverishness, chills,

I O4 ACUTE POLIOMYELITIS

loss of appetite, and has been alternately restless and drowsy. Did not
mention any of these symptoms to anyone because of brother’s illness.
Temperature 103°. Physical examination shows hypermsthesia, spine
Sign and rigidity of the neck. Knee jerks absent. Complete paralysis
of all the muscle groups of the legs and thighs, also weakness of the
right arm. Lumbar puncture, at 72 hours, shows clear ﬂuid under in—
creased pressure. Cell count 1420. 15 c.c. of serum was given.

September 14, 1916. 9 PM. Temperature 104°. Increased weak—
ness in the right arm. Had retention of urine; 16 ounces obtained upon
catheterization. No other changes.

September 15, 1916. 9 AM. Right arm completely paralyzed. Be-
ginning respiratory paralysis. Lumbar puncture was performed and 66
c.c. of turbid ﬂuid withdrawn under increased pressure. Cell count 2560.
11 PM. Respiratory paralysis complete on the right side. Patient
cyanotic. Lumbar puncture was again performed and 40 c.c. of ﬂuid
withdrawn. 2 c.c. of adrenalin were intraspinally administered.

September 16, 1916. 4 AM. Patient died of respiratory paralysis.

Discussion.—Paralysis was already present when the patient was giveri
her ﬁrst dose of serum. The cell count was very high at 72 hours. The
case is one of the straggling group, and went on to a fatal issue, the course
being uninﬂucnced in any way.

Case 2.—T. D. Boy. 15 years. Northport, L. I.

September, 12, 1916. Patient awoke with very severe headache.
Stopped work at noon, came home and went to bed. Felt feverish.
Temperature that evening 104°.

September 13, 1916. Temperature 103°. Patient complains of head-
ache, has stiff neck, exaggerated knee jerks, no abnormal reﬂexes. There
is a deﬁnite spine sign. Physical examination, otherwise negative. Lum-
bar puncture, at 24 hours, shows clear ﬂuid under normal pressure. Cell
count 70. 15 c.c. of serum were given.

September 14, 1916. Patient in Huntington Hospital. Temperature
104°. Stiff neck, double Kernig, no change in tendon reﬂexes. Lumbar
puncture: ﬂuid turbid, pressure slightly increased. Cell count 190. 15
c.c. of serum given.

September 15, 1916. Temperature 102°. No other symptoms or signs.

September 17, 1916. Temperature normal. Patient wants to get up.

September 21, 1916. Up and about the ward. No weakness or
paralysis.

September 22, 1916. Patient has continued up every day. Apparently
well.

Discussion.—This patient apparently had a sudden onset, awaking
from sleep with headache. The spinal ﬂuid taken at 24 hours showed 70
cells, a marked contrast to the ﬁndings in Case 1, his sister. He received
two doses of serum intraspinally, 3o c.c. in all. The ﬁrst puncture was
made 24 hours after the onset.

TREATMENT 105

Case 3.—E. H. Girl. 8 years. Northport, L. I.

September 7, 1916. Child had slight temperature. Yomited once.
No other symptoms.

September 12, 1916.. When seen to-day the patient’s temperature was
101°. Vomited to—day. Knee jerks exaggerated. No rigidity of the
neck. No spine sign. No abnormal reﬂexes. Lumbar puncture: 40 c.c.
of clear ﬂuid withdrawn under markedly increased pressure. No cells.

September 13, 1916. Temperature 99°. No new symptoms or signs.

September 14, 1916. Temperature 102°. Slightly stiff neck. Patient
complains of headache. No change in reﬂexes. Lumbar puncture: ﬂuid
clear under normal pressure. Cell count 120. 15 c.c. of serum given.

September 15, 1916. 9.30 AM. Temperature 103°. Child in Hos-
pital. Stiff neck. Knee jerks diminished. Spinal tenderness. Begin-
ning weakness of the left arm, triceps, biceps and deltoid groups. Right
arm markedly weak. Flexor and extensor muscles of forearm involved
also. Lumbar puncture: turbid ﬂuid under normal pressure. Cell
count 160. 15 c.c. of serum given.

September 16, 1916. Flaccid paralysis of the right arm. biceps, triceps
and deltoid, ﬂexor and extensor muscles of the forearm. Temperature
102°.

September 17, 1916. Patient stuporous, drowsy. Temperature
100°.

September 20, 1916. Brighter. Temperature normal. Paralysis
continues.

September 22, 1916. Motion returning in the left arm. No improve-
ment in the right.

September 29, 1916. Uses left arm quite well. Little return of power
in the right. No other muscle groups involved.

Discussion—Here is a case of the dromedary type in which a puncture
was done during the ﬁrst hump. The ﬂuid is a characteristic one for this
stage, large amount, increased pressure and no cells. The globulin de-
termination was not made. After the onset of meningeal involvement the
ﬂuid shows moderate increase in cells. The patient was given two intra-
spinal injections, the ﬁrst within a few hours of the beginning of the second
hump. It is interesting to note what a small increase in cells followed the
ﬁrst serum injection. Paralysis developed.

Case 4.—R. J. Boy. 4 years. Northport, L. I.

September 17, 1916. Patient’s sister had poliomyelitis. First symp—
toms in sister occurred three days ago. Patient sick for the first time this
morning. Vomited. Temperature 102°. Knee jerks exaggerated, right
more active than the left. No other signs. Lumbar puncture: at about
12 hours, ﬂuid clear, under normal pressure. Cell count 120. 15 c.c. of
serum given.

September 18, 1916. Child in hospital. Temperature 103°. Spinal

106 ACUTE POLIOMYELITIS

tenderness. Kernig double. Knee jerks unchanged. Lumbar puncture:
turbid ﬂuid under increased pressure. Cells 200. 15 c.c. of serum given.
September 20, 1916. On attempting to sit up, found that lumbar mus-
cles are weak. Some persistent tenderness. Child kept in bed.
September 29, 1916. Tenderness still present. Lumbar muscle weak-
ness. Temperature normal.

Discussion.——This case with 120 cells in the ﬂuid 12 hours after the on-
set is a mild form. Two doses of serum, 30 c.c. in all, were given. intra-
spinally. Slight weakness of the lumbar muscles developed on the second
day.

Case 5.—L. J. Boy. 2% years. Northport, L. I.

September 8, 1916. Child was feverish and fretful for a day.

September 14, 1916. Child feverish, vomited, does not like to be
handled.

September 15, 1916. Temperature 102°. Seems fretful, restless and
hyperzesthetic. Had a slight stiff neck. Knee jerks hyperactive, the
left more exaggerated than the right. Lumbar puncture, at 24 hours.
shows clear ﬂuid under normal pressure. Cell count 90. 15 c.c. of serum
given.

September 16, 1916. Child in hospital. Temperature 102.5°. Neck
more rigid. Kernig double. No paralysis or weakness made out. Lum-
bar puncture: ﬂuid clear under increased preSsure. Cell count 150.
15 c.c. of serum given.

September 17, 1916. Temperature 101°. Child improving.

September 18, 1916. Temperature 100°. No paralysis or weakness
made out.

September 20, 1916. Temperature 99°. Improving.

September 22, 1916. Temperature normal. No paralysis or weakness.

September 25, 1916. Child up and about the ward. I

\

Discussion—This case is a well—marked dromedary type. Puncture
about 24 hours after the second hump showed 90 cells. Two intraspinal
injections of serum were given, 30 c.c. in all. Recovery took place with—
out any transient or permanent weakness. In this instance the low initial
cell count suggests a favorable prognosis.

Case 6.—L. 1. Boy. 5 years. Northport, L. I.

September 13, 1916. Patient’s sister, is a positive case, showing
the ﬁrst symptoms 5 days ago. The patient has been previously well.
This morning did not want to get up. Temperature 102.5°. Com-
plained of headache and was hyperaasthetic. Reﬂexes normal. N o spine
Sign. N o gastro-enteric symptoms. Lumbar puncture, at about 4 hours,
showed clear ﬂuid, under normal pressure. Cell count 80. 15 c.c. of
serum given.

September 13, 1916. 9 RM. Temperature 103°. Stiﬁ neck. Kernig
double.

TREATMENT 107

September 14, 1916. 9 A.M. Stiff neck. Knee jerks exaggerated.
Kernig double. Temperature 102°. Lumbar puncture: clear ﬂuid under
normal pressure. Cell count 150. 15 c.c. of serum given.

September 15, 1916. Signs continue unchanged. Temperature 101°.

September 22, 1916. Temperature normal. No weakness or paralysis.
Child up and about.

Discussion.—Another mild case in which the cell count is almost the
only indication of meningitis. As in the previous case its lowness has a
good prognostic value. The ﬁrst treatment was given about 4 hours
after the onset of symptoms at which time 80 cells were found.

Case 7.—E. K. Boy. 4 years. Northport, L. I.

September 21, 1916. Patient taken sick. His cousin (Case 8) has
poliomyelitis whose ﬁrst symptoms were observed September 6th.

September .25, 1916. Patient has been ill during the past 4 days.
Temperature 103°. Kernig, rather marked on both sides. Neck stiﬁ.
Knee jerks present, over-active on the right side, and slightly diminished
on the left. Spine sign present, rather marked. Lumbar puncture:
ﬂuid clear, increased pressure. Cell count 350. 8 c.c. of serum given.

September 26, 1916. Temperature 99°. No change in signs. No new
symptoms. Lumbar puncture: ﬂuid clear under moderate pressure.
Cells 120. 8 c.c. of serum given.

September 27, 1916. Temperature 101°. Child hyperaesthetic, irritable.

September 29, 1916. Temperature normal. No weakness or paralysis
made out.

Discussion—Here the patient had been ill for 4 days when the punc-
ture was done. There is no means of determining how long the meningeal
condition had been present. The marked decrease in cells in the spinal
ﬂuid following the ﬁrst serum injection is interesting. The dose of 8 c.c.
was rather smaller than usual. It was repeated once.

Case 8.——W. K. Boy. 18 years. Centerport, L. I.

September 6, 1916. Patient has chills and fever, headache, and has
vomited twice.

September 7, 1916. Felt better and went back to work on a boat in the
harbor. Headache continued. His condition remained the same during
the following day. 9

September 10, 1916. Headache was very severe and a physician was
called. Temperature 100° at 3 P.M. At 8.30 P.M. it was 102°. Neck
rigid. Knee jerks greatly exaggerated. Kernig double. Spine tender.
There is no paralysis or weakness. No other signs. Lumbar puncture,
at 8 hours, shows clear ﬂuid much increased in amount. Pressure in-
creased. 65 c.c. was removed. Cell count 720. Globulin +++;
Ross-Jones ++; Pandy +. 15 c.c. of serum given.

September 11, 1916. 8 A.M. Temperature 103.2°. Neck more
rigid. Headache increased. Knee jerks exaggerated. Kernig continues.

108 ACUTE POLIOMYELITIS

Spinal tenderness. Lumbar puncture: 60 c.c. of turbid ﬂuid withdrawn.
Cells 850. Globulin; Noguchi ++; Ross—Jones ++. 15 e.c. of serum
given.

September 12, 1016. 0 A.M. Temperature 101°. Patient slept well,
headache much less. Knee jerks obtained. Kernig less marked. N0
paralysis.

November 27, 1016. Almost complete paralysis of the abdomen and
back. Weakness of both legs. Treated at clinic.

Discussion—This case is a dromedary type with not quite complete
remission. The initial spinal ﬂuid count of 720 about 8 hours after the
meningeal invasion is dangerously high. Two doses of serum were used,
30 c.c. in all. Paralysis developed. The patient’s age and the high cell
count are both unfavorable prognostic signs.

Case 9.—M. H. Girl. 4 years. Northport. L. I.

September 10, 1016. No history of exposure or contact was made out.
Temperature 102°. Child fretful, drowsy, loss of appetite and diarrhea.

September 11. 1016. Temperature 101°. Yomited.

September 13, 1016. Child up and well apparently.

September 14, 1916. In afternoon child vomited. Temperature
101.5°. Child fretful and irritable. Neck slightly stiff. Knee jerks,
leIt exaggerated, right diminished. Slight meningeal symptoms. Kernig
on the left. No paralysis. Lumbar puncture at the end of 48 hours,
showed clear ﬂuid under normal pressure. Cell count 425. 15 cc. of
serum were given.

September 17, 1916. Child in hospital. Temperature 102°. Neck
very rigid. Tendon reﬂexes unchanged. Spine sign increased. Lumbar
puncture: ﬂuid clear under pressure. Cell count 630. Child apparently
much better. No paralysis. Some weakness of right arm.

September 18, 1916. 10 A.M. Temperature 101°. Marked weakness
of the anterior tibial and quadriceps group of the left leg. Slight general
hypereesthesia.

September 19, 1916. No new paralysis or weakness. Temperature
10°. 5°. .

September 20, 1916. Temperature 99°. No return of motion in the
left leg.

September 22, 1916. Some beginning of motion in the paralyzed
extremity.

September 26, 1916. Some improvement in paralyzed leg.

September 29, 1916. Continues to improve.

Discussion—T his case belongs clearly to the dromedary group. The
puncture was made 48 hours after the beginning of the second hump,
showing a high cell count. Serum was given at this time. A second
dose was withheld because the muscular weakness had already appeared.
The puncture in this case was unnecessarily delayed.

TREATMENT 109

Case 1oI—M. L. Girl. 8 years. Northport, L. 1.

September 14, 1916. Child appeared ill. One sister and two brothers
positive cases. Cousin, Case 9, a positive case.

September 19, 1916. Patient was ill again 2 days ago, but no phy—
sician was called until this evening. When seen the patient’s temperature
was 103.4°. Neck stiff. Knee jerks diminished. Kernig double.
Spine sign present. Weakness of the muscles of the left arm. Lumbar
puncture at 48 hours shows clear ﬂuid under increased pressure. Cell
count 510. 15 c.c. of serum given. .

September 20, 1916. Temperature 104°. Paralysis of the left arm,
triceps, biceps and deltoid groups. Lumbar puncture shows turbid ﬂuid
under increased pressure. Cell count 600. 15 c.c. of serum given.
Patient shows difficulty in swallowing and also acute retention.

September 21, 1916. Respiratory paralysis began last night. When
seen at 7 A.M. the patient was cyanotic. Complete respiratory paralysis
of the right side. Lumbar puncture: 75 c.c. of ﬂuid withdrawn under
increased pressure. Cell count 725. 15 c.c. of serum and 2 c.c. of adrena—
lin given. Child died of respiratory paralysis at 12.30.

Discussion.—This case is evidently of the dromedary or possibly of the
straggling type. but the diagnostic puncture with the ﬁrst serum injection
was made 48 hours or more after the second hump; 570 cells were present
then. Furthermore muscular weakness was already present when the
ﬁrst dose of serum was given.

Case 11.—C. L. Boy. 2 years. Northport, L. I.

September 14, 1916. Child became ill. He is a brother of Case 10.

September 19, 1916. Continued ill until to-day. When seen had a
temperature of 102°. Neck was slightly stiff and reﬂexes hyperactive.
Lumbar puncture: ﬂuid clear under normal pressure. Cell count 430.
15 c.c. of serum given.

