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Nervous and Mental Disease Monograph 

Series, No. i6 





of Stockholm 

'I ■ 

Authorized English Translation by 
DR. J. WM. J. A. M. MALONEY, F.R.S.Ed. 








Edited liy 

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z. Outlines of Psychiatry. (4th Edition.) I3.00. 

By Dr. WiUiam A. WUte. 
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By Dr. C. Q. Jung. 

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(ad Edition.) $2.50. By Prof. Bigmund Preud. 

5. TheWassermannSerumDiagnosisinPsychiatry. $a.oo. 

By Dr. Pellz Plant. 

6. Epidemic Poliomyelitis. NewTork,r907. (Outof Print.) 

7. Three Contributions to Sexual Theory. $a.oo. 

By Prof. Sigmund Preud. 

8. Mental Mechanisms. |a.oo. By Dr. Wm. A. White. 

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ro. Handbook of Mental Examination Methods, fa.oo. 

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13. History of Prison Psychoses. $1.35. 

By Drs. P. Nitsche and K. Wilmanns. 

14. General Paresis. I3.00. By Prof. E. Kraepelin. 

15. Dreams and Myths, fz.oo. By Dr. Karl Abraham. 

z6. Poliomyelitis. I3.00. Dr. I. Wickmann. 

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Copyright, 1913, by 
The Journal of Nervous and Mental Disease 
Publishing Company, New York 


The new Era printing Company 
lancaster. pa 



Introduction i 

Pathological Anatomy 13 

Pathogenesis - 29 

Symptomatology 38 

Symptomatology 61 

Diagnosis and Differential Diagnosis "84 

Prognosis 91 

Epidemiology 99 

Prophylaxis and Therapy 120 

Literature 126 

• • • 



Acute Poliomyelitis 




Historical Review. — ^Acute poliomyelitis, for many years known 
as infantile paralysis, has so often of late appeared in epidemic 
for;n that our knowledge of it has been consid^prably amplified. 
We have learned that acute poliomyelitis is much more protean 
in its manifestations than was formerly taught. So variable has 
it shown itself, that even clinicians of wide experience doubt the 
identity of epidemic infantile paralysis with the classical malady 
in which only sporadic cases appeared. 

Wickman has suggested that all forms of disease arising from 
the same virus as acute poliomyelitis should be grouped under the 
one term — ^Heine-Medin's Disease. This nomenclature has been 
adopted, especially in Germany and Austria, by many with consid- 
erable experience in the recent epidemics. 

Infantile paralysis was mentioned first by Underwood at the 
end of the eighteenth century. The credit of diflferentiating the 
disease from more or less similar conditions of cerebral origin 
belongs to Heine, who in 1840 published his masterly article on 
this disease. Duchenne, later, demonstrated the behavior of the 
affected muscles to faradic, and Erb, to galvanic stimulation. 
Surprisingly little further progress in our clinical knowledge was 
made until Medin published his celebfated observations on the 
Stockholm epidemic of 1887. Medin recognized, in addition to 
the already familiar spinal form, a bulbar, a polyneuritic, an 
ataxic and an encephalitic type. The last, from theoretical con- 
siderations, had previously been foreshadowed by Striimpell and 
Pierre Marie. The clinical significance of Medin's work re- 


mained almost unappreciated until the accumulated evidence from 
the recent epidemics emphasized its enormous value. 

The first of these great epidemics appeared in 1905 almost si- 
multaneously in Norway and Sweden. , Wicjcman fully reported 
the Swedish epidemic. He distinguished several new types, — a 
meningitic, an abortive, and a form resembling Landry's paralysis. 
The basis of Larldry's paralysis he found sometimes to be an acute 
poliomyelitis ; but he further noted — what until then had not been 
recognized — that most fatal cases run a course closely resem- 
bling that of a Landry's paralysis. His observations showed that 
the disease was a general infection with specific localization in the 
nervous system. Wickman's work was followed by that of Lee- 
gaard (1909), upon the Norwegian epidemic of 1905; by that of 
Zappert and others (1909),, upon the Austrian epidemic of 1908; 
by theVeport of the American School (1910), upon the New York 
epidemic of 1907 ; and by a particularly valuable contribution from 
Ed. Miiller (1910), upon the Hesse-Nassau epidemic of 1909. 

Although Prevost and Vulpian, in 1865, had described atrophy 
of the anterior horn and of the motor ganglion cells in a case of 
infantile paralysis in which the acute stage of the disease was long 
passed; and Roger and Damaschino, in 1871, had reported the 
changes in the stage of recovery; Rissler, in 1885, was the first 
to give a comprehensive description of the pathologic-anatomical 
processes of the acute stage. He demonstrated the inflammatory 
reaction in the blood vessels and also the degeneration in the 
ganglion cells. Later, isolated cases were reported by Dauber, 
Goldscheider, Siemerling, Redlich, and others. Wickman, in 1905, 
published the first work comprising a large series of recent cases. 
By his, and by the subsequent investigations of Forssner, Sjovall, 
Harbitz and Scheel, Marburg, Beneke, Strauss and others, the 
pathological anatomy of the acute stage was conclusively demon- 
strated to be an acute meningoencephalopoliomyelitis. 

Thanks, not only to the researches above mentioned, but also 
to those of Charcot and Joffroy, Roth, Fr. Schultze, and others, the 
changes in the chronic stage, however, had then long been known. 

The first attempt to explain the morbid process was made by 
Charcot. He conceived it to be a primary degeneration of the 
ganglion cells with secondary involvement of the vessels. This 
was a simple and apparently adequate conception and it confofmed 


to the clinical picture presented by the malady. Most observers 
of recent cases — which were just beginning to be recognized-^ 
believed the process to be a true inflammation. Some regarded 
the degeneration of the ganglion cells as a sequel to the inflamma- 
tion, while others looked upon the degeneration and the inflam- 
mation as simultaneous processes. Following the lead of Pierre 
Marie, most considered that the anterior horns were always 
affected because of implication of the arteria centralis. Wick- 
man, on the other hand, maintained the lymphatic spread of the 
disease, and the latest experimental researches confirm the cor- 
rectness of his opinion. 

Very inexact ideas were prevalent concerning the nature of the 
disease until Striimpell and Pierre Marie, from its general char- 
acter and its onset with fever, recognized it to be an infection. 
Their opinion was supported by the 'fact that infantile paralysis 
sometimes appeared in epidemics. 

The first epidemic of infantile paralysis to be described was 
that reported by the Swedish physician, Bergenholtz, in 1881. 
Subsequently, several others were recorded, but most of them 
consisted of relatively few cases. The most celebrated were 
those which occurred in 1887 and 1895, in Stockholm. They 
were reported by Medin. Neither in these, nor in any other out- 
break, however, was it possible to ascertain how the disease 
spread. During the Swedish epidemic of 1905, through the ob- 
servation of indisputable abortive forms," and through the study 
of all possible means of communication, Wickman succeeded in 
proying that Heine-Medin's disease spreads from person to per- 
son in exactly the same way as other contagious maladies. This 
has, in subsequent epidemics, partly been confirmed by Ed. 
Miiller, P. Krause and others. 

Although many problems of this malady have been elucidated, 
many are still unsolved. The cause of the disease is not yet 
known. Of late years, quite a number of very interesting experi- 
mental investigations of poliomyelitis in monkeys have been pub- 
lished and have greatly increased our knowledge of this disease. 
Landsteiner and Popper were the first successfully to infect mon- 
keys. From the work of Flexner and Lewis, Landsteiner and 
Prasek, Knopf elmacher, Leiner and Von Wiesner, Romer, Romer 
and Joseph, Levaditi and Landsteiner, Netter and Levaditi, and 


others, we must conclude that the cause of acute poliomyelitis 
does not belong to the class of the common bacteria, but is a 
filterable virus, and is present in the spinal cord. 

Epidemic and Sporadic Acute Poliomyelitis, — It may not be 
inappropriate to refer here to the relation between epidemic and 
acute poliomyelitis. Some assert that both conditions are not 
identical. The following are the principal reasons for this as- 
sertion: (a) the clinical picture of Heine-Medin's disease is much 
more variable than that of the classical infantile paralysis; (b) in 
a number of cases of the former disease the cranial nerves are 
specially involved, whereas cranial nerve lesions usually do not 
occur in infantile paralysis; (c) adults are more liable to be at- 
tacked in epidemic poliomyelitis ; (d) sporadic poliomyelitis seldom 
runs a lethal course, whereas the epidemic variety has a consid- 
erable mortality; (e) and, finally, the epidemic occurrence itself 
is a characteristic distinction. 

The difference in symptomatology is more apparent than real. 
Obviously very different opportunities for clinical observation 
exist when hundreds of cases can be examined together than 
when only isolated cases are available from year to year. In 
epidemics, connections can be clearly traced between symptom 
complexes, which in isolated cases may appear unrelated, and the 
fact must be emphasized that the spinal type (the classical infan- 
tile paralysis) forms the nucleus of Heine-Medin's disease. From 
the most recent observations as to the localization of the paralysis, 
it is evident that the extremities — especially the legs — are oftenest 
affected. No doubt of the complete correspondence of the dis- 
ease with the ancient infantile paralysis can endure. The changes 
in the acute and chronic stages have been shown to be absolutely 
identical in both. Netter and Levaditi have procured further and 
remarkably interesting evidence. They were able to prove in a 
case of sporadic acute poliomyelitis in which the acute stage had 
occurred three years previously, that the serum " in vitro " de- 
stroyed the virus of the epidemic poliomyelitis. 

I wish, nevertheless, to refer here to certain peculiarities of 
Heine-Medin's disease, and to some circumstances which may ex- 
plain why the epidemic and the sporadic forms have been regarded 
as distinct. 

Heine-Medin's disease shows a striking variability whfch is 


evident not only in the different epidemics ; not only in the various 
foci of the same epidemic; but also even in the different cases 
within a single focus. Its protean character may be gathered 
from the reports of different observers. Thus, one observer sees 
none but the typical ; while another, of mature experience, reports 
a number of atypical cases. I can refer to no better examples than 
Medin, Nonne and Spieler, who, according to present ideas, had 
at their disposal very scanty material and yet recorded unusual 

Later I shall also show that the prognosis of sporadic acute 
poliomyelitis and that of epidemic acute poliomyelitis differ rela- 
tively less than was formerly alleged ; and that the epidemic beha- 
vior is in no way distinctive, as was shown by my observations 
upon the Swedish epidemic, and presents all possible degrees 
from apparently isolated sporadic to accumulated and more or 
less pronounced epidemic cases. The map of the distribution of 
acute poliomyelitis in the Swedish outbreak shows that the disease 
occurred in foci, within each of which usually a continuity of 
spread could be demonstrated. Such was the case in those parts 
of the country in which the disease appeared not in epidemic form 
but only as isolated sporadic cases. From what I have said there 
can be little doubt that epidemic and sporadic poliomyelitis are 
one and the same disease. 

Etiology. — Infantile paralysis has from earliest times been at- 
tributed to a variety of causes; e. g., trauma, cold, teething, etc. 
Infectious diseases, such as scarlet fever, measles, and pneumonia, 
rarely were alleged to be the cause, and a belief arose that under 
certain circumstances their toxins could produce infantile paralysis. 

In 1887, Striimpell — and later Pierre Marie — stated that in- 
fantile paralysis was a disease per se, independent of other infec- 
tious maladies. Experimental research and the study of epidemics 
have since adequately confirmed this statement. Naturally, a 
specific organism was early sought but as none was found either 
in cultures or in spinal cord sections, the morbid changes were 
attributed to the action of a toxin. During the last decade several 
microorganisms from the spinal fluid in this disease have been 
announced. Fr. Schultze, Concetti, Looft, Dethloff and others 
whose examinations were restricted to single cases, and Geirsvold 
and Potpeschnigg who investigated large series, all reported such 


findings. Usually an organism resembling the Weichselbaum 
micrococcus was incriminated. Other investigators with similar 
material have however failed to obtain corroborative evidence of 
these discoveries. The efforts to demonstrate organisms in sec- 
tions of affected tissues have likewise proved unsuccessful. Bon- 
hoff by means of the Mann stain demonstrated in the glia cells, 
bodies which he alleges to be specific. The results of experi- 
mental investigation have shown that the bacteria found have 
absolutely nothing to do with Heine-Medin's disease, and that in 
those cases in which they arose not from faulty technique, such 
bacteria must be regarded as having had an accidental and not a 
causal relation to the malady. 

Experimental Poliomyelitis in Monkeys. — Before discussing 
the recent successful inoculation experiments in monkeys, I shall 
first refer to earlier experimental researches upon acute polio- 
myelitis. Roger, Gilbert and Lion, Vincent, Enriquez, and Hal- 
lion ; Thoinot and Masselin, Crocq fils ; Ballet, Charrin, and Qaude 
have produced poliomyelitis with various bacteria. But as I have 
already mentioned no one has succeeded in reproducing more than 
a vague semblance of the disease. I, myself, notwithstanding the 
extensive material employed, could obtain only negative results 
with streptococcal injections. The time has fully arrived when 
such experimental investigations should be discarded from the 
literature of this disease. 

Landsteiner and Popper were the first experimentally to repro- 
duce indisputable poliomyelitis. They took a piece of the spinal 
cord of a boy who had died of acute poliomyelitis and introduced 
it into the peritoneal cavity of a monkey. They were able to re- 
produce a disease characterized by paralysis and associated with 
the pathologic-anatomic changes of acute poliomyelitis. The re- 
sults of Landsteiner and Popper were extended and corroborated 
by several observers. Similar investigations by Landsteiner and 
Prasek, Flexner and Lewis, Knopf elmacher, Leiner and von Wies- 
ner, Romer, Romer and Joseph, Levaditi and Landsteiner, and 
Netter and Levaditi were carried out about the same time "prac- 
tically independently of each other. 

It should be mentioned, in passing, that similar experiments 
have been made with many other animals, but no constant results 
have been obtained. Thus, Flexner and Lewis — who have done 


most work in this field-— failed in numerous experiments to cause 
the disease* by intracerebral inoculation of guinea pigs, rabbits, 
horses, calves, goats, pigs, sheep, rats, mice, dogs, and cats. Most 
observers have found animals other than monkeys to be refrac- 
tory. But Krause and Meinecke, also Lentz and Huntemiiller, 
have reported as many successful transmissions in rabbits by in- 
oculation through the blood stream, as in monkeys by intraspinal 
inoculation. Insignificant pathologic-anatomic changes were found 
in the spinal cord of the rabbits. Meinecke explains most of the 
negative results of other experimenters on the grounds of varia- 
tion in the susceptibility of different breeds of rabbits and of in- 
sufficiency in the amount of the infective material injected. 
These features are, however, negligible factors in monkeys in 
which a minimal dosie suffices to produce the disease. It seems to 
me, with so many contradictory statements about poliomyelitis in 
rabbits, that until we have further information only monkeys 
should be used for clinical research purposes, for= failure to repro- 
duce the disease by inoculation is in them exceptional. 

The clinical picture of monkey poliomyelitis corresponds very 
closely to that in man. The most important distinctions are the 
absence in monkeys of the initial fever, and the frequency with 
which the disease is characterized throughout its course in them 
by subnormal temperature. Prodromal symptoms sometimes 
usher in the paralysis but are often absent. The paralytic signs 
develop in rapid succession. The brunt of the attack falls upon 
the legs; and a flaccid paralysis develops which is characterized 
by atrophy and loss of reflexes. The mortality among monkeys 
is very high. In Flexner and Lewis' experiments the death rate 
among 8i monkeys was 54.3 per cent. According to these ob- 
servers the incubation period, from the injection until the onset 
of paralysis, is 9-10 days; its minimum is 4, and its maximum 
33 days. 

The pathologic-anatomic picture — apart from the results of 
Leiner and von Wiesner — corresponds with that which we find 
in man. The most important results yielded by experimental in- 
vestigation are, however, those which relate to etiology and path- 
ogenesis. Examination of sections of human and of monkey's 
tissues and the study of the cerebrospinal fluid, blood, etc., by 
every conceivable method have given uniformly negative results. 


These failures led many to the belief that poliomyelitis is a tox- 
aemia. Experimental investigation has now proved the incorrect- 
ness of this belief. The virus occurs in the spinal cord. By 
injecting virulent material into the brain the spinal cord is made 
virulent and we can then reproduce the disease in monkeys by 
intracerebral inoculation with this virulent spinal cord tissue. 
The virus has thus been propagated through many generations of 

The virus shows a special affinity for the spinal cord. Wher- 
ever it be injected it will be found mainly localized in that organ. 
But it has not been demonstrated in the blood, spleen or any other 
organ of the monkey. Yet it seems to be eliminated by several 
channels, for after intracerebral injection it has been found in 
the salivary and mesenteric glands and in the nasal mucous mem- 
brane. In the spinal cord its potency is preserved for some time 
but soon diminishes and finally disappears; at least Levaditi and 
Landsteiner observed that the spinal cord about six weeks after 
infection was no longer virulent. 

The interesting fact has, moreover, been established that the 
virus of acute poliomyelitis cannot be classed among the common 
bacteria, for it passes through bacterial filters such as the Berk- 
feld. When fluid containing ordinary bacteria is so filtered, the 
filtrate is sterile: in poliomyelitis the filtrate is infective; hence the 
virus belongs to that class which we usually designate filtrable. 
It closely resembles, in many of its characters, the virus of rabies. 
One property which both enjoy is resistance to the action of 
glycerin. This resistance distinguishes them from all ordinary 
bacteria. Romer and Joseph found the virus after almost five 
months in undiluted glycerin potently infective; but other ob- 
servers have recorded an attenuation of the virulence under simi- 
lar conditions. 

The poliomyelitis virus is also markedly resistant to other 
agents. Flexner and Lewis, for example, found the infectivity 
still preserved after exposure for forty days to a temperature of 
from — 2° to — 4° Celsius; and, after fifty days, at — 4° C. 
During the exposure autolysis appeared in the preserved pieces of 
the cord which were covered with mould, and yet the virus re- 
mained unimpaired. Even to drying, the virus is most resistant. 
The experiments of Leiner and von Wiesner show, however, that 


if the virus be allowed to dry in thin layers of infected tissues, if 
it be allowed to desiccate therefore under conditions which ap- 
proximate to actual experience, it rapidly decreases in virulence. 
The poison is more sensitive to high than to low temperatures. 
At 55 "* C. it loses its virulence, and at 45° C. it is perceptibly 

Much of the experimental research has been directed towards 
the question of acquired immunity and many interesting facts 
have been discovered. Flexner and Lewis, Landsteiner and Leva- 
diti, and Romer and Joseph demonstrated that monkeys which 
recovered frdm one infection with the virus of poliomyelitis are 
immune. According to Joseph and Romer this immunity is pres- 
ent even when the first infection produces no clinical symptoms. 
Moreover, antibodies can be demonstrated in the blood of such 
immune monkeys. These Antibodies can neutralize the action of 
the virus in vitro (Romer and Joseph, Landsteiner and Levaditi, 
Flexner and Lewis). Netter and Levaditi, and Flexner and 
Lewis have further shown that in the serum of children who have 
recovered from infantile paralysis, antibodies are present; and 
Netter and Levaditi have also established that these antibodies 
can be demonstrated in the abortive forms of the disease. Wol- 
lenstein, Romer and Joseph, and others failed, however, to demon- 
strate the presence of amboceptor (komplementbinden Antikor- 
per) in the cerebrospinal fluid or in the blood serum of patients 
who were suffering from, or who had recovered from poliomye- 
litis. From similar investigations on monkeys they obtained neg- 
ative results. Romer and Joseph call attention to the fact that 
if in highly immunized animals this absence of amboceptor is 
shown to occur, the analogy already recognized between polio- 
myelitis and rabies would be reinforced; for amboceptor has not 
as yet been demonstrated in rabies. 

In has already been stated that no culture has been obtained 
from the spinal cord. Flexner and Lewis and Levaditi have, how- 
ever, given us an impulse to the further study of the propagation 
of the virus outside the body for in bouillon prepared from the 
clear, bacterial- free, virulent spinal cord filtrate they have seen 
arise a cloudiness which was not due to any contaminating bac- 
teria. With the aid of Borrel's modification of the Loffler method, 
Levaditi thought that he further observed in the cloudy bouillon 



minute staining bodies of oval form. Romer and Joseph have 
found in examining these filtrates (Berkfeld) by means of the 
ultramicroscope, extremely small round oval bodies which were 
not demonstrable in the filtrates from normal spinal cords. 
Benecke, and Krause and Meinecke have also published similar 
results which they obtained in working with the blood of infected 
children. The results of experimental research in pathogenesis 
and other matters will be dealt with later. 

Predisposing Factors. — From our experience of conditions in 
epidemics and from the results of experimental research, we are 
compelled to regard Heine-Medin's disease as a specific infection. 
A number of cases have been observed in which the disease has 
developed during the course of a common infectious malady. It is 
extremely probable that such cases are merely coincidences, and 
that the infectious malady is to be regarded in them only as an 
agent in the production of the favorable moment for the polio- 
myelitis invasion. 

There is practically only one predisposing factor — ^the age. 
As is emphasized in the name, infantile paralysis, the disease usu- 
ally attacks children. In order to show the incidence of the dis- 
ease at different age periods, I shall quote some figures from 
various epidemics : — 







Sammelbericht. ... 



Lindner u. Mally. 

Stockholm, 1887, 1895 
Stockholm, 1899 
G6teborg, 1903 
Schwedcn, 1905 
New York, 1907 
Massachusetts, 1908 
N.-Osterreich, 1908 
O.-rtsterreich, 1908 
Osterreich, 1909 
( Steiermark ) 



^ ! 











183 214 


















■ ft ■ 










• • • 


• • • 


• • • 























Leegaard during the two epidemics he reported found the fol- 
lowing figures : — 


0-4 Years 




i(» t4 Vrars 


Over 15 Years Total 

30 54 

179 794 



The experience of Ed. Miiller in Hesse-Nassau was that not 
less than 96 per cent, of the total cases occurred within the first 
decade. Children over five years of age were relatively seldom 
affected : nine tenths of the cases occurred in those less than five 
years old. The disease incidence was markedly greatest in the 
latter half of the second yeiar. Gases in the second or third 
decade were quite exceptional. Of seventy-six sporadic cases 
collected by Byrom Bramwell, forty-one occurred between o and 
3 years; eighteen between 3 and 6; four between 6 and 9; one 
between 9 and 12; and four between 12 and 15; five were over 
15 ; and in three the age was not ascertainable. 

Heine-Medin's disease is therefore principally a disease of 
childhood. Celebrated writers have even stated that acute polio- 
myelitis does not occur in adults. But the statistics of Wickman 
and Leegaard, however, show that adults are by no means im- 
mune. Fr. Schultze, Rissler, Taylor, van Gehuchten, Wickman 
and others had already by pathologic anatomic examinations 
proved that the disease affects adults. Wickman saw a man of 
46 years suffering from a typical attack, while his nine children 
living in the same house with him remained unaffected. It is 
possible that conditions change from epidemic to epidemic, so 
that the frequency of attacks upon adults varies. On the other 
hand, the great diversity of existing statements upon this point 
may partly be due to a lack o£ uniformity in the thoroughness 
of the reports. 

Besides the age, no other predisposing factor is positively 
known to us. As regards sex, the cases during the various epi- 
demics, of which I have data, occurred as follows : 

Medin (1887) 


Leegaard (1899) 

Wickman (1899) 

Wickman (1903) 

Wickman (1905) 

Leegaard ( 1905) .^ 

Zappert (1908) 

Lindner and Mally (1908)... 

Lovett (19071 

Lovctt (1908) 

Emerson (1908) 

Ed. Mailer (1909) 


These figures show that the male sex is somewhat oftener 
attacked than the female. But the source of this difference eludes 
us. Of Byrom Bramwell's cases, 43 per cent, were male ; 56 per 
cent, female. 

Dejerine has asserted that a neuropathic disposition is an im- 
portant etiological factor in the development of acute poliomye- 
litis. Wickman, Medin and Leegaard, however, could not sub- 
stantiate this assertion. 

Even when I elicited proof of a neurotic tendency in a patient's 
family, I could not attribute any causal significance to it. Ed. 
Miiller also calls attention to the fact that in his experience the 
children affected by acute poliomyelitis were free from neuro- 
pathic taint, and, as a rule, were physically and mentally normal. 
Johannessen, however, found various mental diseases among the 
families in several of his cases. 

Occasionally, infantile paralysis has been reported in those 
whose relatives (uncle and aunt) had previously been affected 
(Wickman, Fiirntratt). Leegaard attributes a certain importance 
^to chills and reports strikingly numerous cases which followed 
exposure to cold and wet. Perhaps, however, we ought rather to 
consider such exposure as belonging to the general condition 
under which the people live. It is difficult to determine if over- 
exertion is a predisposing cause, but I am convinced that at least 
once the disease has begun, over-exertion has an unfavorable 
influence upon its further course. 

Hochhaus and others have occasionally observed the disease 
to follow vaccination. This association is most probably accidental. 

Finally, an acute atrophic paralysis may rarely arise from a 
variety of causes other than the virus which produces Heine- 
Medin's disease. A few cases are recorded of acute poliomyelitis 
probably due to syphilis ; e. g,, J. Hoffmann's case. Some may be 
classed as cases of partial transverse myelitis. Typical Heine- 
Medin's disease has been observed to develop in a case of an ex- 
isting luetic infection. Injury may cause a hematomyelia local- 
ized to the anterior horns, and thus simulating acute poliomyelitis 
(Beyer) ; but the history and onset serve readily to identify this 


Pathological Anatomy 

To understand the various clinical forms of the disease, an 
exact knowledge of its pathological anatomy is indispensable. As 
research in recent years has enabled us definitely to ascertain the 
nature of the morbid changes, I shall in this chapter somewhat 
fully discuss them, particularly those peculiar to the acute stage. 

A. Acute Stage, — ^As far as I know, the following are the ob- 
servers who have published reports upon the acute stage. 

Rissler (1888) 3 cases (s-8 days). 

Dauber (1893) i case (5 days). 

Goldscheider (1893) i case (12 days). 

Siemerling (1894) i case (8 days). 

Redlich (1894) i case (10 days). 

Bickel and Roeder (1898) i case (12 days). 

Biilow-Hansen and Harbitz (1899) 2 cases (resp. 5 and 7 days). 

Matthes (1899) i case (8 days). 

Monckeberg ( 1903) i case ( 12 days) . 

Batten ( 1904) i case (.13 days) . 

Schmaus ( 1905) i case (3 days) . 

Neurath (1905) i case (2 days). 

Wickman (1905 and 1910) 14 cases" (2-9 days). 

Forssner and Sjovall (1907) 2 cases (resp. i and 2 days). 

Harbitz and Scheel (1907) 13 cases (2 and 10 days). 

Barnes and Miller (1907) 13 case (8 days). 

Cadwalader ( 1908) 3 cases (3-6 days) . 

Marburg ( 1909) 6 cases. 

Hoffmann (1909) i case (7 days). 

Hochhaus ( 1909) 2 cases (each 2 days) . 

Strauss ( 1910) 8 cases (2-13 days) . 

Benecke ( 1910) 3 cases. 

Pirie ( 1910) i case (5 days) . 

Marchand ( 1910) i case. 

Macroscopic C/taw^^.?.— tAs Heine-Medin's disease is an infec- 
tious malady, symptoms of a general infection are to be expected. 
Enlargement of the spleen has been present in some cases; and 
sometimes, cloudy swelling, even distinct inflammation, appears 



in the kidneys. Rarely, subpericardial and subpleural hemor- 
rhages have been observed, which may, in part at least, have arisen 
from terminal respiratory conditions. More often, a hyperplasia 
of the lymphoid tissue of ,the intestines occurs. Rissler was the 
first to describe the enlargement of Peyer's patches and of the 
solitary follicles. It is doubtful whether this lymphoid reaction 
is due to a local or to a general action of the virus. Beneke ob- 
served moderate enlargement of the tonsils with suppuration. 

But the important and essentiar characteristics of the disease 
are the changes in the central nervoUs system^ 

The cerebrospinal fluid was found always clear and often in- 
creased. The only noteworthy change in the pia mater was 
hyperemia. No cellular exudate was ever noticed, in spite of the 
fact that microscopic investigation, showed implication of the pia 
mater. Rissler reports two cases of hyperemia of the dura», also, 
with hemorrhages upon its external surface. 

The changes in the spinal cord are usually obvious to the un- 
aided experienced eye. If they are at all marked, the cut surface 
protrudes, the gray substance is hyperemic, either as a whole, 
when it appears as a red H, or only in circumscribed areas, espe- 
cially in the anterior horns. Besides this diffuse coloring, gener- 
ally, tiny blood specks and streaks also are perceptible; they re- 
semble capillary hemorrhages and have been so reported. But in 
most of the cases they are actually only vessels distended with 
blood. As mentioned already, these macroscopical changes are 
most marked in the anterior horns, especially in the protuberances ; 
but they occur also in the posterior horns and occasionally in the 
posterior horns alone ( Monckeberg) . In the white matter usu- 
ally edema and occasionally vascular distention are seen. The 
edema may be so great as to appear to the naked eye like a general 
softening of the cord. (Harbitz and Scheel report areas of 
softening of the spinal cord.) But on microscopical examination 
no "softening" in the ordinary acceptance of the term can be 
detected (Wickman). In certain cases, the cord seems practi- 
cally normal to the unaided eye, but microscopic examination in- 
variably reveals the presence of morbid changes (Rissler). 

In fatal cases edema and hyperemia are found in sections at 
higher levels of the central nervous system. These changes may 
be so marked in the brain as to render the dura tense and the con- 


volutions flat (Wickman). The pia may be hyperemic and very 
edematous (Daubert). The brain substance may also be hyper- 
emic. The gray matter may occasionally show flecks of red 
(Redlich). Cerebral changes may be invisible to the naked eye, 
and microscopic alterations yet be present (Wickman). 

The macroscopic changes in the transitional and end stages 
may be very slight. But if the destruction is extensive, the 
anterior horn appears shrunken at first and smaller than normal 
later, after a scar has formed. If only one side be affected, on 
cross section the cord is asymmetrical; the bundles of nerve 
fibers adjacent to the aflFected anterior horn appear smaller than 
normal and the roots arising from it are atrophied. . 

Microscopic Changes. — ^The pia mater. The pia is the seat of 
a round-celled infiltration. (Plate II, No. i.) The majority of 
the round cells appear to be lymphocytes. But another kind of 
cells (Maximov's polyblast) — which I shall describe more fully 
in discussing the round cells of the spinal cord — also occurs in rela- 
tively great numbers. The Unna Marshalko plasma cells, large 
lymphocytes and fibroblasts are seldom seen. More frequent than 
these, though also rare, are typical polynuclear leucocytes with 
lobed nuclei and neutrophilic granules. 

