The official version of Lenin’s malady
The official report of Lenin’s disease is actually that of
Professor Viktor Osipov, a famous Russian psychiatrist
who treated Lenin in 1923. In his opinion, the period of
evident illness should be divided into three periods
(Osipov, 1990). In the first (March–December 1922),
short episodes of loss of consciousness occurred followed
by numbness on the right side of the body
affecting initially the right hand. The numbness was
sometimes accompanied by transient right-hand paresis
and motor dysphasia. These attacks occurred about
twice a week, lasting from 20 min to 2 h. Osipov
interpreted these attacks as fatigue with no serious
organic disease (Osipov, 1990). After convalescing in
the village of Gorky, his condition ameliorated
remarkably. In August 1922, he resumed regular
activities at full steam for several months.
The second phase of Lenin’s disease began in
December 1922, when he was suddenly inflicted with
right hemiparesis without dysphasia. He had to dictate
his articles as he was unable to write. In February 1923,
he composed his last political declaration (Osipov,
1990).
The terminal period of Lenin’s disease started in
March 1923, when he suffered irreversible right hemiparesis
with both motor and sensory aphasia and alexia.
In May 1923, he was taken again from the Kremlin to
Gorky village where his condition improved slightly
and he received speech therapy but, in June 1923, his
condition deteriorated. He suffered from throbbing
headaches, restlessness, hallucinations, sleep disturbance
and loss of appetite. A month later, his condition
improved and his wife mediated between him and the
outside world. At that point Lenin was able only to
express a feww ords, although his ability to undertake
verbal repetition was relatively preserved. His reading
ability improved slightly and he could name objects in
pictures presented to him. He began practising writing
with his left hand (Osipov, 1990). Yet, Lenin’s illness
gradually relapsed. In mid-October 1923, episodes of
syncope occurred, lasting 15–20 s each, initially
occurred three to four times per week and later more
frequently. Subsequently epileptic seizures appeared,
with at least one noted in the medical records. The
epileptic seizures worsened inexorably. He became
lethargic and was bedridden until his death on
24 January 1924. The terminal event was status epilepticus,
which lasted 50 min. Finally his face became congested
and reddened during a final, cardiorespiratory
arrest. Resuscitation attempts failed (Osipov, 1990).
The pathological findings
Autopsy was performed the next day by Professor
Alexei Abrikosov in the presence of the Commissar of
Health, Dr Nikolai Semashko. In the USSR, treating
physicians had to participate in the autopsy and sign
its report, but of the 27 physicians who had treated
Lenin (including eight foreigners) only eight signed:
seven Russians and a German (Fo¨ rster) who knew no
Russian. Two pathologists also signed the protocol.
Notably the famous director of the Brain Institute in
Petrograd, Professor Vladimir Bekhterev (1857–1927),
who had examined Lenin at least once, was not invited
to the autopsy (Nikiforov, 1986; Arutyunov, 1999).
The significant autopsy findings were: an ulcerated
atheromatotic plaque severely stenosed the abdominal
aorta. Minor changes were observed in the coronary
arteries, and the left heart ventricle was hypertrophied.
Complete obliteration of the left internal carotid artery
was noted, with diffuse atheromatotic changes and
stenosis of all intracranial arteries, especially the
ascending and inferior frontal branches of the middle
cerebral artery. The vertebral and basillary arteries were
thick and sclerotic.
The brain weighed 1340 g with the left frontal lobe
smaller than the right. The left hemisphere contained
multiple foci of yellowsoftening with cystic changes.
Two areas of softening were noted in the right occipitotemporal
border. On external examination the left
hemisphere contained four degenerative areas with
cystic changes adjacent to the cortical surface and
invading the subcortex – in the paracentral gyrus, in the
high parietal gyri, near the occipital pole and in the
temporal gyri. The lateral ventricles were relatively
widened, more remarkably in the left hemisphere, and
contained transparent liquid. Blood vessels above the
corpora quadrigemina were congested with blood with
signs of hemorrhage. Cerebellar section through the
vermis revealed transparent liquid (Osipov, 1990;
Petrovskii, 1990).
Abrikosov formulated the diagnosis as diffuse
atherosclerosis, most remarkable in the brain arteries.