September 20, 1916. Neck still stiff. Slight spine sign. General
hyperzesthesia. Lumbar puncture: turbid ﬂuid under increased pres—
sure. Cell count 500. 15 c.c. of serum given.

September 21, 1916. Temperature 101°. No paralysis or weakness.

September 23, 1916. Temperature normal.

September 29, 1916. Temperature normal. Child up and about the
ward.

Discussion—This patient is a brother of Case 10, and represents the
straggling type. Puncture, probably within 12 hours of the meningeal
invasion, showed ﬂuid with 430 cells. The patient received two doses of
15 c.c., each intraspinally. Both these children presented severe clinical
pictures and both had high cell counts. The question arose as to whether
they were peculiarly susceptible, especially as they were ill about the
middle of September when there was very general evidence that the disease
was on the wane.

I IO ACUTE POLIOMYELITIS

Case 12.—M. M. Girl. 9 years. 'Northport, L. I.

September 7, 1916. Slightly feverish.

September 8, 1916. Temperature 102°. Child vomited in the after-
noon after taking calomel.

September 9, 1916. Temperature normal.

September 10, 1916. Temperature 101° to 104° during the afternoon.
Slight frontal headache. No other symptoms. When seen temperature
103°. Physical examination negative, except for hyperactive knee jerks.
No spine sign and no hyperaesthesia. Lumbar puncture, 6 hours after
the meningeal invasion: ﬂuid clear, pressure +, cells 40. No serum
given because meningeal involvement is slight.

September 11, 1916. Temperature 103°. Neck stiff. Kernig on
right side. Knee jerks exaggerated on the left side and normal on the
right. Lumbar puncture, at 18 hours. Cell count 140. Globulin:
Noguchi ++; Ross—Jones ++; Pandy ++. 15 c.c. of serum given.

September 12, 1916. 10.30 A.M. Temperature 103.5°. Stiffness of
the neck much increased. Kernig double. No other abnormal reﬂexes.
Lumbar puncture: increased pressure. Cell count 180. 15 c.c. of
serum given.

September 12, 1916. 9.30 P.M. Child delirious. Apparently
beginning respiratory paralysis. Acute retention. Temperature 104°.

September 13, 1916. 9.30 A.M. Condition continues much the same
except the temperature is 102°. Frequent clonic contractions of all the
muscle groups. Neck extremely stiff. Extremely hyperzesthetic. Knee
jerks, both markedly hyperactive. Lumbar puncture: ﬂuid turbid,
much increased pressure. 60 c.c. of ﬂuid was obtained. 15 c.c. of serum
given. The cell count at this time was 300.

September 13, 1916. 8.30 P.M. Temperature 101°. Patient con-
tinues to have retention. Less muscular twitching. Still rational.
Beginning seropurulent vaginitis. Inability to swallow. Patient begin—
ning to have pressure symptoms. Lumbar puncture was performed at
this time and 40 c.c. of ﬂuid removed. No cell count.

September 14, 1916. 9 A.M. Temperature still 101°. Voided spon-
taneously. Less muscular twitching. Stiﬂness of the neck less marked.
Knee jerks continue hyperactive. Not so hyperzesthetic.

September 15, 1916. Temperature 99. 5°. Vaginitis increased in
severity in spite of treatment.

September 16, 1916. Temperature normal. No weakness or paralysis.
Very marked muscular tenderness in the calves and thighs. I

September 18, 1916. Temperature normal. Child much brighter.
Vaginitis clearing up. Only complaint is tenderness on manipulation of
the legs.

September 22, 1916. Temperature normal. Child continues to be
bright and cheerful. No new signs or symptoms.

September 29, 1916. Temperature normal. N o weakness or paralysis.
vaginitis cured. Slight muscular tenderness.

TREATMENT I I I

Discussion.—T his case of the dromedary type is especially interesting
in View of the slow development of the meningeal irritation as indicated
by the ﬁrst two punctures. The child became increasingly ill and it was
thought 'she would die, especially when swallowing and respiratory em-
barrassment set in. Under these conditions there is some doubt as to the
advisability of having given the 15 c.c. of serum on September 13. Pos-
sibly by its mechanical action it served to increase the pressure on cells
already the subjects 'of pathological effect. At all events great relief of
symptoms followed the removal ‘of 40 c.c. of ﬂuid some hours later.

Case 13.—K. M. Girl. 2 years. Northport, L. I.

September 13, 1916. Patient’s brother has poliomyelitis, showing his
ﬁrst symptoms September 5, 1913. Patient has temperature 102°. No
other symptom or signs.

September 14, 1916. Temperature normal, 1 day interval.

September 15, 1916. Patient feverish and irritable. Temperature
101.8°. Very slight spine sign. Knee jerks on left side hyperactive, on
right side diminished. Lumbar puncture, under 12 hours, shows clear
ﬂuid under increased pressure. Cell count 130. 15 c.c. of serum given.

September 16, 1916. Temperature 104°. Child refuses to swallow.
Apathetic. Spine sign marked. Knee jerks as previously stated. Lum-
bar puncture: clear ﬂuid under increased pressure. Cell count 150.
15 c.c. of serum given.

September 17, 1916. Temperature 102°. No paralysis. Hyperazs-
thesia persists.

September 19, 1916. Temperature normal. Child apparently well.
Has no tenderness.

September 22, 1916. Temperature normal. No weakness or paralysis.

September 29, 1916. Child up and about.

Discussion.——In this instance the initial puncture and treatment was
carried out in less than 12 hours after the onset of the second hump of a
clear-cut dromedary type. Note the very slight increase in cells following
the ﬁrst treatment.

Case 14.—~H. M. Boy. 7 years. Northport, L. I.

September 5, 1916. Child was feverish and felt sick. Was consti-
pated. Felt better next day. No further symptoms for 7 days until
September 12, 1916.

September 12, 1916. At 1 RM. quiet, did not want to play. Was
feverish and constipated at this time. At 8 RM. temperature was 102°.
Child had headache, no other symptoms. When seen complained of
headache. Temperature at that time was 101. 5°. Had slight stiffness
of the neck. Very slight spine sign. Knee jerks were hyperactive. There
was a. question of a possible double Kernig. No paralysis. No other
signs. Lumbar puncture, at 9 hours, showed clear ﬂuid under normal
pressure. Cell count 120. 15 c.c. of serum was given.

I I 2 ACUTE POLIOMYELITIS

September 13, 1916. 8.30 P.M. Temperature 102°. Stiff neck.
Double Kernig. Spine sign. No paralysis or weakness. Lumbar punc-
ture, ﬂuid turbid under increased pressure. Cell count 150. 15 c.c.
of serum given. .

September 14, 1916. 11 A.M. Temperature 101°. Marked hyper-
aesthesia. Signs as previously stated.

September 15, 1916. Temperature and signs continue as above. No
paralysis or weakness.

September 18, 1916. Temperature normal. No weakness or paralysis.

September 28, 1916. Child up, and about the room. No weakness or
paralysis.

Discussion.—A brother of Case 13; this individual had been carefully
watched and his temperature taken twice daily through the 7—day
quiescent period. The puncture and ﬁrst treatment were done 9 hours
after the onset of the second hump. These three cases, 12, 13, 14, all
lived in the same family and were most carefully observed daily by a
competent nurse and the physician in charge.

Case 15.—L. M. Boy. 6 years. Northport, L. I.

September 9, 1916. Patient’s two cousins, Case 12 and Case 14, both
have poliomyelitis. Patient has temperature 102°. Was very quiet and
said he felt sick. Better the following day and showed no symptoms until
the 14th, an interval of 5 days.

September 14, 1916. Temperature 100°. Child nauseated, but did
not vomit. Severe headache.

September 15, 1916. Temperature 103°. Neck slightly stiff. No
change in tendon reﬂexes. No weakness or paralysis. No hyperacsthesia.
Lumbar puncture, 24 hours after the second hump, showed clear ﬂuid
under normal pressure. Cell count 140. 15 c.c. of serum given.

September 15, 1916. 10 RM. (10 hours later). Temperature 103°.
Increased stiffness of the neck. Knee jerks hyperactive. Double
Kernig. Beginning hyperaesthesia. Lumbar puncture: turbid ﬂuid
under slightly increased pressure. Cell count 180. 15 c.c. of serum given.

September 16, 1916. 10 A.M. Temperature 104°. No new symptoms
or signs, except a cough and signs of a diffuse bronchitis. .

September 16, 1916. 4 RM. Child refuses to swallow food or nourish—
ment. Acute retention. Respirations increased in rate, but no evidence
of respiratory paralysis. Great diﬂiculty in raising mucus which seems
to obstruct breathing.

September 16, 1916. 9 RM. Child still refuses to take nourishment,
but when a little ﬂuid is placed in his mouth he does swallow it.
Murphy drip started. Compound tincture of benzoin given. Atropine
16000 g. 4 hours. Mucus which is right from the throat is prune-juice
color. Chest is full of diﬂ’use rales. Cardiac condition poor. No actual
respiratory paralysis made out.

TREATMENT I 1 3

September 16, 1916. 11 RM. Spasms of bronchi cause great difﬁculty
in breathing. Sibilant and a few sonorous rales occurred in both lungs
after the asthmatic attacks. Child was quite cyanosed and the cardiac
condition poor.

September 17, 1916. 3 A.M. During one of these asthmatic attacks
the child died of cardiac failure. Child died on third day of respiratory
failure.

Discussion—This case is most unusual in its manner of death. Appar-
ently there was some weakness of swallowing, but also disturbance of the
bronchial musculature. The possibility of bronchopneumonia cannot
be ruled out. He received his ﬁrst treatment 24 hours after the onset of
the meningeal stage.

Case 16.—M. S. Girl. 3 years. Northport, L. I.

September 9, 1916. Child is feverish, fretful and constipated.

September 10, 1916. Temperature‘is down and remained down until
the 13th.

September 13, 1916. Child fretful, feverish and did not want to eat.
No gastroenteric symptoms. No sore throat, no vomiting.

September 14, 1916. When seen temperature was 102°. Child very
irritable, hyperzesthetic. Knee jerks exaggerated. Beginning stiff neck
and very slight spine sign. Lumbar puncture, 24 hours after meningeal
invasion, shows ﬂuid clear under increased pressure. Cell count 320.
15 c.c. of serum given.

September 15, 1916. 9.30 A.M. Child in hospital. Temperature
102.5°. No new symptoms or signs. Lumbar puncture; ﬂuid turbid
under slightly increased pressure. Cell count 400. I 5 c.c. of serum given.

September 16, 1916. Temperature 101°. Hyperzesthesia continues.
Knee jerks hyperactive. Spine sign.

September 17, 1916. Temperature normal. Hyperzesthesia continues,
also irritability.

September 20, 1916. Temperature normal. No paralysis or weakness.

September 29, 1916. Temperature normal. Child up and about.

Discussion.——This case was punctured about 24 hours after the onset of
meningeal symptoms and showed 320 cells. The same treatment was
given as in Case 15 and at about the same stage.

Case 17.—M. S. Boy. 2 years. Northport, L. I.

September 11, 1916. Child was feverish, vomited once and was
constipated.

September 12, 1916. Fever continues, temperature not taken.

September 13, 1916. Child apparently well, up and about to-day and
the following day.

September 15, 1916. Temperature 103°. Child vomited last night.
Knee jerks, left hyperactive, right diminished. Neck slightly stiff.
Slight spine sign. N0 paralysis. Slight weakness of the right leg in

8

114 ACUTE POLIOMYELITIS

sural group and anterior tibial. Lumbar puncture, at 18 hours, showed
ﬂuid clear under increased pressure. Cell count 640. 12 c.c. of serum
given.

September 16. 1916. Temperature 101.5°. Neck stiff, spine sign. No
paralysis or weakness. Knee jerks'unchanged. Lumbar puncture shows '
clear ﬂuid under increased pressure. Cell count 700. 12 c.c. of serum
given.

September 18, 1916. Temperature 995°. No new symptoms or signs.

September 23, 1916. Child stuporous. No paralysis or weakness.

September 26, 1916. Weakness of the right leg came on this morning.

September 29, 1916. No return of power in the paralyzed leg.

Discussion.——This was a very sick child. The puncture showed 640
cells and was done 18 hours after the onset of the second hump. Two
doses of serum were given, 24 c.c. in all. An interesting feature is the
delayed appearance of the paralysis, 1 1 days after the onset of the second
hump.

Case 18.—-\V. R. Boy. 8 years. Northport, L. I.

September 10, 1916. Temperature 104°. Child drowsy and markedly
constipated.

September 1 I, 1916. Temperature 101°. No other symptoms or signs.
Remained normal until the 15th.

September I5, 1916. Child complained of being tired. Loss of appe~
tite. Temperature 99. 5°. When seen by the local physician there was
no rigidity of the neck. No spine sign, and no reﬂex changes.

September 16, 1916. Temperature was 103°. Very slight rigidity of
the neck. Hyperactive reﬂexes. Slight spine sign. Lumbar puncture,
at 30 hours, shows clear ﬂuid under normal pressure. Cell count 325.
15 c.c. of serum given.

September 17, 1916. 9.30 A.M. Temperature 102°. Neck stiﬂ.
Knee jerks hyperactive. Paralysis of the biceps, triceps and deltoid
groups of the right arm. Lumbar puncture: clear ﬂuid under increased
pressure. Cell count 490. 15 c.c. of serum given.

September 17, 1916. 3.00 P.M. Fluid regurgitated through the nose
on attempts to swallow. Signs of beginning respiratory paralysis. Tem-
perature 104.5°. Lumbar puncture showed turbid ﬂuid; 40 c.c. were with-
drawn under slightly increased pressure. Cell count 520.

September 17, 1916. 5.30 P.M. Complete left respiratory paralysis.
Cyanosis. Child died of respiratory paralysis.

Discussion.—This case is an example of the dromedary type with a
rather long interval of four days. The meningeal stage began with very
inconspicuous signs so that puncture was not requested until nearly 30
hours later. ,At this time there were 325 cells. The patient received two
injections, 3o c.c. in all.

TREATMENT I I 5

Case 19.—A. C. Boy. 5 years. Inwood, L. I.

August 26, 1916. Brother of patient has been ill with poliomyelitis
ﬁve days. To—day patient began to vomit—was very drowsy and. irri—
table. Complained of headache and pains in the spine. Temperature
101.4°, pulse 136, respiration 16. Bowels regular, slightly constipated.
Physical examination shows the child in bed, of slender build and rather
pale. Eyes normal. Throat reddened. Tonsils large. Small cervical
glands palpable. Slight spasm of the neck muscles. Lungs normal.
Heart, soft systolic murmur, heard at the apex, transmitted to the axilla.
Extremities, very slight weakness of the right leg. Knee jerk, faintly
present on the left, absent on the right. Slight Kernig present. Other
reﬂexes normal. Puncture within 12 hours shows clear ﬂuid, not under
pressure. Cell count 250. Treatment, 15 c.c. serum.

August 26, 1916. Patient presents marked meningismus and pro-
nounced Kernig on both sides. No paralysis present. Temperature 99°.
This P.M. there is some improvement. No serum.