The spread of the infiltration in all of my cases showed con- 
siderable uniformity. The infiltration was especially marked in 
the lumbar and sacral regions of the cord, where it generally im- 
plicated the entire circumference. In the upper parts of the cord, 
it was less severe and could usually be seen only at the entrance 
of the anterior fissure, chiefly in the anterior fold of the pia. The 
infiltration was especially pronounced over the front of the cord. 
But in sections at higher levels, circumscribed areas of marked 
accumulations of cells also occurred in the pia. Forssner, Sjovall, 
and Marburg and Strauss observed further that the infiltration 
was particularly localized to the lower part of the medulla spinalis. 
In the cases reported by Harbitz and Scheel, the infiltration, 
although generalized, yet predominated in the lower parts and over 
the anterior aspect of the cord. 

Some special peculiarities of the infiltration of the pia have yet 
to be mentioned. The contiguous bundles of meduUated nerve 
fibers are rarely implicated. The infiltration of the pia is con- 
fined to the area around the vessels. At higher levels, where the 



The representations of microscopical preparations are taken from tny 
" Studies of Acute Poliomyelitis " and " Further Studies," etc. 

Plate I, No. i. Round-cell infiltration of the ganglion cells of the 
lateral group of the gray matter, in the sacral region of the cord, from a 
case two and a half days after the onset. ^ 

Plate I, No. 2. Ganglion cells from the same region in the same case, 
almost destroyed by phagocytic neuroglia cells (Neurophages). 

Plate I, No. 3. Infiltration of the lymphatic space of a central vessel 
from the lumbar cord of the same case. 

Plate I, Ho. 4. Infiltration of a vascular space and of the surrounding 
tissue in the anterior horn of the lumbar cord in the same case. 

Plate II, No. i. Round-cell infiltration of the pia in the antero-lateral 
gray matter of the sacral cord, from a case of three to four days* duration. 

Plate II, No. 2. Area of round-cell accumulation in the posterior root 
entrance zone of the sacral region, in a seven-day case. 

Plate II, No. 3. Right anterior horn from the upper dorsal region of 
the same. Apex of the anterior horn is directed downwards. To the 
right and left of the section can be seen the much less infiltrated white 

Plate II, No. 4. The greater part of the gray matter of the spinal 
cord in the upper lumbar region of the same case. Marked infiltration of 
Clark's column (to the right). The infiltrated anterior system with the 
entering central vessels below and to the left. Posterior columns below 
and to the right. 

Plate II, No. 5. Left anterior horn, apex downwards, from the dorsal 
regioil of the same case. The larger vessels chiefly infiltrated. Below, to 
left and right, can be seen the white matter, which is here very slightly 

Plate II, No. 6. Circumscribed area of disintegration from Clark's 
column in a two-day case. 

Plate II, No. 7. Hypoglossal nucleus of the same case. Round-cell 
infiltration of the vessels and of the supporting tissue with normal ganglion 

Plate II, No. 8. Area of round cells in the brain cortex from a seven- 
day case. 

Plate II, No. 9. Anterior part of the anterior horn, in the cervical 
enlargement, from a three weeks* case. The supporting and nerve tissue 
has been destroyed and absorbed. Only the vessels surrounded by multi- 
nuclear cells still remain. 

Plate II, No. 10. Anterior horn, apex downwards, of lumbar enlarge- 
ment, from an eight weeks* case. The whole lateral half (left of plate) 
of the anterior horn is destroyed. 


pia in the lateral and posterior parts of the cord is free from round 
cells, the infiltration around the vessels stops at the periphery of 
the spinal cord and does not involve the pia. It is noteworthy 
that in the dorsal and cervical regions, where the implication of 
the pia on the external aspect of the cord generally is either very 
slight or completely absent, the infiltration of the pia is still most 
obvious towards the bottom of the anterior fissure. Considerable 
infiltration may occur here and around the entrance of the central 
vessels, although the pia elsewhere escape. These facts are of 
importance, for they enable us to realize the relation of the changes 
in the pia to those in the spinal cord. 

On microscopical examination, the pia is seen to be infiltrated, 
and its blood vessels are found to be dilated and congested. In- 
flammatory changes have been observed in the pia mater of the 
brain, also. The implication of the pia mater in infantile paral- 
ysis was noted first by Dauber, and subsequently by Bickel (Roeder 
and Schultze). Wickman established, and Harbitz and Scheel 
and others have since corroborated, that changes in the pia are a 
constant phenomenon of this disease. 

The affection of the pia mater is of special interest, as it ex- 
plains the meningeal symptoms, which, in the initial stages of 
otherwise typical spinal infantile paralysis, are sometimes ob- 
served. The affection of the pia is also the basis of the meningeal 
form of Heine-Medin's disease. 

As a rule, the dura is not implicated. Harbitz and Scheel suc- 
ceeded in demonstrating a slight cell infiltration of the dura mater 
in only two cases. 

Spinal Cord. — The changes in the spinal cord are most evident 
in the interstitial tissue and in the vessels. Of these changes 
Rissler has written a classical description. The vessels are dilated 
and congested. The vascular changes are especially marked in the 
veins but are not confined to the larger vessels if the process is at 
all advanced. The capillaries are often greatly distended and tor- 
tuous. Siemerling and Matthes allege that a formation of new 
capillaries occurs. The contents of the vessels are red blood cor- 

Wickman, Harbitz and Scheel, and Strauss, in spite of most 
careful search, failed in all their numerous cases to find any evi- 
dence of thrombosis, or embolism, in the first stage of the disease; 


and, as far as I know, all other investigators have similarly failed. 
Mott and Batten have each reported thrombosis in a single case. 
These cases, however, were respectively of 17 and 13 days' dura- 
tion, and I believe it was a secondary phenomenon. Tiny hemor- 
rhages in conjunction with the hyperemia occur not only in se- 
verely aifected areas, but also in areas which otherwise show 
but little change. These hemorrhages are partly attributable to 
the inflammatory process. They may, however, partly be agonal 
changes, dependent upon the terminal respiratory paralysis. Sie- 
merling's case showed, both in the lumbar and cervical regions, an 
extensive hemorrhage, which implicated the greater part of the 
anterior horn. 

Hemorrhages are occasionally seen in the anterior horn, which 
explain the quite apoplectic type of paralysis sometimes observed. 
Motor disturbances may, however, develop with extreme rapidity 
solely from the inflammatory process. 

More important than the hyperemia and hemorrhage is un- 
doubtedly the cellular exudate. The cells are derived partly from 
the vessels and partly from the tissues. The first is the more 
constant source and in some sections the cellular exudate from the 
vessels is the only, or, at least, the principal pathologic change. 
(Plate II, No. 5.) The round cells which compose the exudate 
(in Fig. II, No. 5) are situated in the adventitial lymph spaces of 
the vessel wall. 

The infiltration of the advent itia is most marked around the 
entrance of the central vessels into the spinal cord at the bottom 
of the anterior fissure, where it is directly continuous with the 
infiltration of the pia. 

It has been stated that the arteria centralis is the most severely 
implicated. But Wickman maintains that in his cases, so far as 
any difference in severity existed, the veins were more gravely 
affected than the arteries. Between the central and the peripheral 
vascular systems, with the exception of the severity with which 
the larger central vessels tend to be affected soon after entering 
the spinal cord, no evidence of any discrimination exists. Harbitz 
and Scheel, and Strauss also state that the veins are the more 
affected. Marburg, on the contrary, in his recent report of his 
cases, states that eveil at the very onset of the disease, the anterior 
horn shows dense infiltration around the arteria centralis. In rare 


instances, quite independent of other changes, relatively slight 
infiltrations occur around the peripheral vessels, especially the 
veins. Besides this infiltration of the adventitia, a perivascular 
exudate is sometimes seen. The round cells penetrate the sur- 
rounding tissues and enclose the vessels like a wall. 

In the supporting tissue itself, masses of round cells often col- 
lect. These cells are derived from the vessels. Thus, in Plate 
II, No. I, the upper left hand portion of the picture (anterior 
horn) shows the exudate to consist principally of perivascular cell 
groups surrounding the minute blood vessels and capillaries, 
around whose branches they are massed like clusters of grapes on 
the stem of a vine. When an area of dense cellular infiltration is 
present (Plate II, No. 3), its extent can be demonstrated by serial 
sections, to be limited to the area of distribution of a blood vessel. 
In other cases, the infiltration, however, is diffused through the 
supporting tissue and is without any apparent relation to the vas- 
cular supply. In some areas, an unmistakable relation to the 
ganglion cells can be observed. Forssner and Sjoval demon- 
strated that many of the small masses of cells are only the remains 
of neurophages, which have completely devoured the ganglion 

The morbid changes we have been dealing with occur chiefly 
in the anterior horn. But in the posterior horn, analogous altera- 
tions are almost constantly present. In most of my cases such 
changes were especially marked in Clarke's column in the lower 
dorsal and upper lumbar regions. (Plate II, No. 4, right.) Oc- 
casionally I was able to prove that the infiltrations were connected 
with the vessels of the posterior system. But recently I have 
sometimes found Clarke's column scarcely affected. In Marburg's 
experience, Clarke's column was invariably less affected than the 
anterior horn. As a rule, the changes in the posterior are less 
marked than in the anterior horns. But this rule has exceptions. 
For instance, the morbid process may extend with the same sever- 
ity throughout the greater part of the gray matter ; or it may, as 
in the lower dorsal region in the majority of my cases, affect 
mainly the boundary zone between the anterior and posterior horns 
and gradually diminish in intensity towards the front and the back 
of the cord. Rarely the posterior horn is affected to a greater 
degree than the anterior. Cellular infiltration may occur in the 



white matter, as well as in the anterior, posterior and lateral 
horns ; it is most constantly observed in relation to the sheaths of 
the blood vessels but, as Redlich first recorded, it may be seen 
also in small groups within the nerve tissue. I, myself, demon- 
strated in almost all of my early cases minute and rare foci of cell 
infiltration among the white nerve fibers. (Plate II, No. 2.) 
Such a small focus is pictured in the entrance zone of the pos- 
terior root. Diversity of opinion still prevails concerning the na- 
ture and origin of these round cells. While Rissler, Redlich, 
Schmaus, Harbitz, Scheel and others described them as migrated 
leucocytes, Goldscheider, recently joined by Strauss, maintains 
they are proliferated fixed tissue elements. The former have 
focused their attention principally upon the glia cells; the latter, 
upon the cells of the adventitia. According to Marburg, all are 

In my latest study of the pathologic anatomy of this disease, I 
think I have solved the problem of the nature of these cells. The 
principal cells are not leucocytes, nor proliferated connective tissue 
elements, nor are they simply lymphocytes. They represent a 
further stage in the development of the lymphocyte and are what 
Maximov has described as polyblasts. The distinguishing fea- 
tures of these cells are shown distinctly in the preceding plates. 
Plate I, Fig. 3, represents the exudate around the wall of a large- 
sized vessel. To the left can be seen only one cell, whose proto- 
plasm remains unstained (stain, Pappenheim's methyl, green and 
pyronin) ; four are obviously poly nuclear leucocytes. The re- 
maining round cells can be divided into two groups, one of typical 
lymphocytes, encircled by a small amount of pink staining proto- 
plasm and containing a dark staining nucleus, rich in chromatin, 
which is aggregated at points into masses, the other of cell ele- 
ments which evidently are derived from lymphocytes, in which the 
nucleus stains lightly, in which a dainty network distinctly appears, 
and in which the protoplasm has increased. These cells later 
develop into types — as is evident from three or four of the larger 
forms in this figure — which have no resemblance to the mother 
cells, to which, however, numerous intermediate forms link them. 
The origin of these cells from lymphocytes may. therefore be con- 
sidered as proved. 

Let us now pass to the infiltration around the small vessels and 


in the supporting tissue. The same cell elements occur but they 
are now characterized mainly by the increase in the amount of 
their protoplasm (Plate I, Fig. 4). This figure consists of two 
parts, which are separated by a diagonal light zone due to shrink- 
ing of the preparation. The upper part shows a tissue infiltration ; 
the lower, in which the round cells are denser, shows an exudate 
around a small branch of the same central vessel, from which the 
infiltration of the lymphatic space depicted in Fig. 3 was obtained. 
These infiltrations are continuous and arise from the same infiltra- 
tion. The same cells as have already been mentioned, lympho- 
cytes, leucocytes and polyblasts, are present in this figure. The 
polyblasts now consist of immense cell masses, possessing a light 
staining reticulated nucleus and abundant protoplasm; they are 
here in greater number and show a still higher develppment than 
before. In the tissue infiltration, two isolated glial nuclei and 
one leucocyte can be observed, but no typical lymphocytes. Lym- 
phocytes can, however, be seen in the adjoining vascular infiltration. 

Obviously, the relative numbers of lymphocytes, leucocytes and 
polyblasts are not everywhere the same as is here depicted. In 
some places the lymphocytes are in the majority; in others, the 
leucocytes. As a rule, however, in the tissue infiltration, the mass 
of the round cells consists of polyblasts. Pirie and I arrived at 
this conclusion almost simultaneously. 

Another interstitial change which plays an important part in 
the appearance and disappearance of the symptoms has yet to be 
considered, namely edema. To the naked eye, in many cases, 
edema is obvious. Indeed it is generally easier to detect macro- 
scopically than microscopically. It is at least partly responsible 
for the appearance, which the glial tissue often presents, of being 
permeated by or converted into a finely granular substance. Some- 
times the tissue seems to be loosened, so that the glial meshwork 
appears wider. In a few of Wickman's cases, circumscribed foci 
of softening were present in Clarke's column. In the lighter parts 
of Plate II, Fig. 6, only the remains of the delicate glial reticulum 
can be perceived. Biilow-Hansen, Harbitz, Forssner, Sjovall and 
others also describe a sponginess of the tissues. I think the edema 
is of no slight importance from a clinical point of view, as it affords 
a plausible explanation for the rapid disappearance of a paralysis. 
The dread change which gives rise to the paralysis has its seat in 


the ganglion cells of the anterior horn. Strauss, by means of 
Bielschowsky's method, has recently shown atrophy to be the 
initial change in the intracellular network of the neurofibrillae. By 
the use of Nissl, Von Gieson and other methods of staining, the 
cell body has been proved to swell and to become more globular. 
With this swelling a disintegration of the Nissl granules occurs 
and often extends throughout the whole cell. If a section of such 
a swollen cell does not implicate the nucleus, the entire cell appears 
to be changed into a homogeneous anuclear structure, frequently 
without a single process. But serial sections usually demonstrate 
that this appearance is deceptive, for the nucleus and the cell pro- 
cesses can be found in contiguous sections. In many cases, the 
nucleus retains its normal appearance for a remarkably long time. 
Generally, it also conserves its normal position in the middle of 
the cell. When a severer change occurs in the cell body the nucleus 
is converted into a deeply staining, irregularly shaped structure. 
Sometimes complete karyolysis happens. Occasionally vacuoles 
in varying number are studied through the protoplasm. 

The severity of the ganglion cell changes usually is in direct 
ratio to the intensity with which the interstitial tissue is affected. 
No nerve cells, as a rule, are visible, in the largest infiltrations, but 
slightly altered ganglion cells are sometimes present in the midst 
of a markedly infiltrated area. On the other hand, degenerated 
cells unaccompanied by interstitial changes have never yet been 
found in man. The interstitial changes do not necessarily consist 
of pronounced cell accumulation ; edema may prevail. Degenera- 
tion of the ganglion cells without inflammatory reaction occurred 
in a case of Cestano-Savini and Savini, but this particular case 
clinically as well as pathologically differed so widely from all 
others hitherto described, that I fully agree with Strauss that it 
was not a case of acute poliomyelitis. 

Remarkably numerous neurophages were described by Forssner 
and Sjovall, who attributed to them considefable importance in 
the degeneration of nerve cells. In my later cases I have fully 
confirmed these observations. As shown in Plate I, Figs. 1-2, 
round cells invade and ingest the ganglion cells till only a clump 
of round cells with greatly increased protoplasm remains to mark 
the site of the ganglion cell. In this process the polynuclear leu- 
cocytes and the polyblasts are the chief, if not the sole, agents. 


According to Wickman, each acts quite differently. The poly- 
blasts alone are active neurophages. In the middle of many gan- 
glion cells, degenerating polynuclears lie ; but around the periphery 
the polyblasts are situated and generally show no retrogressive 
changes. Tho difference in behavior of the polynuclear leucocytes 
and of the polyblasts is especially noticeable in places where the 
ganglion cells have already been ingested. In Fig. r, the two poly- 
nuclear leucocytes, which are somewhat to the left above and to 
the right below the center of the field, remain quite passive; 
whereas, the protoplasm of the polyblasts is swollen and laden with 
tiny particles of fat. In addition, other ingested material, appar- 

Fio. I. Neuronophagies, in which the difference in importance between 
polynuclear leucocytes and polyblasts is plainly shown. 

ently decaying ganglion cells, is present. These fat-laden poly- 
blasts develop later into typical fat cells. 

The neurophages also occur in poliomyelitis in monkeys (Land- 
steiner and Levaditi, Landsteiner and Prasek) and are, I think, 
a feature especially peculiar to the most acute cases. In cases 
of slower course, the changes earlier described are evident. In 
perhaps not a few, a degeneration which I described in my first 
work on this subject, occurs; the peripheral part of the cell body 
degenerates and dissolves, but the nucleus is spared. If such cells 
are situated in areas of infiltration, the appearance may resemble 
a complete absorption of the ganglion cells, unless a careful exami- 
nation with a high power lens be made, when the presence of the 


ganglion cells will be detected. Strauss has since confirmed these 

In general, the nerve filaments of the gray matter are faintly 
stained and of irregular contour. Sometimes they show little 
swollen nodes like a chain of pearls ; usually they are degenerated; 
sometimes only fragments can be recognized. 

The parenchymatous changes in the posterior are analogous 
to, but not so marked as, those in the anterior horn. The differ- 
ence lies in the slighter interstitial changes and the lesser implica- 
tion of the nerve cells in the posterior horn. 

In the region of the central canal, Wickman observed round 
cells, which in places penetrated between the ependyma cells ; but 
the evidence of inflammation in this neighborhood was scanty. 

In the bundles of white nerve fibers round cell accumulations 
are few and contain no nerve filaments. The changes in the white 
matter are very slight, and are due chiefly to edema. Swelling of 
individual axis cylinders has been noted; but with Weigert's 
method, at least in my cases, only imperfect staining was demon- 
strable. Rissler observed degeneration and tortuosity of the axis 
cylinder. In the acute stage, the changes in the posterior and 
anterior roots are very mild : they consist chiefly of the invasion 
of the fasciculi of the anterior root by the pial exudate penetrat- 
ing between the nerve fibers. The vessels of the roots may also be 
infiltrated. Enlarged axis cylinders in the anterior and posterior 
horns have been observed. Siemerling found that the Marchi 
stain produced an appearance of black dots in the extramedullary 
portion of the anterior and posterior roots. Redlich and Moncke- 
berg described degenerative changes in the peripheral nerves. As 
these changes were slight, and as no evidence of local inflamma- 
tion was observed, the degeneration must be considered as secon- 
dary. This secondary degeneration is not often present. 

Forssner and Sjovall were the first to examine the cells of the 
intervertebral ganglia. They were able to prove inflammatory 
changes. Their observations were later confirmed by Marburg 
and Strauss, but Harbitz and Scheel found the ganglion cells 

Microscopic examination of the spinal cord has not yet re- 
vealed bacteria. Bonhoff, however, has demonstrated, by Mann's 
method, nuclear enclosures in the neuroglia cells, which he believes 
to be foreign bodies of a specific nature. 


C, Medulla Oblongata and Pons, — Changes in the medulla ob- 
longata have hitherto been found in every fatal case of Heine- 
Medin's disease in which they have been sought and in which death 
was not due to an intercurrent malady. The nature of the lesions 
here, as was first shown by Rissler, is identical with that found in 
the spinal cord. Wickman, however, has pointed out that the 
findings in the spinal cord differ regularly from the findings in the 
bulb; that in the bulb, the degenerative are less marked than the 
infiltrative changes; the lesions tend to be disseminated; and no 
preponderating localization in the motor areas — such as is seen in 
the spinal cord — occurs. The most intense changes in the bulb 
appear often apart from the nerve nuclei, in the substantia reticu- 
laris tegmenti. Exudates are visible in the most diverse areas; 
e. g., in the cranial nerve nuclei of the olive ; in the nuclei of the 
columns of Goll and Burdach ; in the nucleus pyramidalis ; in the 
substantia nigra; in the central gray matter in the neighborhood 
of the aqueduct of Sylvius ; in the anterior and posterior corpora 
quadrigemina ; in the raphe; and elsewhere. Forssner and Sjo- 
vall, Harbitz and Scheel, Strauss, J. Hoffmann, and others subse- 
quently corroborated these observations. 

In the gray matter, morbid changes are conspicuous in the 
larger vessels running beneath the floor of the ventricle. The 
tissue infiltration has an inconstant relation to the nerve nuclei. 
Sometimes the round cells congregate about the nuclei ; sometimes 
they are grouped in the vicinity of and only slightly encroach upon 
the nuclei ; and sometimes they leave the nuclei wholly untouched. 
Occasionally, a densely infiltrated vessel may be seen wandering 
through an otherwise intact nucleus; or almost the whole cross 
section of a nucleus may be normal and free from infiltrating cells 
except in one part where an exudate accompanies a vessel. 

In general, the alterations of the ganglion cells are slight and 
are mainly chromatolytic. Where interstitial changes are absent 
the ganglion cells always appear normal, even when stained by 
toluidin blue. This m.ay often be observed in the immediate 
neighborhood of infiltrated vessels, and, also, in places where infil- 
trations are not intense (Plate II, Fig. 7). .Usually the more evi- 
dent the infiltration the more do the ganglion cells suffer. But it 
is remarkable how exceptionally well preserved the ganglion cells 


may be in the midst of a densely infiltrated zone (Wickman, Forss- 
ner and Sjovall, Harbitz and Scheel, Strauss). 

An exact knowledge of these relations of the interstitial to the 
nerve cell changes is of great importance as regards pathogenesis. 

D. Brain. — ^Redlich was the first to demonstrate that exudate 
around the vessel walls and small foci of round cells— evidences 
of inflammatory reaction — occur also in the brain. In all hitherto 
examined cases these brain lesions have been minute. Harbitz 
and Scheel made the most thorough investigations of the nature 
and site of the cerebral lesions in acute poliomyelitis. They 
found the basal part of the brain, particularly the neighborhood 
of the Sylvian fossa and the central ganglia, as a rule, to be more 
intensely inflamed than the surface convolutions; and that the 
central was the gyrus most often implicated. They further noted 
the involvement of the cerebral meninges, especially in the region 
of the Sylvian fossa. I shall later refer to two cases of encepha- 
litis reported by them. 

In five cases, in which Wickman had an opportunity thoroughly 
to examine the brain, much milder changes were present, espe-' 
cially in the pia. But even in these cases, scattered small foci, mostly 
in the central ganglia and in the central gyri, were observed 
(Plate II, Fig. 8). 

The cerebellum presents analogous pathologic changes. 

E, Other Organs, — The internal organs have seldom been in- 
vestigated. Parenchymatous degeneration of the heart, liver and 
kidney — occasionally even a distinct nephritis — has been reported. 
Inflammatory changes outside the nervous system have been ob- 
served in the pericardium only, and in but a single case (Wick- 

Reparative and Cicatrising Stage. — I shall describe this stage 
very briefly as from every point of view it is of much less in- 
terest than the acute stage. I have. already related how, even at 
the height of the small celled infiltration granule-containing cells, 
which develop from the polyblasts, appear between the small round 
cells. Absorption thus commences. After a while, if the process 
were diffuse and severe, one can no longer speak of the tissue 
proper ; the tissue is dissolved, melted and ingested by these granu- 
lar cells (Plate II, Fig. 9), which lie partly scattered, but mainly 
concentrated around the lymphatics of the vessels. The support- 


ing tissue and the neural reticulum are replaced by a granular 
substance, which is intersected, as by coarse threads, by processes 
of newly formed glial cells. Not even debris of the nerve ele- 
ments may be detectable in these severely affected areas (Plate 
II, Fig. lo). 

The small cell elements do not behave in this as in the acute 
stage. Besides the granular, typical Unna-Marschalko plasma, 
and distinctly proliferating glia, cells are present in great numbers. 
Spindles and other derivatives of- the adventitial cells occur. 
Later, the granular cells gradually retreat till they are chiefly 
restricted to the lymph sheath of the vessels, where they may occa- 
sionally remain, even as long as two years after the onset of the 
disease (Roger and Damaschino, Lovegren). The neuroglia be- 
comes more distinct and its cells develop so many wide and much 
branched processes that they resemble seaweed-covered ^ stones. 
These processes gather together and the neuroglia loses its normal 
delicate felt-like appearance. The change advances. Naturally, 
the appearances observed in cicatrization depend upon the extent 
and severity of the destruction in the acute stage. If the entire 
anterior horn were then implicated to a degree which resulted in 
complete destruction, it would now appear atrophied even to the 
naked eye ; and on microscopic examination, only neuroglia would 
be seen. In some cases such definite gliosis is present only in 
limited foci and normal areas still persist in the anterior horn. 
But if the destruction during the acute stage were not so intense, 
a more or less marked thickening of the neuroglia with rarefac- 
tion and atrophy of the nerve elements ensues. Obviously all 
possible degrees of transition between these various conditions may 

The changes in the ganglion cells originally reported by Prevost 
and Vulpian were later confirmed by Lockhart, Clarke, Charcot, 
Joffroy and subsequent investigators. It was observed in some 
cases that ganglion cells were affected in groups (Sahli, Dejerine 
and Huet). But within the affected groups, isolated normal gan- 
glion cells still persisted in varying number at different levels of 
the cord. In one case Lovegren noticed that the boundary of an 
inflammatory focus ran across a ganglion cell group. Kawka, 
Goldscheider and Kohnstamm were able to demonstrate that the 
sclerosed areas are associated with thickened vessels. Groups of 


round-cell infiltration have also been found in the posterior horn 
and in Clarke's column (Parrot, Joffroy, Dejerine, Huet, v. Kahl- 
den and Praetorius). 

The sequelae of the initial destruction in the anterior horn are 
most evident: they consist of degeneration and atrophy of the 
intraspinal tracts, of the anterior roots of the motor nerves, and 
of the muscles. 

Jagic, Bing and Mott have demonstrated by the Marchi method 
secondary degeneration in the antero-later^l and cerebellar tracts 
and in the posterior columns. The same changes can be seen in 
the anterior roots. The degeneration is followed by atrophy, 
which is usually well marked in the region of the antero-lateral 
tracts (Cornil). 

The muscles, also, atrophy. Occasional hypertrophied fibers 
occur between the atrophied (Dejerine, Lovegren). Sometimes 
the muscle fat is increased. 

Bing and Jagic were able to demonstrate in the pons, during 
the transition stage, morbid changes of slight extent. Eisenlohr 
observed in a doubtful case of several years' duration, a patch of 
sclerosis with degeneration of the ganglion cells in the facial 

Similar changes have been noticed in the brain : Lamy found, 
in addition to the usual changes in the spinal cord, four small 
sclerotic foci in the cortex of the left hemisphere, one in the 
parietal, the others in the frontal lobe. In Rossi's case, the re- 
mains of the encephalitic process were much more diffuse; part 
of the frontal lobe, the inner surface of the paracentral lobule on 
both sides, and the greater part of the corpus callosum were 

In the cases reported by Sander, Rumpf, Colella and Probst, 
a flaccid paralysis of the extremities was associated with atrophy 
of the central convolutions. This cerebral atrophy was explained 
as secondary to the destruction of the peripheral neurons. 



Charcot and Joffroy, who were among the first to investigate 
the pathology of the disease, taught that acute poliomyelitis was 
a parenchymatous process ; that the ganglion cells attacked by the 
virus were destroyed ; and that an inflammatory reaction followed. 
This teaching was based upon observation of a case in which 
several years after the initial attack the principal lesion discovered 
was destruction of the ganglion cells. This conception of acute 
poliomyelitis as a systemic disease corresponds completely with 
the clinical picture. In Charcot's day, as only cases of long stand- 
ing were examined, the opinion prevailed that the disease produced 
a purely motor paralysis. Hence, little attention was paid to the 
observations of Roger and Damaschino, who laid special stress 
upon the interstitial nature of the changes, but who left open the 
question why the changes were limited to the anterior horns. 

Rissler and v. Kahlden strongly advocated Charcot's theory. 
Rissler supported his advocacy by citing one special case in which 
the infiltration of the vessel and of the interstitial tissue was less 
marked than the degeneration of the ganglion cells. I should like 
to emphasize that he was the first to record and depict these inter- 
stitial changes. Further, he did not blindly adhere to Charcot's 
tenets, but admitted the possibility that the disease virus might 
simukaiteously implicate the ganglion cells and the vessel walls. 
As von Kahlden relied solely upon observation of chronic cases, 
his horizon was limited. 

All recent observers agree that Charcot's doctrine is untenable. 
The changes beyond the motor region, for example, in the pos- 
terior columns and in the pia, are not explicable as secondary to 
degeneration of ganglion cells ; nor is there, at least in many areas, 
a primary affection of the ganglion cells. Thus, in the bulb, in 
distinctly infiltrated areas, even with our modern delicate staining 
methods, the ganglion cells appear normal. At first sight, such a 
condition as is depicted in Plate I, Fig. i, where neurophages occur 
in the midst of a densely infiltrated tissue, seems to support Char- 




cot's theory. But if the figure be more closely examined, even 
here, all the larger vessels are seen to be infiltrated, and the 
process must be regarded as inflammatory. Its inflammatory na- 
ture becomes still less open to doubt if, in such a case, different 
parts of the central nervous system be examined. Indeed, inflam- 
matory changes only in the vessels and in the interstitial tissue 
may occur. But the importance of the activity of the neurophages 
must not be overlooked. As I have said, their activity,. especially 
in the most acute cases, undoubtedly plays an essential part in the 
degeneration of the ganglion cells; but pathologic examinations 
have already shown that even in individual cases this is by no 
means true for all parts of the central nervous system. Nor is it 
tenable in those cases in which extensive and well marked paralysis 
disappears completely in a very short time, for a neurophagocytic 
action of considerable degree is quite incompatible with speedy 
return of function. 

