An Investigation Into Post-Encephalitic Parkinsonism

66 Pages·09.969 MB·English

by  McPhater, Archibald

T H E S I S .
AN INVESTIGATION INTO POST-ENGEPHALITIG PAEKINSONISM
BY
AEGHIBALD MGPHATEE, M.B., Ch.B.(HN1VERSITY Off GLASGOW).
1936.
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Pag© 1•
AN INVESTIGATION INTO F03T-ENGEPHALITIC PAEKINSONISM.
FOBEViPBD.
The layout of this thesis is given in the foreword so that the contin­
uity may be as complete as possible.
F irstly ,there is a general introduction giving the history of the disease
Encephalitis Lethargica. This chapter traces the disease from the acute
epidemics to the chronic stages of the disease with special referehce to
Post-encephalitic Parkinsonism and is rounded off by the bibliography re­
lating to it .
Secondly there is a brief chapter on the sedimentation rate of the red blood
corpuscles which was one of the tests used in the investigation. This chapter
is also followed by its own bibliography
Thirdly there is a chapter on the examination of the cerebro-spinal fluid
which was the other line of investigation. The bibliography also follows this
chapter.
Fourthly, before going on to the actual case results, a resume of the scope
of the investigation is given. Again the bibliography follows its relevant
chapter•
Fifthly the case results are given one page being allotted to each case. The
sedimentation rates being given graphically and the cerebro-spinal fluid re­
sults in tabular form.
Sixthly the results of a control series of cerebro-spinal fluid is. giVen in
tabular form. Again this is followed by a bibliograpiiy.
The case results are then summarised with relevant bibliographies appended
and the thesis completed by a chapter giving the conclusions drawn from these
summaries•
Page 2.
GENERAL INTRODUCTION.
During the Great War of 1914/1913 it was inevitable, with the unnatur­
al living conditions,that infections of a ll types should become more pre­
valent. Of these infections probably the most important was influenza with
its attendant disease Encephalitis Lethargica.
This thesis deals with the Post-encephalitic Syndrome of Parkinsonism*
1
In the month of April, 1917* Vienna, Von Economc described cases of
a new disease with the signs and symptoms of a diffuse brain infection. Then
2
Netter, the french neurologist, described sim ilar cases in a military base
hospital in Prance.
Prom this sporadic beginning the disease took on an epidemic form and
finally became pandemic, spreading to a ll corners of the earth in a short
space of time.
Although described by Von Economo and Netter as a new disease there is
historical evidence that a disease with similar characteristics had been chron-
icaled several times as w ill be seen from the following history.
3
In 1580 there is record of a serious epidemic affecting the whole of
Europe which was described as " Morbus epidemicus per totam fere Europa
Schlafkrankheit dictus”,non tarn leta lis n isi accidental alio rnorbo"• Again in
London from 1673 to 1&75 there ms an epidemi* of a disease which Sydenham
describes as "febris comatose”, this disease was often associated with
singultus .
The next record of a disease characterised by somnolence and nerve symp­
toms is by Albrech of Hildesheim in 1695* This was an isolated case described
by him under the title of " de febre lethargiea in strabismo utriusque oculi
desinente” which would agree with the modern somnolent ophthalmoplegic form
of the disease•
The next mention of febrile disease with somnolence was at Tubingen in
1712 but there is dubiety about the occurrence of somnolent states in this
disease.
From 1723 to 1727 an epidemic occurred in London described as "febris
soporosa et apoplectics". Then in 17&3 hepecq de la Cloture described a
11 coma somnolentum" occurring during an influenza epidemic in Rouen, and
again from i~]3Q to 1732 there was an influenza epidemic with marked cerebral
manifestations. Prom 1330 to 1833 there was an influenza epidemic in Paris
characterised by somnolence.
Page 3.