August 29, 1916. Child much improved. Temperature 99°. Neck
slightly stiff. No paralysis.

August 31, 1916. Child seems ill. Temperature 98°. No paralysis.

September 8, 1916. Child well. Up and around and playing in the
yard last week. General condition good. No paralysis or weakness of
muscles. Puncture within 12 hours. Cells 2 5o. Headach‘e. Serum one
dose. Recovery without paralysis.

Case 20.—H. K. Boy. 19 months. Valley Stream, L. I.

August 26, 1916. Mother noticed that the child felt feverish and later
in the day began to vomit.

August 27, 1916. Child very irritable, complains of pain in the back
of the neck and head, extremely drowsy. No diarrhea or constipation.
Physical examination shows the child lying in bed with slight retraction
of the neck. Very irritable and evidently having some pain. Eyes nor-
mal. Throat Congested. Cervical and inguinal glands are palpable.
Lungs and heart negative. Slight weakness of the abdominal muscles.
Extremities show no apparent weakness. Knee jerks absent. Other re-
ﬂexes normal. Slight Kernig on both sides. Marked meningismus.
Temperature 102°; pulse 140; respiration 18. Puncture, after 36 hours,
showed slightly turbid ﬂuid under slight pressure. Cell count 9 50.
Globulin +. Treatment, 15 c.c. serum.

August 28, 1916. Patient not so well. Diaphragm paralyzed. Res-
pirations rapid and difﬁcult. Child slightly cyanotic. No further paraly-
sis. Treatment, 15 c.c. serum.

August 29, 1916. Child extremely cyanotic. Respirations rapid,
shallow and irregular. Pulse 160, very weak. General condition of the
child grew worse and death ensued at 3 RM. Cause of death, respira-
tory failure. Lumbar puncture was made probably 36 hours after the

1 1 6 ACUTE POLIOMYELITIS

onset of meningeal symptoms.- Weakness was already present. Cell
count 9 50.

Case 21.—F. H. Boy. 25 months. Valley Stream, L. I.

September 1, 1916. Mother states that present illness dates back two
weeks. The child has been more sleepy than usual and has run an irregu-
lar temperature which has never been over 100° until to—day, when it
jumped to 104°. The child gagged several times this morning but did
not really vomit. Bowels constipated. During the last 24 hours the
child has been quite peevish and fretful. Physical examination shows a
well-developed and well-nourished child, in bed. Mucous membranes
normal. Temperature, rectal, 104°, respirations 24, pulse 160. Child is
very apathetic and looks extremely toxic. The glands of the neck and
groin are enlarged. Child presents a very marked meningismus, and
weakness of the rector spinaa. No Kernig. Heart and lungs normal.
Extremitics, no paralysis or weakness of the muscles could be ascertained.
Knee jerks, slightly increased. Other reﬂexes, normal. Lumbar p‘unc?
ture: 20 c.c. of clear ﬂuid were withdrawn under slight pressure. Cell
count 400. Globulin +. 10 c.c. of serum given.

September 2, 1916. Child still very drowsy. Very marked meningis—
mus. Child very toxic and muscles twitch at frequent intervals during
sleep. Temperature 103°, pulse 154, respiration 20. 10 c.c. were given
24 hours after the ﬁrst dose.

September 4, 1916. Temperature 102°, pulse 130, respiration 18.
Child looked and acted better. No paralysis or weakness of the muscles
noticed. No serum was deemed necessary at this time.

September 8, 1916. General condition much improved. Still slight
spasm of the neck muscles. During the past three days there has been
apparently some paralysis of the bladder sphincter. To-day the bladder
is distended to the umbilicus, and the urine passed is evidently an overflow.
Four (lays ago the child developed paralysis of the quadriceps extensors
of the left leg.

Discussion—About 15 hours after an abrupt rise in temperature in a
straggling course the cells were 400. Serum was given then and again
after 24 hours. Two days later paralysis developed. There was some
weakness of the back muscles, however, at the time of the ﬁrst puncture.

Case 22.—O. N. Boy. 19 months. Hempstead, L. I.

August 19, 1916. Child became very restless and irritable. The day
following was drowsy all day long and his mother stated that he had fever.
He had not vomited.

August 21, 1916. Yesterday and this morning the child’s arms have
twitched convulsively at times. Temperature 100.6°. Physical examina-
tion shows a well-nourished white child lying on his back in no apparent
pain. His face is ﬂushed and eyes unusually bright. Neck extremely
rigid, and child cries out when it is flexed. Throat red. Cervical and

TREATMENT 1 1 7

inguinal glands palpable. Chest and abdomen negative. Muscles of the
face and eyes are in a semi—spastic condition. Knee jerks are'very slug—
gish. Kernig is mild. When placed on his feet the patient is markedly
ataxic. Lumbar puncture shows a clear ﬂuid under slightly increased
pressure. Cell count 620. Noguchi +++; Pandy +++; Ross-Jones
+++. Patient was very sick and apathetic. At 3.30 the same day a
lumbar puncture was performed and 15 c.c. of clear ﬂuid withdrawn. 15
c.c. of serum was injected intraspinally. Child appears bright to-day.
No deﬁnite paralysis, but knee jerks are absent. Wanted the child re-
moved to the hospital but had no place to take it at the time.

August 22, 1916. 9.30 AM. Lumbar puncture: 15 c.c. of clear
ﬂuid withdrawn. 15 c.c. of immune serum were given intraspinally.
Child appears brighter today. No deﬁnite paralysis but knee jerks are
absent. _

August 27, 1916. Not drowsy now. Paralysis of left lower extremity
(partial paralysis).

August 31, 1916. 4 PM. Temperature 98°. Paralysis of the left
extensor groups continued. Weakness of the same group in the right
leg. Ankle and knee jerks are absent. Slight spinal tenderness.

Discussion.—Here the diagnostic puncture showing 620 cells was done
about 30 hours after the onset of symptoms. Serum was not given until
35 hours after. The case is a very severe one. Paralysis did not appear
until the seventh day. Two doses of serum were given, 30 c.c. in all.‘

Case 23.——R. M. Boy. 9 years. Freeport, L. I.

August 16, 1916. Child had headache and nausea but did not vomit.
No diarrhoea. Rather drowsy. Not irritable at any time. Complained
of slight pain in the back of the neck on ﬂexion.

September 17, 1916. Patient somewhat apathetic with ﬂushed face.
Eyes unusually bright. At times spasmodic twitching of the facial mus—
cles. Throat extremely red. Neck very rigid, pain being caused on
attempt at ﬂexion. Spine rather rigid. All reﬂexes present. Lumbar
puncture. Cell count 220. 15 c.c. of serum were given. Pandy,
Noguchi and Ross—Jones, all +.

August 18, 1916. At 12 M. 15 c.c. of immune serum were given. Cell
count 50.

August 18, 1916. At 8 RM. 15 c.c. of immune serum were given.
Cell count 440.

August 20, 1916. Slight weakness of the deltoid appeared yesterday,
but is absent to-day.

November 25, 1916. The paralysis of the eye and deltoid were tem-
porary. No permanent paralysis.

Discussion—At 36 hours 220 cells were found. There was temporary
weakness of the right deltoid on the 4th day. The patient received three
doses, 45 c.c. in all, of serum intraspinally.

I 18 ACUTE POLIOMYELITIS

Case 24.—J. G. Girl. 14 months. Oyster Bay, L. I.

August 22, 1916. About 6 o’clock the patient’s parents noticed that she
did not appear well. She was unusually drowsy and fretful and seemed
to feel hotter than usual. No vomiting or diarrhoea. Does not‘seem to be
in pain. Physical examination shows the child apathetic, in bed, but in no
apparent pain. Eyes negative. Upper teeth widely spaced. When
crying the right side of the face is drawn over to the right slightly. Throat
is very red and contains an accumulation of glairy mucus. The cervical,
axillary and inguinal glands are enlarged. Neck is rather rigid. Reﬂexes
are all present. Lumbar puncture: 15 c.c. of ﬂuid were withdrawn under
increased pressure. Cell count 50. Noguchi +; Pandy +; Ross-Jones
+ -—. 15 c.c. of serum were injected. Slight facial paralysis. The child
was removed to the Locust Valley Hospital.

August 28, 1916. Slight facial paralysis still persists. Child seems
very well.

Discussion.—The patient was seen when a facial paralysis was present.
Puncture done at this time, which was about 7% hours after the onset of
symptoms, according to the mother, showed a ﬂuid containing 50 cells.
One dose of serum was given.

It is interesting to note that this combination of a low cell count with an
isolated facial paralysis was a very frequent ﬁnding.

Case 25.—-W. E. Boy. 13 years. Hempstead, L. I.

August 23, 1916. Boy does not feel well.

August 25, 1916. Mother noticed that the boy had fever and was
rather drowsy. He complained of headache and some pain in the chest
when the head was bent forward. Not irritable. No vomiting or diar-
rhcea. Physical examination shows temperature 102.3°. Patient is' a
well-developed boy of 13 years. Cheeks are ﬂushed, skin hot and dry.
Eyes negative. Tongue coated. Throat slightly redder than normal.
Neck quite rigid and patient complains of pain over the sternum
when the head is bent forward. Chest and abdomen negative. Knee
jerks very sluggish. Lumbar puncture: 20 c.c. of cloudy ﬂuid was with-
drawn under increased pressure. Cell count 1200. Noguchi ++++;
Pandy ++++; Ross-Jones ++++. 9.45 P.M. Lumbar puncture:
15 c.c. of cloudy ﬂuid withdrawn. 15 c.c. of immune serum given intra-
spinally. Cell count 1600. Patient complains of headache to-day. Neck
extremely rigid. N0 paralysis. Marked resistance to extension of the
Legs with thighs ﬂexed.

Note.——Patient’s brother has poliomyelitis, recognized 3 days ago.

September 1, 1916. Temperature normal for the past three days. Up
and about. No weakness or paralysis. Complains of muscle pains,
especially at night. Had serum 1 week ago.

' Discussion.—This patient presented the very high cell count of 1200
about 12 hours after the onset of drowsiness and pain on anterior ﬂexion of

TREATMENT 1 1 9

'the head. Besides this he was very toxic and much prostrated. There
was marked meningeal irritation following treatment. He received two
doses of serum, 30 in all. The ﬁrst injection was given at about 15 hours.

Case 25a.—C. L. P. Boy. IO months. Sayville, L. I.

August 24, 1916. Child had green stools and a temperature of 102°.
Oil was given.

August 25, 1916. Child appeared much better. Temperature 98.6°.
No vomiting.

August 26, 1916. Child rather drowsy and irritable.

August 27, 1916. Temperature 103.2°. A well—developed boy of 10
months. Fontanelle not bulging. Eyes negative. Throat rather red.
No rigidity of the neck. Cervical and inguinal glands enlarged. Chest
and abdomen negative. Knee jerks exaggerated, especially on the right
side. Apparently some weakness of the right quadriceps and psoas.
Lumbar puncture: clear ﬂuid under increased pressure. Cell count so,
at 72 hours.

August 29, 1916. 10 c.c. of serum given at 11 A.M., at 72 hours. Tem-
perature at this time 103°, and respirations about 80 per minute. Tem-
perature rose in a few hours to 104° and respirations became more shallow
and at 7 A.M. it was thought that death would supervene. InTa short
time it was thought that the child could not swallow well. Since this
time there has been a progressive improvement.

August 31, 1916. Child is reported as seemingly perfectly well.

September 1, 1916. Complete recovery. Paralysis of the pharynx was
only transitory.

Discussion.—This case showed 50 cells at 72 hours. IO c.c. of serum
was given at 78 hours. There was transient weakness of swallowing. The
child was much worse following serum. Patient was breathing 80 per
minute at the time the serum was given. The serum should have been
withheld, but the father, a physician, insisted that it be given.

Case 26.—B. G. Girl. 13 years. Great Neck, L. I.

August 25, 1916. Patient had a temperature of 101.5° and felt poorly.

August 26, 1916. Temperature was normal and the patient was up and
around all day.

August 27, 1916. Temperature continued normal and she went in
bathing, but in the evening complained of headache and at midnight had
marked spinal tenderness.

August 28, 1916. Patient vomited and had a temperature of 101. 5°.
She was seen at II A.M. She is a large girl for her age and is menstruat-
ing. She is a healthy child and does not appear particularly sick. She '
has a headache when she moves her head. Slight spine sign. Reﬂexes:
biceps ++. Knee jerks and ankle jerks absent. No weakness. At 4
P.M. Temperature 101°, headache better. Spine sign the same. Spinal

I 20 ACUTE POLIOMYELITIS

puncture at 24 hours shows ﬂuid clear, under increased pressure. Cell-
count 180. 12 c.c. of serum were given.

August 29, 1916. Patient has had a good night and feels better. Tem-
perature normal.

Discussion—This patient was not very toxic, but 24 hours from the
onset of the second hump had 180 cells. She received one dose of serum
which did not set up any meningeal irritation. She then followed an un-
eventful and short course to recovery.

Case 27.AL. G. Boy. 7 years. North Hempstead, L. I.

August 21, 1916. Child had a poor night. No vomiting but slight
temperature. Was given catharsis which was successful. Was not
drowsy.

August 22, 1916. Seen at 7.45 A.M. this morning. Child ﬂushed,
slightly sore throat, acute febrile picture. Deﬁnite spine sign. Knee
jerks ++. Spinal puncture: made under 24 hours shows ﬂuid clear,
pressure 10w. Cell count 430. Globulin +. 15 c.c. of serum given.
Patient grew worse during the morning and embarrassment of the respira-
tion began on the right side, and weakness of the right arm with
distinct weakness of the neck muscles. At 5 RM. 15 c.c. of ﬂuid was
withdrawn. Pressure at this time was 6 mm. of mercury. 15 c.c. of
serum was run in. Cell count was 770. Vomiting followed. There was
no sign of respiratory paralysis at this time. Knee jerks +-+—. Tem-
perature 103.

August 23, 1916. 7.00 A.M. Temperature 101.2. Paralysis of the
right arm has increased. Patient has had a restless night, but is resting
easily this morning. Spinal pressure very low, only about 5 c.c. being
removed. Cell count 120. 15 c.c. of serum were injected. No vomiting
followed.

August 23, 1916. 9.45 PM. Left arm has become involved, so that
patient is unable to lift it from the side to any extent. Neck does not seem
so rigid. Temperature about the same as this morning. 15 c.c. of
immune serum given with 116 c.c. of adrenalin chloride. Cell count 180.

August 24, 1916. At 10 A.M. Patient distinctly better. Tempera—
ture lower, left arm not so helpless. being able to raise it to the right—angle
position. His general appearance is better. Had a restless night.

August 29, 1916. The child is doing very well, but has paralysis of
both arms. The paralysis of the left arm is only of the deltoid muscle.

Discussion—Puncture and ﬁrst treatment, just under 24 hours. Cell
count 430 cells. There was slight transient embarrassment of the respi-
ration during the next 6 hours; then involvement of the arms. The
patient received four doses of serum, 60 c.c. in all. This was a very
sick case. Possibly a fatal issue was prevented.