There is reason to expect that experimental investigation will 
thrdw some light upon this question. Unfortunately, at present, 
we have extensive microscopic observations only of poliomyelitis 
in monkeys. Leiner and v. Wiesner have reported some cases of 
degenerative processes in the ganglion cells unaccompanied by in- 
flammatory reaction. We must here admit that there is a strong 
direct action of the virus upon the ganglion cells. It is also cer- 
tain, however, that no parenchymatous process can adequately ex- 
plain the known changes in man. The descriptions of Land- 
steiner and Popper prove, moreover, that a purely parenchymatous 
affection rarely occurs even in monkeys. Leiner and v. Wiesner 
acknowledge that in a large number of cases infiltrations exist; 
they suppose that the parenchymatous and interstitial processes 
develop synchronously; and they maintain in their writings a 
position intermediate between the extremists of both parties. I 
may here remark that the apostles of the inflammatory nature of 
the malady do not attempt to deny the direct action upon the gan- 
glion cells. As I belong to this category, allow me to quote from 
my latest work on the pathology of this disease. Emphasizing 
the fact that, in man, many factors undoubtedly point to the inter- 
stitial, as the more important changes, I call attention to the unde- 
niable possibility of a direct influence upon the nerve tissue. It 
is possible that under certain conditions this influence may even 


be very marked, although, as a rule, it is slight. Among such con- 
ditions, extreme virulence of the infection ranks first. 

It would not be surprising if an increase of virulence influenced 
the toxic peculiarities of the virus. Such a circumstance, how- 
ever, can hardly affect our conception of the nature of the changes. 
Probably passage from monkey to monkey enhances the virulence. 

Most recent investigators believe the changes in acute polio- 
myelitis to be inflammatory. Goldscheider, Redlich, Biilow- 
Hansen and Harbitz, Wickman, Harbitz and Scheel, Benecke, and 
others regard the degeneration of the ganglion cells as a special 
consequence of the interstitial inflammation. Ernst, Schwalbe, 
and others consider the parenchymatous and interstitial changes 
as synchronous.* Many pathologists, however, believe that here, 
as elsewhere, it is immaterial whether an inflammation is discern- 
ible first in the parenchyma or not. The essential points to be 
determined in either case are the same: First, why the malady, 
which from a pathological standpoint is a strictly localized affec- 
tion, develops clinically as a systemic disease; and, second, why 
the effects are limited practically to the anterior horn, and are not 
distributed as in a transverse myelitis. 

Pierre Marie thought that Kady's experiments upon vascular 
distribution in the spinal cord solved the whole problem. Kady 
proved that the anterior horns are supplied from the central artery 
which, at the bottom of the anterior fissure, enters the spinal cord 
and turns forward to ramify within a restricted zone. Pierre 
Marie supposed the morbid process to consist of embolism pr of 
thrombosis of the central artery. His theory received some sup- 
port from the experiments of Hoche and Marinesco. It was 
generally accepted. I, however, felt compelled to raise the follow- 
ing objection to it: 

1. In recent cases, neither embolic nor thrombotic processes 
have been demonstrated. Mott, Money and Batten have, it is 
true, each reported a case where thrombosis was present. But 
the most recent of these cases had already lasted thirteen days and 
such thrombosis may better be interpreted as a secondary process. 
In more recent cases, in spite of eager searching, thrombosis has 
not been found. And the isolated observations ju&t reported are 
totally inadequate to permit a generalization. 

2. The changes in Heine-Medin's disease are radically different 


from those of an embolic process. The necrotic area which is 
characteristic of embolism is never observed in poliomyelitis. 

3. Experimental embolism in the spinal cord does not substan- 
tiate Marie's hypothesis. Occasionally lesions restricted to the 
gray matter have been produced ; whereas, usually the white mat- 
ter is extensively implicated. 

4. In ulcerative endocarditis, caisson disease, and other mala- 
dies in which demonstrable embolic processes do occur in the 
spinal cord, no preferential selection of the gray matter can be 
seen. 9 

Proof has not yet been given that the changes in Heine-Medin's 
disease are referable to embolic or thrombotic processes; and, 
further, the pathology of the spinal cord comprises no analogous 
conditions to lend support to this view. 

I have also emphasized facts — apart from the nature of the 
process — which seem to me to contraindicate any preponderating 
influence of the central artery : 

I. In recent cases the most marked changes usually appear 
within, but never coincide with, the area of distribution of the 
central artery. Beyond this particular vascular zone, in the pos- 
terior horns, in the white matter, and in the pia, round-cell infil- 
tration generally occurs. Clearly, since the central artery sends 
no branches either to the posterior horns or to the pia, the central 
artery cannot be implicated in lesions in these situations. Lesions 
of the white matter have been alleged to be distributed exactly 
within the area of supply of the central artery, but I believe other- 
wise. Kady's experiments show that in a transverse section of 
the spinal cord, three vascular zones can be distinguished: a 
peripheral zone, which is supplied exclusively by the peripheral 
artery ; a central, limited to the gray matter, supplied by the cen- 
tral artery ; and an intermediate, which is supplied from each side 
in such a way that the capillaries of both systems intermingle. If 
the central artery determined the local distribution of the disease, 
one wouia expect that the lesions would radiate from the gray, far 
into the white, matter ; and that they would appear wedge-shaped 
on cross section. Such lesions, however, have never been ob- 
served. The morbid changes commonly cease precisely at the line 
of demarcation between the gray and white matter ; and when, as 
occasionally happens, the disease encroaches further, it extends 


by the direct implication of the contiguous tissue, and not by prop- 
agation along the branches of the central artery. 

2. Occasionally I found the round cells accumulated about the 
peripheral veins and associated in occurrence and distribution with 
the peripheral vessels. Around a fork-shaped peripheral vein, 
which is ramifying in the lateral part of the anterior horn, such an 
infiltration appears in Plate II, Fig. 3. This section seems to me 
to demonstrate distinctly how easily a false conception may arise. 
The focus here is wholly confined within the anterior horn. It is 
therefore within the extent of the region supplied by the central 
artery. But serial sections showed that the infiltration was asso- 
ciated only with this peripheral vein and not with the central 

3. I found, as a rule, infiltrations occurred in connection with 
the distribution of the largest vessels (or of the lymphatics). 

I assert not that the central artery plays no part, but that it 
plays not the most important part, in the pathogenesis. The 
round cell accumulations are sometimes associated with it; but 
they are also associated with the central vein, and sometimes with 
the peripheral vessels. I believe that these cells are directly de- 
rived not from the blood vessels, but from the lymphatics of the 
blood vessels. In my earliest publication on this subject, I main- 
tained that the specific pathologic changes could best be explained 
as a lymphatic infection. If we regard the disease as a blood 
infection, it is undoubtedly difiicult to account for the continuity 
of the changes in the long axis of the cord in fatal cases ; for in a 
vascular condition one would expect the scattered foci of inva- 
sion to be separated by normal areas. The continuity of the 
lesions and the tendency of the paralysis to spread from below 
upward seem to me to indicate a diffusion of the virus within the 
spinal cord and its membranes. And this diffusion obviously fol- 
lows not the blood but the lymph channels — the lymph vessels and 
the lymph spaces. In corroboration of this opinion, I may adduce 
the marked infiltration of the lymphatics of the large blood vessels 
in Plate II, Fig. 5, and the fact — still more convincing — that, at 
least in several places, the earliest infiltration appears in the lym- 
phatics. In a blood infection, one would expect the capillary 
region to be the first attacked ; whereas, here, initial implication of 
the capillaries has been shown not to occur. 



The conditions existing in rabies support my contention of the 
lymphatic ^read of infantile paralysis. I proved that the changes 
in both diseases were completely in harmony; and that, from a 
pathological aspect, each had an equal right to be called an acute 
poliomyelitis. In rabies the spread of the virus was proved to 
occur by way of the nerves. But Homen,by his studies, has since 
shown that the way of the nerves is the path of their lymphatics. 

Experimental investigations in monkeys have now practically 
confirmed the hypothesis of the lymphatic spread of acute polio- 
myelitis. It has already been mentioned that the disease can be 
produced by intravascular, subcutaneous, subdural, intracerebral, 
intraneural and intestinal inoculation. These various procedures, 
however, are of unequal value. The most reliable are intracere- 
bral and intraneural inoculation. 

How does the poison reach the spinal cord from an inoculation 
not infecting the blood ? Most of the workers upon experimental 
poliomyelitis in monkeys have come to the conclusion that the 
virus spreads from the site of inoculation especially by way of 
the nerves; the infection extends along the lymphatics, which 
accompany the nerves. I can hardly do better than quote Leiner 
and V. Wiesner, who have directed special attention to this ques- 
tion: "In the vast majority of our experiments — omitting for 
the moment those which were intracerebral — we observed a defi-- 
nite relation between the site of the inoculation and the seat of 
the paralysis, analogous to that already established in inoculation 
experiments with tetanus. Flexner and Lewis, Levaditi and 
Landsteiner, and we, have already demonstrated that the inocu- 
lated extremity is the first to become affected with the disease. 
In proceeding with further experiments, we almost invari 
proved that an inoculation in a nerve of a posterior extre 
produced paralysis which was situated in, and tended to rei 
restricted to, the hind end of the body ; and similarly, an inoi 
tion in the median nerve primarily affected the fore part. Ii 
tion through the digestive tract causes paralysis of the poste 
that through the respiratory tract, of the anterior half of 
body." These investigators conclude : " Our results, as a w 
indicate clearly that the seat of the paralysis depends upon 
site of the inoculation ; and that the virus of poliomyelitis rea 
the spinal cord by the shortest route. We are thus able to 


firm the view which we had previously stated and to which Romer 
and Kraus lent their authority, viz., within the organism the virus 
travels along the nerves, undoubtedly by way of the accompanying 
lymphatics. As what we have experimentally shown frequently 
occurs in accidental infections in man, these observations may 
be of importance in enabling us to determine the path of infec- 
tion in human beings." 

Landsteiner and Levaditi, by successful inoculation of the an- 
terior chamber of the eye, and also by demonstrating that inocu- 
lation through the nasal mucous membrane renders the olfactory 
bulb virulent, have further established the probability that the 
nerves are the conducting channels for the virus. 

As a control experiment Leiner and v. Wiesner clamped the 
sciatic nerve in an animal and injected the virus into the nerve 
distal to the clamp. They then thoroughly isolated and ligatured 
the nerve at the point where it had been clamped. Poliomyelitis 
did not follow the inoculation ; the animal remained healthy. 

Krause and Meinicke, contrary to other experimenters, assert 
that infection occurs through the blood stream ; or, at least, that 
at a certain stage, a blood infection occurs. They actually found 
the blood and spleen of children, who had succumbed to infantile 
paralysis, contained the virus. Other investigators have failed 
to demonstrate the poison in the blood of infected monkeys. 

The foregoing observations seem to add experimental ratifi- 
cation to the doctrine of lymphatic infection which I enunciated. 
Against this doctrine are two facts : first, that intracerebral inocu- 
lation may cause paralysis which sets in first in the lower extremi- 
ties, and, second, that experimental poliomyelitis may be* pro- 
duced by intravenous injection. 

Concerning the first, investigation is still being made : Leiner, 
Wiesner and Romer have already shown that here no essential 
contradiction necessarily exists. 

Concerning the second, I think we must clearly distinguish 
between the way in which the poison reaches the spinal cord and 
the mode in which the changes of poliomyelitis originate. These 
are by no means one and the same. Let us take an elementary 
example. Suppose a certain amount of virus settles in, for in- 
stance, the region of the posterior horn. The changes which here 
occur produce no picture typical of the disease. If, however, the 


poison Spread to any extent, from the area first attacked, so that 
the characteristic appearances of acute poliomyelitis later develop, 
although the lesion in the primary disease focus in the cord be 
due to an infection by way of the blood, the subsequent and typical 
lesions certainly are not. 

Leiner and v. Wiesner state that in monkeys, inoculation of 
the blood only exceptionally is successful. They have never, 
during the incubation period, been able to demonstrate the pres- 
ence of the virus in the blood. Their observations sharply con- 
trast with those of Krause and Meinicke who, as I have men- 
tioned, state that in rabbits the most effective site of inoculation 
is the blood and who have demonstrated the virus in the blood, 
as well as in other tissues, during the initial stage of the disease. 

Harbitz and Scheel arrive at a conclusion similar to my own, 
except that they maintain that the virus reaches the pia by way 
of the blood, and then invades the spinal cord along the sheaths 
of the vessel. Fr. Schultze, indeed, had already dwelt upon this 
possibility. He, however, considered it as an accidental phenom- 
enon, which might happen in the course of a cerebrospinal menin- 
gitis, and which infrequently afforded an explanation of the char- 
acteristic pathologic picture, or of the symptom complex of the 
disease. Leiner and v. Wiesner, while not clearly recognizing 
the principal point of the problem — the peculiar localization, with 
marked participation of the gray matter, especially in the anterior 
horn — yet acknowledged the lymphatic origin of the morbid 
changes in the nerve substance. The double step in the infection 
seems to me not very probable; and microscopical examination 
fails to substantiate that the inflammation, as a rule, diffuses in- 
ward from the pia. 

The point at which the virus enters human beings is still to 
be determined. Many different sites have been incriminated; 
e, g., because of diarrhea in the initial stage, the alimentary canal 
was accused ; because of angina, the throat ; and because of bron- 
chitis, the respiratory tract. Experimental research, especially by 
Romer and Joseph, proved that diarrhea might occur after intra- 
cerebral infection. Diarrhea, angina and bronchitis may, there- 
fore, be accepted as consequent upon the elimination, and not 
upon the invasion of the virus. If it be permissible to deduce 
from animal experiments the mechanism of morbid changes in 


human beings, then my belief that human infection takes place by 
way of the alimentary canal is not without foundation, for the 
paralysis almost always attacks first the legs and often remains 
confined to them. 

Hoche believes the central canal of the nervous system plays 
a part in the pathogenesis, but it is difficult to understand the rea- 
son for his faith. If the morbid changes have any relation to the 
special infective process, presumably, a communication must exist 
between the site of infection and the central canal. Otherwise, only 
diffusion of the process within the spinal cord itself could be 
ascribed to the central canal. But the facts satisfactorily * show 
that the central canal has no great importance. In some cases of 
acute poliomyelitis, elderly people in whom the central canal was 
obliterated, have been attacked ; and in cases where the canal was 
patent, in and around it, extremely slight and not always definite 
pathological changes occurred. As in my early investigations, I paid 
special attention to the central canal and myself demonstrated 
these points. I consider there is no sound basis for Hoche's opin- 
ion. The tendency to attack children is peculiar to all infectious 
diseases and can hardly be connected with the patency of the cen- 
tral canal. 




The GeneraLClinical Aspect of the Disease. — ^As a rule, Heine- 
Medin's disease begins quite suddenly, with fever and malaise. 
Tenderness is a frequent and prominent feature. Pain, headache, 
stiffness of the neck and spontaneous pains in the limbs appear. 
In some cases vomiting and diarrhea are present; in others, the 
disease commences with sore throat, coryza or bronchitis. 

These symptoms, which are in no way peculiar to, or dis- 
tinctive of, the disease, may constitute the whole clinical picture. 
After a few days the patient may recover without further symp- 
toms : such is the typical course in abprtive cases. 

In others, again, after the malaise has lasted one or more days, 
paralysis appears. Paralysis is the only sign which is character- 
istic of the disease; and it is the only sign which conclusively 
establishes the diagnosis. Paralysis generally attacks the limbs — 
most often the legs — but it may also affect the trunk and head. 
It develops rapidly and within a few days attains its maximum 
extent and severity. In a number of cases complete recovery of 
function occurs, but usually in certain areas the paralysis dimin- 
ishes to some degree and then remains stationary. It shows the 
characteristics of a flaccid paralysis, diminished reflexes, changes 
in electrical excitability, and atrophy. Subsequently, in cases in 
which the paralysis is persistent and extensive, paralytic contrac- 
tures, faulty positions and deformity develop, and more or less 
incapacitate the patient. 

According to the course of the disease, the seat of the paral- 
ysis, the predominance of isolated symptoms, and other features, 
I have distinguished the following forms of Heine-Medin's 
disease : 

1. The spinal poliomyelitic form. 

2. The form resembling Landry's paralysis. 

3. The bulbar or pontine. 

4. The encephalitic. 



5. The ataxic. 

6. The polyneuritic (resembling neuritis). 

7. The meningitic. 

8. The abortive. 

Zappert gives the following classification : 

1. Cases in which spinal paralysis preponderates (poliomye- 
litis in the restricted sense) with ultimate implication of the re- 
spiratory musculature (Landry's paralysis). 

2. Cases with marked cerebral symptoms, especially referable 
to implication of the cranial nerves, more rarely, of the cerebral 

3. Cases without special aifection of the central nervous sys- 
tem, but with more or less marked meningeal, gastrointestinal or 
general febrile symptoms. 

P. Krause differentiates : 

1. Spinal form (poliomyelitis acuta). 

2. Bulbar form. 

3. Cerebral form : (a) Meningitic; (&) encephalitic; (c) ataxic 

4. Abortive form. 

5. Recurrent or relapsing form. 

Although I recognize that a simplification of my classification 
would be desirable, I cannot perceive that the grouping either of 
Zappert or of P. Krause marks any advance. They differ from 
one another : the ataxic Zappert includes with the bulbar, Krause 
with the cerebellar; the meningitic Zappert places in the same 
group as the abortive, Krause as the cerebral. Neither of these 
groupings seems to me to have much purpose. Indisputably, 
meningitic cases occur which prove fatal, and a whole series of 
cases run a course typical of spinal meningitis without affording 
any clinical evidence of implication of the brain. From my per- 
sonal experience and from my intimate knowledge of recent lit- 
erature, I believe that my classification is not only correct but also 
that its nomenclature gives the physician the best survey of the 
various clinical aspects of the disease. Zappert has acknowledged 
the didactic value of my classification. I might even assert that 
from my classification, one could picture the general features of 
the symptomatology of the disease. 

B. Details of the Initial Symptoms and of the Various Forms. 


(a) Heine-Medin's disease usually attacks those in perfect health 
and begins acutely with fever and malaise, speedily followed by 
paralysis. Many earlier observers have asserted that the paral- 
ysis develops without preceding symptoms. Occasionally mothers 
make similar assertions and allege that the child, having been well 
when put to bed in the evening, awoke the next morning with a 
paralyzed leg or arm. West created for those particular cases a 
special name, "morning paralysis." The wide experience of re- 
cent years has shown the extreme rarity of such cases. Careful 
inquiry reveals that most of those children present prodromal 
^mptoms, which sometimes, however, are so slight as to evade 
notice till the attention of the relatives is specially directed to them. 
The cases in which sudden paralysis is alleged to happen occur 
chiefly among the very young. Older children and adults rarely 
give such a history. But veridical examples can be cited in which 
the initial symptoms were extremely slight. 

Occasionally the disease begins so insidiously that a vague 
un>yellness, without any positively localized signs, gradually de- 
velops. But, as a rule, after this ill-defined prodromal period, 
acute symptoms arise. 

Occasionally, as the disease develops, an intermission occurs. 
The patient recovers more or less completely from the first attack, 
only to be re-attacked. This second invasion must be considered 
as a relapse, if in the interval the patient were quite well. Even 
when paralysis has been established, relapses have occurred. 

The most constant symptom of the initial stage certainly is the 
fever. Simultaneous with the acute onset, the temperature, as a 
rule, rises rapidly. It usually reaches 38°-39° ; according to Ed. 
Muller a temperature of 40°-4i° Celsius may rarely occur. Gen- 
erally, the fever is maintained for a few days or even a week, and 
it falls, either gradually with rnarked occasional oscillations, or 
rapidly, as in a crisis. Ed. Muller observed that the subsiding 
temperature did not reach merely a normal, but sometimes even 
a subnormal level, which persisted . for a certain period. In some 
cases he noticed, almost always after four days, a second rise, 
which, in general, was associated with evident increase of the 
paralysis. Zappert reported cases in which the temperature per- 
sisted at about 40° for 8-14 days. I have rarely observed pro- 
longed fever. 


Wickman, and subsequently Ed. Miiller, Zappert, Spieler, and 
others have especially emphasized that neither the height of the 
fever, nor the severity of the other initial symptoms, foretell the 
nature of the subsequent course. After mild initial symptoms, 
some patients develop extensive and severe paralysis; some even 
die. Others, after an alarmingly severe onset, soon recover, with- 
out a trace of the affection they have undergone. 

Rarely the disease is ushered in by a rigor. . 

Besides the fever, there are other initial symptoms, such as 
headache and malaise, which have no special characteristics, but 
which may sometimes awaken suspicion. Drowsiness, general 
tenderness, stiffness of the neck and marked perspiration often 
appear. The drowsiness in most cases is very marked. Mothers 
frequently narrate that the patient has slept for several days and 
has, awakened only to eat and to void. Spieler and several other 
observers have reported deeper disturbances of consciousness. 
Very rarely actual coma occurs ; sub finem vitae, in lethal cases 
it may appear; complete unconsciousness may also arise, even in 
favorable cases. Zappert showed that coma may appear syn- 
chronously with the fever at the onset of the illness. Starr states 
that delirium generally accompanies the fever. Fiirntratt re- 
corded maniacal outbursts ; and others reported delusions. 

More characteristic than drowsiness is diffuse tenderness, 
which perhaps is the most noticeable symptom that in the initial 
stage directs our attention to the likelihood of Heine-Medin's 
disease. The mother notices that a mere touch is evidently pain- 
ful to the child. Sometimes, if she only approaches the patient's 
bed, anxiety and protests are expressed by the little sufferer. The 
patient may hardly be able to tolerate either the pressure of the 
bed clothes or the same position for any length of time. In the 
early descriptions of the disease this tenderness which was known 
to Heine, Duchenne, and others, was scarcely mentioned. Medin 
emphasized its frequency and also its prominence in the clinical 
picture of the disease. Wickman, Starr, Zappert, Foerster, Ed. 
Miiller, Netter, and others, confirmed his observations. This 
hyperesthesia is in many instances the most marked symptom in 
the initial stage. It is usually increased by passive movements, 
especially in my experience, by movements of the vertebral 
column, such as rising. Spontaneous pains exist, in some cases, 


in the neck, back and extremities. Occasionally the pain has been 
observed to show itself only in the extremity which later becomes 
paralyzed. The pain is often excessive, and generally diffuse and 
continuous. Older patients sometimes describe it as radiating. 
Such pain usually persists only for a short time and disappears 
with the subsidence of the acute symptoms. It may, however, 
last for weeks and arouse a suspicion of neuritis. 

Many cases on examination show an actual hyperesthesia of 
the skin, but others do not. This hyperesthesia, which, in my 
experience, is most marked over the spinal column, has its origin 
in the tenderness elicited by the movement. Again, in other 
cases, sensitiveness to pressure over the muscles and nerve trunks 
may be present and may persist, even as the spontaneous pain. 
Foerster, Spieler, and others have reported numerous cases of 
spontaneous pain in the limbs and pain on pressure over the mus- 
cles and nerve trunks. Byrom Bramwell demonstrated in several 
instances that the sporadic do not differ from the epidemic cases 
with regard to the occurrence of pain; and he pointed out that 
such pain is often mistakenly attributed to rheumatism. 

I shall later consider objective disturbances of sensibility. 

The explanation of the sensory irritability is somewhat uncer- 
tain. I, myself, am inclined to refer it to implication of the pia. 
But most observers tend to regard it more as a neuritic process. 
The possibility of such a process cannot be denied, but, at present, 
pathological evidence of its existence is lacking. I shall later 
return to this question; but the signs of irritation could undoubt- 
edly be due to the meningitis, which is invariably demonstrable. 
To the changes in the pi^ a series of symptoms, usually ascribed 
to meningitis, are referable. In the mildest cases, only pain in 
the neck develops. Frequently, however, rigidity of the neck, 
demonstrable only on bending the head forward, is also present. 
Sometimes a distinct contraction may be observed ; the head then 
is retracted. Head retraction may, however, be present without 
marked contraction of the muscles. Not seldom these symptoms 
are associated with pain and stiffness in the back; occasionally 
with orthotonus; more rarely with opisthotonus. In some cases, 
increased sensitivity of the spinous processes is present. Occa- 
sionally Kernig's sign has been noted (New York epidemic, Foer- 
ster, Ed. Miiller) ; and occasionally the sciatic phenomenon (Wick- 
man, Lindner and Mally). 


Medin, Pierre Marie, Fr. Schultze and others have called atten- 
tion to the occurrence of signs of meningeal irritation during the 
initial stage. Spinal infantile paralysis may therefore at the onset 
closely resemble meningitis. The frequency of these symptoms 
has only become known during the epidemics of late years. 

The signs of meningeal irritation usually are evident, but not 
well marked. Sometimes, however, in the initial stage, they are 
so pronounced as to dominate the clinical picture. 

Foerster has called attention to the reflex hyperextension of 
the vertebral column, which he frequently observed on attempting 
to raise recumbent children. He believes this sign to be somewhat 
characteristic of the disease. In Foerster's cases, and in Spieler's, 
the meningitic s-igns were unmistakable and persistent. Occa- 
sionally typical scaphoid retraction of the abdomen was also pres- 
ent (Foerster). 

Starr, Kraiise and Ed. Miiller state that sweating is an impor- 
tant early sign. Ed. Miiller observed sweating quite at the onset 
or during the first days, in three fourths of his cases. Sometimes 
Miiller's patients for weeks continued to perspire. Miiller sug- 
gested the possibility, in such cases, of a lesion of the sweat cen- 
ters or of their subdural tracts. Although I have not particularly 
referred to this sign in my own report, I can, however, confirm 
these observations; sweating is often profuse and its amount is 
not always dependent upon the height of the fever. 

In early descriptions convulsions occupied a prominent place 
among the initial signs. Medin, however, stated that convulsions 
rarely occurred, except in cases which later proved to be encepha- 
litic. In the epidemics I described, twitchings of individual limbs 
occasionally appeared, but convulsions rarely. During the Aus- 
trian outbreak Zappert observed convulsions and twitchings in the 
extremities among the early signs; he further noted that these 
signs were not restricted to the cases which later developed cere- 
bral symptoms. Zappert does not state the seat of the irritation 
in these cases — if irritation of the cerebrum or of the spinal cord 
was responsible for these convulsive movements. During the epi- 
demic in Hesse-Nassau, epileptiform seizures without uncon- 
sciousness, or spasms of a more tonic nature, were observed. Ed. 
Miiller, however, noted only one case of severe epileptic convul- 
sions with unconsciousness. In some cases, during the initial 


stage, Wickman observed a tremor which was occasionally very 
marked, which, resembled a mild intention tremor and which was 
absent in repose. 

Quite frequently gastrointestinal disturbances appear at the 
onset. Vomiting, of no great violence, usually occurs alone ; but 
intestinal disorders, sometimes constipation, oftener diarrhea, may 
also be present. The stools may be watery, green and fetid. In- 
deed, the diarrhea is sometimes such as suggests an acute gastro- 
intestinal catarrh. 

Medin, Wickman, Zappert, Krause and others have empha- 
sized the frequency of gastrointestinal symptoms in the initial 
stage of acute poliomyelitis. Diarrhea is the usual manifestation ; 
but in Spieler's cases and in the New York epidemic, obstipation 
was commoner. 

Post-mortem examination has demonstrated that gastrointes- 
tinal symptoms arise from changes in the intestinal mucosa ; swell- 
ing of the solitary follicles, of Peyer's patches, etc. Marie and 
some writers believe the changes in the intestinal tract to be symp- 
tomatic of a general infection; others consider the intestinal 
changes to be due to the primary action of the virus. Diarrhea 
in monkeys mostly occurs at the stage of paralysis. In man, the 
gastrointestinal signs appear as a rule at the onset of the disease 
and may precede all other signs of the infection. No one has yet 
been able to demonstrate the presence of the virus in the intestinal 

The respiratory tract also may contribute symptoms to the 
initial stage. Ed. Miiller reported the occurrence of respiratory 
symptoms in more than one half of his cases; some had severe 
persistent coryza; others sore throat, and a few conjunctivitis. 
But more frequent than these manifestations was severe bron- 
chitis, which sometimes led the physician to diagnose influenza. 
Occasionally bronchopneumonia was observed. Romer, in several 
cases of initial angina, examined cultures from the throat and 
tonsils without finding any specific microorganism. In a propor- 
tionally great number of Eichelberg's cases, an initial affection of 
the air passages (sore throat, bronchitis, etc.) was observed. 
Lindner and Mally found in many cases marked fetor of the 
breath in association with the throat affection. 

Skin eruptions, such as herpes labialis and varieties of ery- 


thema, have been observed during the initial stage. Among one 
hundred cases Ed. Miiller noted herpes thrice on the lips and once 
on the knee. Herpes is therefore rare. In other cases, he ob- 
served vesicular, measly, or scarlatiniform exanthemata. He also 
noticed similar appearances a week or more after the onset. The 
New York epidemic was peculiar inasmuch as skin eruptions oc- 
curred in 6i cases. The type of eruption was inconstant, but 
herpes appeared only twice. The rarity of herpes labialis is im- 
portant in the differentiation of Heine-Medin's disease from cere- 
brospinal meningitis. 

Very few other general symptoms have been observed. Iso- 
lated instances of swelling of one or more joints have been reported 
by Wickman, J. Hoffman, and Spieler. As the swelling was asso- 
ciated with general tenderness it was actually mistaken for acute 

In rare cases, enlargement of the spleen has been noted (Ed. 

Recently, Ed. Miiller established the fact that leukopenia is 
tolerably characteristic of the initial stage of Heine-Medin's dis- 
ease. He reported that in no instance either among fifteen cases 
in man, or among a series of infected monkeys, had he found an 
increase in the number of leucocytes during the febrile period. 
In the minority of the cases the count was normal, but in the ma- 
jority only 3,000-5,000 leucocytes were present. Miiller also 
proved that in monkeys leukopenia may occur long before the 
appearance of the paralysis and even in cases which remain free 
from paralysis. Krause, also, in such cases found leukopenia 
with a slight increase of lymphocytes. On the other hand, during 
a New York epidemic in six cases, leukocytosis ranging from 
13,400 to 20,600 was reported. If further investigations confirm 
Miiller's observations, the leucocyte count will prove a valuable 
aid in differential diagnosis. 

In an epidemic the character of the initial symptoms may pre- 
sent much variety. During the Swedish epidemic of 1903, Wick- 
man, however, observed that in a disease focus the general aspect 
of the initial symptoms might show considerable constancy. Thus, 
in one neighborhood, meningitic symptoms predominated ; and in 
another, gastrointestinal. Exactly the same observation was made 
in the German epidemic of 1909. Ed. Miiller, in the Hesse- 


Nassau epidemic, observed severe intestinal s)rmptoms only in the 
minority of cases, while Krause reported that about two thirds of 
the cases in Westphalia were initially afflicted with severe diar- 
rhea. Yet Miiller and Krause were reporting merely different 
foci of the same epidemic. 