The previously mentioned diseases characterised by fever, somnolence
and other cerebral manifestations are only put forward hypothetically aa
being Encephalitis Lathargica, but in 1346 there was described by Dubinni
the electric chorea in Northern Italy which is generally recognised as having
been myoclonic encephalitis. Again from 1839 to 1390 there was an epidemic
4
of influenza in Italy and from 1390 to 1991 the disease called "Nona" was
seen in Italy: this had many of the characteristics of Encephalitis Lethar­
gica •
The first name associated with the modern epidemic of Encephalitis
Lethargica is that of Constantin Von Economo of Vienna. In the winter of
1916/1917 there came to the Vienna Psychiatric Clinic many cases which could
not be classified under any definite heading but a ll of which showed lethargy
combined with ocular paralyses which led him to associate it with the disease
"Hona" which had occurred in Northern Italy in the nineties of the previous
century. This knowledge of "Nona" was derived from the fact that he had
spent his youth in Southern Austria where tales of this disease were o till
prevalent•
Although Von Economo was the first to classify this disease as Ence­
phalitis Lathargica, Cruchet in Prance, claimed to have seen cases in the
winter of 1915/1916 and Urechia of Eoumania described similar oases but did
not associate them with any recorded disease. More cases continued to be de­
scribed but it was not t ill after the influenza epidemic of 1913 that Ence­
phalitis Lethargica assumed a pandemic form instead of localised epidemics•
After the pandemic stage of the disease had passed off localised epid-
5,& 6
emics again made their appearance, three of such being, at Sheffield in 1924,
7,&3.
at St. Louis in America during 1933 » present, the disease
in the acute form is only seen in sporadic cases, but with the advent of
world-wide h ostilities and the possibility of similar conditions to those
of the War of 1914/1918, there is the fear of sporadic cases of Encephalitis
Lethargica becoming localised epidemics or even pandemic.
During theyepidemic and pandemic stages of Encephalitis Lethargica it
it was first thought to be an acute inflammatory disease which subsided by
in the recovering cases, but as time passed and the after effects
became more obvious, there were two schools of thought as to the cause of the
after effects.
Pago 4.
The first school of thought stated that these after effects were due
to consequent degeneration following damage done in the acute stage and lab­
elled the after effects sequellae, In 1924, discussing these sequallae, Ivy
9
Mackenzie stated that in his opinion, there was no active inflammation but
changes bore a resemblance to Inflammation in the basal nuclei of the brain.
10
Abro in Beaumont’s text book of medicine refers to chronic cases, but says they
11
are due to the previous destruction of nerve cells. The Ministry of Health, in
a memorandum published in 1929* described the after effects as sequallae and not
as chronic infective processes.
The second school of thought favours the theory of a s till active infect­
ion in a chronic stage. Prom the literature this has a greater following, and
the proof of this can be grouped under three headings:- clin ical,pathological
and epidemiological.
12 to 19 20 21 22 23 24
On the clinical side Von Economo, Wimmer, Hall, MciNalty, Duncan, Gross-
25 26
man, and Preeman support the view that the infection is s till active, but in a
27, 23
chronic state. In addition, several of the observers liken chronic Encephalitis
Lethargica to General Paresis of the Insane, which is a definitely proven chron­
ic infective Encephalitis due to the presence of the Spirochaeta Pallida in
29
the brain tissu e. Also, one observer finds a sim ilarity between chronic
Encephalitis Lethargica, General Paresis and Disseminated Sclerosis, which is
a chronic Encephalitis characterised by recurrences of activity.
30, 31
Pathologically, many are found to support the chronic infective theory;
32 33 34 33 36
these include Muir, MeAlpine, Vegni, Carmichael, Preeman, Hunt & Cornwall,
37
^Reynolds & Slater. Their findings are a ll based on histopathology and are the
results of post-mortem examinations on Post-Encephalitic cases at varying in­
tervals of time from the first attack.