Case 28.—E. E. L. Girl. 3 years 10 months. Oyster Bay, L. I.
August 21, 1916. Suddenly at 10 o’clock this morning the child was

TREATMENT I 2 I

seized with pain in the back of the neck. She continued to play until 12
o’clock when she gave up and began to be feverish. Became rapidly
worse. At 3 P.M. her temperature was 102.6. At 7 45 P.M. it was
102.4. Physical examination shows a well—nourished child. She pre-
sents an acute febrile picture, with deﬁnite ﬁne ataxic tremor on motion.
Knee jerks are absent. Patient is apprehensive and nervous. There is
no weakness. Spinal puncture: ﬂuid hazy. Pressure normal. Cell
count 2430. 15 c.c. of serum given.

August 22, 1916. At 7 A.M. The child is slightly improved. Has had
a fair night with 6 hours sleep. Bowels have not moved and no food has
been taken since the last visit. Physical examination shows stiffness
and tenderness of the neck and spine, and a positive Kernig in each leg.
There are no paralyses or weaknesses made out. Temperature is 102.2.
Lumbar puncture: 20 c.c. of cloudy ﬂuid was withdrawn under normal
pressure. Examination of this ﬂuid at the bedside shows it to contain
2220 cells and no red cells. The Globulin reaction is very marked.
Fehling’s reaction positive. V

August 22, 1916. 9.30 P.M. Patient has rather suddenly assumed an
opisthotonos position. Temperature 103. Face is quiteﬂushed,breathing
somewhat rapid. 15 c.c. of serum together with 1% c.c. of adrenalin
chloride were given intraspinally. Cell count was not made.

August 24, 1916. Temperature is about .1° lower than on the previous
day. Opisthotonos still continues and paralysis of the right arm with
weakness of the left. Cyanosis of the lips and face and evidence that
the accessory respiratory muscles are involved. Spinal puncture: 15
c.c. of serum together with 1% c.c. of adrenalin were given. Cell
count 2 50.

August 25, 1916. 10 A.M. Patients condition is very poor. Tem—
perature is high, pulse rapid, appearance cyanotic. 2 c.c. of adrenalin
chloride were administered intraspinally. Child died at 1 1.30.

Discussion.—Overwhelming infection. Puncture and ﬁrst treatment
IO hours after the onset of meningeal symptoms showed 2430 cells.

It is interesting to note that after 2 months the mother remembered
what she had failed to mention at the time of the child’s sickness, that the
child had been feeling poorly on the previous day. Possibly this case,
then, which has been reported in the group of sudden meningeal onsets
belongs to the group of straggling courses with a very short duration.

Case 29.——]. L. Girl. 6 years. Garden City, L. I.

August 23, 1916. This morning before breakfast the patient seemed
not to be well. During the morning she was drowsy and vomited but
ate her lunch. In the afternoon her temperature was 100. At 7 P.M.
it was 102.5. The patient is a large girl for her age. There is a light
tremor of the face and hands on motion. Spinal sign is fairly marked.
Patient is ﬂushed and acutely sick. Knee jerks and ankle jerks ++.

I 2 2 ACUTE POLIOMYELITIS

No muscular weakness. Spinal puncture: ﬂuid clear, pressure slightly
increased. Cell count 490. Globulin ++++. Patient was given
15 c.c. of serum at 9 P.M. after the removal of 20 c.c. of ﬂuid; she was
relieved by the injection. This was followed by cramps in both legs.

August 24, 1916. 9. A.M. Patient had a good night, some twitching,
no vomiting. Temperature 100.6. Slight headache. Knee jerks, both
positive. Cells 2540. 15 c.c. of serum given after the removal of 20 c.c.
of ﬂuid. Again cramps in the legs. .

August 24, 1916. 7 P.M. Following the last injection the patient
complained of pain in the bladder. She is very alert, trembling and
nervous. Respiration rapid, pulse rapid. Knee jerks +; the Achilles
jerk in the left ankle is negative. Right Achilles jerk is present. Spinal
puncture: ﬂuid turbid, pressure increased. 15 c.c. of ﬂuid removed and
10 c.c. of serum given. Cell count 2962. Patient was drowsy and nearly
went to sleep while the serum was being given.

August 25, 1916. Patient in stuporous condition most of the day. Is
ﬂighty when aroused. Temperature 103. Possibly slight weakness of
the deltoid, shown as early fatigue. Knee jerk ++. Ankle jerks both
present.

August 26, 1916. Patient had good night. Temperature 100.4. This
morning after exertion caused by changing the bed, the patient went into
collapse. Recovery was prompt. Pulse very weak, rapid. When seen
at 9 o’clock patient was prostrated, pulse fair, respiration very shallow.
MacEwen ++. Knee jerks ++. Ankle jerks, right plus, left negative.
Heart action and sounds good. Puncture was done to relieve pressure.
Fluid clear, pressure ++. Cell count 2 5. Globulin +. About 20 c.c.
of ﬂuid removed. MacEwen’s sign disappeared. During the day the
patient was in a stupor. She is probably a case of the true encephalitic
type. Reﬂexes are all double plus. There is a tendency to spasticity.
Respiration became deeper after the removal of the ﬂuid. When fed
swallows only on order. Makes violent grimaces on opening the mouth,
some twitching and athetoid motions. Respiration irregular.

August 27, 1916. Patient awoke early in the morning and spoke
clearly to the mother. Temperature 100, pulse 120, rather poor force
but not bad. General condition shows some improvement. Still somno-
lent and psychically detached. Eats better but still with violent mouth
opening. Temperature began to rise this afternoon.

August 28, 1916. Patient continues in'semi-stupor. Puﬂiness of the
eyelids this morning. Takes nourishment automatically. Temperature
101, pulse 112, good quality. Twitching less. In the afternoon the
temperature began to rise again. Patient still refuses to answer and looks
blankly at her mother without recognition.

August 29, 1916. Patient much clearer mentally. Temperature 99.
Marked exaggeration of all reﬂexes, slight unsteadiness and general weak-

TREATMENT ‘ I 23

ness of the arms on raising, but probably not due to cord lesion. It
seems more like general disability.

August 30, 1916. Last night the temperature rose as high as 102.6.
Patient was somewhat distended and was given castor oil. Good results
in the morning. Temperature now 101.4. Patient is quiet, clear men-
tally and relaxed. Physical examination shows the eyes apparently nor-
mal, but there is slight puﬂiness of the lower lids. Throat a little red.
Uvula appears to be absent. The lymph nodes, both the anterior and
the posterior cervical are palpable. Bladder is markedly enlarged,
especially on the right side. The axillary nodes are also markedly
enlarged, as well as the epitroclear and inguinal glands. Heart and lungs
are apparently normal. The liver is felt in the anterior axillary line about
a ﬁnger’s breadth below the costal margin. The spleen is not felt.
Reﬂexes are all present except the ankle jerks, which are not obtained
this morning. There is no muscular weakness made out.

August 31, 1916. Patient’s temperature has been rising slowly and
steadily. This morning there is a positive MacEwen sign. Another
puncture was suggested on the possibility of increased intracranial
pressure. The family wished to postpone this. At 6 P.M. the tem-
perature was 104.6. Patient seemed in good condition and bright, and
not as sick as temperature would indicate. Spinal puncture: ﬂuid clear,
pressure low. 15 c.c. of ﬂuid withdrawn. Cell count 105. All but a
very few of the cells are small lymphocytes.

September 1, 1916. Patient is apparently in the same condition as
yesterday. Temperature has dropped to 102.6. She is complaining now
of a great deal of pain and tenderness in her joints, shoulders and knees,
especially. Midday temperature again arose to 103. Aspirin was
ordered, 5 grains every 3 hours. The patient has had pains all day
and last night in her joints and muscles. Marked palpitation was noted.
Patient is tender and when touched has many pains. Temperature 104. 5.
She eats well and seems in good condition generally. She is not as sick
as her temperature would indicate. Pulse full and of good quality. At
noon she was given 5 grains of aspirin; 2 hours subsequently she per—
spired freely and went to sleep. At 3 PM. temperature has fallen to
101.3.

September 3, 1916. Temperature continues high, between 102 and 104.
General condition remains unchanged.

September 7, 1916. Patient’s temperature has been normal for 3
days. She seems very much better in all respects though considerably
prostrated. N0 weaknesses are made out. Reﬂexes are all present, ex-
cept the left ankle jerk. The neck is no longer stiff.

Discussion—This is a most unusual case in the length of its course.
The marked meningeal irritation following treatment and the profound
psychic disturbance are interesting features. There is no doubt that the
respiratory embarrassment was relieved by the withdrawal of ﬂuid.

I 24 ACUTE POLIOMYELITIS

The ﬁrst treatment -was given about I4 hours after the onset of symptoms.
The cells at this time were 490.

Case 30.—R. L. Boy. 7 years. Roslyn, L. I.

July 27, 1916. Patient seemed rather quiet during the morning and
instead of his usual activities was lying about on chairs and sofas. At
this time he complained of headache and feeling lazy. Eyes were deﬁ-
nitcly puffy. There were no weaknesses made out. Reﬂexes were pres—
ent and slightly exaggerated. Spine sign was positive but not marked.
Heart and lungs were normal. Lumbar puncture, at 6 hours. showed
hazy ﬂuid, under increased pressure. Cell count 530. At 12 midnight,
about 12 hours after the onset, patient was given 20 c.c. of serum from a
recovered case. Next morning the spine sign was very much more marked.
Patient tended to assume the opisthotonos position. Marked and in-
'creased rigidity of the spine. Patient very tremulous and somewhat
ataxic in the arms.

July 28, 1916. Patient given 20 c.c. of serum intraspinally. Fluid
withdrawn is cloudy. Cell count about 3000. Condition the same with
spinal tenderness and rigidity of the neck. Marked exaggeration of all
the reﬂexes. During the night there was severe twitching of the arms,
legs and face. Patient vomited once.

July 29, 1916. 9 A.M. Patient punctured again. 20 c.c. of ﬂuid
withdrawn. 15 c.c. injected. The cell count has dropped to 77. During
the injection the patient had a very considerable nose-bleed, and com-
plained of abdominal pain. The same signs of meningeal irritation are
presented. There is slight weakness of the left deltoid. At 10 PM. the
patient was given the fourth injection of IO c.c. of serum. Cell count
lost. Spastic condition continues.

July 30, 1916. 9 A.M. Patient is given the ﬁfth injection of 7 c.c. of
serum. The ﬂuid is perfectly clear. Cell count 50. Patient continues
spastic with a continued spine tenderness, maintaining a marked contrac-
tion of the neck, and ﬂexion of the face and knees. Reﬂexes all exagger-
ated. No weakness made out. The weakness of the deltoid has appar-
ently disappeared. During the night there were severe contractions of
the muscles. Patient complained again of abdominal pain during the
injection of the serum. Temperature came to normal on this date, and
remained so subsequently. The tender spine and spastic condition per-
sisted until the middle of August, and gradually disappeared.

Discussion.—The patient was very toxic from the start and showed a
high cell count within 12 hours of the onset of the headache and
drowsiness. He developed intense meningeal irritation following the
treatment, shown both by the high cell count and extreme spasticity and
opisthotonos. He received ﬁve intraspinal injections, amounting to 77
c.c. This case was one of the earliest ones to be treated and received the

TREATMENT I25
1
largest doses—20 c.c., and also the greatest number. Later on smaller
and fewer doses were given.

. Case 31.—B. N. Girl. 8 years. Westbury, L. I.

July 29, 1916. Patient was ill with tonsillitis which lasted three days.
There was then a 4-day interval with normal temperature and the
patient seemed better.

August 5, 1916. This morning the patient complained of headache,
and was found to have a stiff neck. Lumbar puncture, within 6 hours,
was done by Dr. DuBois from the New York City Department of Health.
A small amount of ﬂuid was obtained, and the cell count by the dry
method. indicated an increase above normal. Albumin was also positive.
At 7.40 PM. About 12 hours later, the patient was punctured a second
time. 25 c.c. of ﬂuid was removed under moderate pressure. Cell count
420. The patient was given 20 c.c. of serum. Patient is large, rather
fat type of girl. Knee jerks are very hard to get. The biceps jerk is not
obtained. She has a painful spine.

August 6, 1916. In the afternoon the patient was punctured again.
Fluid was clear, pressure, normal. Cell count 380. 7 c.c. of serum was
administered. Knee jerks were present.

August 7, 1916. Neck still stiff. Kernig sign present. No weakness.
Biceps jerks were not obtainable. Knee jerks were present. T empera-
ture 100.3. Lumbar puncture: under ether. Fluid clear, slightly tinged
with red cells. Pressure normal. Cell count 290. 1 2 c.c. of serum given.

August 8, 1916. Patient seems much better to-day. Meningismus
marked. Knee jerks are present, but hard to get. This is the end of the
fourth day or the beginning of the ﬁfth.

August 12, 1916. Meningismus practically gone. Right knee jerk
present, but much less than the left.

Discussion.—This case is a well—marked dromedary type in which the
ﬁrst hump is deﬁnitely associated with a tonsillitis. A number of such
cases were seen. There was very little response to treatment so far as
the meningeal irritation was concerned. The child was very sick during
the whole course of the treatment. She recovered without any weakness
having appeared. Her ﬁrst puncture was made within 6 hours of the
onset of meningeal symptoms and the ﬁrst injection of serum at about
I2 hours.

Case 32.—R. N. Boy. 4 years. Westbury, L. I.

August 6, 1916. Brother of Case 31. Similar in looks. Sudden onset,
with restlessness during the night. At 7 A.M. vomited and had stiffness
of the neck. Physical examination at 10.30 A.M. showed the spinal
ﬂuid clear under low pressure. Cell count 2000. 7 c.c. of serum were
given. The serum entered with difficulty and cramps of the legs followed
the injection. At midnight the child was chloroformed and 25 c.c. of

I 26 ACUTE POLIOMYELITIS

ﬂuid removed under slightly increased pressure. Fluid was cloudy. Cell
count 4500 (mononuclears). 15 c.c. of serum was given.

August 7, 1916. Patient again etherized and puncture performed.
Fluid very turbid. Cell count 1800. Pressure normal. 26 c.c. of serum
was given. During the night breathing became very bad, 50 per minute
and very shallow. The condition seemed more like respiratory center
involvement, for the diaphragm and thoracic muscles were working.

August 8, 1916. Patient shows a slight tendency to favor the right
thigh and leg. No deﬁnite paralysis, but slight weakness of the extensor
groups, above and below. Patient was given 12 c.c. of serum. Fluid
was clear. Pressure normal. Cell count 177.

August 9, 1916. Patient had rapid breathing during the night. This
morning markedly prostrated. Declines to move the right leg.

August 1 1, 1916. There has been slow but progressing weakness of the
respiratory center, but no paralysis. Deltoids are apparently ﬂaccid.
There is also great weakness of the thighs.

August 12, 1916. Breathing better this morning. Both groups acting
more extensively. Spontaneous ﬂexion of the left foot in sleeping.

August 16, 1916. Patient much better. Generally stronger. Both
respiratory groups acting more forcible. Continues to demand constant
changing of position. No change in ﬂaccid muscle. Neck is stronger.