(b) Paralytic Signs and Special Forms of Heine-Medin's Dis- 
ease, — In many cases only the onset of paralysis makes the diag- 
nosis certain. Paralysis appears after the initial symptoms have 
lasted from one to several days. It is the sign most characteristic 
of Heine-Medin's disease. It may attack different parts of the 
body and may produce most diverse clinical pictures. The com- 
monest type, the type which predominates in our conception of 
the disease, is the spinal, poliomyelitic form which is identical 
with the long-known infantile paralysis. 

I. The Spinal Poliomyelitic Type, Infantile Paralysis, — The 
paralysis attacks mainly the extremities, and one or more limbs 
may be affected. The muscles of the trunk and neck in varying 
degree and combination, also, may be implicated. Cranial nerve 
palsies may occur in this type, but they are a negligible feature. 
Three stages of the disease may be distinguished : an acute stage, 
a stage of repair, and a chronic, definitive stage. Here I shall 
discuss the first two stages together and the chronic stage separately. 

The paralysis either immediately follows the febrile stage, or, 
more commonly, develops during the course of the fever ; increases 
rapidly in extent and severity and then partly diminishes, or, more 
rarely, completely disappears; and as a rule, is a purely motor 
paralysis of a flaccid type, with diminished muscular tonicity, 
muscular atrophy, and absence of reflexes. 

Motor disturbances generally appear within the first three 
days. Very seldom complete paralysis is present from the begin- 
ning. Usually the initial signs are those of a palsy; the move- 
ments still preserve their normal range, but the muscles are mark- 
edly weak and easily fatigued. Adults are conscious of the pro- 
gressive development of their muscular weakness: children may 
complain of it; or their elders may note the increasing feebleness 
of the child's attempts to move in and out of bed. In infants and 
little children the paralysis is usually not observed until it is far 
advanced : even then, to determine its nature is often difficult. 
In infants who have not yet learned to walk a diagnosis may some- 

' ««*«>«K ^* 


times be more easily reached by observing the lack of resistance 
to passive movements, the flaccidity of the muscles and the loss 
of reflexes, tlian by relying upon the absence of active movement 
which, of course, on more prolonged observation will also be evi- 
dent. It must be borne in mind, however, that consequent upon 
the attempt to elicit a deep reflex in a child, an inhibitory degree 
of muscular tension may be induced, and thus a loss of reflex 
may be simulated. Sometimes great patience, therefore, is nec- 
essary to determine whether a reflex actually exists or not. 
Special care is needed when spasm of the muscles is present, or 
when no normal stc^ndard remains owing to the real or apparent 
loss of the reflex on the first examined side. The motor func- 
tions of the body become more limited as the paresis advances. 
If the legs are aifected, the child may perhaps be able to move 
them in bed; but if he attempts to stand, he collapses; to walk 
now is for him impossible. If only one leg be attacked, the child, 
still able to stand upon the healthy leg, falls if he tries to support 
himself upon the affected leg. But occasionally one is deceived 
in this experiment by children who maintain their upright posture 
upon the weakened limb by hyperextending it at the knee joint 
so as to immobilize and fix it — just as if it were a wooden leg. 
The strength of the arms may also be reduced and the normal 
range of movement lost. If movement be retained, it is limited 
in range and so feeble in power as to be prevented by very slight 
resistance. # 

If the paresis progresses, complete paralysis results and the 
afflicted extremites become motionless. Later, a slight motility 
may be observed in a few muscles. When the paralysis affects 
several limbs, as a rule muscles of the trunk also are affected, and 
the neck muscles, too, may be implicated. A patient in such a 
condition presents a pitiful picture of helplessness. He is a mass 
without motion. When he is lifted out of bed, his head and limbs 
loosely hang suspended as pendulums. In a few cases, even if 
the paralysis be extensive, it more or less completely disappears, 
occasionally within a very short time. 

Neurath observed a case in which the usual rapid development 
and subsequent amelioration of the paralysis were absent; in- 
stead, a sudden onset was followed by a progressive course for a 
few months. It seems to me to be improbable that this case was 


really an example of Heine-Medin's disease. Foerster, however, 
observed cases where the paralysis reached its maximum extent 
only after 12 days. 

Character of the Paralysis. — Before I discuss the localization 
of the paralysis, I shall first refer to its characteristics. Typically, 
the paralysis is flaccid and is associated with loss of reflexes, hypo- 
tonicity, changes in the electrical irritability and atrophy. 

Usually, the reflexes disappear. Medin, however, showed that 
in sporadic cases the knee jerk may even be increased. Later 
investigators have also reported variations in the reflexes. As 
the legs are most commonly affected, let us first discuss the altera- 
tions of the knee jerk. 

1. Absence of the knee jerk is the rule. It is noteworthy that 
the loss of the patellar reflex may be the only demonstrable ob- 
jective sign of the disease (Wickman, Ed. Miiller, Zappert). 

2. An initial increase with subsequent disappearance may 
occur (Wickman, Ed. Miiller). 

3. If the arm be affected, or if the bulb be implicated, an other- 
wise normal leg may show an increase of the patellar reflex (Wick- 
man, Neurath, Zappert, Foerster, Ed. Miiller). 

4. Paralysis and loss of reflexes in one leg may be associated 
with apparent healthiness and increase of reflexes in the other 
(Wickman, Zappert). 

5. The patellar reflexes may be increased in a paralyzed and 
obviously atrophied leg (Wickman). 

These variations cannot with certainty be interpreted. The 
initial increase with subsequent diminution may I think be ex- 
plained by supposing that in the earlier stage of the disease the 
inflammatory process increases the irritability of the spinal cord. 
As the disease advances the stimulation gives place to the destruc- 
tion of nerve cells and this irritability diminishes till the reflexes 

More interesting are the cases in which an increase of the leg 
reflexes coexists with flaccid paralysis of the arm of the same 
side, or with a lesion at a still higher level. Evidently, the pyra- 
midal tract, in its course through the segments of the affected 
cervical cord or bulb, is injured, but to so slight an extent that the 
injury is manifest not as a paralysis of the leg but only as an in- 
crease of its reflexes. Ankle clonus also may be observed in such 


cases (Wickman, Neurath). Foerster found this sign in the 
very acute stage. 

These observations are important, as, also, are those of the 
sensory disturbances which will later be mentioned, because they 
together constitute the clinical expression of the localization of 
the morbid changes. 

The same explanation may suffice for categories 3 and 4. 

Increase of the knee reflex accompanying paralysis of the leg 
seems almost inexplicable. In the very rare cases which show 
this phenomenon implication of the pyramidal tract at a level 
higher than that of the lesion causing the atrophic paralysis, must 
give rise to an overcompensation of the reflex excitability of the 
paralyzed limb. 

Other tendon reflexes, also, undergo corresponding changes. 
Usually, in paralysis of the leg, the tendo Achillis reflex disap- 
pears; and in paralysis of the arm the arm reflexes are lost. 
Varying reports exist upon the nature of the tendo Achillis reflex 
in this disease; according to Zappert, in the same extremity, ab- 
sence of the knee jerk is not seldom associated with increase of the 
tendo Achillis reflex. Occasionally the arm reflexes may be ex- 
aggerated (J. Hoffmann). 

Oppenheim has reported a case which shows how the tendon 
phenomenon may differ even in the same patient. The shoulder 
muscles were paralyzed on the left, the quadriceps on the right, 
and the sural triceps, the peronei and the extensor communis digi- 
torum on the left. The tendon reflexes were as follows : Absence 
of right knee jerk; right tendo Achillis reflex distinctly, even 
markedly, present; left knee jerk conspicuously present; but left 
tendo Achillis completely absent. 

The superficial reflexes also may disappear. Wickman and, 
later, Lindner and Mally reported that the abdominal reflex even 
in pronounced paralysis of the abdominal muscles is preserved. 
Babinski's sign, also, has been observed. Strange to say, Foerster 
found it present either on one or on both sides in all cases ; it was 
not continuously demonstrable but disappeared occasionally only 
to return ; at times it persisted for a month. 

The affected limbs are markedly hypotonic. The hypotonicity 
does not show itself only by abnormally slight resistance to pas- 
sive movements, but also by a flaccidity of the muscles to touch 



which sometimes exists in limbs in which no paresis can be de- 
tected. Hypotonicity is often an invaluable aid to diagnosis. In 
little children this sign, especially when associated with loss of 
reflexes, is of great value, for paralysis and still more paresis is 
often difficult to establish in them. But hypotonicity, however, is 
not of invariable occurrence. Occasionally, in a paretic limb, one 
group of muscles may be hypertonic. 

A further important sign of paralysis in the spinal type of 
Heine-Medin's disease is alteration in the electrical irritability of 
the muscles. These electrical changes appear mostly during the 
course of the second, occasionally even toward the end of the 
first week. Jagic's case, which was confirmed microscopically, 
showed normal faradic excitability eighteen days after the onset. 
The change may be merely quantitative, a decrease or complete 
loss of irritability to faradism. A partial or complete reaction of 
degeneration may develop. 

After the illness has lasted for several weeks, a more or less 
pronounced atrophy of the paralyzed muscles gradually appears. 
It progresses more rapidly and markedly in the muscles which 
later remaiji paralyzed. The atrophy is caused not only by the 
trophic disturbances, arising from the changes in the nervous sys- 
tem, but also in part by disuse. 

Distribution of the Paralysis, — The paralysis in diflferent cases 
greatly varies in its extent, its combinations and its forms. It 
has been proved that the legs are most frequently affected, and 
that no muscle area is secure from attack. 

. During the Swedish epidemic of 1905 the distribution of the 
paralysis was as follows : 


1. Paralysis of one or both legs 353 

2. Paralysis of one or both arms 75 

3. Combined paralysis of leg and arm 152 

4. Combined paralysis of leg and trunk 85 

5. Combined paralysis of arm and trunk 10 

6. Isolated paralysis of trunk muscles 9 

7. Paralysis of the " whole body " 23 

8. Ascending paralysis 32 

9. Descending paralysis 13 

10. Combined paralysis of spinal and cranial nerves 34 

11. Isolated paralysis of cranial nerves 22 

12. Localization of paralysis not mentioned 60 


*<^ o 



Probably only the first two categories are accurately counted ; 
the figures relating to the lower extremity affections are espe- 
cially reliable. The nurhber of the combined paralysis of arm 
and leg, however, is, in my opinion, too high. When I had an 
opportunity to examine such cases in the early stage of the attack, 
I found that in addition to the affection of the arm and leg, the 
trunk muscles, especially the abdominal, were implicated, also. 
In category 6 I included 3 cases of paralysis, confined to the neck 
muscles. Category 7 comprises cases which might just as well 
be included in 4 or 5, and others, also, which might be classed 
with the ascending or descending paralysis. Finally, as many of 
the cases in 8 and 9 had cranial nerve palsies, they could be re- 
ferred to category 10. The figures show that the legs are most 
frequently attacked. In 353 out of 808 cases, 43.69 per cent., 
paralysis was confined to the lower extremities. If we now add 
together the cases in which one or both legs were involved (all, 
in categories 3, 4, 7, 8, 9; and 24, in category 10), we find not less 
than 692 cases out of 808^85.64 per cent. — in which the lower 
extremity was attacked. Analogous results, with slight variation, 
occurred also in other epidemics. Leegaard found paralysis con- 
fined to one or both of the lower extremities in 58.2 per cent, of 
311 cases; whereas, in 83.6 per cent. (260 out of 311) the lower 
limbs were implicated alone, and in association with other areas. 
Ed. Miiller stated that in four fifths of all cases the lower extremi- 
ties were attacked. In Medin's epidemic, a similar incidence of 
the paralysis prevailed. In discussing the relation' of epidemic 
to sporadic poliomyelitis, mention might have been made of the 
fact that the earliest observations of the disease emphasize the 
frequency with which the legs are affected. 

Lovett and Lucas, in 628 polyclinic cases, found both legs 
affected in 130; right leg, in 216; left leg, in 239; right arm, in 5; 
left arm, in 5 ; all four extremities, in 3 ; both legs and one arm, in 
2; trunk muscles with other area, in 6; in 15 hemiplegia existed, 
and in 7 crossed paralysis. In order of frequency, paralysis of 
the arm is generally believed to follow paralysis of the leg. 
Miiller, however, states that affection of the trunk is more fre- 
quent than of the arms and is second only to that of the legs. He 
noted in over two thirds of his cases that the trunk muscles were 

Par«stft ct die crmfe nnmad» al^^iFay^ accDmnsmiBf acvscs 
I>ftr^y<«!( of die Ihwer cgtrgrnirigff. 3ixt wsa traaaH^ rraiErazntL 
Z^^pett caOft acsenncu tD t^ act drat 31 ':ns capgrimug r^ lied: 
$iiie was ^otprangfj mcas: ctrtfx sna/dksd than die rignt • am 
paTmie* — 4 rpg^c, ro jcfc: igr palMS — J2r> rigftt.. 3* lefcr aaniB- 
pfegia* — ?i r^^iv 14 feS: . Daring: tie Xcw York ggiifffmnr. 29» 
left,. » rig^x arm. pallHKs; rjx fcr::. r33- r5^rt jc^ palsies^ ssd rj 
left aiuf r6 ri^x Ii<srr7pfeg3» were repcrtecL I zrT^eif ritanf 54^ 
left,, aiuf ^4;. rlgjir arm palsies; ♦^^r lefr. 60 rjg^ Leg: palsaes ami g. 
lefr,. ami ^ rigfet HetraiJegsi^ Lccgaarf gr^ics ere frllbwig 
f^jre*: AnFT^^ « r5^^ :2rr left: !cg5. 56 r^x 44 -J^ft ♦ "^grrfrreggy 
7 rilq^fit, ^ left. 

ft iA e-^irfert that every part o-f tie JCtrsLl c:r i niay 5e arracked 

Ti tlv>^ arf^tcrxn. Clinical'j. t±e disease occasccaZj seers to be 

er.ndr.ei^ to a i:rtt:rr.3cr:c,eii area^ Tz£: ^reat ^rariaiiliry of ±e 

para';'^U L"^ of>vicriJ* nrx only wtjen. d'Le i«rb:''e bccy ls ariTrhrkeil. but 

%W> ir. :T.:(trj:'w.rA ^*'7'.i7:r^ *fr.^ Irnh.*> In tie e^rrer r^t ie?^ even 

^::;r:r.^ the £rit perxd, wher. the pardLlyiis £s of greatest inrergary 

ar.^ extent, actrrrate co'terratij'.n seiiom rereals a cctrrlete ztmoo- 

p!<»^a or parap'e^ia. Eren Ts^heti the -xr'jole le? lies rz-zdccLess* 

the ti'.e:^ rr.ay ^til^ r>e capa-Me of rr.OTemer.t which, biwcTer. £5 more 

^xr-^^iic or I<^^-i free than n-orrnaL An anal't^-.tis o:ni:t£-:c occtrrs 

nof rar-*:'/ ir. the arrr.. After ^orr.e time ha^ elap^el. the tmeqtral 

/1i^*r:r/r*ion of the parah>-,:,% :» rr.ore e'/iient, Alihiuzh a great 

varief'/ of c/'/'r.hir^t:or.i of oaralvr:.? rrav -ieveltt). certain t^"t?cs 
^ * ^ ^ ^ • ^ 

ap;>ear rr,ore often than others. In the lez. the per-z-neal group 
krA certain Tr/::vyA of the thf^'h — in rrr/ experien :e the qna-iriceps 
fenr/>r;i e^pecrahy— t^:r.d to :^ rrroh-^jited, Altho'jgh die paralysis 
jieerr,^ U^ f^ I^'/^a'ized y> the-e n:v:r.',Ie^, ethers are to s^:n:e degree 
^ff^Atf'/l a!*o, Iy>vf:tt and L'.'ca-, showed that in n:t less than 355 
fya of 47H ca^e% in which the legs were impli rated, the quadriceps 
tithes alone or in corn hi nation with other muszles was affected. 
\'ext JR frtf\uency to the quadriceps, comes the tibialis anticus, 
which j% oftener attacked than the peroneal group. Of the flexors 
of the th:gh, the medial ir.u^Ies are more frequently paralyzed 
than the lateral. In the upj^er>', an analogous condition 
exj«»t^ ; i. e., in htriuency and distinctness, paralysis of the deltoid 
and of the uifptt arm preponderates CE. Remak). 

Sometime* the mr/tor disturbances assume the form of an 



upper or lower plexi^s palsy (Oppenheim, Cestan and Huet, De- 
jerine, Cruchet, etc.). 

The experience that the proximal parts are the more severely 
attacked, is in accord with the observations of early writers, such 
as SeeligmuUer, Baumanns and others. Cases occur, however, 
in which the distal are more implicated than the proximal parts. 
Very often, according to Ed. Miiller, second in frequency only 
to the affection of the legs, when severe paralysis exists, the trunk 
muscles are involved. The patient then may not be able to turn 
in bed or to change his position without help. The paralysis of 
the muscles of the back prevents sitting up in bed. When made 
to assume an upright position, the patient falls forward or to one 
or other side. From a bending forward attitude the patient can- 
not sit upright. Later, in consequence of the paralysis of the 
back muscles, scoliosis and kyphosis may be especially marked. 
If the abdominal muscles are attacked, the patient cannot rise 
from a recumbent position. When an attempt to rise is made the 
abdominal muscles remain quite flaccid; and the abdomen pro- 
trudes during the effort owing to the contraction of the diaphragm 
upon the intestines. In the acute stage, as the paralysis is usually 
bilateral and diffuse, all the muscles of the abdominal wall, as a 
rule, are attacked. But cases occur in which the paralysis is only 
unilateral : a protuberance of the abdomen then appears upon the 
paralyzed side, and the umbilicus is drawn to the healthy side. 
Rarely, after the disease has lasted some time, only isolated mus- 
cles may remain paralyzed, and a circumscribed hernial protuber- 
ance of the abdominal wall then appears which often closely 
resembles a lumbar hernia. Duchenne mentioned this implica- 
tion of the abdominal muscles in acute poliomyelitis, but Medin, 
Ibrahim and Herrmann, Oppenheim, Wickman, Petren, Ed. 
Miiller, Foerster and others particularly studied it. Strassburger 
and Foerster report cases in which the only motor disturbance 
was paralysis of the abdominal muscles. In Foerster's cases, this 
paralysis was associated with obstinate constipation which he con- 
sidered was due to a paralysis of the intestinal muscles, secondary 
in some cases to that of the abdominal muscles. 

Ed. Miiller noted that the abdominal muscles were affected 
next in frequency to the legs. This is of interest to me as it 
shows that even in non lethal cases conditions prevail which re- 


semble exactly those which I have established in fatal cases, 
namely, that the changes in the spinal cord during the early stage 
are continuous and extend longitudinally. Generally, the paralysis 
of the trunk later disappears and the disease often assumes the 
outward semblance of a disseminated myelitis. 

The respiratory muscles may also be involved. The inter- 
costal muscles are more frequently affected than the diaphragm. 
Paralysis of either produces functional disturbance which, in my 
experience, is especially marked when the diaphragm is paralyzed. 
When the attack falls upon the intercostal muscles, the chest may 
slightly move or remain motionless. Breathing may be carried on 
exclusively by the diaphragm. 

The intercostal paralysis is generally bilateral, but, as Medin, 
Foerster and Spieler observed, it may be unilateral. 

The functional disturbances resulting from paralysis of the 
diaphragm are marked and characteristic. The epigastrium during 
inspiration is drawn in ; during expiration, protruded. 

Paralysis of the respiratory muscles is of special importance 
for prognosis. If the intercostal muscles and the diaphragm are 
severely attacked, danger of asphyxia threatens; and the existence 
of an affection of the respiratory muscles later predisposes to 

Not rarely the neck muscles are affected. They are oftener 
implicated in the ascending type of the disease. The functional 
disturbances are characteristic if the flexor and extensor muscles 
are attacked; the patient cannot lift his head from the pillow; 
when he is raised his head and legs hang down backwards ; if his 
body is bent a little forward, his head falls forward or to one or 
other side and, controlled only by gravity, remains completely 
passive. This paralysis of the neck is usually accompanied by 
paralysis of the extremities, but during the Swedish epidemic of 
1905 at least 3 cases of isolated paralysis of the neck muscles 
occurred. Wickman in the Stockholm epidemic of 1899 reported 
another case in which only the neck muscles were affected; this 
case was interesting for, as it showed increased knee jerks and 
ankle clonus, the pyramidal tracts were probably injured in their 
course through the cervical cord. 

Erb classified as acute superior-anterior poliomyelitis those 
cases in which the disease is situated in the cervical region of the 


cord as high as the first cervical segment and partly invades the 
medulla oblongata to attack isolated cranial nerves. Foerster had 
previously described this form. 

Oculo-pupillary signs such as narrowing of the palpebral fis- 
sure and contraction of the pupil have occasionally been observed 
(Wickman,Oppenheim, J. Hoffmann, Spieler, Lindner and Mally). 

Rectal and Bladder Phenomena. — ^Although Heine observed 
that a temporary weakness of the bladder and rectum might occur, 
it was supposed that bladder disturbances did not arise in infantile 
paralysis. Medin, however, during the fever stage of several 
cases, observed retention of urine, which occasionally demanded 
catheterization. During the Swedish epidemic of 1905 I recog- 
nized many cases of retention, but only isolated examples of incon- 
tinence of urine. Zappert, also, has reported bladder disturbances. 
Ed. Miiller considers that they are among the commonest of the 
signs of the early stage of the disease and that their frequency is 
underestimated because they are so transient and slight. They 
soon disappear and only rarely persist for any length of time. 
These disturbances of micturition may be a febrile epiphenomenon ; 
but, as among children who have already learnt to control their 
sphincters, such disturbances seem to be commoner in Heine- 
Medin's than in any other infectious disease, I believe they more 
probably are due to changes in the nervous system. Moreover, 
their organic nature is confirmed by their long duration in quite 
a series of cases and by their almost exclusive association with 
paralysis of the legs (Krause and Ed. Miiller). Spieler, however, 
observed persistent severe retention of urine associated with 
paralysis of one leg, and Peiper reported a case in which it was 
associated with paralysis of an arm. Oppenheim considers that 
the rare occurrence of sphincter paralysis in this disease favors 
the view of L. R. Muller that the centers for the bladder and 
rectum lie not in the spinal cord but in the sympathetic ganglia. 
Foerssner, Sjovall, and others, also, have reported sphincter 
trouble in Heine-Medin's disease. As the ganglion cells often are 
slightly or not at all affected, whereas the interstitial tissue usually 
suffers severely, the evanescent nature of the bladder disturbances 
may perhaps be deemed in harmony with the anatomical change. 
The transient bladder troubles are probably analogous to the fleet- 
ing muscular palsies already discussed. 



Sensibility. — Generally, poliomyelitis shows no objective dis- 
turbances of sensibility. However, there are a number of cases 
known where sensory disturbances were proved. Medin observed 
a child who had a transient complete anesthesia of the legs. -A 
similar case was noted by Krause. A patient of Wickman showed 
a distinct diminution of sensibility to pain over the legs ; the tem- 
perature sense in this case was also impaired and it persisted 
unimproved for at least one year after the commencement of the 
illness. Diminution of sensibility to the faradic current has been 
reported by Vulpian^ Seeligmiiller and Oppenheim. Wickman 
observed that this disturbance very regularly occurred and that it 
was not associated with any other impairment. Ed. Miiller 
thought that in adults he could demonstrate at the beginning of 
the disease a widespread diminution of sensibility, mainly to pain 
and temperature; he alleges that this analgesia is very common in 
the initial stage, but that on account of its transient character, and 
of the early age of most of the patients, it generally escapes ob- 
servation. In one of his cases the sensory changes were marked. 
Dissociated disturbances of sensibility imply a posterior horn 
lesion — ^an implication in harmony with pathological findings. 

Cerebrospinal Fluid. — The marked meningitic symptoms and 
the constant round-cell infiltration of the pia lead us to anticipate 
some deviation from the normal in the cerebrospinal fluid. . Miiller 
invariably found the fluid to be at high pressure, even a few weeks 
after the beginning of the. disease. The fluid was clear and quite 
sterile; its albuminous content was increased; the addition of 
silver nitrate gave distinct indications of chloride ; the cell content 
consisted of lymphocytes so few as not to be visible as a sediment 
on centrifugalization. Wollstein obtained practically the same 
results. Other investigators, Guinon and Paris, Triboulet and 
Lippman, Achard and Grenet, Brissaud and Londe, Starr, Petren 
and Ehrenberg, reported an increase in the number of lymphocytes. 
Leucocytes as well as lymphocytes have been found in some cases, 
but only very exceptionally (Raymond and Sicard, Netter) were 
the leucocytes in the majority. The results of cytological exami- 
nations correspond therefore with the microscopical investigations, 
which showed a lymphocytic infiltration of the pia. In isolated 
cases (Spieler and Netter), the clear fluid on standing coagulates. 



In the chapter on etiology I have already discussed the results 
. of bacteriological investigation of the cerebrospinal fluid. 

In several cases, WoUstein, and Romer and Joseph studied 
the complement fixation properties of the cerebrospinal fluid, but 
obtained negative results. 

Final or Atrophic Stage, — Reference has already been made 
to the occurrence of partial or even of complete disappearance 
of the paralysis. The period within which, under proper treat- 
ment, involution or recovery is still possible, is about one year, 
or, according to some authors, even longer. Finally a time arrives 
when the existing paralysis remains stationary. The disease has 
then attained the chronic or final stage. Heine, Duchenne, Char- 
cot, Seeligmiiller and others exhaustively studied this stage. 

In addition to the changeless paralysis and the atrophy of mus- 
cles, secondary phenomena, such as deformities, alteration in the 
bones and joints, anomalous development, and vasomotor disturb- 
ances characterize this stage. Atrophy of varying degree is pres- 
ent in the permanently paralyzed muscles. Occasionally this 
atrophy is cloaked by a pseudohypertrophy. But the atrophy and 
the consequent change in the configuration of the limb is generally 

Fibrillary twitchings have occasionally been observed in the 
atrophic muscles (J. Hoffmann). 

The most frequent deformity is pes equinus, which, in patients 
confined to bed, arises from the drooping of the foot and the pres- 
sure of the bed clothes. Reducible at first, the foot later becomes 
fixed by retraction of the muscles. The contracture of the non- 
paralyzed flexors of the foot aggravates the deformity. 

The pes equinus may develop gradually from an attempt to 
compensate for the diminished growth of the affected leg. 

More rarely than pes equinus, pes varus results. Quite fre- 
quently the deformity is neither a pure pes equinus, nor yet a pes 
varus, but an equino-varus. Pes valgus and pes calcaneus also 
may develop. I shall not discuss the origin of these deformities, 
nor the bone and joint changes, for they more closely concern the 
orthopedist than the neurologist. These deformities disclose that 
the paralysis does not affect all the muscles of any group. When 
muscle groups are completely implicated, loose joints result espe- 
cially at the ankle, shoulder or hip. 


At the knee joint hyperextension may occur and produce a 
more or less distinct genu recurvatum. Hyperextension is often 
detectable in cases in which the paralysis is very slight; in my 
experience it is without diagnostic importance. More rare than 
genu recurvatum is genu valgum or genu varum. In certain cases 
a flexor contracture develops at the knee joint, A great number 
of patients present scoliosis. The scoliosis may be static — sec- 

Fic. 2. Spinal form of poliomyelitis with parafyses and atrophy of 
the left arm since childhood. (The muscles of the shoulder girdle mostly 
involved. After Bryom Bramwell.) 

ondary to a paralysis and shortening of a leg — or it may be a 
sequel to a partial paralysis of the back muscles. Messner, Kir- 
misson, Vulpius and most other investigators state that the con- 


vexity is generally directed towards the healthy side. Carles, 
however, has described a number of cases where the convexity 
was directed towards the affected side. In spite of the many in- 
vestigations of scoliosis, its mechanism has not yet been explained. 
Lordosis may arise from paralysis either of the back muscles or 
of the abdominal muscles arid kyphosis may also occur but both 
are rarer than scoliosis. 

If — as seldom happens — the neck muscles be only partially 
paralyzed, a torticollis may arise from contracture of the sterno- 
cleidomastoids of the healthy side. 

Although contractures and deformities have gradually passed 
into the realm of orthopedic surgery, they yet merit minute atten- 
tion from physicians and neurologists who alone are in a position 
to prevent their development. The avoidance of these deformi- 
ties is of prime importance for they tremendously increase the 
difficulty of the surgeon's task. The accompanying pictures depict 
the extent to which such deformities may 6xist. 

If the extremities be severely affected, their growth is generally 
retarded. Heine demonstrated by palpation that in this disease 
the bones may become atrophied ; recently his observation has been 
confirmed by means of X-ray examination by Johannesen, Achard 
and Levi, Oppenheim and others. 

In a few cases, however (Seeligmiiller, Kalischer, Neurath, 
Oppenheim), an elongation of paralyzed extremities has been ob- 
served. Various explanations have been given of this paradoxical 
behavior of the bones. Seeligmiiller supposed that the freedom 
from use might promote elongation, whereas Kalischer blamed 
trophic influences. According to Neurath, the elongation is only 
apparent and transient; only rachitic children suffering from re- 
cent poliomyelitis are said to show it; in them, if the paralysis 
be unilateral, the rachitic process — which retards growth — is made 
more obvious in the non-paralyzed limb. The growth of the para- 
lyzed leg sometimes is surpassed by that of the non-paralyzed leg 
only after the rickets has disappeared. 

Vasomotor disturbances manifest themselves in cyanosis and 
in lowering of the surface temperature. Heine described these 
changes and showed that the difference of temperature between 
the paralyzed and sound extremity might be considerable. 

Higier, in a few cases, noted a striking dryness restricted to 
the skin of the paralyzed extremities. 


Another vasomotor change, first observed by Oppenheim, is an 
indurated edema, which may be so marked as to simulate an 
hypertrophy of the paralyzed leg. 

Among other anomaUes of Heine-Medin's disease, Oppenheim 
mentioned immoderate development of the penis and the pre- 
cocious appearance of hair upon the mons veneris in the yoiing. 

Fig. 3. Fia 4 

Figs. 3-4. Spinal form of poliomyelitis with extensive paralyses and 
deformities. (After Johannessen.) 