The epidemiological evidence is scarcer than either the clinical or path-
33
ological, but Preeman writing in the Journal ©f the American Medical Association,
quotes seven cases of probable contagion of Encephalitis Lathargica from pat­
ients suffering from post-Encephalitic Parkinsonism. Steifler suggests that
acute exacerbations of a chronic case of Encephalitis Lethargica may be a source
of new infections.
Prom these paragraphs the evidence would seem to point to the persistence
of Encephalitis Lethargica as a chronic infection, and this paper is based on
work done with thirty such cases of post-Encephalitis* Parkinsonism over a period
of six months, in an effort to prove that the infection was s till in existence
in these cases. The investigation was directed, firstly to the sedimentation
/sedimentation rate of the red blood corpuscles and to an examination of the
cerebro-spinal fluid. In the cerebro-spinal fluids, special attention was
paid to the albumen-globulin ratio. Before proceeding to the actual investi­
gation, it was found necessary to study the literature on the sedimentation
rate of the red blood corpuscles and to practical methods of analysing cerebro­
spinal fluids; thus the following notes on the history and application of the
red blood corpuscle sedimentation rate to infective proeesses and the import­
ance of the albumen-globulin ratio in the cerebro-spinal fluid of cases of
nervous disease became essentially a part of the investigation.
BIBLIOGRAPHY.
GENERAL INTRODUCTION.
1. Von Economo G. Encephalitis Lethargica its Sequellae and Treat­
ment* Vienna - translated by K.O, Newman,
Oxford, 1931 *
2* Netter. Bulletin de Societe Medicin des Hopitals de Paris*
Vol. 22 March,1913.
3* Abrahams I. Lethargica Encephalitis. New York. 1935*
4* MLa Nona" The so-called New Disease. The British Medical
Journal. Vol.1. 1890. p*p*743.
3. Memorandum on Encephalitis ^ethargica. Ministry of Health publication.
1929*
6. Medical Research Council: Special Report Series No. tOS.
The Sheffield Outbreak of Encephalitis in 1924.
7* Epidemic of Encephalitis- St. ^ouis Outbreak. Journal of American Medi­
cal Association* Vol. 101. P*P* 923.
3. -do- St. Loui s Outbreak. Journal of American Medi­
cal Association. Vol.103. P*P* 462*
9* Mackenzie I. Encephalitis Lethargica. British Medical Journal.
Sept. 24th. 1927*
10. Beaumont. System of Medicine. 1934. p*p*3ot.
It* Memorandum on Encephalitis Lethargica. Ministry of Health Publication 1929*
12* Scottish Board of Health, 8th. Annual Report. 1926. p.p.5.
13# Epidemic Encephalitis* Journal of American Medical Association.
Vol. 73 p.p.716.
14. Epidemic Encephalitis. Journal of American Medical Association.
Vol. 73 p.p.1767.
13» Epidemic Encephalitis. Journal of American Medical Association.
Vol. 79* p*p»2tt.
16. Epidemic Encephalitis. Journal of American Medical Association.
Vol. 80. p .p.1833.
17* Epidemic Encephalitis. Journal of American Medical Association.
Vol. 91* p.p.f33.
13. Lethargica Encephalitis. British Medical Journal. Vol.t 1920. p.p.732.
19* Ministry of Health Reports. Reports on Public Health and Medical Subjects.
P.P.139*
20. Von Economo C. Encephalitis Lethargica-its Sequellae and Treat­
ment. Oxford University Press. 1931.
21. V&ramer A. Chronic Encephalitis Lethargica. Heineman 1924.
22. Hall A.J. Schorstein Lecture. British Medical Journal.
Novr. 7th.I93I. p.p. 333.
23* MciNalty A.S. Chronic Encephalitis. British Medical Journal.
June, 26th. 1926. p.p. 1075.
24. Duncan A.G. Encephalitis Lethargica. "Brain" Vol. XLVII.
Part 1. P»P»95«
25«Grossman M. Follow up of Encephalitis Lethargica. Journal
of American Medical Association. Vol.73 p.p.359»
Page 7 .