August 18, 1916/ Left forearm all right. Deltoid, biceps and triceps
ﬂaccid. Right deltoid, biceps and triceps weak. Right forearm weaker
than the left. Lower right quadriceps very weak or absent. Anterior
tibial group weak. Left tibial group weak, but much more active than
the right. Breathing almost back to normal. Spinal tenderness still
very marked.

September 6, 1916. Since last note the patient has continued to im-
prove in general condition. Spinal and muscular tenderness which has
persisted until a day or two ago at almost its original intensity has only
just begun to diminish. Diminution of this tenderness has made it possi-
ble to determine that the paralyses are improving. There is practically
complete use of all the muscles below the knee on both sides. The quad-
riceps on both sides, however, are apparently gone. The ﬂexion of the
thigh is possible through the action of the psoas. The upper extremities:
on the left side there is almost complete use of the forearm and hand
muscles, also of the biceps. The triceps and deltoid, however, are still
practically useless. There seems to be a slight return of power to the
deltoid. The right arm: there is marked weakness of the ﬂexors of the
ﬁngers. There is much greater weakness of the biceps than on the left
side. Like the left side there is almost complete uselessness of the triceps
and deltoid, but here is also apparently a slight return of power in the
deltoid.

Discussion—This case was by far the sickest patient of any that lived.
He was profoundly toxic and had intense meningeal involvement. The

TREATMENT 1 2 7

exhaustion of the respiratory mechanism was very unusual for it was ap-
parently a central affair. Whether the fact that the two worst slumps in
his breathing followed intraspinal injections is of signiﬁcance or not is
open to discussion. The ﬁrst puncture and treatment came within 8 hours
of the onset of meningeal symptoms, disclosing the very high count
of 2000.

Case 33.—A. L. Male. 32 years. Oyster Bay, L. I.

August 21, 1916. Patient felt poorly.

August 22, 1916. He felt all right.

August 23, 1916. He felt feverish and somewhat “dopey.”

August 24, 1916. Complains of headache, feverishness, and slight
stiffness of the neck. Temperature 102°. Patient is a large, bony indi—
vidual. Pharynx is congested and he has a slight cough. Heart and
lungs are negative and there is no explanation of the temperature except
the onset of an attack of polibmyelitis. Knee jerks are present. Neck is
slightly rigid. Spinal puncture: ﬂuid clear and shows no cells. Pressure,
3 mm. of mercury. Globulin +. No history of vomiting or constipation.

August 25, 1916. Temperature 101°. Patient still has cough, complains
of headache and feels weak. Spinal puncture: ﬂuid is clear with no cells
and no increase of pressure. Neck is distinctly stiff but not markedly
so.

August 26, 1916. Temperature 100.8°. Neck more rigid. Did not
sleep well last night, feels restless. There is considerable tremor of both
hands, especially of the right side. No kernig or clonus. Knee jerks
still present. Spinal ﬂuid, at about 48 hours, is clear, but shows about so
cells. Globulin +. 15 c.c. of serum were given with 1% c.c. of adrenalin
chloride. The patient was then taken to the Locust Valley Hospital.

August 27, 1916. Running a slight temperature. 15 c.c. of serum were
administered.

August 29, 1915. Temperature normal. Patient feels well and would
like to get up. There is evidently very slight weakness of the muscles of
the right leg.

Discussion—This patient is the father of Case 28. The case is espe-
cially interesting because of the series of punctures, the slight meningeal
involvement, so cells, and the partial and transient weakness. It was not
until about 48 hours that cells ﬁrst appeared in the spinal ﬂuid and serum
was injected.

Case 34.——A. M. Boy. 8% years. Great Neck, L. I.

August 28, 1916. Patient complains of headache. Lay down for quite
a while during the day.

August 29, 1916. Child was in bed all day but had a good appetite.

August 30, 1916. Felt better to-day.

August 31, 1916. Had a temperature and complained of pain in the
neck. Mother says he has been running wild and eating almost anything

I 28 ACUTE POLIOMYELITIS

he could get his hands on, such as raw cucumbers and fruit of all kinds.
His general condition, therefore, has not been very good. Temperature,
by mouth, 101. Neck is moderately rigid. Kernig, positive on both sides
but especially on the right side. Knee jerk is exaggerated on the right
side, present on the left. There is no history of vomiting. Bowels have
been moved thoroughly by two doses of castor oil. Throat is red. Child
is rather poorly nourished, very dirty. Spinal ﬂuid pressure 12 mm. which
was reduced to 4 by the removal of 30 c.c. of clear ﬂuid. Cell count 80.
IO c.c. of serum were given. The child was sent to the Neighborhood
House, Roslyn.

September 7, 1916. 11.30 A.M. Beginning respiratory paralysis
noted this morning. Respirations, shallow, frequent (32) labored. Lum-
bar puncture——2o c.c. of blood-stained ﬂuid removed. Pressure not
increased. 2 c.c. of adrenalin hydrochloride (I—Iooo) was introduced.
No improvement during the afternoon. Atropine 1/f50 q. 4 h. 8 P.M.
Complete diaphragmatic and intercostal paralysis of left side. Right side
accessory respiratory muscles being used. Lumbar puncture: 5 c.c. san-
guinous ﬂuid withdrawn. Pressure not increased. Patient died of
respiratory paralysis.

Discussion—This case is one of the dromedary group with a very mild
ﬁrst hump. Puncture a few hours after the second rise in temperature
showed only 80 cells. This patient received one intraspinal dose of serum
and one of adrenalin. The outstanding features are the low cell count, the
poor physical condition of the boy, and the fatal issue.

Case 35.—M. M. Girl. Westbury, L. I.

August 20, 1916. Child developed fever, became irritable and com-
plained of pain in her legs. Had not been well for about a month. Has
had no appetite. Previous to this time she has been strong and very
active. Child appears ill and has a ﬂushed face. Cries when touched and
complains of pain in her ankles when her legs are manipulated. Knee
jerks, barely present. Kernig sign, positive. Stiffness of the neck.
Temperature 101.2°. Cell count 485 at 18 hours. Refused to send child
to the hospital.

August 21, 1916. At 4 P.M. Patient had been admitted to the Roslyn
Hospital an hour before. Cell count at this time was 300. Temperature
102.6°. There is more stiffness of the neck and a suggestion of spasticity
of the legs. Face is ﬂushed. Child seems quite comfortable, however
except when her legs are moved or touched. Cervical lymph nodes
enlarged. Spinal puncture. At about 30 hours 25 c.c. of ﬂuid was
removed under slightly increased pressure. 15 c.c. of immune serum were
injected.

August 22, 1916. 11 A.M. Deﬁnite paralysis in the right leg and begin-
ning loss of function of the left. No knee jerks. Child complains of pain
in the region of the hip joint when a Kernig is attempted. Cell count 280.

TREATMENT I 29

15 c.c. of ﬂuid withdrawn. Spinal pressure is 8 mm. of mercury, measured
by the manometer. 15 c.c. of serum injected. Splints applied to the legs
to overcome the tendency to toe drop. ’

August 23, 1916. Condition is advancing. Both legs are paralyzed.
Rigidity of the neck more marked. No involvement of the respiratory
muscles of the arms. Pressure 9 mm. of mercury, reduced to 1 mm. with
the removal of 30 c.c. of spinal ﬂuid. 10 c.c. of immune serum injected.
Temperature 102.4°.

August 24, 1916. 4 RM. Temperature 103°. Patient is cyanotic and
breathing with difﬁculty. There is probably paralysis of the respiratory
muscles. Arm is paralyzed. I 5 c.c. of ﬂuid withdrawn. Cell count 50.
Pressure low. No serum was given.

August 25, 1916. Patient died, apparently of paralysis of the respira-
tory center.

Discussion.—This patient received her ﬁrst dose of serum 25 to 30 hours
after the onset of symptoms pointing to meningeal invasion. The cells
were 485. She pursued a steadily downward course, displaying signs of
general prostration in addition to the advancing paralysis. The manner
of death was not purely a respiratory muscle failure, but there seemed also
to‘be an additional element of central nature.

Case 36.—M. B. Girl 5.16 years. Oyster Bay, L. I.

September 3, 1916. At 11 A.M. Temperature was 105°. Child was
drowsy, irritable, constipated, complained of frontal and occipital
headache.

September 3, 1916. 3 P.M. Spinal sign positive. Vomiting at 2.30.
Temperature 104° per rectum. Headache in the temporal and occipital
region. Spinal puncture, within 6 hours, showed a cell count of 240. 15
c.c. of serum given. Child was not quite so apathetic. Spinal sign not
quite so positive. Temperature 103.4° at 8 o’clock. At midnight tem-
perature was 100 per rectum.

September 4, 1916. At 8 A.M. Temperature 101.4°. At noon 100.8°.
At 4 RM. 102°. At 5 PM. 103°. At 5.30 spinal puncture was done.
Pressure negative. Cell count 200. 15 c.c. of serum given. There is
increase of spine sign and general depression.

September 9, 1916. Patient looks wilted and heavy-eyed, is irritable
and rather restless. There is a marked MacEwen’s sign. The knee jerks
and the ankle jerks are absent. The right biceps jerk is obtained, the left
doubtful. Lumbar puncture: about 12 c.c. of clear ﬂuid not under pres-
sure was removed. Cell count 200. Patient is running a high tempera—
ture. No paralysis. Slight weakness of the abdominal muscles.

Discussion.—This case with apparent sudden meningeal onset was
punctured within the ﬁrst six hours. Cells were 240. She received two
doses of serum. Following the second dose she seemed generally de-
pressed and weak. She recovered with a very slight abdominal weakness.

9

I30 ACUTE POLIOMYELITIS

It is interesting to note that the very marked MacEwen’s sign was not
associated with increased pressure of the spinal ﬂuid.

Case 37.—H. McC. Girl. 8 years. Freeport, L. I.

August 27, 1916. At 6.30 this morning the patient complained of
headache and vomited at 9.30 o’clock. At 11.30 A.M., temperature
was 103. At 4 P.M. 102. At 5 P.M. 100.4 per mouth. There was
slight pain on ﬂexion of the neck. Pulse 138. N o patellar reﬂexes.

August 28, 1916. Physical examination showed the posterior neck
muscles slightly rigid. Temperature 101. No .other signs present.
Spinal puncture at 24 hours showed a slight increase in pressure.
Fluid ﬂocculent, not cloudy. Cell count 240. Temperature 102. At
2 P.M. 15 c.c. of serum was given. The cell count was the same as
above.

August 29, 1916. Temperature 101. At 10 o’clock 100.8. 15 c.c. of
serum was given at 10 A.M. Cell count was not made as child kicked
over the tube. General condition of the child much improved. Slept
well the night before. Family physician does not think it necessary to
repeat the serum, but child will be seen at 9 o’clock to—morrow night, and
if necessary serum will be given.

August 30, 1916. At 10 A.M. 15 c.c. of serum was given. Tempera-
ture at this time was 100.4.

August 31, 1916. Temperature 99. Child’s general condition good.

September 1, 1916. Child has no paralysis and is otherwise in good
condition.

Discussion.—Puncture at 24 hours showed 240 cells. The child was
very sick. The patient received two doses of serum, 30 c.c. in all.

Case 38.—A. S. Boy. 12 years 9 months. Huntington,L. I.

August 20, 1916. Temperature 105. Child is irritable, constipated,has
slight rigidity of the neck muscles, no vomiting and very uncomfortable.

August 21, 1916. Temperature 103. The same symptoms with slight
increase of stiffness of the posterior muscles of the neck. Physical ex-
amination shows anxious facies. Kernig, slight on the left side. There
is a decided spasm of the posterior neck muscles. Child is very irritable,
constipated, no vomiting. Spinal puncture, at 24 hours, shows ﬂuid
under increased pressure. Cell count 222. 15 c.c. of serum were given.

August 22, 1916. Temperature 103.5.

August 23, 1916. General condition of the patient improved. Slept
well night before last. Irritable. Knee jerks, present on the right side.
Less spasm of the posterior muscles of the neck. Temperature normal.
Appetite fair. Child had a good night. 15 c.c. of serum given. Cell
count 70. Fluid came out very slowly, drop by drop. The posterior neck
muscles not so stiff. Back ﬂexible. Reﬂexes positive. No abnormal
temperature. Patient had a very slight right lateral abdominal weakness.

TREATMENT 13 1

Discussion.—This patient had 222 cells at about 24 hours. He received
two doses, 30 c.c. Observe the unusual drop in cells following treatment.

Case 39.—C. S. Girl. 5 years. Freeport, L. I.

August 30, 1916. Seen at 1 P.M. when the child complained of head-
ache which she had had during the morning. At 2 P.M. she vomited
once. Later on in the afternoon she vomited three times.

August 31, 1916. Temperature, by mouth, 100.6. Neural examina-
tion was negative, except for slight pain in the cervical region of the cord
when the head was ﬂexed. This symptom was very slight. Spinal
puncture at 12 hours, showed a cell count of 170. Pressure was increased.
Fluid clear. Child had been sick just 12 hours. 15 c.c. of serum were
given.

September 1, 1916. At 10 A.M. Temperature was 101. Cell count
960. 15 c.c. of serum was given. Child complains of no headache and
feels much better.

September 2, 1916. No abnormal temperature. Headache has sub-
sided. Child slept well the night before. Appetite was good. Child
was up and playing about, so that no serum was deemed advisable. No
paralysis.

Discussion.—This patient was not very ill and wanted to get up and
play. At 12 hours after the onset puncture showed 170 cells. This
patient received two doses of serum, 30 c.c. in all.

Case 40.—F. S. Girl. 15 years. Mineola, L. I.

August 21, 1916. Child complained of vertigo. Restless that night.

August 22, 1916. Child complained of vertigo, headache and nausea.
Vomited ﬁve times and was constipated. Complains of anorexia. Very
severe pain in both legs, from hip down. Temperature 104.6.

August 23, 1916. In the morning complained of cold legs, anorexia,
very severe pain in both legs. Vomited, nausea, intense frontal and
occipital headache. Posterior neck muscles stiff. Constipated. Nys—
tagmus; ankle clonus on both sides. Double patellar clonus on both
sides, also a delayed patellar clonus on both sides. Spinal puncture, at
36 hours, showed ﬂuid under slightly increased pressure. Cell count 130.
Temperature 103.6.

August 24, 1916. Temperature 104.8, per mouth. One-half hour
later, 104.4 per rectum. Nystagmus and symptoms of the previous day
increased in severity. Dr. Dalton gave 15 c.c. of serum at 1 P.M., 60
hours after the onset. Muscles of the lower maxilla stiff. Slight right
facial paralysis. Has difﬁculty in speech, thick and indistinct. Child
lay all day in profound stupor.

August 25, 1916. Nystagmus less marked than on the previous day.
Slight facial paralysis. Tendo Achilles reﬂexes positive on both sides.
Posterior neck muscles not stiff. Patellar reﬂexes not decreased. Speech
improved, mentally clear. Temperature, per rectum, 104.4. No head-

I32 ACUTE POLIOMYELITIS

ache, appetite good. Menstruated this morning seven (lays ahead of
time. Usually has pain and duration of two or three days. No pain this
time. Profuse amount. Slight nystagmus.