Relapses. — The initial symptoms — as I have already said — may 
develop in two relays. The second relay, as if it were a relapse, 
occasionally occurs after the patient has recovered from the first. 
Paralysis may also follow an analogous course. Medin, Auerbach, 
Leegaard, Neurath, Foerster and Schwartz (New York epidemic) 
and others have mentioned such cases. The interval between the 
attacks may be weeks or months. These relapses contradict clin- 
ical, epidemiological and experimental experience which indicate 
that a single infection produces immunity. 



The So-called Laitdry's Paralysis Type 

Reference has already been made to distinct and continuous 
progression of the paralysis from one part of the body to another. 
If in such cases respiratory disturbances arise, death follows fast 
and a symptom complex, known to literature as Landry's paralysis, 
thus evolves. 

In 1859, Landry described a disease, characterized by flaccid 
paralysis, beginning in the legs, progressing upwards and termi- 
nating in respiratory paralysis. Sensibility remained intact or was 
only slightly diminished; the electrical reactions were unaltered, 
and the post-mortem findings were negative. The last two fea- 
tures were later disproved. In an array of cases, microscopical 
examination demonstrated morbid changes — usually a multiple 
neuritis or acute myelitis, occasionally an acute poliomyelitis (Im- 
mermann, Monckeberg, Schmaus). 

Later Wickman showed that the fatal cases of acute poliomye- 
litis ended in exactly the same clinical picture as Landry's paral- 
ysis and that many cases, which were recorded as Landry's paral- 
ysis with myelitic changes, were merely acute poliomyelitis. These 
statements were corroborated in subsequent epidemics. 

This type affects mostly the leg. After initial general symp- 
toms, paralysis in the legs develops and progresses upwards to at- 
tack first the muscles of the abdomen and back, then the arm and 
neck, and finally bulbar symptoms appear. Cranial nerves are 
attacked, and as the respiratory center is implicated, dyspnea ap- 
pears. Death occurs on the third or fourth day. Generally, con- 
sciousness remains clear until the very end; more rarely, coma 
precedes death; occasionally, Cheyne- Stokes' respiration appears. 
Sensibility is either normal or only slightly reduced. 

If the disease progresses so far as to produce respiratory dis- 
turbances the issue is usually fatal. If recovery does take place, 
signs of a widespread spinal type of the disease occasionally asso- 
ciated with paralysis of isolated cranial nerves persist. 



Rarer than the ascending is the descending type. According 
to Landry's original description, the symptoms appear in the re- 
gion of the bulb and thence extend downwards. This descending- 
type is very rare. But such forms as begin in the arm, attack 
then the leg and finally the bulb. Forms intermediate between 
ascending and descending paralysis are usually classified as " de- 
scending.*' Occasionally the legs may be spared altogether, and 
the arm paralysis be immediately succeeded by respiratory diffi- 
culty. The patient then quickly sinks. 

This progressive course with terminal disturbance of respira- 
tion is most evident in adults, as they can themselves observe the 
advance of the disease. Most lethal cases so evolve. In older 
children the progress may readily be traced; in those of tender 
years the difficulty of following the evolution is naturally greater, 
but not insurmountable. 

The negative results originally obtained on electrical examina- 
tion by Landry have been corroborated ; such patients generally die 
before electrical changes have time to develop. 

During the Swedish epidemic of 1905, of 159 patients who 
died during the first two weeks, 45 conformed with the picture 
of Landry's disease (32 ascending, 13 descending paralysis). As 
most of the fatal cases were not described in detail but were re- 
ported only as having shown widespread paralysis, these figures 
are too low. I do not mean that this is the only mode of death 
in poliomyelitis. The meningitic symptoms may predominate, but 
such cases are more rare. In the Austrian epidemic, among 29 
deaths, Zappert found 14 cases of Landry's paralysis. He stated 
that older children were so attacked; whereas, among children 
under five years of age, cerebral signs predominated. Zappert's 
experience may have been peculiar to the epidemic he observed; 
I am, however, of the opinion that the difference in great part 
depends not upon variations in the course of the disease at the 
several age periods, but upon the greater ease with which the 
course can be determined in older individuals. 

That fatal cases usually run a course resembling Landry's 
paralysis is amply corroborated by numerous reports from the 
latest epidemics. 

3. The Bulbar (Medin) or Pontine Type {Oppenheim), — If 
we ignore isolated observations (Eisenlohr) not quite free from 


objection, Medin was the first to mention the involvement of the 
cranial nerves as a not uncommon complication of infantile paral- 
ysis. He further recognized the etiological connection of certain 
isolated cerebral nerve palsies with infantile spinal paralysis. 

In discussing the spinal type, it has been mentioned that not 
infrequently the cranial nerves are attacked. Either the spinal or 
the cerebral component may be emphasized in the clinical picture. 
Sometimes the cerebral may be so transient and ill defined as to 
rank only as a complication of the spinal symptom complex. 
Sometimes the spinal is the less obvious and symptoms of involve- 
ment of the bulb or of the brain stem predominate. There is, 
however, no sharp line of demarcation between these two compo- 
nents ; in a case of ES. Miilier, for example, a facial palsy coex- 
isted with marked hypotonia of the muscles and loss of knee jerks 
on one side. 

Yet there are cases which show only symptoms of infection of 
the bulb, pons, or brain stem — the bulbar, or pontine type. The 
seventh nerve is the most frequently attacked and as a rule the 

Fig. S. Fig. 6. 

Figs. 5-6. Bulbar form of poliomyelitis with paralysis of the left facial 
and the left hypoglossus. 

upper as well as the lower branch is implicated. The paralysis 
may be combined with atrophy and loss of electric excitability 
(Wickman and Oppenheim). The prognosis of facial palsy in 
this disease is usually good. The paralysis may be only partial; 
complete or practically complete recovery may then ensue. The 


facial palsy, which appears as a complication of the spinal type 
of Heine-Medin's disease, seems to have an especially good prog- 
nosis. Wickman showed microscopically that such transient pal- 
sies depend upon a not inconsiderable nuclear affection. As a 
rule the facial paralysis is partial ; rarely has an affection of both 
sides of the face been observed (Medin, Ed. Miiller). Spieler 
described a case where the facial paralysis was associated with a 
homolateral disturbance of taste. 

In several cases the paralysis of the seventh was associated 
with paralysis of the hypoglossal. The affected half of the tongue 
was flaccid to the touch; later, it atrophied. The patient had a 
feeling of difficulty in moving the tongue. Unilateral paralysis 
of the hypoglossal does not, however, cause much inconvenience. 
So far as I know the recovery of a case of bilateral paralysis has 
not yet been reported. Bilateral hypoglossal paralysis may have 
occurred in fatal cases in which paralysis of swallowing was 


Paralysis of the abducens and of the oculomotor nerve is not 
uncommon. The abducens in my experience is more frequently 
affected than the oculomotor. Medin and Wickman have reported 
cases of paralysis of both the abducens and the oculomotor in 
which ultimately the trochlear shared so as to produce a more or 
* less complete ophthalmoplegia. The paralysis is generally partial. 
During the epidemic in Breslau, in 1909, I saw, however, in 
Czerny's clinic for children, a child affected by bilateral external 
ophthalmoplegia after a short initial stage in which sweating was 
conspicuous. The completely motionless eyes were directed for- 
wards; distinct though partial ptosis was present on both sides, 
but accommodation and convergence were preserved. Takahashi 
reported an analogous case in the Vienna epidemic: paralysis of 
the external oculomotor and of the trochlear nerves on both sides 
was present, together with a slight paralysis of the facial and of 
the left hypoglossal. 

In cases of unilateral ophthalmoplegia the seventh fibers to the 
levator palpebrse were unaffected. Yet, in Heine-Medin's disease, 
ptosis may occur and may be the only sign of affection of the eye 
muscles. Nystagmus occasionally may also be observed (Medin, 
Ed. Miiller, Netter). 

I may appropriately here mention that the optic nerve also is 



in rare cases affected. Tedeschi found complete blindness with 
optic atrophy in the left eye of a chronic case and Wickman dem- 
onstrated optic neuritis in a recent case. Ed. Miiller, however, 
found the fundus always quite normal. 

As observed by Medin, Wickman, J. Hoffmann, Lindner and 
Mally, implication of the trigeminal may cause a paralysis of the 
jaw muscles. 

The ninth, tenth and eleventh nerves may also be affected. In 
several, mostly fatal, cases difficulty in swallowing was present, 
but isolated paralysis of the pharynx has also appeared in a few 
cases. Wickman recorded as the only symptom in one case, a 
unilateral paralysis of the velum palati. If the palsy is incom- 
plete, the injury to the muscular apparatus may still be recog- 
nized from the striking tendency of the patient to swallow "the 
wrong way." 

Involvement of the laryngeal muscles may produce hoarseness 
or aphonia (Medin, Huet, Wickman, J. Hoffmann). Respira- 
tory disturbances may depend upon either an affection of the 
.center for the intercostal muscles or a lesion of the nucleus of the 
vagus. It is sometimes impossible to distinguish the precise origin 
of the disturbance^ One kind of respiratory disturbance, which 
in all probability is due to involvement of the vagus, is the spells 
of respiratory difficulty described by Wickman and Medin ; tachy- 
cardia accompanies these spells. 

Cheyne-Stokes' respiration, which has been observed in a few 
cases, is certainly due to an affection of the respiratory center. 
I have already mentioned a case in which the accessorius almost 
alone was involved. During the epidemic in Sweden, in 1905, 
paralysis localized to the neck muscles was noted in a few cases. 
Besides these paralyses of cranial nerves, the bulbar type of 
Heine-Medin's disease sometimes presents symptoms which arise 
from implication of nerve tracts which merely pass through the 
brain stem or bulb. Wickman described such cases; in one, be- 
sides paralysis of the eye muscles and of the left side of the face 
and right side of the tongue, cerebellar ataxia was present ; another 
showed paralysis of the left facial and hypoglossal, slight scan- 
ning, syllable-stumbling speech, some ataxia of the arms and exag- 
geration of the deep reflexes of the legs. Zappert and Spieler 
enumerate analogous cases. J. Hoffmann observed in two cases 



dizziness which he thought was of bulbar pontine origin. The 
following figures may serve to show the frequency of cranial 
nerve affections. Medio found among 64 or 65 cases, nine cases 
of involvement of the facial, in three of which no other symptom 
of the disease was present. Paralysis of the hypc^lossus was 
noted in five cases, and, of the abducens, in six. The accessorius 
was implicated in four cases, the oculomotorius in three, the 
trigeminal in one, and the vagus in two. 

During the Swedish epidemic of 1905, 1 collected the following 
figures: c-«i.i Nerv= Aff«,i™, 

AMOclalcd wiih SplDil CnDlalN.rvn 

VII . 

42 34 

As shown in this table 42 different paralyses occurred in 34 
patients; the 34 affections of cranial nerves, alone, occurred in 
22 patients (vide page 63) ; therefore, it is evident that in a num- 
ber of patients paralysis of the cranial appears in combination 
with paralysis of the spinal nerves. Leegaard in 311 cases of 
paralysis twice found the facial alone implicated (0.64 per cent.) 
and thrice, facial combined with spinal paralysis ; once ptosis ap- 
peared associated with' an affection otherwise confined to the 
spinal cord. Ed. Muller observed no fewer than 13 facial and 
3 unilateral abducens palsies among 100 cases, but he detected no 
implication of the other cranial nerves. 

Zappert collected 25 instances of combined cerebral and spinal 
nerve affections out of about 290 cases. During the Austrian 
epidemic, cases occurred in which only the. cranial nerves were 
attacked, but with reference to these Zappert gives no exact 
figures. Spieler gave a more detailed report upon • • '■•■•^ -.-^=- 
from this epidemic. Cranial nerves were involved i] 
the facial in eleven, hypoglossal in five, the ocuio 
and the vagus in two. Bulbar disturbances of spt 


nystagmus appeared twice, and difference of the pupils four times, 
twice due to spinal cord lesions, for the oculopupillary symptom 
was present. Three of these cases were almost exclusively bulbar- 
pontine in type, one showed associated cerebellar ataxia, four had 
spinal cord symptoms, and three were of the encephalitic type. 

Among the 752 cases of the New York epidemic, involvement 
of the cranial nerves is reported to have occurred as follows: 
Facial palsy 27 (14 right, 4 left side, bilateral 2, side not specified, 
7) ; eyelids, 18; strabismus, 26; difficulty in swallowing, 18; and 
speech affection, 28. 

The inconsistency of these statements arises partly because re- 
ports of epidemics mostly are the result of collective investiga- 
tions, in which the primary data may be imperfect, and partly 
because in regard to cranial nerve involvement as to other par- 
ticulars, the features of the disease vary in different epidemics. 
In 1887, during the Stockholm epidemic, the keen observation of 
Medin detected 8 instances of facial palsy among 44 or 45 cases, 
but in the 1895 epidemic only i. 

Inflammatory changes are the basis of the signs of affection 
of the bulb and brain stem. Clinically the alteration in the cranial 
nerve nuclei is the most evident change, yet according to the cur- 
rent nomenclature these cases must be regarded as polioencepha- 
litis. We must, however, distinguish superior polioencephalitis 
from inferior polioencephalitis. In superior polioencephalitis we 
must further, I believe, differentiate two forms — ^the recognized 
Wernicke form and one which I suggest should be named the 
Medin form. These two forms differ not only in their etiology 
but also in their general course. 

Wernicke's form arises principally from intoxications, the 
most usual of which is alcoholic. It is generally accompanied by 
mental changes which may culminate in delirium tremens, and it 
usually pursues an afebrile, sometimes a subnormal temperature 
course. Hemorrhage is the common morbid change found in 
this form. 

Entirely different are the conditions in the Medin form. 
Here, in harmony with the infectious nature of Heine-Medin's 
disease, we find inflammatory changes in the brain stem. The 
disease is, moreover, febrile and usually shows none of the psychic 
disturbances peculiar to the Wernicke form. There are resem- 


blances between the Wernicke and Medin forms, but there are 
also distinct differences. I am of opinion, however, that cases of 
Heine-Medin's disease have been published under erroneous des- 
ignations. Still more certainly has this occurred with regard to 
the second principal division — acute inferior polioencephalitis. 
Several maladies are included here which have in common that 
they, although of different origin, are all due to infectious proc- 
esses ; that they are characterized by similar pathological changes ; 
and that they further correspond from the point of view of symp- 
tomatology. One of these varieties is nothing more nor less than 
the bulbar type of Heine-Medin's disease. The etiology, there- 
fore, is the key to the differential diagnosis. All cases of Heine- 
Medin's disease with bulbar localization are cases of acute inferior 
polioencephalitis, but all cases of acute inferior polioencephalitis 
are not cases of Heine-Medin's disease. 

As Heine-Medin's disease, during an epidemic, may express 
itself as a facial palsy, we may accept that, in sporadic cases, the 
disease may assume the same guise. Hence, some facial palsies 
which have been attributed to lesions of the seventh nerve trunk 
may really be due to inflammatory changes in the seventh nerve 

Oppenheim has repeatedly observed an initial febrile stage of 
one to three days' duration in young children, in whom facial 
paralysis acutely developed. He raised the question whether these 
paralyses were or were not sometimes of pontine origin. I, my- 
self, observed a sporadic case of facial palsy which in great proba- 
bility was due to Heine-Medin's disease, for the little brother of 
the patient was attacked about the same time by an abortive type 
of Heine-Medin's disease. 

4. The Cerebral Encephalitic Type. — Although Vizzioli had 
already established the relationship of spinal and of certain forms 
of cerebral paralysis in children, Striimpell was the first to give 
us a complete description of the cerebral type of Heine-Medin's 
disease, which he called "Acute Encephalitis in Children (polio- 
encephalitis acuta)." Pierre Marie in France also recognized this 
symptom complex as a disease entity. 

Striimpell describes the disease as follows: "After an initial 
stage, in which fever, vomiting and well marked convulsions occur, 
paralysis develops. It may be a hemiplegia, a monoplegia, or a 


facial paralysis, but it has the usual characters of a cerebral paral- 
ysis. In a number of cases, signs of motor irritation persist. 
Many patients show symptoms of epilepsy through life. In some 
the epileptic convulsions are confined to the afflicted side, but 
more frequently they are generalized epileptic seizures. Atheto- 
sis, chiefly of the hands, follows more often than epilepsy. Dis- 
turbance of speech sometimes appears; more often, a diminution 
of intelligence and moral deterioration are observed.'* 

This acute polioencephalitis must be deemed a special form 
of cerebral infantile paralysis. Just as in acute poliomyelitis, 
here, also, the distinguishing and specific character is the short 
febrile initial stage. Medin's observations and other facts seem 
to establish the accuracy of Striimpeirs teaching. Several physi- 
cians, however, have pointed out that the great recent epidemics 
apparently afford no indubitable substantiation of Striimpeirs 
views. I shall here briefly discuss the results which have sup- 
ported Striimpeirs doctrine and also the objections which have 
been urged against it. 

I shall first consider the pathological findings. Foci of en- 
cephalitis have been detected in all the recent cases which have 
been examined (Redlich, Wickman, Harbitz and Scheel). It was 
contended that as these foci were always very small, and as they 
produced no symptoms during life, they could be regarded only 
as symptomatic of a widespread affection of the central nervous 
system. Such a contention is quite correct, for the patient dies 
showing the usual spino-bulbar symptoms long before more ex- 
tended encephalitic processes have time to develop. Two cases 
of Harbitz and Scheel ran a different course and as they are of 
great importance I may perhaps be allowed more fully to refer 
to them. 

I. The patient was a man, 39 years old; the disease began 
with headache, fever and excessive sweating. A few days later 
stiffness of the neck, vomiting, delirium and general convulsions 
followed; in four days a left-sided hypoglossal paresis, rigidity of 
the limbs, exaggerated patellar reflexes, and, later, twitching of 
the left forearm and of the fingers appeared ; coma was replaced 
by death on the thirteenth day of the disease. On macroscopic 
examination of the organs after death, no change was visible ex- 
cept a marked inflammation and softening of the right temporal 


lobe, which at the frontal pole and over the under surface was 
so soft as almost to be diffluent. The changes were most marked 
in the cortex, but penetrated 2-3 cm. into the white matter, and 
effaced completely the line of demarcation between the cortex and 
the white substance. The process extended to the Island of Reil, 
also, and its surface was likewise softened, but only to a depth of 
2-3 mm. A similar softening 8-10 cm. in extent, and 2-3 mm. 
deep, spread in a sagittal plane, on the mesial surface of both 
hemispheres, corresponding to the gyri fornicati. Microscopical 
examination revealed an acute inflammatory infiltration at these 
sites, in the central ganglia, pons, medulla oblongata; and a pre- 
cisely similar change was present in the gray matter of the anterior 
horns of the upper cervical segments, such as has been often ob- 
served in cases of Heine-Medin's disease. A pial infiltration was 
found elsewhere in the spinal cord. 

2. In the other case, a child seven years old suddenly developed 
fever, vomiting, drowsiness, twitching in the left elbow, knee and 
hip joints and rigidity of the neck muscles. Death occurred in 
four days. In this case, an acute encephalitis of the left optic 
thalamus was found. Otherwise, even upon microscopical exami- 
nation, no abnormal condition could be detected except a hypere- 
mia most marked in the neighborhood of the aqueduct of Sylvius 
and of the cervical region of the cord. 

These two cases were observed in Christiania during the Nor- 
wegian epidemic of 1905, but their relation to the epidemic was 
left undecided by Harbitz and Scheel, as only 13 cases of acute 
poliomyelitis occurred in the whole city. The similarity of the 
morbid changes in each, and in the first the coexistence of unmis- 
takable evidence of poliomyelitis, although not absolute proof, yet 
convince me that both were cases of Heine-Medin's disease. 

Macroscopical findings have also been collected in cases of 
longer duration. Lamy found besides poliomyelitic changes in 
the lumbar' enlargement, four foci in the cortex of the left cere- 
bral hemisphere; one was in the parietal lobe, the others in the 
frontal. Still more extensive destruction of brain substance was 
established by Rossi in a man, 34 years old, who since childhood 
had suffered from paraplegia; the right leg was spastic and the 
left flaccid. On post-mortem examination, Rossi found a patch 
of sclerosis in the anterior horn region of the lumbo-sacral cord; 


and, in addition, a widespread, bilaterally symmetrical destruction 
of the brain, implicating particularly the frontal lobe, the inner 
surface of the paracentral lobule and the great part of the corpus 
callosum. . 

In view of these proofs of the occurrence of extensive cerebral 
lesions in Heine-Medin's disease, I think that objections based 
upon the smallness of such lesions in most recent cases are not 
quite tenable. 

The etiological identity of acute poliomyelitis and of Striim- 
peirs polioencephalitis is supported first by the fact that flaccid 
and spastic palsies may occur in one and the same patient ; and, 
second, that occasionally an epidemiological connection may be 
proved between cases of poliomyelitis and of encephalitis. 

Williams, Neurath, Calabrese, Negro, Oppenheim, Pierre 
Marie and Wickman have reported cases of combined flaccid and 
spastic paralysis. Although it may be argued that the spasticity 
was due to a lesion of the pyramidal tract in the spinal cord, the 
case just quoted from Rossi shows that it may also be due to a 
cerebral lesion. Still more convincing in my opinion are the facts 
concerning the occurrence of spasticity during epidemics. Mobius 
observed a sister and brother affected with fever and malaise which 
they developed almost simultaneously. The one had a flaccid 
paralysis, as a sequel ; the other a spastic hemiplegia with choreic 
movements. During the epidemic in Stockholm, Medin saw three 
cases which presented an acute febrile onset, somnolence, twitch- 
ing and paralysis of one side of the body, and spastic symptoms. 
In one case, athetotic, in another, choreic movements appeared. 
Twice a paralysis of the abducens was observed. Concerning a 
fourth case, Medin admitted he was uncertain if it were a menin- 
gitis or a polioencephalitis, but its subsequent course with its rapid 
improvement and complete recovery convinced him it was a polio- 
encephalitis. It corresponded perhaps more to the meningitic 

Several other cases of Medin showed symptoms indicative of a 
brain lesion. One case in which the etiological relationship to 
Heine-Medin's disease seems to me to be placed beyond doubt is 
especially interesting: A small boy was feverish and somnolent; 
his legs and arms became paralyzed; and five days later, appar- 
ently after the appearance of respiratory difficulty, he died. The 


physician considered the case to be meningitis, until the patient's 
brother a few days later developed fever and pain in the back. 
In this second case, after some time, a paralysis of the lower 
branch of the seventh nerve appeared, and then disappeared ; and 
the knee jerks markedly increased. A contracture in the thigh 
muscles could be demoitstrated by passive movement. The gait 
was spastic, broad-based, and uncertain. On account of this last 
symptom, Medin recorded the case as an acute ataxia. But I 
believe that here also was a case of encephalitis. 

Against Medin's cases one might protest — as has been done — 
that they were merely coincidences and had no etiological relation 
to the prevailing epidemic of poliomyelitis. Anyone experienced 
in the pathology of children knows, however, that cases such as 
those described by Medin are extremely rare; and, besides, the 
death in the one case was typical of acute poliomyelitis. 

Further observations have been made by Buccelli upon the 
synchronous occurrence of encephalitis and poliomyelitis. He 
studied, in 1897, in a restricted locality in Genoa, a small epidemic 
of 17 cases. Some of the cases were of a cerebral, others of a 
spinal type. In one house, where several children were ill, one 
developed spinal and two cerebral infantile paralysis (cited from 
Starr). Buccelli collected the cases of polioencephalitis treated 
in the polyclinic at Genoa, and found that they had been most fre- 
quent during summer. But neither Neurath in the Vienna, nor 
J. Hoffmann in the Heidelberg epidemic, was able to establish 
this connection. 

Aug. Hoffmann reported the simultaneous illness of two chil- 
dren, one of whom presented a flaccid paralysis; the other, a 
spastic hemiplegia with athetosis, ankle clonus and Babinski's sign. 

If now we turn to the larger outbreaks, we have to admit that 
they afford only meager corroboration. 

During the Swedish epidemic, among all the hundreds of cases 
which I personally examined, I observed no case of spastic hemi- 
plegia. It is, however, quite possible that among those I did not 
examine spasticity occurred. The reports made to me by my col- 
leagues, in many instances, dealt mainly with the localization of 
the paralysis, and omitted to mention the condition of the reflexes. 
Only once a spastic paralysis of the arm was observed. -Quite a 
number of my colleagues, however, reported the occurrence of 
aphasia which invariably proved transient. 


Leegaard reports only two cases of encephalitis. 

No case of spastic hemiplegia was recorded from the American 
epidemic. In one family, however, one child was said to be at- 
tacked by the spinal, and another by the cerebral type, but no 
further information was given ; and aphasia was reported only in 
one case. 

Ed. Miiller, who had an opportunity to examine over one hun- 
dred . patients, believes that there undoubtedly is a clinical form 
of Heine-Medin's disease, which may be called cerebral infantile 
paralysis, but that it is very rare. In four of Miiller's cases only 
spastic paralysis developed; and in two, a spastic was combined 
with a flaccid paralysis. Another case, which Miiller thinks was a 
brain lesion, showed a right-sided spastic paresis of the extremi- 
ties, with implication of the right side of the face. 

During the Austrian epidemic, Zappert observed three cases 
probably of an encephalitic nature. In one of these, the remains 
of a right-sided hemiplegia and an atrophic paralysis of the left 
leg coexisted. 

I9 another, according to the statement of the attending physi- 
cian, "a severe, febrile, acute encephalitis with left-sided paral- 
ysis " ended in recovery, and the third showed clinically and patho- 
logically a combination of encephalitis and poliomyelitis. 

In spite of the meager data, Zappert is disinclined to deny the 
essential relationship of encephalitis to Heine^Medin's disease. 
Spieler records three cases of encephalitis among the 44 patients 
admitted to the Karolinen-Kinderspital. Another case observed 
during the Vienna epidemic, but not reported by Zappert, is re- 
corded by Schlesinger as belonging to the encephalitic type of 
Heine-Medin's disease. 

In the neighborhood of Hamburg, Nonne observed in four vil- 
lages, in 1905, a small epidemic of 22 cases. In most of the cases 
the common type of poliomyelitis occurred. In a few, however, 
unusual symptoms appeared : Nonne observed in two adults a uni- 
lateral encephalitic paralysis ; both recovered without residues. 

Krause also observed one case of encephalitis during the 1909 
epidemic in Westphalia. 

The testin^ony of the great epidemics upon this point has ob- 
viously been very slight. But in judging these facts we must con- 


sider, first, that most of the material has merely been gathered 
from general reports; and, second, that the disease from time to 
time and from place to place not inconsiderably varies. 

The first circumstance implies the possibility of lack of com- 
pleteness in the primary data. Often in cases of hemiplegia, no 
reference was made to the patellar reflex. And further, if a 
spastic hemiplegia occurred, it depended upon the knowledge and 
personal opinion of the attending physician whether it was in- 
cluded with the other cases of poliomyelitis, or considered as an 
independent disease. In the latter contingency, the case was prob- 
ably omitted from the statistics. On the other hand, encephalitis 
in the initial stage often simulates meningitis and usually is then 
so diagnosed, for practitioners are better acquainted with the na- 
ture of meningitis than of encephalitis. 

The second circumstance, the variability of the disease, must 
not be undervalued, but I have already dwelt upon it in the 

The greatest difficulty seems to me to lie in the results of ex- 
perimental poliomyelitis. In monkeys, after intracerebral injec- 
tion, a poliomyelitis^ not an encephalitis, regularly appears. 

From all facts at our disposal, it is probable that in man the 
virus of Heine-Medin's disease may cause encephalitic changes. 
Symptoms may, therefore, arise in this disease of a very variable 
but distinctly encephalitic character. Occasionally, the encepha- 
litic affection may assume the form of a hemiplegia, but this is 
rarer and of better prognosis than was formerly thought. Further 
exact observations are much needed on this subject. 

Finally, I may mention Petren's view that encephalitis is caused 
by a special virus, which occasionally gives rise to poliomyelitis. 
For lack of fundamental facts we shall not at present discuss this 

5. Ataxic Type. — Medin observed during an epidemic of in- 
fantile paralysis that some cases showed only or chiefly ataxic 
symptoms. He compared these motor disturbances with those of 
Friedreich's ataxia. The child's walk is uncertain, staggering and 
wide-based. There is evident difficulty in maintaining balance: 
the child stumbles and falls often and readily. Medin's cases, 
however, showed symptoms which distinguished them from the 
typical spinal infantile paralysis: in none did atrophy of the 


muscles develop ; and in many the patellar reflexes were increased. 

Wickman also observed instances in which ataxic symptoms 
were especially conspicuous. The ataxia was sometimes of a dis- 
tinctly cerebellar type, but here paralysis of cranial, and, to a lesser 
degree, of spinal nerves also occurred. In other cases, the only 
demonstrable sign, besides the ataxia, was either diminution or 
loss of the patellar reflexes. These cases did not present the dis- 
tinctive features of a cerebellar ataxia. Occasionally, the dis- 
turbances, although evident, were not prominent in the picture of 
the disease. 

Ataxia .was more frequently observed in subsequent epidemics. 
Its presence was mentioned by Zappert and Spieler in several cases 
in which it seemed to be associated with cranial nerve lesions. 
Lindner and Mally reported a case of cerebellar ataxia, paresis, 
and atrophy of the left thigh, marked increase of both patellar 
reflexes, and ankle clonus. The cranial nerves were not implicated. 

A case of aphasia, paralysis of the right arm, and ataxia was 
described by Netter. 

Nonne saw in a child during the Heidelberg epidemic a severe 
status hemiepilepticus, which was followed by a high degree of 
general ataxia of the acute cerebellar type. The case pursued a 
favorable course and ended in complete recovery. 

The pathologic basis of the ataxia in my opinion is inconstant. 
Medin thought a neuritic process was concerned, but such seems 
hardly probable, for in all cases the tendon reflexes were increased. 
In cases which present cranial nerve signs, the ataxia may be due 
*to an interruption in the coordinating tracts of the midbrain. 
Perhaps the ataxia may also arise from changes in the cerebellum, 
which have been found in almost every recent case examined. In 
other cases the lesion may be situated in the spinal cord — in Clarke's 
column, perhaps. 

Zappert thinks it undesirable to consider ataxic cases sepa- 
rately. He prefers to include them with the bulbar, or pontine 
type. Although some undoubtedly belong to the bulbar type, 
there are many others in which the ataxia is not distinctly cere- 
bellar in character, and in which all signs of either bulbar or 
pontine implication are absent. The fundamental site of the 
changes in these cases still evades us, but to imply for a whole 
group of cases certain changes which are perhaps not common to 
all, seems to me undesirable. 