26 • Freeman • Encephalitis Lethargica. Journal of American
Medical Association. Vol. 37 p*p.l601.
27* McGowan & Cook. Chronic Encephalitis uethargica. Lancet Vo.2 1927*
p.p.361.
23* Freeman. Encephalitis Lethargica. Journal of American
Medical Association. Vol. 37 p.p.l601.
29* Editorial Note. Encephalitis Lethargica. British Medical Journal.
Sept. 24th. 1927* P*P*537«
30. Nelson’s ^©ose-^eaf Index of living Medicine. Vol. 6(VI) p.p. 269.
31. Henderson & G illespie. Text-Book of Psychiatry. 1927* P*P* 323*
32, Muir R. Text-Book of Pathology, 1924. p.p.727'
33- MeAlpine D. Pathology of Parkinsonism. "Brain" Vol XLVI.
Part 3 P*P*279*
34. Vegni. Pathology of Parkinsonism. Journal of the American
Medical Association. Vol. 30 p.p. 1333*
33. Carmichael. Pathology of Parkinsonism. Journal of Neurology and
Psychiatry. Vol. IX. p^p.229.
36. Hunt & Cornwall. Pathology of Parkinsonism. Journal of the American
Medical Association. Vol. 34. p.p. 29.
37* Reynolds & Slater. Pathology of Late Manifestations of Encephalitis
Lethargica. Journal of Neurology and Psychiatry.
Vol. 10 p.p. 242.
33. Freeman. Chronic Encephalitis,Lethargica. Journal of the
American Medical Association. Sol. 37 p.p. t601 •
Page 3.
THE SEDIMENTATION SATE OF THE HEP BLOOD CORPUSCLES.
A iiefi-nition of the sedimentation rate of the red blood corpuscles is
1
difficult to give but that given by Panton is concise " a non specific test
for the presence of an active infection*.
Although the clinical application of the test in its present form is
comparatively recent sedimentation has a long history with its beginnings
in the writings of Hippocrates and A ristoteles, who held that the four funda­
mentals of life were Air, Water, Fire and Earth. These in varying proport­
ions composed all things living and dead. Similarly in the human body there
were four fluids? intimately mixed forming the contents of the blood vessels
and the body fluids. The Ait corresponds to the blood, Vfeter to phlegm, Fire
to yellow bile and the Earth to black b ile. These fluids were known as the
Humours•
This theory of four Humours was supported by venesection which was the
only method of blood examination then known. The shed blood,after standing,
differentiated itself into several layers, the dark coloured lower portion;
of the blood clot represented the black b ile, the red portion represented in
the upper part of the clot was the blood proper while the yellow bile was the
serum expressed from the clot. Finally, in pathological bloods the phlegm
collected as a whitish layer above the blood clot and was called the "Febria*
content. Thus this whitish layer was taken as an evidence of the presence of
fever.
In therapeutic venesection it was customary to measure the amount of
phlegaaa in the!shed*blood and to base the prognosis on the amount present.
The presence of phlegm in the blood of patients who were i l l led to it (the
phlegm) being regarded as the causal agent of disease. Thus in the Grecian
theory of medicine phlegm was held t© be the most important causal factor in
disease. Galen gave the name "Buffy Coat" to this layer of phlegm.
Until the advent of Paracelsus in the sixteenth century this fcheory held
sway. He stated that the increase of phlegm was the result and not the causal
factor of the illness but his theory did not replace the old one. In the seven­
teenth century Harvey's discovery of the blood circulation in l628 and Malpighi’s
discovery of the capillaries and red blood corpuscles also helped to undermine
the old theory but did not completely replace it.
Sydenham (1624/1639) believed that" i^lammation;;Of:t1^i«Sr/]tJl©©J,1was the basis
of disease and the two signs of this were fever and the formation of a "buffy