August 26, 1916. Temperature of the patient is normal. Posterior
neck muscles not stiff. Slight facial paralysis of the right side‘ clearing
up. Child’s speech is now normal. No headache. Complains of a
little pain in the right temporal region when she touches it with her hand.
Patellar reﬂexes present on the left side, slightly delayed on the right
side. Kernig, negative. Child walks fairly well.

September 1, 1916. Temperature normal. Child up and about. No
stiffness of the neck or spinal tenderness. Right facial weakness. Speech
normal. Occasional neuralgic pains on the right side of the face. No
paralysis of extremities. Tendon reﬂexes present.

Discussion—This patient was punctured at about 36 hours following
the onset. At this time had 130 cells. She developed profound stupor,
nystagmus and slight facial weakness. One dose of serum was given at
about 60 hours. Note the menstrual disturbance.

Case 41.—K. McL. Boy. 18 months. Northport, L. I.

August 17, 1917. Child has slight diarrhoea. Sister has the disease.

August 19, 1916. Child in bed sleeping with no history other than the
slight diarrhma for 2 days. Constitutionally he seems well and was
awakened for the purpose of examination and temperature. Physical
examination at 1 A.M. shows temperature 105. Eyes, ears, nose, throat,
heart, lungs, and abdomen normal. Neck and spine stiff and tender.
The head will not ﬂex upon the chest. Suspension by the head and but-
tocks caused arching of the back and pain. Kernig positive in both legs.
No paralyses made out in any part of the body. Reﬂexes normal. Spinal
puncture shows clear ﬂuid under normal pressure with a moderate globulin
test. Cell count 320. This child was well on going to bed after playing
all day. 15 c.c. of serum was given intraspinally after drainage of the
cord.

August 20, 1916. At 2.30 P.M. the child seemed better and took food
fairly well. Bowels about the same as before. Temperature has dropped
to 103. Child seems less toxic.

N0te.—Upon the 18th the temperature shows a critical drop to 99.
Where it remained for about 8 hours. On the 20th the temperature was
98. Child feels better and shows no paralysis.

August 21, 1916. At 2.30 P.M. Lumbar puncture was performed and
the cell count found to be 540. 15 c.c. of serum was given intraspinally.

September 6, 1916. A telephone from the boy’s father stated that the
boy showed a normal temperature 3 days after he was seen last and
that he had made a perfect recovery with no paralysis.

Discussion—This case is interesting because of the unusual way in
which the disease was recognized. The meningeal' invasion must have

TREATMENT I 33

occurred between the previous evening and 1 A.M., when 320 cells were
found. This patient received two doses of serum, 30 c.c. in all. The
ﬁrst treatment was not later than 7 hours after meningeal invasion.

Case 42.—C. W. Boy. 4% years. Lawrence, L. I. ,

September 6, 1916. Appetite poor brit seemed to have no temperature.
His bowels moved and he complained f no pain or other distress. His
mother says he did not seem very ill during this period, though not quite
himself. ‘

September 9, 1916. After eating tomatoes the child suffered an abrupt
rise in temperature which has remained. until he was seen by physician.

September IO, 1916. Was seen by physician at noon. Temperature
103. Has vomited on three or four occasions after taking food. Bowels
have been constipated. Has no cold in [the head, cough, sore throat, pain
in the chest, abdomen, or joints. He has had no earache. Mother
thought the child favored his neck in mdvements. No history of a rise in
temperature previous to 4 days agoL Physical examination shows
temperature 103. Eyes, ears, nose and hroat negative. Cervical glands
normal. Neck slightly stiff and tender, cannot place chin on the chest.
Suspension by head and buttocks shows the neck and back to be straight.
Heart, lungs and abdomen normal. No paralyses are made out. Knee
jerks are present. Kernig is absent. Spinal puncture, at 30 hours, 15
c.c. of cloudy ﬂuid withdrawn. Cell coulnt 280. No red cells. Globulin
+. 5 c.c. of serum injected slowly. \

September 11, 1916. Temperature 104. Child had had a restless night.
Has vomited incessantly. Bowels have not moved. Mother noticed
much twitching of the eye, eyelids and hands; she thinks he is much
worse. Physical examination shows the child looks worse, more toxic.
Lips and tongue dry and cracked. Left eye seems to be turned slightly
inward, although all movements of bothl eyes are obtainable. The neck
is the same as on the last visit. Knee jerks very active. Kernig positive
in both legs with pain. Paralyses other than the left external rectus are
not present. Child is to be removed immediately to the hospital, and
further serum treatment though indicated is postponed until his arrival
there. A second dose of serum was givlen. Following this the patient
became much worse, there being intense meningismus and opisthotonos.
Child very toxic. Twenty-four hours afier the second dose, the patient
appeared to be going to die, but his condition changed and rapidly im-
proved and he had a normal temperature in 5 days. There remained
a weakness of the masseters and slight ‘deglutition weakness.

Discussion.—This patient seemed to ibecome much worse following
treatment, very toxic and showing intense meningismus. His ultimate
recovery was good with slight weakness. l The ﬁrst treatment was about
30 hours following the second hump onset. The cells were then 280.

_——l—_—

I34 ACUTE POLIOMYELITIS

Case 43.——W. C. Boy. 4 years. Inwood, L. I.

August 24, 1916. This afternoon the patient complained of not feeling
well. Did not want to play. Did not have any pain. No vomiting.
Bowels moved only after medicine. Temperature 101. Pulse 150.
Pupils unequal, slow in reacting. Child apathetic and hyperaesthetic.
Knee jerks present, but slight. Kernig slight. Neck stiﬂ and painful.
Lumbar puncture at 8 hours shows clear ﬂuid under pressure. Cell count
215.

August 25, 1915. Temperature 101. Child said to be about the same
as above. The neck and back are stiff and tender with a considerable
retraction of the former. There is no Kernig or paralysis. Child appears
toxic and deﬁnitely of the meningeal type. Spinal puncture. 15 c.c.
clear ﬂuid were withdrawn. Cell count 150. 15 c.c. o'f reddish
serum from a cured case received from Willard Parker injected into the
spine.

August 26, 1916. 12.30 P.M. Temperature 101. Child appears to
be more toxic and considerably worse than the day before. Has had
two or three greenish, watery movements, which show undigested grape
and pear. He vomited once after serum injection; it was not projectile
in type. Physical examination shows neck and back markedly retracted.
Kernig marked. Lips and tongue are very dry and cracked. Child is
very toxic. No paralysis. Spinal puncture. 15 c.c. of very cloudy ﬂuid
obtained. There is no evidence of reddish color. Cell count 5600.
Leukocytes present. No red cells. Globulin +++. Differential count:
Polynuclcars 81 per cent., lymphocytes 19 per cent. Film stained by
Gram stain shows no organism. Culture remained sterile 48 hours. 15
c.c. of serum injected intraspinally.

August 27, 1916. Temperature 100. Child much better. Stiffness
of the neck and retraction. Kernig present, but less marked. No paraly-
sis. Bowels better. Appetite good. Cord tapped and drained. 15
c.c. of clear ﬂuid. Globulin +. Cell count 580. No serum injected.

August 29, 1916. Child improved. Temperature 99. Neck slightly
stiff.

August 31, 1916. Neck slightly tender, otherwise normal. Tempera-
ture 98. No paralysis.

September 8, 1916. General condition good. Up in wheeled chair.
Slight weakness of legs. When walking there is a slight give at the knees.
Knee jerks present.

September 15, 1916. Interossei and lumbricales of the right hand
paralyzed and slight claw—like contracture.

Discussion—The initial puncture in this case was made about 8 hours
after the onset of symptoms and shows 215 cells. The child was very ill.
At 26 hours a second puncture was done, showing 150 cells. 15 c.c. of
serum were given. Note the increase of cells to 5600 following this pro~
cedure, and also the marked opisthotonos. After the second injection the

I

TREATMENT 135

cells dropped to 580. This patient, as inany others, became much more
acutely ill following the intraspinal injection.

Case 44.—G. S. Boy. 6% years. Ntirthport, L. I.

September 11, 1916. Patient at this time vomited. Temperature 102,
lasting 12 hours. Constipated. The . well until the 18th, a 7-day
interval. nl

September 19, 1916. Patient complained of pain in the right leg and
headache. Temperature 101.5. Righ‘ knee jerk exaggerated. Slight
rigidity of the neck. Physical examin tion shows: temperature 101.5.
Muscle tenderness of both thighs. Spine sign present. Reﬂexes normal.
Lumbar puncture, at 17 hours, press‘pre increased. Cell count 270.
Globulin + —. 10 c.c. serum given.

September 20, 1916. Temperature 1 2. Spine sign present. Double
Kernig. Stiff neck. Lumbar punctuile: ﬂuid turbid under pressure.
Cell count 300. Acute retention. Relieved by catheterization. 15 c.c.
of serum given. '

September 21, 1916. Temperature nolmal. No weakness or paralysis.
Voided spontaneously.

September 29, 1916. Child up and {Thout the ward. No paralysis or
weakness.

Discussion—This case was treated 17 hours after the onset of the second
hump. There were then 270 cells. No further treatment was given.
The unusual length of the free interval is a striking feature of the case.

Case 45.—A. H. Boy. 2% years. W‘estbury, L. I.

September 15, 1916. Patient had a lemperature of 104. Tonsils en-
larged and red with white spots. Lumbar puncture was done at this time.
Pressure was normal. Cell count 5. lTemperature was normal for 3
days following.

September 18, 1916. A colitis came on and the patient’s temperature
rose again, reaching 104. ‘

September 20, 1916. Temperature 103. No spine sign. Reﬂexes
normal. Tonsils normal. Lumbar puncture was done at 48 hours and
slightly increased pressure was foundl Cell count 39. Globulin +.
No weakness of any muscles.

September 21, 1916. Physical exa ination shows weakness of the
right deltoid. Spine sign present. Ne k quite stiff. Temperature nor-
mal. Lumbar puncture: pressure +. 30 c.c. of ﬂuid were withdrawn.
Cell count 33. 10 c.c. of serum were gi en.

September 22, 1916. Temperature 1 st night was 101. Temperature
this morning was 99. Spine sign still marked. Right arm weaker than
yesterday. Knee jerk and Achilles slightly increased. N 0 other paraly-
sis. Lumbar puncture: ﬂuid, pressure +. 10 c.c. of serum given.
Child to be sent to the Garden City Hospital to-day.

September 25, 1916. Temperature nbrmal since last night. Paralysis

136 ACUTE POLIOMYELITIS

of the right arm marked. Slight weakness of the anterior tibial muscles
on one side.

Discussion.—This case belongs to the dromedary group, but the stage
of meningeal invasion is not sharply marked, nor are the signs of meningeal
invasion great. The ﬁrst puncture, at 48 hours after the second onset
showed 39 cells and no serum was given in consequence. The next day
weakness of the right deltoid appeared. Two doses of serum were then
given, 20 c.c. in all. There was no doubt that the serum was delayed in
this case owing to the very slight reaction found in the spinal ﬂuid at the
ﬁrst puncture.

A REPORT OF TWENTY-SIX CASES

By Drs. Amoss and Chesney
From Journ. of Exp. bled” [917, XXV, 58!

Group I. Cases Showing Paralysis at the Beginning of the Treatment
Class I. Paralysis Extending

Case 1.——Male. Age 33 years.

September 2, 1916. Malaise, headache, and vomiting. Sept. 3.
Unable to bear weight 011 legs. Sept. 4. Admitted to hospital. Legs
completely paralyzed. No tendon reﬂexes. Cerebrospinal ﬂuid shows
280 cells per c.mm. and increased globulin. Bladder, bowels, diaphragm,
abdominal and thoracic walls, and upper extremities normal. Sept. 5.
Bladder paralyzed; no abdominal movement during respiration; using
accessory muscles of respiration; deltoids weak; cyanosis.

On Sept. 5, 10 c.c. of serum were injected intraspinally and 20 c.c.
intravenously. The cyanosis gradually increased, and death resulted from
respiratory paralysis IO hours after the injection. No obvious inﬂuence on
the course of the disease was exerted by the injections of serum.

Case 2.—Fernale. Age 10 years.

September 22, 1916. Headache, nausea, fever, and abdominal pain.
Sept. 23. Temperature 103°F. Pain in back and in right leg; drags
right foot. Sept. 25. Admitted to hospital. Temperature 102.6°F.;
pulse 112; respirations 3o. Neck and back muscles stiff; ﬂaccid paralysis
of both legs; bladder functions. Sept. 26, 6 RM. Left deltoid paralyzed;
dyspnoeic; employs accessory muscles of respiration; no, respiratory move-
ment of abdominal wall; bladder paralyzed. Cerebrospinal ﬂuid contains
270 cells per c.mm.; globulin increased.

On Sept. 26, 20 c.c. of serum were given intraspinally and 60 c.c.
subcutaneously. Sept. 27, 8 RM. Temperature 99.8°F.; pulse 102;
respirations 30. Abdominal muscles move with respiration. Sept. 28.
Abdomen moves freely; left deltoid responds but not yet normally;
bladder inactive. Sept. 30. Bladder acting; no change in leg condition.

The history of the acute stage of this case readily divides itself into two
periods. The ﬁrst (a) takes in the time up to and including the paralysis

TREATM NT ~ 13 7

of the legs, followed by a brief interval when (b) the abdomen, diaphragm,
shoulder, and bladder became paralyzed It was during the second period
that the serum was administered. Coi cidently with the administration
there was no further progress, but rath r a rapid recession of the recent
paralysis; the older paralytic condition was not obviously affected.
Whether the phenomena described are of the nature of cause and effect
cannot certainly be determined.

Case 3.—Male. Age 3 years.

September 26, 1916. Fever and vomiting. Sept. 27. Difficulty in
swallowing. Sept. 28. Admitted to hospital. Temperature 101°F.;
pulse 112; respirations 38. Paralysis if muscles of deglutition. Sept.
29. Complete paralysis of right side?> of face. 12 M. Temperature
104.2°F.; pulse I38; respirations 62. Very ill. 2 RM. Cerebrospinal
ﬂuid, 208 cells per c.mm.; globulin slightly increased.

On Sept. 29, 15 c.c. of serum were ministered intraspinally, 2o c.c.
intravenously, and 40 c.c. subcutanagusly. Sept. 30. Temperature
99°F .; pulse 102; respirations 68. Mar‘ ed improvement in general con-
dition but no change in the degree of paralysis of the face or muscles of
deglutition. Before discharge the paralysis had almost disappeared.

Whether the prompt Subsidence of th severe general symptoms in this
case is to be ascribed to the serum treatment cannot be stated positively.
The fact that no extension of the paralysis occurred in spite of the severe
symptoms may or may not have been due to the treatment. But in this
instance, as in Case 2, the paralysis wa extending at the time the serum
was given and no further extension occuried. It is obvious that in the ﬁrst
case of this series, no result was accomplished. It should be mentioned,
however, that as compared with the more energetic treatment subse-
quently employed that case received a cry small quantity of the serum,
which was administered late in the courle of the disease.

Class II. Paralysis Present

Case 4.—Female. Age 33 years.