6. The Polyneuritic Type. — In the description of the initial 
symptoms, pain and general tenderness were mentioned as usual 
features of Heine-Medin's disease. If the pain be severe and be 
accompanied by tenderness on pressure over nerve trunks, we 
have a picture which corresponds completely with the disease 
described in all text books as peripheral neuritis. When these 
symptoms sporadically appear, a diagnosis of peripheral neuritis 
is made. 

Medin first observed in an epidemic of infantile paralysis cases 
which resembled neuritis ; and during the epidemic of 1905 I and 
numerous other Swedish physicians encountered similar cases. 

The observations of later epidemics confirmed the occurrence 
of this form of the disease (Hartmann, Schlesinger, Foerster, Ed. 
Mijller, V. Stark, Netter, Sachs and others). In all of Foerster's 
cases the nerve trunks in the limbs were hypersensitive, and ten- 
derness was present on passive movements. Foerster found, also, 
in several patients the sciatic sign, which is mentioned by Wick- 
man, Lindner and Mally. These cases may progress to recovery 
or remain permanently paralyzed. If recovery occurs, harmony 
with the t'ext book description of acute neuritis becomes still 
more perfect. Rarely, disturbances of sensibility appear. Close 
examination has shown that these sensory disturbances have a dis- 
sociated character. Obviously, this fact can hardly be demon- 
strated in little children, in whom sensory examinations are per- 
force restricted exclusively to the pain sense. 

It is still undecided if these clinically polyneuritic forms 
really arise from inflammatory changes in the nerves. I person- 
ally am of opinion that they are exclusively produced by central 
changes and therefore it would, from my point of view, be more 
correct to designate them pseudo-neuritic. Rut post-mortem ex- 
amination in Heine-Medin's disease has never revealed the pres- 
ence of neuritis. Objective disturbances of sensibility are usu- 
ally lacking; and it is difficult to reconcile in such cases the exist- 
ence of a widespread paralysis and a lack of objective sensory dis- 
turbances upon the basis of a neuritis. 

Indeed, microscopical examinations of fatal cases of Heine- 
Medin's disease have not yet disclosed any changes in the periph- 
eral nerves. But on the other hand, such examinations have been 
restricted in extent and few in number; and so far as I know 


have not been made upon cases which from the distinctness of 
the neuritic symptoms definitely belong to this group. Although 
we can, therefore, say that the existence of a neuritis in Heine- 
Medin's disease has not been histologically demonstrated, we can- 
not completely exclude its possibility. 

It is, however, quite certain that Heine-Medin's disease is fre- 
quently indistinguishable from spontaneous, infective, acute poly- 
neuritis and it cannot be differentiated from the "amyotrophic 
plexus, neuritis of infancy," described by E. Remak. As in each 
of these, the paralysis directly follows a febrile initial stage, both 
stand, in all probability, in direct etiological relation to Heine- 
Medin's disease. I think it is of practical importance to distin- 
guish a neuritic or pseudo-neuritic type of Heine-Medin's disease. 

7. The Meningitic Type. — The signs of meningeal irritation, 
which can often be observed in Heine-Medin's disease, may, under 
certain conditions, attain such prominence as convincingly to re- 
semble some form of meningitis. Vomiting, headache, pain and 
rigidity in the neck and back, opisthotonus,* Kernig's sign, tonic 
and clonic spasms, strabismus, coma, etc. — all the symptoms of 
an acute meningitis in all degrees and in all possible combinations 
may be added to the picture of the disease. Only in the chronic 
stage does the course differ from that of a meningitis. In most 
cases, the signs of irritation cease and the characteristic palsies of 
Heine-Medin's disease become evident. In some, the disease, 
even after it has assumed a most threatening aspect, disappears in 
a tolerably short time and an astoundingly complete recovery en- 
sues. In others, under a more or less stormy aspect, the malady 
runs a lethal course. 

During the Swedish epidemic, numerous transitions from dis- 
tinct meningitis to ''typical poliomyelitis were observed. Upon 
this clinical basis and upon the epidemic connection of these men- 
ingitic cases with proven poliomyelitis, Wickman established a 
special meningitic form of Heine-Medin's disease. The following 
are two typical examples of this meningitic form : 

The first developed convulsions, marked somnolence, stiffness 
of the neck, opisthotonus, hyperesthesia, persistent tonic spasm 
of the limbs, strabismus, inequality of the pupils and retention, 
with subsequent incontinence, of urine. All these symptoms dis- 
appeared within two weeks and left no trace. 


The second, an adult, had fever, headache, vomiting, pain and 
stiffness in the neck and tonic spasms iti some of the muscles of 
the shoulders and arms. Later, cramps in the legs appeared; 
then, opisthotonus; and, finally, difficulty in speech and in swal- 
lowing developed and death came three days after the illness 
began. As this patient was pregnant, the physician thought she' 
suffered from eclampsia. He therefore induced premature labor. 
Post-mortem examination showed in the spinal cord the changes 
typical of acute poliomyelitis. In connection with this case, some 
others of a transient nature are mentioned on page JT, Upon 
epidemic, clinical and pathological grounds, the meningitic type 
is in established relation to Heine-Medin's disease. This has been 
confirmed by others. Leegaard in his statistics of the Norwegian 
epidemic reports cases which he enumerates as cerebrospinal men- 
ingitis, but which undoubtedly belong to this group. Zappert 
states that according to his observations during the Austrian epi- 
demic the existence of this type is beyond doubt. Spieler's state- 
ments about similar cases are of such great interest that I shall 
here quote them literally : In 8 out of 44 cases of Heine-Medin's 
disease, admitted to the Karolinen-Kinderspital in Vienna, more 
or less pronounced and typical meningeal symptoms were present. 
The picture of the disease in four of these eight so resembled a 
tuberculous meningitis that not until some time had elapsed was 
its relation to Heine-Medin's disease suspected. For a week or 
more the well known prodromal symptoms — change in disposi- 
tion, tiredness, nocturnal restlessness, screaming, occasional vomit- 
ing and obstipation — suggestive of commencing basic meningitis 
were present. This suggestion was reinforced by the sudden 
appearance of convulsions, which were associated with marked 
rigidity of the neck, irregularity of the pulse, Kernig's sign, transi- 
tory increase of the patellar reflexes, strabismus, general cuta- 
neous hyperesthesia, vasomotor disturbances, and typical cerebral 
facies. The deception was still further enhanced, for lumbar 
puncture yielded a clear fluid which was under increased pressure, 
which formed a distinct diffuse, non-reticular, fibrinous clot ; and 
which, on cytological examination, showed only numerous lympho- 
cytes. At length, the noteworthy retrogression of the signs of 
irritation, and, later, of the cranial nerve symptoms ; the complete 
disappearance of the fever; the more or less localized, flaccid 



paralysis of limb, of abdominal, and — as occurred in a private 
case — of isolated neck muscles, together with the appearance in 
them of the reaction of degeneration, and recovery either com- 
plete or associated with permanent, more or less diffuse, flaccid 
paralysis and atrophy of the muscles, permitted no doubt that 
these were cases of Heine-Medin's disease. 

In the epidemic in New York, a case occurred in which con- 
vulsions, rigidity of the neck, Babinski's sign and Kernig's sign 
led a distinguished pediatrist to diagnose meningitis (Schwartz). 
Hochhaus saw two cases in which post-mortem examination dem- 
onstrated conclusively Heine-Medin's disease, although the clin- 
ical course had been that of an acute meningitis. Netter called 
attention to the striking and frequent occurrence of signs of 
meningeal irritation during the Paris epidemic of Heine-Medin's 
disease. Kernig's sign was very often noted. One child was sent 
to the hospital with a diagnosis of cerebrospinal meningitis. 
Netter observed one case in which the spinal fluid was somewhat 
cloudy and yielded a fine cobweblike coagulum; but in another, 
the ftuid was clear. Netter further noted that in one third of his 
cases the disease began with distinct meningeal symptoms. He 
was able to prove in Paris, synchronous with the epidemic of 
poliomyelitis, the prevalence of a benign form of meningitis 
which he considered — correctly, I believe — to belong to the menin- 
gitic type of Heine-Medin's disease. 

Occasionally the spinal fluid coagulates (Netter and Spieler). 
Its other characters have already been discussed in dealing with 
the acute stages (page 29). 

How closely Heine-Medin's disease may resemble ordinary 
meiningitis has just been narrated. The knowledge of this men- 
ingitic form helps us to explain the statements of observers such 
as Caverley and Macphail, and Mackenzie, who reported that 
cerebrospinal meningitis and poliomyelitis may occur simulta- 
neously. It also bares the foundation of the belief that these two 
diseases are related. Wickman proved^ that where exact data 
were available no such relationship existed and he suggested that 
in both of the recent American outbreaks numerous and definite 
cases of the meningitic form of Heine-Medin's disease, alone, 

The Abortive Form. — During the Swedish epidemic of 1905, 



in the immediate neighborhood of well-defined cases of poliomye- 
litis, and in distinct etiological connection with them, many pa- 
tients were discovered who showed only general symptoms of 
being ill and presented no signs of paralysis. Such cases Wick- 
man designated Abortive Cases, Between the definitely abortive 
case running a course characterized merely by malaise, or by slight 
and fleeting palsies, and the completely typical and, even, some- 
times, fatal case, the existence of transitional forms was clearly 
established. Indeed, these various forms were occasionally ex- 
emplified among the respective members of one family. 

The picture of the abortive type corresponds in general with 
that of the initial stage of typical infantile paralysis. The attack 
as a rule is acute and accompanied by fever, headache and general 
malaise. In some cases these symptoms are associated with 
others, such as rigidity of the neck ; pain in the Aeck, back, loins, 
and limbs ; and paresthesia ; which point to implication of the ner- 
vous system. But these symptoms are not followed by paralysis. 
The patient usually recovers within several days and no trace of 
the disease remains except prostration which may be protracted. 
The abortive case thus presents only symptoms of a general infec- 
tion and no real localizing signs. Even if the disease sets in sud- 
denly, vague, ill-defined prodromal symptoms, such as exhaustion, 
mark its commencement. But after a few days generally the 
symptoms become acute. In discussing the initial stage it was 
mentioned that the height of the fever and the severity of the 
other signs are not significant of the further course of the disease. 
In abortive cases simultaneous with the usual complaint of head- 
ache is that of pain in the neck. Rigidity of the neck muscles is 
often then detected. In the abortive case not infrequently symptoms 
perhaps attributable to meningeal irritation arise. More or less 
marked opisthotonus even may occur. The disease then closely 
resembles meningism. Such cases are a link with the definite 
meningitic type of the disease. Among other signs of irritation 
pain in the limbs is especially marked. Usually several extremi- 
ties are tender but sometimes only one. Sometimes the severity 
of this tenderness is extreme. In such cases, for want of a better, 
a diagnosis of influenza is often made. 

Nausea, vomiting, diarrhea and other gastrointestinal symp- 
toms have frequently been observed in association with the abortive 


type ; sometimes so marked were they that gastrointestinal catarrh 
was suspected. 

Wickman distinguishes the following varieties of the abortive 
type : 

1. Cases running the course of a general infection. 

2. Cases in which signs of meningeal irritation are especially 
prominent ( " pseudo-meningism '* ) . 

3. Cases accompanied by distinct tenderness ("pseudo- 

4. Cases with gastrointestinal disturbances. 

Sometimes cases belong exclusively to one, more often to sev- 
eral of these varieties. As cases in which weakness or paralysis 
of the extremities or of the cranial nerves appears and quickly 
disappears might also be included among the abortive, this form 
obviously cannot be sharply differentiated from the others. These 
transient palsy cases Ed. Miiller calls " rudimentary " ; those I 
have described as " abortive " he calls " masked." As an example 
of how gradual the transition between the various forms may be, 
Wickman relates an indubitable Case in which the only objective 
sign was diminution of one patellar reflex. On the other hand, 
Wickman also observed abortive cases in which the patellar re- 
flexes were increased. Leegaard in his report of the Norwegian 
epidemic estimated that more than one third of all his cases were 
of the abortive type. Similar cases, although rarely reported, 
occurred in subsequent epidemics. The reasons for the rarity of 
reported abortive cases are, first, that reports are based upon col- 
lective investigations, the primary data for which are furnished 
only after the acute stage has passed ; and, second, that physicians 
as a rule are unaware that such symptoms belong to Heine-Medin's 
disease. Yet the existence of the abortive type can be proved in 
these epidemics. Records of the New York epidemic mention that 
cases with symptoms of a severe general infection with or without 
temporary paralysis were observed by various physicians. Zap- 
pert definitely states that, within small infected localities, he was 
able to establish the occurrence of a number of cases of obscure 
fever synchronous with the appearance of poliomyelitis. Physi- 
cians remarked frequently upon the cases of " influenza " and 
upon the gastrointestinal symptoms which developed in the vicinity 
of the cases of poliomyelitis. Zappert reports further a small 



localized epidemic in which about 20 persons were attacked by 
symptoms resembling influenza; in 10 of these people developed 
characteristic paralysis; no paralysis appeared in the others. 

Ed. Miiller particularly studied the abortive forms in tHe epi- 
demic in Hesse-Nassau. He verified the varieties I described, 
and, in addition, found cases evolving as bronchitis, or as sore 
throat. He, also, observed the connection between the several 
varieties. For instance, he saw one family in which three chil- 
dren were attacked with gastrointestinal symptoms. In the first 
child the symptoms all disappeared; in the second, only loss 
of tendon reflexes persisted; while in the third, typical paralysis 

Krause, who noted many cases of the gastrointestinal variety, 
mentioned that often the other members of the family suffered 
from diarrhea. " In one family," he reports, " seven persons were 
thus attacked." 

Records of abortive cases have accumulated recently, especially 
from the American epidemic (Lovett, Armstrong Davis, Ball and 

It may, therefore, be safely asserted that the occurrence of 
abortive forms during epidemics is a regular phenomenon. 

Abortive cases represent a considerable proportion of all the 
cases in any epidemic. Their exact ratio we cannot yet determine. 
Wickman's statistics of the Swedish epidemic of 1905 contain 
968 paralytic and 157 abortive cases. But as the abortive cases 
could be accurately enumerated only in limited districts, their total 
is underestimated here. In the several areas carefully examined, 
the proportion was quite inconstant. In one epidemic center, of 
31 cases, II (35 per cent.) were abortive. In another, where 
every case was detected, 49 cases were observed, of which 23 (46 
per cent.) were abortive. In yet another, which was studied by 
Wickman, 56 per cent, were abortive. It is not impossible that 
the frequency of those abortive cases, under certain conditions, 
may be even greater. 

A large number of abortive cases have been observed and de- 
scribed by Brorstrom, who believes that they are more frequent 
than the paralytic cases. He considers, however, acute poliomye- 
litis as a variety of influenza and admits, therefore, many cases 
which have no claim to discussion here. 


Leegaard, among 952 cases, found 358 of the abortive type. 
He remarks that this figure is too low ; that such cases are to a 
great extent overlooked, and that, without exaggeration, the abor- 
tive forms might be estimated at about one half of the total cases. 

Ed. Miiller is of the opinion that the abortive are far more 
numerous than the typical casesj especially among adults. Miiller 
thinks it possible that the abortion of the disease is due to an 
acquired immunity. I can neither confirm nor deny Miiller's 
statements,' but, at least, within the foci I studied a relatively 
greater frequency of the abortive type in adults was not evident. 
If acquired immunity had any practical importance in this ques- 
tion some great epidemics must be presumed to have occurred and 
to have conferred protection on the large number of people who 
now enjoy it. But epidemics of former years are unheard of in 
Germany. Miiller's hypothesis, however, is highly interesting, 
and will be more accessible to examinatipn when serological meth- 
ods of investigation are simplified. 

The common origin of the abortive and paralytic forms was 
established by clinical and epidemiological observations in Sweden. 
Further evidence of this etiological identity has lately been ob- 
tained by Levaditi and Netter. In the blood of a girl who was 
attacked by an abortive variety of Heine-Medin's disease, and 
who developed no paralytic symptoms, these observers found sub- 
stances exercising a specific neutralizing action upon the polio- 
myelitis virus. This child's brother was attacked at the same time 
by typical infantile paralysis and similar antibodies were found in 
his blood. • 

Finally, in the experimental poliomyelitis of monkeys, also, 
abortive varieties have been observed. 

The abortive type is of great importance, especially as regards 
the epidemic behavior of the malady. Obviously, the spread of 
the disease presents a totally diflFerent aspect if we consider not 
only the typical but also the abortive cases. 


Diagnosis and Differential Diagnosis 

As a general rule, a diagnosis of Heine-Medin's disease is 
justifiable if, after a short, acute, febrile, initial stage, paralysis 
of flaccid type develops. The paralysis attacks usually the leg, 
trunk or arm muscles ; rarely, the muscles supplied by the cranial 
nerves. During the initial stage, symptoms such as general ten- 
derness, rigidity of the neck, sweating and somnolence are to a 
certain extent characteristic. 

As Heine-Medin's disease often presents at the onset only the 
general characters of an ordinary infectious disease, we must be 
prepared to distinguish it from similar conditions due to other 
infections. If well-marked general tenderness be present a sus- 
picion either of influenza or of a rheumatic affection may arise. 
The latter, as a rule, is easily excluded; the tenderness in rheu- 
matic affections is usually localized to joints; whereas, in Heine- 
Medin's disease such a localization, although it may occur and be 
associated even with joint swelling, is extremely rare. 

To differentiate from influenza is more difficult. Clinically 
influenza has become as a lumber room in which most hetero- 
geneous conditions are lodged. Heine-Medin's disease may be 
separated from a real influenza produced by Pfeiffer's bacillus: 
in Heine-Medin's disease catarrhal symptoms, although generally 
present, are less, whereas sensory irritability as a rule is more 
severe than in influenza. Yet, a bronchitis, a conjunctivitis, or 
other catarrhal inflammation may appear in the course of infantile 

If gastrointestinal symptoms are present, or if they predomi- 
nate, an intestinal catarrh may be suspected. But in such cases, 
usually, some symptom, such as tenderness, or sweating, suggests 
that the nervous system is implicated. 

What has just been said applies to the abortive forms. These 
can be diagnosed with certainty only if they appear during an 
epidemic, or if they are associated with cases either of paralysis, 
or of indubitable implication of the nervous system. Among the 




most important of the signs of involvement of the nervous system 
is alteration pf the reflexes. The alteration may consist either of 
an increase or of a decrease. Hypotonus without actual paralysis 
has been described occasionally. Any unilateral alteration of the 
refleXej must be regarded as abnormal. We have to guard, how- 
ever, against concluding too hastily that the reflexes are absent, 
especially in children in whom, owing to muscular tension, deep 
reflexes are often difficult to elicit. 

In the initial stage, marked and occasionally persistent menin- 
geal symptoms may easily be mistaken either for epidemic cerebro- 
spinal or for tuberculous meningitis. But Heine-Medin's disease 
very rarely presents a herpes labialis such* as so often occurs in 
cerebrospinal meningitis; and psychic disturbances are more 
marked usually in cerebrospinal meningitis. Petren is of the opin- 
ion that the tendency to an exclusive spinal localization of the 
meningitic symptoms in Heine-Medin's disease differentiates it 
from cerebrospinal meningitis ; but although cerebral symptoms do 
predominate in cerebrospinal meningitis, yet each of these dis- 
eases has shown such great variation in this respect that selective 
localization, even when well defined, may mislead. The most re- 
liable means of discriminating lies in the use of lumbar puncture. 
In cerebrospinal meningitis, the cerebrospinal fluid appears cloudy ; 
presents a leucocytosis ; and may contain the intracellular men- 

In tuberculous meningitis, and in Heine-Medin's disease, lum- 
bar puncture yields no such distinctive features ; in both the fluid 
is clear, shows lymphocytpsis, and coagulates; but in tuberculous 
meningitis the clot forms a characteristic central thread. The 
rapidity of onset of each disease is very variable but tuberculous 
meningitis tends to develop more slowly. Indeed, as was shown 
in Spieler's description, the similarity of these two conditions may 
be extraordinary. The diagnostic difficulty is especially great in 
the pure meningitic types, but if tubercle bacilli can be demon- 
strated, or if characteristic palsies appear, the nature of the case 
becomes at once apparent. 

The existence of motor disturbances is by no means always so 
evident as to be obvious immediately. Sometimes, in the begin- 
ning of the disease, careful search is necessary. Especially in 
little children, repeated and skilful observation may be needful to 



establish the precise nature of the disturbance. In older children 
and in adults the diagnosis of paralysis is easier. If paralysis be 
demonstrable, then we have its character and the anamnesis to 
enable us to decide whether the disease is or is not Heine-Medin's. 
If it is, we shall learn that the patient became suddenly ill with 
the well-known initial symptoms. But we must bear in mind that 
painstaking investigation is sometimes necessary in order pre- 
cisely to ascertain the history of the development of the illness ; 
and further, that the initial symptoms may, although rarely, be 

The differential diagnosis from multiple neuritis is of some im- 
portance. A sharp distinction has here to be made between the 
various forms of neuritis — the toxic, the infective, and the post- 
infective. Of the toxic forms of neuritis the most common are 
those due to alcohol, arsenic and lead. The paralysis which ap- 
pears in any one of these, as a rule, is symmetrical ; diminishes in 
severity centripetally ; and develops much slower than, and lacks 
the febrile initial stage of, Heine-Medin's disease. The exciting 
causes can generally be ascertained in alcoholic neuritis and lead 
palsy. Both of these, in consequence of their special etiology, 
occur exclusively in adults. 

Among the post-infective forms of neuritis, diphtheritic poly- 
neuritis in children may closely resemble Heine-Medin^s disease. 
The resemblance may be so great — especially if no history be 
obtainable and the paralysis be extensive — that, at first, it may be 
practically impossible to differentiate between them; moreover, 
Heine-Medin's disease may begin with sore throat. In the last case, 
however, paralysis develops immediately when the throat affection 
occurs and not, as in diphtheritic palsy, some time afterwards. 
Diphtheritic palsy almost invariably affects the soft palate and the 
muscles of accommodation. Patients suffering from diffuse diph- 
theritic palsy look cachectic and often have a tolerably character- 
istic grayish yellow complexion. Symptoms, such as irregularity 
of the heart's action and cardiac dilatation, may be present in 
diphtheria but not in Heine-Medin's disease. One of the most 
important distinguishing features is the gradual development of 
diphtheritic palsies. If ' a recent case present combined bulbar 
and spinal symptoms — a picture common in diphtheritic paralysis 
and possible in Heine-AIedin's disease — and if the history of the 



development of the affection be vague and meager, the disease is 
probably Heine-Medin's. The symptoms of Heine-Medin's dis- 
ease may reach their maximum in a sick, recumbent child so rap- 
idly as to escape the notice of the child's parents; whereas, in 
diphtheria the motor disturbances are noted usually before they 
become so widespread as to give rise to the suspicion of Heine- 
Medin's disease. 

Epidemics have taught us that the clinical entity known as 
infective neuritis may be produced by the virus of acute polio- 
myelitis, that there is a neuritic type of Heine-Medin's disease. 
I believe we cannot diff'erentiate this type of Heine-Medin's dis- 
ease from many of the cases of so-called idiopathic infective poly- 
neuritis. No distinction exists between them; they are identical 
conditions. If in immediate relation to a short febrile stage, 
paralysis suddenly develops, and if no sensory disturbances exist 
except spontaneous pain and tenderness on pressure especially 
over nerves, Heine-Medin's disease is probably present. No other 
virus, apart from that of rabies, is known to attack the nervous 
system in such a fundamentally specific manner as the virus of 
Heine-Medin's disease. The existence of sensory disturbances 
has been looked upon as a distinguishing feature between acute 
polyneuritis and the spinal form of acute poliomyelitis. But sen- 
sory changes are not constant in the former and they have been 
observed in the latter disease. When sensory loss, however, does 
occur in Heine-Medin's disease, it is not marked ; it is seldom per- 
sistent; and it affects only the sensations of pain, heat and C9ld. 
These sensory changes arise from implication of the posterior 
horn. They can be satisfactorily demonstrated only in adults. 
In children, as dissociated sensory loss is difficult to determine, the 
disturbance is usually charted as a complete anesthesia. But if 
decreased perception of all forms of sensation really exist, or if 
the sense of touch be diminished and tenderness on pressure be 
present, the case is one of neuritis. If a neuritis be encountered its 
exciting cause remains to be discovered. It may be produced by 
the virus of Heine-Medin's disease or by other infective agents. 
Pathological investigation, mainly because of the limited extent 
to which recourse has been had to it, has not yet yielded any means 
by which we may differentiate these various infective agents. I 
think it necessary to separate the pathologic from the etiologic 


aspect until their relationship be made clear by our own experience 
in epidemics. No text book, as yet, advocates my attitude on this 
point. Contrary to custom, I hold that the outcome of the disease 
ought not to determine the diagnosis ; and a recovery from paral- 
ysis should indicate in dubio a polyneuritis. In a number of cases 
of poliomyelitis also recovery assuredly occurs. The most that 
may be said is that the persistence of paralysis is presumptive evi- 
dence of poliomyelitis; whereas, a benign course may equally 
indicate either a polyneuritis or a poliomyelitis. 

The occurrence of dissociated disturbance of sensibility, com- 
bined with flaccid paralysis — to which reference has just been 
made — raises the question of the differential diagnosis from syrin- 
gomyelia, but the essentially chronic course of syringomyelia at 
once distinguishes it from Heine-Medin's disease. Rarely, a case 
of hematomyelia presents the clinical aspect of acute poliomyelitis ; 
but striking disturbances of sensibility usually exist in the former, 
together with a history of a trauma, and of an afebrile development. 
Other varieties of myelitis, such as syphilitic myelitis, com- 
pression myelitis, and caisson paralysis, vary in symptomatology 
according to the localization of the disease focus. They chiefly 
differ from acute poliomyelitis in their sensory changes in which 
usually all forms of sensation are impHcated. In addition, bladder 
trouble is commonly conspicuous in these varieties and their clin- 
ical picture is that of a transverse myelitis. Rarely, syphilis, prin- 
cipally through vascular changes, causes a paralysis which in dis- 
tribution and in other respects corresponds to that arising from an 
acute poliomyelitis. From cases of such paralysis we must dis- 
tinguish instances of Heine-Medin's disease occurring in luetic 
subjects and evolving in the customary manner. 

A closer resemblance exists between labor paralysis, myatonia 
congenita, and Heine-Medin's disease. 

In labor palsies the deciding factor is again the anamnesis. 
Heine-Medin's disease may assume the characteristic localization 
of a plexus paralysis. If no history be obtainable, a differential 
diagnosis may be almost impossible, especially when the paralysis 
has persisted for years. 

In myatonia congenita (Oppenheim) great weakness with flac- 
cidity of the muscles and joints rather than actual paralysis is 


present. Myatonia congenita extensively implicates the extremi- 
ties, is congenital, and seems usually to be degenerative. 

In the suddenly developing pseudo-paralysis of rickets only 
extreme feebleness of the limbs is evident: the electrical reactions 
remain unimpaired. But according to Oppenheim atrophy may 
occur here, also. . 

In older children and in adults the question of hysteria arises 
sometimes. In hysteria sensory changes occur often; the reac- 
tions are normal, and atrophy is absent. 

Hip disease may simulate paralysis but examination will readily 
enable the one to be distinguished from the other. 

The so-called paralysis of Parrot which occurs occasionally in 
congenital syphilis must also be mentioned here. It is not a 
paralysis; the immobility in this affection is maintained because 
of the pain fulness of the diseased bones; the electrical reactions 
are normal; the condition usually appears during the first weeks 
of life and other symptoms of inherited lues, such as " snuffles " 
or eruptions, etc., are present also. 

Progressive muscular atrophy may be confounded with the 
chronic stage of Heine-Medin's disease, but, whereas the latter 
remains stationary, progressive muscular atrophy and poliomyelitis 
chronica advance. Difficulties in diagnosis ought therefore to 
arise here only if all information concerning the onset and course 
of the disease be denied. It has already been mentioned that pro- 
gressive muscular atrophy attacks occasionally a person previously 
-afflicted by infantile paralysis. 

Heine-Medin's disease may run a course resembling Landry's 
paralysis. I am of the opinion that a clinical differentiation of 
these conditions is impossible at present. 

In the accepted nomenclature the bulbar and pontine types of 
Heine-Medin's disease may be designated, according to the site 
of the lesion, acute superior, or acute inferior polioencephalitis. 
It has already been remarked that we have at least two types of 
acute superior polioencephalitis, Wernicke's and that which I 
have named Medin's type. Further research is required to deter- 
mine if still others exist. 

Wernicke's type is characterized by very well defined psychic 
symptoms, profound alterations in consciousness, delirium tremens, 
etc., and by an afebrile onset ; the ocular muscles are usually para- 



lyzed symmetrically or in groups. The history discloses an etiology 
in which intoxication, especially from alcohol, plays an important 

Medin's type, in contradistinction, shows the febrile onset, 
characteristic of an acute infectious disease. Psychic symptoms 
are, as a rule, absent;. and when they are present they usually con- 
sist of drowsiness and not of delirium. Rarely is the distribution 
of the ocular palsies symmetrical ; frequently it is very irregular. 

The bulbar type of Heine-Medin's disease may sometimes be 
differentiated by means of the history from acute inferior polio- 
encephalitis. But further investigation undoubtedly is necessary 
in order definitely to separate these conditions. 

Special reference must be made to the occurrence of facial 
palsy in Heine-Medin's disease. When such a palsy appears spo- 
radically it is invariably considered as a peripheral paralysis. 
Clinically to differentiate a facial nerve palsy from a facial nucleus 
palsy due to Heine-Medin's disease in many cases is scarcely 
possible. Usually the former is more marked than the latter, but 
the febrile stage of the latter is the only practical distinction. It 
is perhaps unnecessary' to state that in children the first step in 
the diagnosis of a facial palsy is to exclude the most common of 
its causes — middle ear-disease. 

Loss of reflexes, atrophy, and electrical changes distinguish the 
hemiplegic type of spinal infantile paralysis from a cerebral in- 
fantile paralysis. The encephalitic variety of Heine-Medin's dis- 
ease when it assumes a hemiplegic form is distinguished by its 
febrile onset from other foniis of cerebral paralysis in children. 



When we speak of the prognosis of Heine-Medin's disease we 
must, more than in most other diseases, distinguish between the 
prognosis quoad vitam and the prognosis quoad valetudinem com- 
pletam. That infantile paralysis never or hardly ever ran a fatal 
course, and that permanent paralysis always ensued, had formerly 
the weight of a dogma. Medin and Rissler proved that infantile 
paralysis could end fatally. Wickman later showed that, under 
certain conditions, the prognosis quoad vitam ought to be guarded ; 
that a high mortality might prevail ; and that the disease was more 
fatal to adults than to children. The Swedish epidemic of 1905 
demonstrated further that the prognosis quoad valetudinem com- 
pletam is more favorable than was credited formerly. 