The attending physicians concluded overwhelming
372 V. Lerner et al.
2004 EFNS European Journal of Neurology 11, 371–376
impairment of cerebral blood circulation; and
haemorrhage around the corpora quadrigemina
(Lopukhin, 1997; Arutyunov, 1999; Danilov, 2000).
Neurosyphilis as a possible diagnosis
Syphilis is ignored as a possible diagnosis in the official
report (Volkogonov, 1994). However, it is our hypothesis
that Lenin suffered from neurosyphilis from the
first decade of the 20th century, and probably even
earlier when the young Lenin lived in Zurich, Geneva,
Munich, Prague, Vienna and London. Despite the
myths, Lenin was not a puritan (Roslyakov, 1997;
Arutyunov, 1999). On 18 July 1895, he was admitted for
2 weeks to Borhardt’s clinic in Switzerland (Danilov,
2000). Lenin did not disclose the reasons for this but he
wrote to relatives that he had: a good time and found
myself … in a Swiss resort (Lenin, 1970).
Returning to Bremen after examining Lenin in
Russia, the renowned German syphilis specialist
Professor Max Nonne hinted in response to a question
about Lenin’s illness everybody knows for which brain
disorders I am called (Flerov, 1987).
The famous Russian physiologist Ivan Pavlov was
quoted to assert that Lenin suffered from syphilis while
at the helm of the Russian Government … he was a
typical patient suffering from progressive paralysis.
Moreover, Pavlov was acquainted with several
researchers who studied Lenin’s brain and confirmed
finding changes consequential of syphilis and progressive
paralysis in Lenin’s brain (Flerov, 1987).
Professor Kramer, who attended the autopsy,
thought that the pathological findings were most compatible
with neurosyphilis. His signature and that of
Dr Kozhevnikov, who also suspected neurosyphilis,
were missing from the official protocol (Witztum and
Lerner, 2002; Lerner, 1979, unpublished observations).
Specialists who gained access to Lenin’s archives noted
that the results of urine tests but not of blood tests were
present, although records showthat blood tests were
taken repeatedly (Lopukhin, 1997).
Dr Hu¨ nter Hesse, a German specialist in the history
of medicine who studied Lenin’s illnesses, also pointed
at Lenin’s sterility, suggesting combined infection with
syphilis and gonorrhea (Hesse, 1998). He also mentioned
that Lenin was treated for 6 weeks in the outpatient
clinics of Berlin’s Moabit hospital for unknown
reasons and that his wife was affected by a feminine
disease (Hesse, 1998).
The Commissar of Health Semashko reported in his
memoirs that the damage to the blood vessels in Lenin’s
brain was so extensive that a metal sound was elicited
by the touch of forceps and that the lumina of vessels
were narrower than a hair (Osipov, 1990; Volkogonov,
1994; Arutyunov, 1999; Danilov, 2000). This, and the
massive sclerosis of cerebral blood vessels described
in Lenin’s autopsy (Osipov, 1990; Freeman, 1991;
Lopukhin, 1997) are compatible with neurosyphilis in
its meningovascular form (Victor and Popper, 2001).
The clinical picture also strongly suggests neurosyphilis
as general paresis occurs typically 10–20 years
after the primary syphilis infection (Roos, 1999). The
personality and cognitive changes can mimic atherosclerotic
cerebrovascular disease (Stoudemire et al.,
2000). Moreover, symptoms such as headache, vertigo,
insomnia and irritability, that inflicted Lenin could be
the clinical manifestation of the slowly progressive
vascular syndrome of meningovascular syphilis
(Lukehart and Holmes, 1994).
There are many versions of Lenin’s autopsy protocol;
some claim a minimum of three (Lopukhin, 1997)
others of eight (Lerner, 1979, unpublished observations),
but no version is authorized. The official version
was publicized shortly after Lenin’s death, to counter
widespread rumours that he had died of syphilis but
this failed to stop them. Therefore, an additional protocol
with histological analyses was issued to prove that
Lenin had not suffered from syphilis. The anatomical
loci chosen to make this claim were atypical and typical
organs heavily affected in syphilis, such as the carotid
and vertebral arteries or the aortic arch, and typically
affected brain areas were ignored (Lopukhin, 1997).