October 16, 1916. Chilly sensationl; abdominal pain; difﬁculty in
walking. Oct. 17. Stiffness of neck; legs weak. Oct. 18. Admitted
to hospital. Temperature 103°F.; pulse 104; respirations 34. Neck and
back stiﬁ; weakness of muscles of abd men and left leg. None of the
muscle groups are completely paralyz d. Cerebrospinal ﬂuid, 50 cells
per c.mm.; globulin increased.

On Oct. 18, 2o c.c. of serum were given intraspinally and 50 c.c.
intravenously. Oct. 19. Paralysis sta ionary. Oct. 21. Temperature
99. 6°F. No extension of the paralysis.

The serum was administered 1n this ase probably within 24 hours of
the onset of deﬁnite paralysis, but whether or not it inﬂuenced the progress
cannot be stated. ‘

I 3 8 ACUTE POLIOMYELITIS

Case 5.——Male. Age 2 years.

September 13, 1916. Fever and headache. Sept. 18. After an
apparently normal interval, vomiting occurred and the neck and back
became stiff. Sept. 20. Weakness of legs noticed. Admitted to hos-
pital. Temperature 98.2°F.; pulse 108; respirations 44. Neck and back
stiﬂ; face slightly asymmetrical; abdominal wall relaxed; no reﬂexes;
partial paralysis of muscles of legs. Cerebrospinal ﬂuid, 37 cells per
c.mm.; globulin increased. ,

On Sept. 20, 5 c.c. of serum were given intraspinally and 30 c.c. sub-
cutaneously. The paralysis did not extend, but there was no immediate
improvement of the paralyzed muscles.

The treatment in this case was given probably at the end of the 4th day
of illness at a time when the paralysis had already been arrested. Appar-
ently nothing deﬁnite was accomplished. Case 6, a sister of this patient,
should be used for comparison.

Case 6.—chale. Age 4 years.

September 19, 1916. Fever, headache, and constipation. Sept. 20.
Temperature 101.4°F.; vomiting. Facial asymmetry. II P.M. Ad-
mitted to hospital. Temperature 102°F.; pulse 140; respirations 32.
Neck and back stiff; slight left facial paralysis; weak hamstring and quad-
riceps muscles on both sides; knee jerks and Achilles tendon reﬂexes in- -
creased. Cerebrospinal ﬂuid cloudy and contains 920 cells per c.mm.;
globulin increased.

On Sept. 20, 10 c.c. of serum were given intraspinally and 25 c.c.
subcutaneously. Sept. 22. No extension of paralysis. Sept. 23.
Temperature normal.

In this case the serum was given within 30 hours of the onset of the
symptoms and at a time when weakness of the muscles of the thighs
was appearing. The temperature became normal in about 60 hours
and no extension of the paralysis ensued. Within 2 weeks recovery
of all the weak muscles was complete. The striking point in the case
is the large number of cells in the cerebrospinal ﬂuid when the serum
was injected.

Case 7.—Female. Age 2 years.

September 12, 1916. Headache and fretfulness. Sept. 14. Admit-
ted to hospital. Temperature 101.8°F.; pulse 124; respirations 28.
Weakness of ﬂexors and extensors of right hip and of gastrocnemius.
Achilles tendon reﬂexes absent. Cerebrospinal ﬂuid contains 99 cells per
c.mm. and increased globulin.

On Sept. 14, 5 c.c. of serum were injected intraspinally and 30 c.c. sub-
cutaneously. Sept. 15. Temperature normal; paralysis stationary.
There was never any extension, but gradual improvement of the partially
paralyzed muscles. The temperature curve shown in Text-ﬁg. 18.

TREATMENT

Case 8.—Male. Age 22 months.
September 9, 1916. Child ill. Sept.

perature .102.6°F.; pulse 136; respirations 36.

ceps anterior.

I39

10. Admitted to hospital. Tem-

Weakness of left quadri-

On Sept. IO, 5 c.c. of serum were acministered intraspinally at home

before removal to the hospital. Sept.
20 c.c. of serum given subcutaneously.
Partial paralysis unchanged.

Case 9.—Female. Age 3 years.
October 12, 1916.
partially paralyzed. Oct. 15.
99.8°F.; pulse 120; respirations 32.
back, weakness of the extensors of the

spinal ﬂuid contains 115 cells per c.mm

On Oct. 15, 15 c.c. of serum were
subcutaneously. The temperature ﬂu
and 100°F. for 2 weeks. The weakness
what.

tibial group was completely paralyzed.

The serum was injected in this case
appearance of any symptoms and at a
paralysis existed. Nevertheless, the

Child feverish a
Admitted to hospital.

One month later some degree of
quadriceps, hamstrings, peroneals, and

11. Left thigh muscles weaker.
Sept. 13. Temperature normal.

nd irritable. Oct. I4. Left leg

Temperature

There is stiffness of the neck and

left foot, and toe-drop. Cerebro-
; globulin increased.

injected intraspinally and 40 c.c.
tuated irregularly between 98.6°
of the foot and leg increased some- ‘
impairment was present in the left
toe extensors, while the anterior

within about 72 hours of the ﬁrst
time when only slight and limited

 

muscular impairment progressed

slowly in the muscles ﬁrst affected andrinto neighboring muscles, but the
degree of paralysis never became sever .

Case 10.—Male. Age 15 months.

September 9, 1916. Child feverish nd sweating; vomited. Admitted
on same day. Temperature 99.6°F.; pulse 132; respirations 36. The
neck and back are stiff and there is dou tful weakness of the right deltoid.
Cerebrospinal ﬂuid shows 30 cells per c.1nm.; globulin increased.

On September 9.5 c.c. of serum were iven intraspinally. There was no
further involvement of the right delto d and the temperature remained
normal during the stay in the hospital.

This child was seen within a few hour of the onset of the ﬁrst symptoms
and the serum injection was given at t e home before removal to the hos-
pital. No paralysis developed.

Case 11.—Female. Age 2 years.

September 27, 1916. At noon the c ild was feverish. IO P.M. Stiff-
ness of the neck and back, weakness f the left quadriceps and peroneal
muscles, and slight weakness of the ntercostals. The patient, whose
brother was already in the hospital, w admitted at once. Temperature
101°F.; pulse 110; respirations 32. Cer brospinal ﬂuid, 30 cells per c.mm.;
globulin increased.

I40 ACUTE POLIOMYELITIS

On Sept. 27, IO c.c. of serum were given intraspinally and 30 c.c. sub-
cutaneously. Sept. 28. After 24 hours the temperature was Ioo°F.;
no extension of muscular weakness. Sept. 29. Temperature normal.
Muscular impairment gone. N0 abnormality on discharge.

The serum was administered to this child within 12 hours of the ﬁrst
appearance of the symptoms, and although a degree of weakness of certain
muscles was already present, it quickly disappeared.

Case 12.———Male. Age 3 % years.

September 12, 1916. Headache and fever. Sept. 13. Temperature
103 . 8°F. Stiffness of neck and back; weakness of muscles of right ankle;
toe-drop. Cerebrospinal ﬂuid, 250 cells per c.mm.; globulin increased.

On Sept. 13, IO c.c. of serum were injected subdurally and 40 c.c. sub-
cutaneously. Sept. 14. Temperature 99.6°F. Weakness of muscles
diminished rapidly.

The serum was administered within 24 hours of the onset of symptoms
and at a time when several muscle groups were impaired. The tempera-
ture quickly fell to normal and the muscular weakness soon disappeared.

In considering Cases 1 to 12 the points that can be made deﬁnitely are:
(1) the diagnosis was clearly established in each; (2) there was some grade
of paralysis present in each; and (3) with the exception of Case 1, 8 and 9,
there was either no increase of the existing muscular weakness or paralysis,
or there was prompt improvement in these conditions.

Group II. N 0 Paralysis at the Time of Treatment

In the following series of fourteen cases, no paralysis was detected up to
the time that the serum was administered. One reservation should, how-
ever, be made: in the early stages of the disease, some of the patients were
too ill to warrant a full examination of all the muscle groups and hencea
degree of weakness or paralysis may have sometimes been overlooked.
Moreover, the quantity of serum administered varied considerably,
depending upon circumstances. The cases will be considered in the order
of the amounts of serum given.

Case 13.—Male. Age 8 years.

September 19, 1916. Headache, fever, and drowsiness. Sept. 20.
Same condition; neck and back stiff. Sept. 21. Admitted to hospital.
No paralysis detected. Temperature 102. 5°F .; pulse 102; respirations
32. Cerebrospinal ﬂuid, 850 cells per c.mm.; globulin increased.

On Sept. 21, 5 c.c. of serum were given intraspinally and 15 c.c. sub-
cutaneously. Sept. 24. Temperature normal. In the interim weakness
of the following muscle groups developed: deltoids, pectorales, major
rotators (outward) of arms, ﬂexors of hip, quadriceps and hamstrings,
and abdominal wall.

The serum was administered within 48 hours of the onset of symptoms.

TREATMﬁLNT 141
The amount given intraspinally was‘ small. Weakness subsequently
developed in many muscle groups, but i none was the paralysis complete.

Case 14.—Male. Age 19 months.

September 19, 1916. Vomiting, attributed to improper food. Sept. 20.
Fever; neck and back stiﬂ'; muscular twitchings. Admitted to hospital.
Temperature 103°F.; pulse 124; respira ions 32. While there was mus-
cular stiffness, no weakness was detect d. Cerebrospinal ﬂuid, 120 cells
per c.mm.

On Sept. 20, 5 c.c. of serum were injected intraspinally and 20 c.c. sub-
cutaneously. The fever persisted, an paralysis developed, involving
ultimately the muscles of respiration. ept. 23. Died.

Obviously no inﬂuence on the course of the disease was exerted by the
serum. The experience gained later ‘ow indicates that the injection
should have been repeated. rj

Case 15.—Female. Age 4 years.

September 23, 1916. Fever and 1headache; irritable. Sept. 24.
Neck and back stiff; muscular twitching Admitted to hospital. Tem-
perature ro3.6°F.; pulse 128; respiratio‘ s 34. No muscular impairment
detected. Cerebrospinal ﬂuid, 360 cells per c.mm.; globulin increased.

011 Sept. 24, 10 c.c. of serum were given intraspinally and 20 c.c. sub-
cutaneously. Sept. 25. Flaccid paral sis of right arm and shoulder
girdle with rapid extension and involvement of muscles of respiration.
Died.

Autopsy showed severe poliomyelitic. lesions of the cervical cord and
medulla.

Obviously this case was not beneﬁte by the serum injection, since pa-
ralysis developed a few hours after the treatment and extended rapidly.

Case 16.—Female. Age 8 years.

September 23, 19I6. Headache; rcistless. Sept. 24. Temperature
Io2°F. Neck stiff. Cerebrospinal ﬂuid, 730 cells per c.mm.; globulin
increased.

Within 6 hours of the onset IO c.c. 0 serum were administered intra-
spinally and 20 c.c. subcutaneously. he temperature fell slowly and
reached normal on the fourth day. During this period weakness of the
muscles of both arms and possibly slight {weakness of the left leg appeared;
complete paralysis was never present. LImprovement was rapid, and al-
most complete recovery of lost strength ‘vas made in a short time.

Case 17.—Female. Age 2 years.

September 17, 1916. Fever; drowsy; muscular twitching; convulsions.
Sept. 19. Admitted to hospital. Cerelirospinal ﬂuid, 60 cells per c.mm.;
globulin increased. Temperature Io4.2°F.; pulse 132; respirations 32.
Neck and back stiﬁ‘; no muscular weakness.

On September 19, 6 c.c. of serum weTe given intraspinally and 25 c.c.

I42 ACUTE POLIOMYELITIS

subcutaneously. Within 24 hours the temperature was normal. No mus-
cular weakness developed.

Case 18.—Male. Age 5 years.

September 14, 1916. Temperature 103°F.; headache; drowsy. Sept.
15. Neck and back stiff. Temperature 104°F. Admitted to hospital.
Temperature 103.4°F.; pulse 126; respirations 50. No weakness of mus-
cles. Cerebrospinal ﬂuid, 379 cells per c.mm.; globulin increased.

Within 24 hours of the onset 5 c.c. of serum were given intraspinally and
25 c.c. subcutaneously. Sept. 16. Temperature 101°F. 5 c.c. of serum
were introduced intraspinally. Cerebrospinal ﬂuid, 249 cells per c.mm.
Sept. 17. Temperature normal. No muscular weakness ever developed.

Case 19.—Male. Age 4 years.

September 17, 1916. Temperature 102°F.; pain in back. Sept. 19.
Temperature 102.4°F. Neck and back stiff. Cerebrospinal ﬂuid, 150
cells per c.mm.; increased globulin. Admitted within 24 hours of onset.

On Sept. 18, 10 c.c. of serum were injected intraspinally and 25 c.c. sub-
cutaneously. 15 hours later the temperature became normal. No mus-
cular weakness developed.

. Case 20.—Male. Age 13 months. Cousin of Case 19.

September 17, 1916. Drowsiness and fever. September 18. Cerebro-
spinal ﬂuid clear and contains 7 5 cells per c.mm. ; globulin increased. The
patient was given 10 c.c. of serum subdurally and was shortly afterward
brought to the hospital. On admission, temperature 101.4°F.; pulse 120;
respirations 26.

Immediately after admission a subcutaneous injection of 2 5 c.c. of serum
was given. The temperature rose to 104°F. and fell to normal 22 hours
afterward. There was no subsequent weakness or paralysis.

This patient was treated about 18 hours after the ﬁrst symptoms. The
temperature previous to treatment is not known. After a rise to 104°F.
the temperature fell rapidly, reaching normal about 22 hours after the
ﬁrst injection (Text-fig. 17). The child-developed no subsequent weakness
or paralysis.

Case 21.—Female. Age 3% years.

September 3, 1916. Headache; temperature 102°F. September 4.
Temperature 104°F. September 5. Temperature Ior.5°F. Stiﬂness
of neck. September 6. Cerebrospinal ﬂuid clear and contains 230 cells
per c.mm.; globulin increased. Admitted to hospital the same afternoon.
On admission, temperature 102.4°F.; pulse 130; respirations 42. Stiffness
of neck and back; no weakness or paralysis noted.

Immediately after admission 5 c.c. of serum were injected subdurally
and 40 c.c. subcutaneously. Temperature reached normal 32 hours after
treatment. No deﬁnite weakness or paralysis developed subsequently.

In this case treatment was begun about 3 days after the initial symptoms
and at a time when paralysis had not appeared. Treatment was followed

TREATMENT 143
by a rapid drop in temperature and no ‘weakness or paralysis developed
during the period of observation.

Case 22.—Female. Age 3% years. l

October 7, 1916. Fatigue, irritability, and vomiting. October 8.
Fever and a mild delirium. October I . Fever persisted; drowsiness.
Admitted to hospital. On admission, t mperature Ior.6°F.; pulse 132;
respirations 28. Stiﬂness of neck and back. Clear cerebrospinal ﬂuid
with 88 cells per c.mm. l

On October 10, 20 c.c. of serum were injected subdurally and 30 c.c. sub-
cutaneously. Temperature rose to 104°F. that night and there was slight
nystagmus. Lumbar puncture yielded A slightly turbid ﬂuid under con-
siderable pressure. About 30 c.c. of ﬂuid were withdrawn from the spinal
canal. On the following morning the nystagmus had disappeared and 36
hours after treatment the temperature reached normal. Cultures of the
turbid ﬂuid were sterile. Turbidity was due to the presence of a large
number of polymorphonuclear leukocytes. No weakness or paralysis
developed subsequent to treatment.