The mortality fluctuates considerably, not only in different 
centers of the same epidemic, but even at the various points of a 
single center. In one small epidemic area of 26 cases, Wickman 
found a mortality of 42.3 per cent. ; in another, of 41 cases, the 
death rate was only 10 per cent. 

The general aspect of an epidemic varies materially according 
as the abortive cases are estimated or not ; and even when they are 
estimated, it changes according to the thoroughness with which the 
estimation is made. 

The following table shows the figures accessible to me from 
European epidemics. 

I reported altogether 1,025 cases with 125 deaths; 868 cases 
showed paralysis; 157 were abortive. For the sake of compari- 
son with other epidemics and because the actual number of abor- 
tive cases was far in excess of those I reported, I have calculated 
the mortality with reference only to the 868 cases of paralysis. I 
have omitted the deaths which occurred after two weeks, for then 
the fatal termination always arose from a complication such as 
pneumonia developing in consequence of the paralysis. Fourteen 
deaths were thus excluded ; one hundred and forty-five remained 
and are inserted in the table. 


« IP 


lyzed s)nnmetrically or in groups. The history discloses an etiology 
in which intoxication, especially from alcohol, plays an important 

Medin's type, in contradistinction, shows the febrile onset, 
characteristic of an acute infectious disease. Psychic symptoms 
are, as a rule, absent ;. and when they are present they usually con- 
sist of drowsiness and not of delirium. Rarely is the distribution 
of the ocular palsies symmetrical; frequently it is very irregular. 

The bulbar type of Heine-Medin's disease may sometimes be 
differentiated by means of the history from acute inferior polio- 
encephalitis. But further investigation undoubtedly is necessary 
in order definitely to separate these conditions. 

Special reference must be made to the occurrence of facial 
palsy in Heine-Medin's disease. When such a palsy appears spo- 
radically it is invariably considered as a peripheral paralysis. 
Clinically to differentiate a fecial nerve palsy from a facial nucleus 
palsy due to Heine-Medin's disease in many cases is scarcely 
possible. Usually the former is more marked than the latter, but 
the febrile stage of the latter is the only practical distinction. It 
is perhaps unnecessary to state that in children the first step in 
the diagnosis of a facial palsy is to exclude the most common of 
its causes — middle ear-disease. 

Loss of reflexes, atrophy, and electrical changes distinguish the 
hemiplegic type of spinal infantile paralysis from a cerebral in- 
fantile paralysis. The encephalitic variety of Heine-Medin's dis- 
ease when it assumes a hemiplegic form is distinguished by its 
febrile onset from other forms of cerebral paralysis in children. 



When we speak of the prognosis of Heine-Medin's disease we 
must, more than in most other diseases, distinguish between the 
prognosis quoad vitam and the prognosis quoad valetudinem com- 
pletam. That infantile paralysis never or hardly ever ran a fatal 
course, and that permanent paralysis always ensued, had formerly 
the weight of a dogxna. Medin and Rissler proved that infantile 
paralysis could end fatally. Wickman later showed that, under 
certain conditions, the prognosis quoad vitam ought to be guarded ; 
that a high mortality might prevail ; and that the disease was more 
fatal to adults than to children. The Swedish epidemic of 1905 
demonstrated further that the prognosis quoad valetudinem com- 
pletam is more favorable than was credited formerly. 

The mortality fluctuates considerably, not only in different 
centers of the same epidemic, but even at the various points of a 
single center. In one small epidemic area of 26 cases, Wickman 
found a mortality of 42.3 per cent. ; in another, of 41 cases, the 
death rate was only 10 per cent. 

The general aspect of an epidemic varies materially according 
as the abortive cases are estimated or not ; and even when they are 
estimated, it changes according to the thoroughness with which the 
estimation is made. 

The following table shows the figures accessible to me from 
European epidemics. 

I reported altogether 1,025 cases with 125 deaths; 868 cases 
showed paralysis; 157 were abortive. For the sake of compari- 
son with other epidemics and because the actual number of abor- 
tive cases was far in excess of those I reported, I have calculated 
the mortality with reference only to the 868 cases of paralysis. I 
have omitted the deaths which occurred after two weeks, for then 
the fatal termination always arose from a complication such as 
pneumonia developing in consequence of the paralysis. Fourteen 
deaths were thus excluded ; one hundred and forty-five remained 
and are inserted in the table. 





i-<cc^&arQ • ••••• ■■••••• 


Lindner and Mally... 



Ed. MUller 



Sweden, 1905 
Norway, 1905 
N. Austria, 1908 
E. Austria, 1 908 
Styria, 1908 
Germany, 1909 

( Arnsberg ) 
Germany, 1909 

Germany, 1909 

Germany, 1909 


Totalof Para- 
lytic Cases 







Total Deaths 




Per Cent. 









These figures of the table show incontestably that during the 
epidemic in Europe a fairly heavy mortality prevailed. The mor- 
tality of the American epidemics was lower. In the New York 
epidemic the case mortality was estimated to be S per cent.; in 
1907 Lovett reported a mortality of 4.7 in Massachusetts ; of 234 
cases II died. In 1908 he collected, in the same part of the State, 
136 cases, but their mortality was only 2.94 per cent. Emerson 
recorded a synchronously occurring epidemic (1908) in another 
part of Massachusetts in which the mortality was as high as 7.24 
per cent. 

The death rate is much greater in adults than in children. In 
Wickman's report the mortality from birth to 11 years (592 cases 
of paralysis, 71 deaths) was 11.9 per cent.; whereas, between the 
age of 12 to 32 years (250 cases of paralysis, 69 deaths) it rose 
to 27.6 per cent. The statistics of Leegaard show this same ratio, 
although the fact seems to have escaped his attention. If Lee- 
gaard's figures be calculated in percentages, they show from birth 
to 14 years a mortality of 12.4 per cent. (404 cases of paralysis, 
50 deaths) ; but between 15 and 30 years a mortality of 25 per 
cent. (132 cases, 34 deaths). If a similar reckoning be made with 
the figures from Fiirntratt's table we find a mortality of 11.05 P^'" 
cent, in the age period from 0-14 years (407 cases, 45 deaths) ; 
but a mortality of 25.53 per cent, above 15 years (43 cases, 11 
deaths). Still more striking are the figures of Mally and Lindner: 
Between o and 11 years, 59 cases of paralysis of which 10 were 
fatal; i. e., a mortality of 16.9 per cent.; above 11 years, 12 cases 
of paralysis, of which 6 were fatal; i. e., a mortality of 50 per 


cent. These several statistics are obviously in harmony on this 
point and those from the other epidemics are not in discord. The 
figures for adults are admittedly too few to permit of any positive 
conclusion. But as the sum of the cases observed by Wickman 
and Leegaard is exceptionally large (1,378 cases of paralysis, 224 
deaths), and as their cases were collected under very similar con- 
ditions, the greater mortality in adults and older children which 
their statistics show may be taken as an established fact. 

With respect to the danger upon different days of the disease, 
there is no uniformity. According to Wickman, life is in greatest 
peril between the third and seventh days, and the fourth is the 
most fatal day. Leegaard's figures show that death occurred most 
frequently on the third or fourth day. Ed. Miiller affirms further 
that on the fourth day severe paralysis most often appears. After 
the lapse of the second or third week, in cases in which the func- 
tion of the respiratory muscles is seriously impaired by paralysis, 
life is especially menaced by pneumonia. 

We have next to consider, in the prognosis, the patient's pros- 
pect either of escaping wholly, or of recovering completely, from 

In the discussion of the symptomatology we mentioned that 
many cases recover rapidly, without ever presenting symptoms of 
paralysis. But as the frequency of these cases seems consider- 
ably to vary, just how great is their proportion cannot be decided 
at present. Nor can we yet determine the influence of age upon 
this aspect of the prognosis for our available data are still too 
meager. Of my 699 patients between the ages of o and 11 years, 
107 — 15.3 per cent. — were abortive cases; whereas, of my 299, 
between the ages of 12 and 32 years, 49 — 16.4 per cent. — were 
abortive. Among Leegaard's 615 cases under 15 years of age, 
34.31 per cent. (211) were abortive; and of the 179 above 15 
years, 26 per cent. (47), were abortive. We cannot extract a 
generalization from these figures, as the census of the abortive 
cases was not sufficiently reliable, yet the numbers are not without 
interest, for omissions occurred among adults as well as among 
children. It is evident, however, that neither adults nor older 
children enjoy in this connection any privilege denied to infants. 

Epidemics have completely changed our ideas with regard to 
the possibility of recovery from paralysis. A little while ago it 


was accepted as an axiom that a person attacked by acute polio- 
myelitis never completely recovered. But now it has been dem- 
onstrated frequently by clinicians in this and other countries, that 
a fairly extensive paralysis may absolutely disappear. The con- 
dition of the patients, reported by me as paralyzed soon after 
the acute stage of their illness, I tried to ascertain one to one and 
a half years later. The returns obtained concern 530 of them, 
and were as follows : 

Paralyzed 297 — 56 per cent. 
Recovered 233 — ^44 per cent. 

These figures have been given, however, only partly by physi- 
cians and partly by teachers and others. They cannot, therefore, 
be considered as wholly exact. They are nevertheless of interest, 
as they show that an unexpectedly high percentage of the para- 
lyzed recovered without appreciable permanent disability. 

Leegaard showed in his report that 26.87 P^r cent, of paralyzed 
cases got well. 

Ed. Miiller had 58 patients under prolonged observation; 10 
of them — 15 per cent. — long before the end of the first half year, 
recovered without obvious impairment of function. Mtiller states, 
however, that this is only the minimum figure for subsequently 
so marked improvement ensued in the other patients that at the 
date of the publication of his report severe and widespread paral- 
ysis remained only in about one third of the whole number. 
Those attacked in the epidemic in Westphalia who recovered with- 
out a trace of the disease were estimated by Krause to number 
15-20 per cent. 

Zappert reported from the Austrian epidemic of 1908, the 
recovery of 37 out of 266 cases. But he mentioned that the actual 
number of recoveries was probably greater, for between the onset 
of the epidemic and the commencement of the general statistical 
investigation only a few months elapsed. A great number of 
cases of marked improvement were known also to Zappert then. 

Foerster, about six months after the onset of the disease, noted 
in fifteen cases which he observed very closely three who com- 
pletely recovered and two who at the time of the report were 
almost well. 

The collective report of the epidemic of 1907 in New York 


shows a less favorable state of affairs. Only in 5.3 per cent, a 
complete, and in 1.8 per cent, an "almost complete'* disappear- 
ance of the paralysis occurred. But even here variation occurred,, 
for, according to Ed. Miiller, Koplik, who observed part of the epi- 
demic, indicated that recovery was the rule. He observed wide- 
spread paralysis completely disappear or persist only in limited 

Age Factor in Prognosis. — Of my 530 cases of paralysis, 384 
were aged from o-i i years. One and a half years after the onset 
of the disease, 198 in this age period — 51.6 per cent. — were re- 
ported as still paralyzed; and 186 — ^48.4 per cent. — ^as recovered. 
Of the paralyzed patients older than 11 years, 99 (67.8 per cent.) 
remained paralyzed a year and a half after the onset; and 47 
(32.2 per cent.) recovered. As the percentage of recoveries is 
lower between the ages of 0-2 years — when disturbances of func- 
tion are more readily overlooked — than between the ages of 3-1 1 
years, the value of my figures cannot be questioned on the ground 
that a residuum is more evident in and to an older individual. 

Leegaard reported between the ages of 0-14 years 404 cases ; 
of them, 281 (69.6 per cent.) remained paralyzed, and 123 (30.4 
per cent.) recovered. 

Of the 132 paralytic cases above the age of 14, there remained 
paralyzed 102 — 77.3 per cent. — and there were cured 30 — 22.7 
per cent. 

Leegaard's statistics, as also mine, show that with respect to 
recovery from paralysis, adults are not so favorably situated a?, 

We must therefore conclude that the prognosis is in every 
respect more unfavorable in adults than in children. 

In comparison with the age factor, none other seems to have 
any demonstrable effect upon the prognosis. Physical condition 
and neuropathic predisposition cannot be shown to have any im- 
portance either in my cases or those of others. Fatal cases often 
occurred among strong and healthy peasants. Exertion during 
the initial stage seems unfavorably to influence the further course 
of the disease and seems to tend to induce a relapse. 

* My previous statements concerning the importance of age in com- 
plete recovery were based upon observations I made upon my own 
patients; whereas these are founded upon all the available data in the 
general report. 


Can we from any clinical data predict the course and termina- 
tion of the disease in a given case? All clinicians agree that the 
intensity of the initial symptoms has no prognostic significance. 
Alarming initial symptoms may usher in a benign or an abortive 
attack; and a njild beginning may be the prelude of a stormy, 
perhaps of a fatal course. 

All text books state that electrical irritability is a prognostic 
index. Oppenheim asserts that muscles which show a complete 
reaction of degeneration, at the end of the first week, will prob- 
ably remain permanently paralyzed; whereas, those in which the 
faradic excitability is not wholly lost after 2-3 weeks probably 
will regain functional activity. Although this may be the usual 
rule, recent experience has taught us that the issue cannot be so 
exactly forecasted. , 

From my somewhat limited electrical investigations, I have 
received the impression that the prevailing teaching upon the 
prognostic value of electrical examinations is not quite accurate 
and that the entire problem needs reinvestigation. Recently Ed. 
Miiller has confirmed this impression. He found the active con- 
traction of muscles to be much better than their electrical reac- 
tions had led him to expect ; and he observed that even after weeks 
of persistent paralysis the reaction of degeneration might be 
absent. Moreover, Foerster maintains that muscles which during 
the acute paralysis show the reaction of degeneration may com- 
pletely recover. Hence, the old law on this point should not be 
accepted too rigidly. 

It is also of importance to know how long improvement may 
be expected. Most of the complete recoveries take place un- 
doubtedly during the first half year; but some not rarely occur 
during the second half; and Petren and Ehrenbergh assert that 
they have succeeded, by prolonged treatment, in procuring recov- ' 
ery of paralyzed muscles even after several years. It is now cer- 
tain that improvement and recovery may be induced by correct 
therapy at a far later period than was believed formerly. 

It is not without interest to consider whether these recently 
established facts relative to prognosis, which contradict earlier 
experience, are actually new, or are merely old features, 
now rightly interpreted. In discussing the identity of the epi- 
demic with the classic sporadic poliomyelitis the difference alleged 


in the prognosis of the two conditions was mentioned. No 
such difference, I believe, exists. We cannot deny that the 
mortality of poliomyelitis is subject to fluctuation. I have ex- 
pressly accentuated and adduced evidence of this variability. Un- 
doubtedly the percentage mortality of sporadic cases is much 
larger than has generally been accepted. Fatal cases in children 
hitherto have been diagnosed as meningitis. Medin and Pierre 
Marie record actual instances of such diagnoses. Among young 
children who die of acute poliomyelitis, meningitic symptoms are 
more marked than among older (Zappert). In former times de- 
fective knowledge of the early stage evidently led to so many 
errors in diagnosis that teaching concerning the mortality in clas- 
sical poliomyelitis was unreliable. In adults all lethal cases were 
formerly diagnosed as " Landry's paralysis " which was regarded 
as a disease sui generis; whereas, we know now that most of the 
fatal cases of Heine-Medina's disease follow the course of a Lan- 
dry's paralysis. 

Referring again to the recovery from paralysis I may say that 
in former times such a result was certainly not unknown; and 
perhaps not rarely happened. When a cure did occur the case 
was diagnosed usually as polyneuritis, in accordance with the doc- 
trine of the unfavorable prognosis quoad valetudinem in Heine- 
Medin's disease, and in harmony with the benignity of polyneu- 
ritis. And when in such benign cases tenderness was marked and 
spontaneous pain and sensitiveness on pressure over nerve trunks 
were present, the diagnosis of polyneuritis seemed incontrovert- 
ible. It is now established that patients may present these symp- 
toms under the action of the virus of acute poliomyelitis, alone. 

I think we may conclude that conditions have not materially 
changed and that the apparent difference between the old and the 
recent observations depends chiefly upon the inaccuracy of the 

Secondary Diseases. — After an attack of acute poliomyelitis 
there seems to remain a certain predisposition to other organic 
nervous affections. A number of instances are known in which in 
a case of poliomyelitis has developed subsequently a chronic spinal 
cord affection. Usually chronic muscular atrophy (Charcot, Ray- 
mond, Vulpian, Cestan, Alessandrini and others) ; more rarely 
progressive myopathy (Cassirer, Rossi) appears. I saw a man 



in Lennmalni'§ clinic at Stockholm who showed remains of a 
spinal infantile paralysis and suffered from a combined posterior 

Crouzon recorded a case of a man who had suffered in child- 
hood from infantile paralysis in the legs and who between the ages 
of 18 and 40 was attacked not less than nine times by sudden tem- 
porary paraplegia. A similar case was reported by Ballet and 

Pierre Marie described as secondary to and developing about 
a decade after acute poliomyelitis, what he calls " scoliose tardive." 

But these cases in which, after complete recovery from acute 
poliomyelitis, secondary disease in later life appears are infre- 
quent. According to Risien Russell, Potts in 1903 could collect 
from the literature only 37 cases. 




Bergenholtz was the first who observed a true epidemic. He 
recorded in the Swedish Public Health reports, i8 cases of spinal 
infantile paralysis which occurred in North Sweden in 1881. In 
1887, Oxholm published the first article on this subject; it com- 
prised five cases of paralysis which appeared almost simulta- 
neously in a limited district of Norway. Although there is now 
no doubt of the nature of the five cases, Oxholm seems not to 
have been quite clear on the point. A small epidemic of 13 cases 
occurred in the south of France in 1885. Cordier in 1888 pub- 
lished such details as after the epidemic he was able to collect. 
Both publications remained unnoticed. Medin's lecture at the 
Tenth International Congress at Berlin in 1890, upon his obser- 
vations during the first epidemic in Stockholm (43, or more cor- 
rectly 44 cases), convinced everyone that spinal infantile paral- 
ysis could appear in epidemic form. Subsequently, other reports 
were made upon groups of cases, but only those described by 
Medin, 1895 (second epidemic in Stockholm, 21 cases) ; Caver- 
ley and Macphail, in America, 1894 (126 cases); Leegaard, in 
Norway, 1899 (54 cases) ; Auerbach, in Frankfort on Main, 
1898 (15 cases) ; Buccelli , in Italy, 1897 (^7 cases) ; Zappert, in 
Vienna, 1898 (42 cases); Platou, 1904 (20 cases), and Nonne, 
in Norway (41 cases), 1904, could be called epidemics. Other 
outbreaks consisted of groups usually of 4 or 5 cases, sometimes 
more, sometimes less. (Brieglieb, Andre, Pierracini, Pasteur, 
Pleuss, M. Taylor, Buzzard, Biilow-Hansen and Harbitz, New- 
mark, Packard, Chapin, and others). 

No reports give us any explanation of the mode of spread of 
Heine-Medin's disease. The only noteworthy observation in this 
respect was Leegaard's. He proved that the disease showed a 
remarkable relation to highways. But to him, also, the precise 
mode of diffusion of the disease remained obscure. The current 
view was expressed in the sentence: "Infantile paraly»i* is of an 



infectious, but not of a contagious nature." As a matter of fact 
no indisputable instance of contagion could be proved. 

Wickman (1907) in his report of the Swedish epidemic of 
1905 (1,031 cases), was the first to show that Heine-Medin's 
disease is conveyed from person to person, partly by those afflicted 
with the abortive type (abortive varieties had till then been over- 
looked), and partly by healthy people acting as germ carriers. 

The disease, as has already been shown, occurred in several 
countries; e.g., in Norway, 1905,952 cases (reported by Leegaard, 
1909) ; in New York, 1907, about 800 cases ;^ in Massachusetts, 
1907, Lovett, 234 cases ; in Massachusetts, 1908, Lovett and Emer- 
son, 136 cases; in Lower, Austria and Vienna, 1908, 290 cases 
(collected 1910 by Zappert) ; in Upper Austria, 1908, 68 cases, re- 
ported by Locker and later by Lindner and Mally ; in 1909, Styria, 
433 cases (Fiirntratt) ; in 1908, Heidelberg, 36 cases (J. Hoff- 
mann) ; and in 1908, Hamburg, 22 cases (Nonne). In 1909, Ger- 
many was seriously invaded by the disease in epidemic form. In 
Westphalia 633 cases occurred (P. Krause) ; in Hesse-Nassau 
over 130 cases (Ed. Miiller), and some smaller attacks occurred, 
in Hanover, 34 cases (Eichelberg), Silesia at least 50 cases (Foers- 
ter), and in Pomerania, 51 cases (Peiper). The German epi- 
demic of 1909 comprised, therefore, at least 1,000 cases and prob- 
ably more. 

The disease appeared in epidemic form in France and Holland. 
Netter reported about 100 cases in and around Paris. 

In addition to these, other epidemics prevailed in America and 
Australia, which, as their reports are not at present at my dis- 
posal, I cannot intimately discuss, but I shall quote Netter and 
Lovett concerning them. 

Australia: Alston, 1895 (14 cases) ; Wade, 1904 (34 cases). 

America: Painter, 1892 (38 cases), in Massachusetts, of which 
Brachett (1894) communicated 10; Bondurant and Woods in 
Alabama, 1900, 15 cases. 

In 1908 the epidemic appeared in several States, among them 
Minnesota (over 150 cases), other than Massachusetts (Lovett 

*In the general report of the American epidemic it is stated that 
data concerning 752 cases existed, but that the reporting committee 
estimated the actual figure as not less than 2,000 cases. The basis for 
this estimate sems to me absolutely inadequate to sustain it. 


and Emerson). More than 200 cases were reported from Ne- 
braska in 1909. 

It was long recognized that acute poliomyelitis prevailed mostly 
during summer and early autumn. This seasonal incidence was 
maintained, as a rule, in the recent epidemics. Not less than 86 
per cent, of the cases in the Swedish epidemic of 1905 occurred 
between July and October. The maximum number, 35 per cent, 
of the total cases, developed in August^ Leegaard observed a 
similar incidence in the Norwegian epidemic. But the maximum 
of the 1907 epidemic in New York occurred in September; and 
in September most cases appeared in the Massachusetts epidemic 
described by Lovett. During the epidemic in Hesse-Nassau (Ed. 
Miiller) the morbidity was markedly less in July, August and Sep- 
tember than in October and November. In these last two months 
over 75 per cent, of the total cases occurred. Miiller explains 
that the disease probably began in the adjacent region of West- 
phalia, reached its height there in September and October, and 
gradually invaded Hesse-Nassau till it assumed epidemic propor- 
tions. The apex of an epidemic, therefore, occurs, as a rule, in 
summer and early autumn ; but in certain districts it has occurred 
in winter. In three adjacent and clearly connected outbreaks, the 
18 cases of the first appeared between June and October ; the 27, 
comprising the second, which occurred to the west of the first, 
from July to December ; and the J2, cases of the third, which ap- 
peared in a contiguous but still more westerly district, developed 
between the end of September and the following February, and 
had their maximum during November and December (Wickman). 
An epidemic which prevailed throughout the winter in North 
Sweden has just been reported to the board of health. From 
October till the following September, 69 cases were observed in 
a relatively small area, by the only physician of the district. They 
occurred as follows: October to December, 13 cases; January to 
March, 25; April to June, 28; and July to September, 3 cases. 
The apex of this epidemic occurred, therefore, in April and May. 
Although Heine-Medin's disease may be deemed a summer malady, 
it may not only occur, it may be even epidemic in winter. Its 
winter occurrence is, as I shall later discuss, not without impor- 
tance from the point of view of the mode of spread of the disease. 

Wickman states that the period of incubation is one to four 


days; Leegaard, one to three. The incubation period was esti- 
mated from the interval which elapsed between the first and second 
case in instances of multiple victims in the same family. As one 
to four days prevailed so markedly, it seems justifiable to accept 
a short incubation. But in some cases, in which apparently the 
disease developed after a visit, Wickman found that the incubation 
lasted six to ten days. As far as can be ascertained at present 
the last is, most likely, the true period. In six cases in which the 
source of infection and the duration of the exposure to infection 
were definitely known the minimum incubation was five days ; and 
the average about seven. P. Krause estimates the incubation pe- 
riod at ten to twelve days. Experimental inoculation of monkeys 
has shown an incubation of nine to ten days with a minimum of 
four and a maximum of thirty-three (Flexner and Lewis). 

But a person, who, for instance, while visiting is exposed to the 
disease, is not necessarily infected then. The virus may lodge on 
the hands, clothes, or elsewhere and only later invade the body. 
The actual infection dates from the invasion of the tissues and not 
from the exposure. These figures, especially the higher, are, 
therefore, not beyond criticism. But in monkeys the incubation 
period is calculated legitimately from the moment of inoculation 
to the first appearance of paralysis — for, as a rule, the character- 
istic initial fever observed in man is usually absent in monkeys. 
The difference between my estimate and the results of experi- 
mental investigation is not therefore so great as appears at first. 

An incubation period of one to two days is indisputably too 
short. When this interval is observed between the first and the 
subsequent case in a family each patient must be infected from a 
common source. I believe that in man, if the onset of the disease 
be calculated from the commencement of the fever- — as it should 
be — the incubation period will be found to be at least three to four 
days. Its average duration might quite probably be even higher.. 
The acceptance of a somewhat longer period of incubation does 
not, in any way, weaken my conclusions concerning the mode of 
spread of. the disease. 

Wickman during the Swedish epidemic of 1905 first established 
the precise manner in which the disease spreads. As no oppor- 
tunity so favorable has since occurred for the study of epidemic 
conditions, I shall give in detail the observations I made then. 


The 1905 epidemic comprised 1,031 cases. Their distribution 
was irregular ; foci of 4 or 5 or more or fewer cases were widely 
scattered. In the regions intervening there was either no instance 
of the disease or only an isolated case. These infected foci oc- 
curred in no relation to the density of the population; ravaged 
rural districts ; and practically spared the cities. Within the large 
groups, it was possible to investigate minutely only restricted areas 
where every case was publicly known, and where the determining 
factor could be sought. In these areas contact between all afflicted 
with the disease could be proved to have taken place ; whereas, no 
other factor which would satisfactorily explain the manner in 
which the malady spread, could be incriminated. The transmis- 
sion may be indirect. It" is not absolutely necessary for direct 
contact of patient with patient to occur. Indeed, the disease seems 
more often to be propagated through the mediation of the healthy. 
As in- many other epidemic maladies, spread occurs in Heine- 
Medin's disease by transmission from person to person. 

I shall demonstrate a few examples of this diffusion. Fig. 7 
illustrates an outbreak within the little parish of Trastena. The 
parish lies some distance from the highroad and has somewhat 
more than 500 inhabitants. The houses, 102 in number, are dotted 
singly over an area of 32.5 sq. kilometers. Each house, almost 
without exception, is occupied by only one family. The inter- 
course between the individual families is limited. Each house- 
hold possesses a spring and, usually, one or more cows. The 
products of their farming supply their simple wants, and from 
the outside world little enters their spheres. In sUch a community 
the spread of an infectious disease can be accurately studied. 

In this parish, between June 28 and August 14, not less than 
49 people, chiefly children, were attacked by acute poliomyelitis. 
In 26 cases paralysis resulted ; in the others motility was unim- 
paired. The dates of affection of the latter are placed in paren- 
thesis in the figure. 

The conditions under which the people lived obviously pre- 
cluded infection from either milk or water ; and the only supplies 
which entered the parish came from a village where the disease 
was yet unknown. 

The search for a common source of infection led to the public 
school of the parish. Not less than seven patients, who in their 


families were the source of infection for new cases, were school 
children. These, Nos. 477, 463, 465, 470, 481, 459 and 472, are 
in the figure connected by lines with the school (X), In one 
family, where four were taken ill (477 to 480), the child first 
afflicted was the only one attending the school. The teacher lived 
in the school house with his four children. Two of them were 
pupils. All were attacked by Heine-Medin's disease (Nos. 455— 


Other groups could be connected also with the school. For 
instance, cases occurred in five families in each of which one or 
more members who showed no symptoms of illness attended 
school. Two affected children (Nos. 498 and 499) of the same 
family neither attended school nor had they brothers or sisters 
of school age; they lived in a single story house with another little 
girl who went to school, but who was not ill. Each of these 
houses is connected in the schema by dotted lines with the school. 
The infection can, therefore, be shared in this as in all other 
infectious diseases by persons who show no morbid symptoms. 
Such intermediaries must act as yirus carriers. 

. The moment of the appearance of the disease in the different 
families harmonized very closely with the hypothesis of dissemi- 
nation by way of the school. Where the disease originated from 
direct infection by sick school children the first cases appeared 
between June 28 and July 12. But where, in all probability, the 
infection was carried to a family by healthy school children, the 
first cases occurred between July 13 and 23. The school was 
closed on July 15. I believe no demonstration of a school epi- 
demic better than this could be found. Of the other cases, four 
or five were traced to infection at the house of Nos. 470 and 471. 
No. 471 was attacked on July 18; No. 484 visited him on July 19, 
and was taken ill on July 22. Later, the disease attacked. the 
two sisters of Nos. 470 and 471. No. 487, a hired laborer on the 
premises of No. 470, became ill on July 29. A man, who had 
one son attacked on July 23 (case No. 497), and another a pupil, 
was also a hired laborer with No. 470; here the possibility of 
infection both from this infected house and from the school exists. 
Only three of the houses attacked in this parish remain to be 
considered. One of these, which No. 481 occupied, was situated 
only a few steps from the house which was first attacked. The 



two families came often in contact with each other during the 
outbreak. In the other cases (Nos. 500, 501, 502 and 503) no 
certain connection with the rest could be proved ; but the dispo- 
sition of the houses is such that direct or indirect infection was 
quite possible. Morieover, the disease appeared in these last 
houses at the end of July. 

In all probability cases 470 and 471 were the source of infec- 
tion for a small focus which developed in a little parish about one 
hundred kilometers from Trastena. A boy, three years old, was 


\^(*n)^^ ^ *V>t 

Fig. 7. School epidemic in Sweden, 1905. Each parallelogram rep- 
resents a house, X is the school. The dates in parentheses represent 
abortive cases. The continuous lines represent the direct infection; the 
broken lines, the indirect infection (by personal contact). 

the first victim. He travelled with his mother, on July 23, to a 
village, adjacent to Trastena, where his grandparents dwelt. The 
way led through infected districts ; and while the child was at his 
grandparents' house, a relative came there who was employed as 
a servant on the farm where Nos. 470 and 471 were ill. On July 
27, the boy was taken ill with the usual symptoms. On July 30, 
the mother set out with her sick child and on the same day arrived 
home. On August 17, the father of the boy was taken ill with 
paralysis in one leg. On August 15, a child living in their house 
was attacked.. The next case occurred on August 21, about one 
kilometer from the infected house, and was followed, on August 



27, by another in the immediate neighborhood. At the beginning 
of September the brother of the last patient was taken ill. 

From Trastena the infection radiated (Fig. 8) to the sur- 
rounding districts. 

Another smaller focus in which communication between nearly 
all the cases could be proved is depicted in Fig. 9. The local 
conditions in this, as in the epidemic centers about to be discussed, 
were very similar to those at Trastena. The spread here, also, 
was partly due to the school. Nos. 136 and 138 and 141 were 
school children. Nos. 135 and 136 lived in the immediate vicinity 
of the school and were accustomed to play with the school chil- 
dren during the recreation hour. No. 140 lived in the same house 








f¥S f9¥ 

Fig. 8. School epidemic in Sweden, 1905. Explanation same as in Fig. 7. 

as Nos. 138 and 139; and 142, 143, 144, 145 and 146 lived in a 
house only a few steps from the house of No. 141. Contact, 
therefore, could scarcely be avoided. The cases numbered 147, 
148, 149 and 150 were distributed in two houses which lay side 
by side ; it was established that contact had occurred between them 
and cases 130 to 134. A similar connection was highly probable 
between No. 151 and Nos. 147 to 150. No. 152 lived with his 
grandparents, who were servants in the household of Nos. 130 to 
134. No contact to explain No. 137 could be proved. The parish 
contained 1,400 inhabitants. The houses were occupied usually 
by one family and were irregularly distributed within the parish 



Fig. 9 demonstrates the mode of diffusion of the disease within 
a group of 19 cases (9 abortive). They all occurred on two 
islands which lie in a large lake. The smaller island, Borgo, con- 
tributed only three cases; the larger, Sirko, five kilometers long, 
and one to two kilometers broad, the others. Most of the patients 
were school children. One case (No. 274) could be connected 
with the school only through a healthy person who acted probably 
as a disease carrier. No. 271, an adult who worked in the fields. 

U12S22SS 26V 

217 27i 


Fig. 9. Contact epidemic in Sweden, 1905. Explanation same as in Fig. 7. 

took her meals during the day at the house where No. 265 was 
already ill. 

The cases on the island of Borgo (Nos. 277-279) could be 
connected with those on Sirko. The parents of the mother of 
the first two children attacked on Borgo lived on Sirko, in a house 
adjoining that in which No. 273 became ill on July 25. Between 
July 25 and August 13, the father of the two children had several 
times visited his wife's parents at Sirko and certainly encountered 
the relatives of No. 273. For the remaining case at Borgo these 
two were evidently the source of infection; their dwellings were 
near one another. Between almost all the cases contact could 
be proved. The longer island is inhabited by 28 families who 
occupy 29 houses. One-family dwellings are therefore the rule. 

It was impossible to find how the disease penetrated the 
island. Only one point was assured; the father of the children 
who were attacked first was the only person who kept actively in 
touch with the surrounding mainland. 



Fig. ID shows another example of a school epidemic. This 
center contained i8 cases; ten of these were abortive and pre- 
sented pronounced general symptoms. Ten of the eighteen at- 
tended school; one (No. 328) of the ten and his brother dwelt in 
the schoolhouse with the teacher's son. The school was closed on 
September 19; two cases subsequently occurred — one on Septem- 
ber 22 and one on September 29. Only for six children, occupy- 
ing four houses, could no contact with the other 52 who attended 
school be traced. The parish comprises over 3,000 inhabitants. 















SS¥ ' 




l^y '%. 1 



X c^*'^ 

Fig. 10. School epidemic in Sweden, 1905. 

Lastly, I shall mention another small epidemic center (Fig. 
11). A woman, 54 years old, was attacked first (No. 714). 
She probably became infected in a district where the disease was 
epidemic, about five kilometers from her own village. Her illness 
began on December 5. Her son (No. 715), 22 years old, was 
taken ill on December 13. On December 18, a man servant (No. 
716) who lived about two kilometers away, and who had several 
times visited the sick No. 715 was attacked. On December 24 a 
little girl of four years was taken ill in the household of No. 716. 
Two cousins of the child lived only a stone's throw away and 
were daily with her; they were taken ill on December 26, 1905, 
and on January i, 1906, respectively. One of the cousins devel- 
oped fever, severe pains in the neck and opisthotonus, but recov- 



ered without paralysis. Two cases seemed to be infected through 
the intermediation of a healthy carrier of the disease. In their 
family a housekeeper was employed who was the sister of No. 
716 and who had visited him daily for a week during his illness. 
She herself showed no morbid symptoms, but the two children 
(cases 720 and 721) of the family were taken ill on December 31, 
1905, and January 10, 1906, respectively. Case 720 showed only 


TPf 7f6 




710 m 

Fig. II. Small focus, showing evident contact between the cases. 

general symptoms and rigidity of the neck. An adult who lived 
about 10 kilometers from this neighborhood was taken ill on 
January 10. He had spent Christmas and the early part of Jan- 
uary at his parents' house close to cases No. 716 to 719. He 
visited No. 715 first on January 3; subsequently, he often visited 
both No. 715 and 716. 

The country where this group of cases occurred is sparsely 
peopled. But in the vicinity of the attacked dwellings, a number 
of houses are situated. It cannot therefore be regarded as acci- 
dental that the disease afflicted only such persons as stood in the 
relation to each other which I have just traced. The possibility 
of the transmission of the disease from house to house by means 
of healthy carriers was proved in numerous other groups, also. 

These small centers were part of large foci in which it was 
impossible always accurately to trace the mode of spread of the 
disease. Yet regarding these large foci certain facts are noteworthy. 


The infection seemed to radiate, as a rule; the cases occurred in 
groups; and in many of the scattered cases the possibility either 
of direct or of indirect transmission existed. The tendency to 
arrangement in groups was expressed by the disease implicating 
members of one family, dwellers in one house, or persons living 
in neighboring houses. The 1,031 cases were distributed as 
follows : 

In each of 627 houses i case occurred. 

In each of 95 houses 2 cases occurred. 

In each of 39 houses 3 cases occurred. 

In each of 14 houses 4 cases occurred. 

In each of 7 houses 5 cases occurred. 

In I house 8 cases occurred. 

These figures seem high compared with statistics of others, 
but abortive cases are here included. All abortive cases were 
omitted, however, except 157, which occurred in restricted areas 
where the diagnosis could be proved beyond cavil. If all the 
aibortive cases were included the resemblance to a contagious dis- 
ease would be greater still. 

The distinct group-like disposition which the cases showed 
within the larger foci was analogous to an attack involving sev- 
eral members of one family. The chronological order of the 
cases within the smaller groups showed that probably the disease 
resulted from a causal agent common to them all. 

Another important observation was the radiate nature of the 
dissemination within the focus itself which I have illustrated by 
remarkable examples. In still other districts as the groups ap- 
peared about the same time they were infected probably from the 
same source. 

Fig. 12 demonstrates foci with radiate spreading. The dis- 
ease appeared here first about June 30, on a large estate, Stora 
Sundiby, which is renowned for its natural beauty and is a favorite 
tourist resort. On June 23 and 24, Sweden celebrates great na- 
tional festivals. The disease was epidemic to the west of Stora 
Sundby. Stora Sundby itself was free before the holidays oc- 
curred. Excursionists probably brought the infection with them 
and an outbreak followed. The figure shows how the disease 
spread in various directions. Towards the north lies the small 
borough of Kungsor, in which 13 cases occurred. The son of 



f t a * ttm 

I I I I * 

Fig. 12. Focus with radiate spreading, Sweden, 1905. 


the only physician of the place was the first afflicted. The physi- 
cian, undoubtedly, may have transmitted the disease to some of 
the others attacked. From Kungsor diffusions in all directions 
took place. Every case shown in the figure presented paralysis. 
In some, direct contact could be traced. In response to our in- 
quiries the physician reported that he had observed a number of 
cases which completely recovered and which showed exactly the 
same symptoms as occurred in the initial stage of the illness of 
those who developed paralysis. Undoubtedly, therefore, abortive 
cases occurred also, and the epidemiological conditions of a con- 
tagious disease might have been demonstrable here if attention 
had been paid to these abortive cases and to the virus carriers. 
These conditions were partly established later. The patient men- 
tioned on page 75, who died with meningeal symptoms, was sus- 
pected of eclampsia and had premature labor induced. The 
woman was taken ill on August 19. Two days previously, her 
son had been attacked with fever and great drowsiness. It was 
alleged that he developed no paralysis then ; as a year afterwards, 
his left leg was thinner than his right, possibly in the acute stage, 
the paralysis was overlooked. On August 24 the midwife, who 
took care of the woman and assisted at the confinement, became 
ill with headache, pain in the back, arms, and legs, nausea, and 
high fever. She recovered without presenting any signs of paral- 
ysis. The boy and the midwife probably were abortive cases (un- 
less the boy be regarded as a paralytic case). 

The intimate association of the disease with the principal high- 
ways was clearly demonstrable. The relation to main roads and 
railways was especially striking in districts in which the cases 
were scattered, either singly or in small groups. A study of the 
local conditions showed that dissemination must be due to the 
busy traffic which permitted more frequent communication be- 
tween the people. 

The Swedish epidemic of 1905 thus demonstrated that the 
mode in which the disease spreads both within the large epidemic 
centers and within the individual components which constitute 
them, so far as it was possible to determine, was essentially anal- 
ogous to that established for a number of other infectious diseases, 
in which transmission takes place from person to person. 

Acute poliomyelitis must, therefore, be included among the con- 



tagious diseases. The lateness of the recognition of this fact is 
due partly to the smallness of former epidemics and partly to two 
factors which nullified all earlier investigations of epidemic con- 
ditions ; viz., first, abortive types were not considered, and, second, 
the possibility of infection through healthy virus carriers was not 

It was rarely probable that infection was conveyed by food or 
by inanimate objects. The following instances I observed during 
the 1905 epidemic in Sweden. They are reported now for the 
first time. In a certain district three cases appeared in one family ; 
two cases in each of two others J altogether six families were at- 
tacked and ten cases occurred. The first patient was a farmer's 
son who was attacked on October 20; his brother and four chil- 
dren of the neighborhood were seized with the same symptoms. 
All the patients were supplied with milk by the farmer. The 
houses were separated from one another by one to two kilometers ; 
and in five cases the illness began on the same day. Under these 
circumstances it seems to me extremely probable that the milk 
convyed the infection. 

In exceptional cases the infection seems to be carried by inani- 
mate objects, also. An adult who was taken ill near Stockholm 
on July 27 acquired paralysis of a leg. Sometime after, she was 
transported to her home in Stockholm. During her convalescence 
she amused herself with sketching and similar work. Early in 
September one of her drawings was sent to a studio to be repro- 
duced. At the studio the person who performed this work, a 
lady, 34 years old, was taken ill on Septemfber 25 and suffered 
from a typical acute poliomyelitis. This lady was the only person 
in the studio who was affected; the population of Stockholm is 
almost 300,000; in the year in question only 11 cases of Heine- 
Medin's disease were reported from Stockholm ; and the lady had 
been exposed to no other source of infection. Such cases are of 
great rarity. They do not prejudice in any way the doctrine of 
the contagious nature of acute poliomyelitis ; analogous cases are 
known to happen in all other infectious diseases. 

Our observations in the Swedish epidemic of 1905 have not 
always been corroborated by those who have studied subsequent 
outbreaks elsewhere. But no other manner of spread has been 
demonstrated; and corroboration was usual when the reporter 


himself had clinically investigated the cases. Yet Leegaard, Avho 
apparently confined his efforts tJo editing the accounts he received 
of the Norwegian epidemic, concludes that the disease is trans- 
mitted from person to person ; and that the infection is conveyed 
more often by healthy carriers than by direct contact witli the 
sick; and he adduces many examples in support of these con- 

In Westphalia P. Krause occasionally observed distinct foci 
of the disease which were particularly linked to certain roads. 
He, also, was able to prove transmission through intermediate 
persons who remained well. But, on the other hand, he exoner- 
ates food, water, milk, insects, etc. 

From the epidemic in Hesse-Nassau Ed. Miiller, who thor- 
oughly studied it, concluded that Heine-Medin's disease is con- 
tagious, and that it is spread less often by the affected children 
than by the healthy disease carriers. Miiller reports several in- 
stances in which persons carried the disease from infected to non- 
infected districts; and instances, also, in which healthy persons 
had, for a short time, visited an infected locality, then returned 
home and spread the virus among their own community. In many 
villages intercourse between infected houses was traced. It is 
noteworthy, as Ed. Miiller remarks, how the first and often the 
only case of poliomyelitis in an otherwise healthy people occurred, 
as a rule, not among the real peasantry but in a family of a person 
who had business relations with people outside the parish ; e, g., 
an innkeeper, a coachman, a letter carrier or a shoemaker. To 
both Miiller and Eichelberg the morbidity among shoemakers' 
children seemed particularly striking. These observers think that 
the infection possibly lurks in the dirt which adheres to personal 
belongings, such as clothing, shoes, etc., of the intermediate car- 
rier. The connection of the first cases with highroads and railways 
Miiller could trace invariably; whereas, localities far from the 
principal communication routes remained free from invasion. 
Ed. Miiller's observations are especially interesting, for the epi- 
demic he studied consisted of a dense aggregation of isolated 
cases. If his investigation had not been so thorough the dissemi- 
nation of the infection would have appeared mysterious and 

Each of a small group of seven cases investigated by Netter 


dwelt far from, and had no dealings with, the others ; but three of 
them, the brother of a fourth, and the cousin of a fifth all attended 
the same school. 

The epidemic in Austria reported by L5cker also seems to 
have been due to contact. Most of the cases appeared in isolated 
and remotely situated houses. Yet, large and smaller groups oc- 
curred; and Locker proved in several districts that the school 
played a great part in spreading the disease. Indeed, in one local- 
ity, practically all the affected children were pupils of the parish 
school. The local conditions in this epidemic greatly resembled 
those in several of the Swedish districts, in which food and water 
as sources of infection could be excluded. Lindner and Mally 
investigated also this epidemic and greatly amplified Locker's de- 
scription of it. They advanced a number of proofs to show that 
infection here took place by contact. 

Emerson proved contact between the cases in the epidemic of 
1908, in Massachusetts ; and Armstrong, in that of 1909, at St. 
Paul. Jones reported 86 cases in the Massachusetts epidemic of 
1909 and stated that most of them were connected with the high- 
ways. In thirteen of the nineteen cases, which occurred within 
34 days at Great Harrington, he traced some association with the 
school. Five of the thirteen were pupils; the rest were sisters, 
brothers or other relatives who were in daily contact with the 

Shidler's observations (quoted by Holt) correspond closely 
with my own. He reported an epidemic of more than 200 cases 
in Nebraska. In six families, two children were attacked; in 
five, 3, in three, 4 ; and in one, 6. Remarkable proof of infection 
was given. The first case in the town of York was a child, who 
was attacked by the disease nine days after his mother and his 
brother returned from visiting an afflicted family in another town. 
All the children of a neighboring family were taken ill soon after- 
wards. A child visited this family and was attacked five days 
later. A boy, who lived outside the town, visited the affected 
locality, became ill, and was transported back to his home in the 
country. His sister was attacked then. A few weeks later a 
child from another town, where no cases were known, visited this 
country family and stayed over night. Five days later he, also, 
was taken ill. A month passed and then another child spent a 


night with the same family; he likewise became ill five days after- 
wards. Shidler is stated to have reported numerous other in- 
stances of infection. 

There still remain many epidemics in which contagion could 
not be established, but in which some of the features we have been 
discussing, such as the occurrence of the cases in groups, and the 
distribution of the disease along the channels of communication, 
were present. Among these is the epidemic of 1908 in Vienna 
and North Austria which was described by Zappert. The disease 
raged in a thickly populated province, traversed by many trade 
routes. To investigate the epidemic conditions here was therefore 
no easy task. Yet, Zappert was able to establish the following 
suggestive facts : The 129 cases in Vienna showed a very irregular 
distribution ; the case incidence did not vary as the density of the 
population; and within any one district the cases tended to ac- 
cumulate in certain quarters and houses. But, on the other hand, 
the relation of the cases to each other could be just as little demon- 
strated as their radiation from a common center. Zappert col- 
lected 137 cases in North Austria. Here also the disease showed 
no uniform distribution but more distinctly and obviously than in 
Vienna the cases developed in groups. Zappert concluded it 
would be incorrect to deny that the disease is contagious, although 
he failed to prove contagion in this epidemic. 

Zappert's statements regarding the discordant time relations of 
the various groups of cases are very interesting. He found the 
group of early cases occurred in Lower Austria in every district 
which bordered Vienna on the south and west ; the groups of later 
cases developed in the north of the province ; whereas, the Septem- 
ber and October cases appeared in the center and in part of the 
southern division of Lower Austria. Zappert seems here to estab- 
lish a very pretty succession of groups. However, he asserts that 
in spite of the evident and striking distribution of the cases, no 
clue could be found to any underlying factor determining the path 
of the epidemic. He bases this assertion, so far as I can judge, 
principally upon the fact that the early cases occurred at the north- 
west, whereas the later appeared at the southwest boundary of the 
province. I believe one ought not to ascribe such great impor- 
tance to cases appearing — so to speak — outside the epidemic, on 
the boundary of Bohemia and Hungary. As very imperfect re- 


ports of the cases of poliomyelitis were issued from these coun- 
tries, one cannpt affirm that the disease there was not connected 
with the other foci of the epidemic. Moreover, in densely popu- 
lated districts with busy traffic an epidemic passes not as a running 
stream, which always must flow through one region before it can 
reach the next; an epidemic spreads by "leaps" and we must 
expect such " leaps." 

I am inclined to ascribe much more importance to the distri- 
bution of the cases and to the time relation shown in the succes- 
sion of the groups than Zappert cares to admit. 

Lovett, whose report on the Massachusetts epidemic of 1908 
was similar to Zappert's, also, found a distinctly perceptible for- 
mation of the cases in groups. These groups occurred along the 
railroad and the disease tended especially to spread along the lines 
of greatest traffic. Lovett observed among the 134 cases of the 
epidemic, eleven instances in which the disease attacked more than 
one dweller in the same house ; and 20 in which acquaintances of 
sufferers were attacked. He estimated that the possibility of 
transmission was demonstrable in 17 per cent, of cases. On the 
other hand Lovett inclines, without valid proof, to accept that the 
virus may occur in milk. But there are observations (New York 
epidemic of 1907) to show that the disease is prevalent among 
breast-fed babies ; and my own work, also, tends to show that we 
may exclude not only milk but even food as a source of infection. 
The epidemics in New York, in 1907; in Styria, in 1909 (Fiirn- 
tratt) ; and in Pomerania (Peiper), give no positive information 
regarding the mode of spread. No method of dissemination 
could be established in these, other than that I advocate. Fiirn- 
tratt stated that at the onset of the epidemic he could confirm my 
observations, whereas, later, he could do so only guardedly. 
Peiper found at least one instance of aggregation of the cases into 
groups but could not trace the infection either directly or by 
healthy carriers. 

It has been pointed out in opposition to my contention that 
acute poliomyelitis is contagious, that the disease appears only 
sporadically ; that during an epidemic only one member of a family 
may be affected, even if adequate opportunity for infection be 
offered to the others ; and that infection in hospitals has not been 
observed. These are the principal objections. How very little 


is their worth, I can best show by analogy. We do not need to 
go far into the past to encounter the time when exactly the same 
arguments were quoted against the contagious nature of cerebro- 
spinal meningitis. Here, also, it had been observed that only one 
child in a family was attacked; that a healthy child might share 
his bed with impunity; and that no hospital infections occurred. 
Probably, no human being doubts now that cerebrospinal menin- 
.gitis is a contagious disease, since the carrier of the micrococcus 
has been demonstrated and contact chains have thence been woven. 
Precisely analogous conditions prevail in Heine-Medin's disease 
and neither the one nor the other differs from contagious diseases 
in its mode of spread. The only distinction which does exist is 
that for other infectious diseases, such as diphtheria, people show 
greater susceptibility than for either cerebrospinal meningitis or 
Heine-Medin's disease. The epidemic factors in these last two 
diseases are very similar. Thus from the New York epidemic of 
1907 it was reported that the occurrence of several cases in one 
family or in one house was observed in the same percentage of 
cases, as in the outbreak of cerebrospinal meningitis which pre- 
vailed there in 1905. Netter, during an epidemic of cerebrospinal 
meningitis affecting more than 180 cases, only five times observed 
more than one case in the same family or in the same house. 

I wish to refer to the possibility of spread by means of insects. 
P. Krause and Ed. Miiller excluded it, after duly weighing the 
evidence they had collected. The prevalence of Heine-Medin's 
disease in summer may be adduced as suggestive of this mode of 
spread. But, on the other hand, insects could not promote the 
continuance into the winter months which occasionally occurs. 
One of the most striking of the winter epidemics, so far as this 
point is concerned, was the north of Sweden epidemic to which 
reference has already been made. There the snow begins to melt 
only in May and the temperature at the time of the scourge was 
far below zero. 

Various authors have also established that Heine-Medin's dis- 
ease in epidemic form never afflicts the same district two years in 
3Uccession. Some insect-carried diseases, such as malaria, recur 
annually with una;bated virulence. 

Moreover, hardly any disease disseminated by insects could 
^how such evident contagious characters as have been . observed 
in certain epidemics of acute poliomyelitis. 


Caverley, Wickman, Peiper, and others have mentioned the 
appearance of paralysis in animals and in fowl coincident with 
epidemics among human beings. But the futile inoculation of 
these creatures shows their affliction has nothing in common with 
that in man. 

Recurrence of acute poliomyelitis in a house after a period 
of one or more years has been reported by Wickman, Fiirntratt, 
J. Hoffmann. It is impossible to determine in such cases whether 
the virus has remained active or a fresh infection has .been 

■ The general trend of the results of recent investigation has 
been to confirm <ny observations concerning the contagious nature 
of acute poliomyelitis. Particularly has this been the case in 
epidemics in which the abortive type and, above all, the healthy 
disease carriers have been ponsidered. But in several other epi- 
demics also one can recognize some of the chief characteristics of 
a contagious disease. 

If recording physicians had personally made all observations 
and if accompanying circumstances had not so greatly compli- 
cated the problem the result would have been more conclusive. 
Yet, Jaeger's words concerning cerebrospinal meningitis may not 
inappropriately be applied to acute poliomyelitis. " The diffusion 
of this scourge appears to us now like a mountain range free from 
mist; only peaks without foundation are visible; yet we are per- 
ceiving now more and more the great bases upon which the peaks 
arise." The more exactly we study epidemics of Heine-Medin's 
disease the more apt will Jaeger's words appear. 


Prophylaxis and Therapy 

As a logical consequence of the doctrine of the infectivity 
of Hein€-Medin*s disease physicians and public authorities should 
enforce the same regulations for the prevention of this as for 
the prevention of other acute infectious maladies; e. g,, isolation 
of the patient, disinfection, etc. Isolation is almost insuperably 
difficult to attain. Not only the paralytic, but also the abortive 
cases, and the healthy virus agents need to be segregated. To 
the last two categories we possess no guides comparable with 
those we can utilize, for instance, in diphtheria, cerebrospinal 
meningitis and other contagious diseases. Hence, effective isola- 
tion practically cannot be accomplished. Under such circum- 
stances we can only warn those suspected of being either abortive 
cases or virus carriers of the menace they may be to the com- 
munity. Schools ought to be closed for several weeks. Isolation 
of the patient seems not to be essential, for experience has taught 
us that infection is seldom direct. The patient may, however, 
become a source of virus carriers and to guard against this possi- 
bility isolation is desirable. Isolation hospitals are the best means 
of segregating such cases, but the present custom of admitting 
fresh cases among others seems to me to be bad. We have no 
exact information yet concerning the isolation time necessary. 
According to Ed. Miiller it is eight weeks. Most physicians in 
the Swedish epidemic were content with three weeks. At present 
we cannot, however, make any positive pronouncement on this 
point. Obviously an attempt must be made to destroy the in- 
fecting germs, even although we are still in the dark concerning 
them. Experimental poliomyelitis in monkeys has shown that we 
may deem the intestinal and nasal mucosae and the salivary glands 
as excretory channels for the virus. It is therefore advisable 
at least in the early stages to disinfect the intestinal and nasal dis- 
charges. Flexner and Lewis found that one per cent, solution of 
hydrogen peroxide destroys the virus; such a solution may be 



used to disinfect the naso-pharynx. Levaditi and Lahdsteiner 
recommend for the same purpose a one per cent, solution of 
menthol, or a powder of the following composition : 

Menthol 0.2 grams, 

Salol 5.0 grams, 

Boric acid 20.0 grams. 

Special attention must be devoted to the disinfection of hand- 
kerchiefs in all maladies in which the germs are present in the 
nasal discharge, but this attention is particularly essential in 
Heine-Medin's disease. According to Romer formalin is suffi- 
cient for disinfecting houses. 

Preventive inoculation has been attempted because of the 
promise of the immunity experiments to which reference has 
already been made. Several investigators have succeeded in 
making monkeys insusceptible to the virus of poliomyelitis. Land- 
steiner and Levaditi were able to produce by subcutaneous injec- 
tion of spinal cord substance, dried as in the Pasteur method of 
attenuating rabies virus, a substance which protected against sub- 
sequent injections. This immunity was obtained by the subcu- 
taneous injection of a mixture of the virus and the serum from 
a sheep, which previously had been treated with virulent emul- 
sions of poliomyelitic cords. Romer and Joseph by means of a 
virus-serum mixture succeeded in establishing a resistance to sub- 
sequent inoculation with unaltered virus. Romer further obtained 
analogous results by heating the virus to 45-50° Celsius, and 
Krause by treating it with 0.5 per cent, carbolic acid, before 
injecting it subcutaneously. These are interesting experiments 
but their practical value has not yet been determined. Inocula- 
tion in the manner of the Pasteur method is not without danger 
and occasionally results in paralysis. 

Therapy.-^— As no specific therapy is yet available, treatment 
in the acute stage must be purely symptomatic. The character- 
istically excessive tenderness demands the greatest possible free- 
dom from disturbance and the most comfortable position for the 
patient. A plaster-of-paris jacket (Hohmann) and a plaster bed 
(Machol) have been recommended to ensure rest. But I agree 
with Ed. Miiller that surgical contrivances in the early stages are 
superfluous. The nerve irritative phenomena soon disappear in 


most cases, and may be treated with internal remedies without 
apparent detriment to the patient. Usually preparations such as 
sodium salicylate, antipyrin, and phenacetin are administered - 
In some cases these drugs are efficacious ; in others they are not. 
Because of the severe pain morphine has been given. Allen Starr 
recommended the use of urotropin ; the local antiseptic affect from 
the formaldehyde which urotropin liberates in the cerebrospinal 
fluid was desired. 

Some advocate diaphoresis. I join with Oppenheim in advis- 
ing that sweating be produced, not by baths which necessitates 
moving the patient, but by packs, hot drinks, etc. 

Retention of urine, constipation, and diarrhea should be reme- 
died in the usual way. Treatment by lumbar puncture has been 
used by Petren and Ed. Miiller. Ed. Miiller recommended it for 
the relief of pressure in rapidly progressing paralysis; and espe- 
cially in the meningeal type of the disease. 

During the reparation stage attention is especially directed to 
avoiding the development of contractures. Precautions must 
early be taken. We must see that the bedclothes do not press 
upon the patient's feet. The feet should be kept at right angles ; 
and the legs extended by splints, bandages, etc. Physicians un- 
doubtedly are careless in this matter, and they thus enhance the 
difficulties of the orthopedist's task. 

Besides preventing such sequelae as contractures, active phys- 
ical treatment should be commenced. Bathing, massage, passive 
and active movements, and electrical stimulation may be useful. 

How soon should such active treatment begin ? In most cases 
at the end of the second or third week active treatment may be 
initiated without harm to the patient. Resorption and reparation 
are then occurring and I hardly think that further advance need 
be feared. The chief aim of the baths is to improve the general 
condition. For this purpose ordinary warm water baths are used, 
but brine, mud, or chalybeate baths may later be serviceable. The 
treatment most effective in restoring the tonicity of the muscles 
is massage, to which passive and active movements are powerful 
adjuvants. Passive movements not only improve the circulation 
in the muscles, but also help to prevent the occurrence of contrac- 
tures. Active movements must be adjusted to the degree of 
paralysis. If only a paresis be present, resistance movements can 


be employed from the beginning. Manual resistance is at first 
preferable as it can easily he graduated to correspond with the 
strength of the muscles. Later, apparatus for exercising may be 
used. Btit if the paralysis be severe, treatment by gymnastic 
exercises becomes more difficult. In such cases the gymnastic 
treatment should he practised in baths. Or the movement which 
normally is subserved by the paralyzed muscle may be passively 
imitated while the patient attempts actively to perform it. By 
such treatment, contractures of years' duration, in completely 
paralyzed and contractionless muscles, have gradually disap- 
peared. We ought, therefore, to practice rational physical therapy 
as early, as thoroughly, and as continuously, as possible. 

Even if we fail to procure recovery, we can at least pave the 
way for the subsequent orthopedic treatment to restore function. 
This manual treatment must be performed by one whose hand 
is skilled. 

Electrical treatment has long been lauded both for spinal and 
for muscular troubles. I doubt if it has caused any material 
benefit. In any case, this method of treatment is not to be com- 
pared in efficacy with the. others. It often causes great uneasiness 
in children and it is questionable if its value materially compen- 
sates for the mental stress it involves. If electrical treatment be 
employed it should be used according to the principle earlier men- 
tioned; if no faradic reaction can be elicited, naturally only the 
constant current should be employed. 

It is difficult to state how long one ought to continue mechan- 
ical and electrical treatment. Probably no essential gain can be 
expected from these methods if improvement is not noticeable in 
a few months. This improvement occurs usually towards the end 
of the first year, often earlier, occasionally later (Risien Russell, 
Petren). Orthopedic surgery is our next resource. In general, 
it is better to consult a surgeon too soon than too late. As a 
suitable operation places paralyzed muscles under better func- 
tional conditions it aids and quickens the recovery of their power. 
The necessary procedures, immobilization of joints, tendon trans- 
plantation, plastic operations on nerves, bandaging, etc., belong to 
the field of orthopedic surgery and mechanical orthopedy. 


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