This patient was treated 3 days after the initial symptoms when there
was no evidence of weakness or paralysis‘, Following the treatment there
was evidence otincreased irritation of the meninges and increased pressure
in the subdural space which was relieve‘ by lumbar puncture and with-
drawal of ﬂuid. The temperature reached normal 36 hours after the
injection and the child did nOt develop any weakness or paralysis sub-
sequently. The serum used in this cllse contained considerable fat;
whether or not this played a part in the reaction following the injection
cannot be stated deﬁnitely. This was th only instance in which any such
reaction was obtained, although other cates were treated with portions of
the same serum.

Case 23.-—Male. Age 5 years. l

October 3, 1916. Vomiting. October 4. Fever; vomiting persisted.
Clear cerebrospinal ﬂuid with 2 so cells per c.mm. Admitted to hospital.
On admission, temperature Ior°F.; pulse 130; respirations 30. Stiffness of
neck and back; no weakness or paralysis.

15 c.c. of serum were immediately given subdurally and 40 c.c. subcu-
taneously. Temperature rose to 103°F. and fell to normal 12 hours later.
There was no subsequent weakness or p ralysis.

This patient was treated about 30 ho rs after what seemed to be the
initial symptoms. At the time of treatment there was no demonstrable
involvement of any muscle group. The‘temperature dropped to normal
12 hours after treatment and the child did not show any weakness or pa-
ralysis at any time. ;

Case 24.——Female. Age 1% years. -l
October 11, 1916. Temperature 101°F. October 12. Stiffness of
the neck and back with muscle tenderness. Temperature Io3°F. No

I44 ACUTE POLIOMYELITIS

demonstrable weakness. Admitted to hospital. On admission, tempera-
ture 103°F.; pulse 118; respirations 28. Clear cerebrospinal ﬂuid with 40
cells per c.mm.; globulin increased.

On October 12, 25 c.c. of serum were injected subdurally and 35 c.c.
subcutaneously. Temperature dropped to normal within 16 hours after
treatment. At no time was there any demonstrable weakness present.

This patient was treated about 30 hours after the mother ﬁrst noticed
fever, and at a time when there was no demonstrable weakness of any
muscles. The temperature became normal in less than 24 hours after
treatment. An older sister of this patient was admitted to the hospital
on the day previous to the one on which this case was admitted. The
sister had been sick for a period of 4 days with temperature as high as
104°F. She was admitted at the end of the febrile period, 4 days after
the onset, and at the time of admission lumbar puncture showed the pres-
ence of a clear ﬂuid with 76 cells and increased globulin. She received no
serum and developed no weakness or paralysis.

Case 25.——\Iale. Age 5 years.

October 5, 1916. Irritability and fever. October 6. Fever persisted;
constipation. October 7. Admitted to hospital. On admission, tempera-
ture 103°F.; pulse 104; respirations 28. Marked stiﬂness of neck and
back; active reﬂexes; positive Kernig. No demonstrable weakness of any
muscle group. Clear cerebrospinal ﬂuid with 260 cells per c.mm. ; globulin
increased. ,

On October 7, 22 c.c. of serum were given subdurally and 45 c.c. subcu-
taneously. The temperature fell to normal within 22 hours after treat~
ment and the patient did not develop any weakness or paralysis.

This patient was treated about 48 hours after onset of the ﬁrst symptoms
and within 22 hours after treatment the temperature was normal (Text-
ﬁg. 19). No weakness or paralysis developed. A younger sister of this
patient was admitted to the hospital 2 days previously with ﬂaccid pa-
ralysis of both lower extremities. In this case onset had occurred 5 days
before admission and the temperature had fallen to normal and paralysis
had already set in when she was admitted.

Case 26.—Male. Age 23 years. ‘

December 9, 1916. Vomiting and headache. Stiffness of neck, hyper-
zesthesia, and asymmetry of patellar reﬂexes. Kernig’s sign present on
right side. Temperature 101°F. No demonstrable weakness of any
muscle group. Clear cerebrospinal ﬂuid with 40 cells per c.mm.; globulin
increased.

38 hours after onset patient received 20 c.c. of serum subdurally and 100
c.c. intravenously. Following treatment the temperature fell to normal
within 48 hours, the hyperaasthesia disappeared within that time, and no
paralysis or weakness developed.

This patient, an adult, was treated within 38 hours after the initial

\

REFERENbEs 145

1
symptoms at a time when there was no demonstrable involvement of the
muscles. His temperature rapidly fell‘to normal, and no weakness or
paralysis developed subsequently. ‘

The more important facts relating to the twenty-six cases described are
collected in Table I.

REFEREN$ES

1 MICHEAL UNDERWOOD: Treatise on Diseases of Children, Phila., 1793.

2JOHN BADHAM: London Med. Gazette 1835, XVII, 215.

3 JAC. v. HEINE, Stuttgart, 1840. l

‘ A. STRUMPELL: Deutsch. Arch. f. KlinJ. Me(l., 1891, 47—53.

5 MEDIN: Arch. med. des enfants, 1898,11—257, 321.

6VVICKMAN, Berlin, 1905.

7 MiiLLER, Berlin, 1910.

8 ZAPPERT, WIESNER and LEINER, Leipsic & Wein, 1911.

9 PROVOST and VULPIAN: Compt. rend. tie la Soc. de Biol., 1865.

1° CHARCOT and JOFFROY: Archives de ,physiologie normale et patholo-
gique, 1870.

11 ROGER and DAMESCENO: Compt. rend.‘ de la Soc. de Biol., 1871.

‘2 RISSLER: Nord. Med. Ark., 1888, XX,l1.

‘3 WICKMAN: Lac. cit. ,

” STRAUSS: The Pathology of Acute l’oliomyelitis. Rep. of Collective
InvestigationComm. on the New Ydrk Epidemic of 1907. p. 68.

15 HARBITZ and SCHEEL: Pathologisch—anhtomische untersuchungen iiber
akute Poliomyelitis, Christiana, 1907, .

'6 WICKMAN: Die Akute Poliomyelitis, e‘tc., Handbuch der neurologie,
Berlin, 1911.

1““ FLEXNER, PEABODY and DRAPER: Jouln. Am. Med. Ass’n, 1912.

1" LANDSTEINER and POPPER: Zeitsehr. f. [Immunitats forsch. Orig., 1909,
II, 377' ‘

‘3 FLEXNER and LEWIS: Journ. Am. Med.,Ass’n, 1909, III, 2095.

19 LANDSTEINER and LEVADITI: Compt. Rend. Soc. de Biol., 1909, 7, XVI,
592-

20 LEINER and VON WIESNER: Wien. Klin. Wochenschr, 1909, XXII, 1698.

2‘ LANDSTEINER and LEVADITI: Compt. ren‘d. Soc. de Biol., 1910, LXVIII,
311.

22 FLEXNER and LEWIS: Journ. Am. Med.‘Ass’n, 1909, L111, 1639.

”3 FLEXNER and NOGUCHI: Journ. Exp. Med, 1913, XVIII, 461.

’4 R. W. LOVETT and M. W. RICHARDSON:,Bull. Mass. State Med. Bd. of
Health, 1911, p. 55.

25 C. S. CAVERLY: Bull. Vermont State Bd. bf Health, 1914, XIV, 3.

26 Report of Med. Director of Mayor’s Special Comm., 1917.

27 H. L. Amoss and ED. TAYLOR: Journ. Ex . Med. 1917, XXV, 507.

28 MATHERS, G.: Journ. Am. Med. Ass’n., 1916, XVII, 1019. Journ. In-
fectious Diseases, 1917, XX, 113. l

10 l

I46 ACUTE POLIOMYELITIS

2" ROSENOW, E. C., TOWNE, E. B. and WHEELER, G. W.: Journ. Am. Med.
Ass’n, 1916, XVII, 1202.

3" PHIL. A. E. SHEPPARD: N. Y. State Journ. of Med., 1916, XVI, 442.

31 Report of New York City Department of Health, 1917.

3’ FLEXNER, CLARK and FRAZIER: Journ. Am. Med. Ass’n, 1913,LX, No. 3.

3“ KLING, PETTERSSON and WERNSTEDT: Rep. of State Med. Institution
of Sweden to XVth International Congress on Hygiene and Demo-
graphy, Washington, 1912.

3‘ KLING, PETTERSSON and WERNSTEDT: Lac. cit.

3‘ FLEXNER and AMOSS: Journ. Exp. Med, 1917, XXV, 539.

3" FLEXNER and Amoss: Journ. Exp. Med., 1914, XX, 249.

37 FLEXNER and AMoss: Journ. Exp. Med, 1917, XXV, 525.

“9 FLEXNER and LEWIS: Journ. Am. Med. Ass'n, 1910, LIV, 45.

‘0 NETTER, JENDRoN and TOURAINE: Compt. Rend. des Séance de la Soc.
di Biologic, 1911, 70, 625.

“ NETTER, A.: Bull. Acad. Med, 1915, LXXIV, series 3. 403.

“NETTER, A.: and SALANIER, 1\I., Bull. et mém. Soc. med. hop, Paris,
1916, XL, series 3, 299.

‘3 R'oMER and JOSEPH: Munch. Med. Woch., 1910, LVII, 568.

“LEVADITI and LANDSTEINER: Compt. Rendu. Soc. Biol., 1910, LXVIII,
311.

‘5 FLEXNER and LEWIS: Journ. Am. Med. Ass‘n, 1910, LIV, 1780 and LV,
662.

‘5 BLANTON, W. B.: Journ. of Med. Research, 1917, XXXVI, 1.

‘7 AMoss and CHESNEY: Journ. Exp. Med., 1917, XXV, 581.

‘3 ZINGHER, ABRAHAM: Journ. Am. Med. Ass’n, 1917, LXVIII, 817.

‘9 ANDERSON, J. F.: and FROST, W. H.: J. Am. Med. Ass’n, 1911, LVI,
663.

5" ZINGHER, A.: Journ. Am. Med. Ass’n, 1917, LXVIII, 817.

5’ PEABODY, F. W.: Boston Med. Surg. Journ., 1917.

52 M011: Lancet, London, 1910, II, 79.

53FLEXNER, S.: Journ. Am. Med. Ass’n, 1913, LXI, 447 and 1872.

lNDliEX

After care, 103
Ataxia, 64

B

Badham, John, I

Blood, 70
differential count, 70
virus in, 25

Bone marrow, virus in, 25

C

Carriers, 16, 20
barnyard fowls, 20
healthy, 16
insects, 20
pet animals, 20
rodents, 20
Case reports 44—61, 103-145
diagnostic series, 44~61
treatment series, 103—145
Cases, mild, 67
Cell count, 71
prognostic signiﬁcance, 72, 73
Cerebrospinal ﬂuid during systemic
phase, 71
cell count, 71
globulin, 71
lange colloidal gold, 71
types of cells, 71
Wassermann reaction, 71
Charcot, 3
Choroid plexus, 26
Clinical classiﬁcation 38, 42, 43
dromedary type, 40
straggling type, 40
sudden onset type, 40
Constipation, 69
Culture media, 29

D
IiDamescino, 3
Diagnosis of paralysis, 78
Diagnostic series, 44-61
Diarrhoea, 62

graper, 3
rowsiness, 67
l E

limotional instability, 76
pridemiology, I 3
group immunity, 20
l milk and food, 22
seasonal occurrences, 17, 18
i winter epidemic, 19
Ftiology, 6
Bixpression, 63
Eyes, 63

i F

Femily susceptibility, Io
Fever, 62, 65, 69
Flexner, 4, 28

l G

Gﬂolmid bodies, 29
()flobulin, 71

, H

Hrarbitz, 3
Heine, 1
Hpspitalization, 87

l I

Immune serum, 28
Flexner, 28
i Lewis, 28
Netter, 28
‘ neutralization test, 28

I48

Immune serum, human, 88
hemoglobin, 88
preparation, 88
red cells, 88

Immunity, active, 28
acquired, 28
passive, 28

Immunity, group, 20

Immunity of previously infected

areas, 21

Infection, propagation of, 4

Infections, contact, 14, I5, 19
group, x4, 15

Injection, time of intraspinal. Ioo

Isolation, 4

I
J offroy. 3

K
’Kissing, 87

L

Landersteiner, 4

Lange gold test, 71

Leiner, 4

Levaditi, 4

Lovette, 103

Lumbar puncture, 88
technique, 88
multiple, 41, 66

Lymph nodes, 68

M

Medin, 2

Meningo-choroid defense, 26
Monkeys, transfer to, 4
Muller, 3

Muscular twitching, 64

N

Nasal irrigation, 85
Nettcr, 28
Neurophage, 31
Neutralization test, 28
Noguchi, 4

INDEX

0

Opisthotomes, 67

Organism, the, 4, II
cultivation and isolation, 4

Oxydase reaction, 35

P

Pain, 68
Paralysis, 75
as central thought, 4
diagnosis, 78
prognosis, 81
progressive, 76
respiratory muscles, 78, 80
Pathology, 30
in experimental disease, 30
in human disease, 35
parenchymatous lesions, 31
Peabody, 3
Pharynx, inﬂammation of, 62
mucous membrane of, 25
Popper, 4
PrognOsis, 81
psychic state in relation to, 82
value of spinal ﬂuid in, 83
Propagation of infection, 4
Prophylaxis, 85
ﬁeld work, 87
hand-washing, 87
hospitalization, 87
kissing, 87
nasal irrigation, 85
quarantine, 86
community, 86
individual, 86
sneezing, 86
Provost, 3
Psychic disturbances, 76

R

References, 145

Reﬂexes, 68

Respiratory paralysis, 78, 80
Rissler, 3

Roger, 3

Scheel, 3
Serum of recovered cases, 38
Spinal ﬂuid, 25
Spleen, 25
Strauss, 3
Strumpell, 2
Susceptibility, individual, 6
age, 9
family, 10
physical type, 6, 8
race, 7, 8
sex, 6
Symptoms, 62
ataxia, 64
circum orbital puﬂiness, 63
diarrhoea, 62
fever, 62, 65, 69
Kernig’s sign, 64
muscular twitching, 64
pharyngeal inﬂammation, 62
shrugging gesture, 63
spine sign, 64
stiﬁ neck, 64
stupor, 64, 76
universal over-stimulation, 64
vomiting, 62

INDEic I49
l
Syphilis of the central nervous sys-
tem, 65
Sbstemic phase, 41
l T
lionsils, 25
l
‘ V
V‘irus, behavior toward chemical
agents, 24

physical agents, 23
l distribution of the tissues, 25
methods of inoculation, 24
nature of, 23
l portal of entry, 24
, of exit, 24
viability, 20
meiting, 62
vtbn Wiesner, 4

‘ W
Wassermann reaction, 71
ickman, 2
Winter epidemic, 19
l 2

Zaippert, 3
l

  

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