Only after the fall of the Soviet regime when secret
archives were opened for a short period, did it became
possible to retrieve documents. It was discovered that
Commissar Semashko unequivocally instructed Chief
Pathologist Abrikosov to prove that Lenin had not had
syphilis (Arutyunov, 1999; Danilov, 2000). For the
first time, these relevant documents are available in
English. The recently disclosed accounts of two foreign
physicians who treated Lenin, further support these
observations.
The last photographs published of Lenin were only
recently revealed to the public (for example Fig. 1). In
contrast to the well-known photographs and pictures,
this picture reflects the rapid deterioration in his condition.
The impression is of a seriously ill person with a
strange extinguished, haunted look.
Stru¨ mpell’s testimony
Dr Adolf von Stru¨ mpell an eminent neurologist and
internist from Leipzig mentioned in his 1925 memoirs
the medical consultation in Moscowjust briefly. However,
sections from his diary were published in 1974 by
his daughters Dr Regina Stru¨ mpell and Dr Anna
Klapheck from Dusseldorf (Strumpell and Klapheck,
1974). There he noted the first medical consultation
The enigma of Lenin’s malady 373
2004 EFNS European Journal of Neurology 11, 371–376
with the Russian professors Kramer and Kozhevnikov:
March 20, 1923 – Endarteritis luetica with softening is
very probable, although the diagnosis of lues is uncertain
. The next day he examined Lenin in his apartment.
Lenin extended his left hand to him in a friendly
manner. Right hemiplegia and near-complete motor
aphasia with right hemianopsia were diagnosed. The
same afternoon, the full team of consultants met and
discussed endarteritis luetica with secondary softening
as the highly likely diagnosis. However, this diagnosis
remained uncertain as the CSF was normal and Wasserman’s
test was negative but in tertiary syphilis
Wasserman’s test in the CSF is false negative in 34–
90%, while as in blood tests only 5% are false negatives
(Sepp et al., 1950; Lishman, 1987; Isselbacher et al.,
1994; Stoudemire et al., 2000). Additional diagnoses
were proposed including cerebral tumour and subdural
haematoma. Dr Stru¨ mpell noted in his diary that the
patient had too many attending physicians and added,
following another examination of Lenin, diagnosis
uncertain and prognosis uncertain (Strumpell and
Klapheck, 1974).
Henschen’s testimony
In 1974, Folke Henschen, Professor Emeritus of
Pathology from the Karolinska Institute published his
personal reminiscences of his visit to Moscoww hile
accompanying his father, Professor Solomon Henschen,
one of the eight European physicians invited in
March 1923 to treat Lenin. The father gave a detailed
report of his visit to Moscowin the meeting of
the Swedish Medical Society on 26 February 1924
(Henschen, 1974).
Upon arrival in Moscow, he participated in a consultation
with six foreign physicians and the two local
attending physicians. During each of the next 4 days
two different physicians examined Lenin, and Henschen
was paired with Stru¨ mpell. During their examination,
Lenin was coherent and cooperative, leaving the
impression of an intact intellect. He performed all the
verbal commands and understood all his examiners
questions but his verbal response was limited to a few
Russian and German words due to motor aphasia. The
examiners noted complete right hemiparesis without
left-sided motor deficit. The consultants concurred
regarding both the medical treatment and the poor
prognosis.
A fewdays later Lenin’s condition worsened and he
became wholly apathetic and unresponsive to verbal
stimuli. Henschen noted regarding the primary etiology
of Lenin’s disease … Perhaps the apparent cause
could be a common and non-specific etiology, since
Wasserman’s serologic test in CSF was negative.
Henschen considered the terminal event, 10 months
later, to be status epilepticus with hyperthermia of
42.3C and respiratory arrest (Henschen, 1974).
Henschen, having received the detailed autopsy
report with Semashko’s diagnosis of erosive sclerosis,
disputed the final diagnosis of intracerebral haemorrhage
for lack of evidence with only a small
haemorrhage near the corpora quadrigemina. Massive
central intracerebral haemorrhage should have demonstrated
ventricular engorgement with blood but the
ventricles were filled with clear fluid. Henschen (1974)
believed that the document was aimed at the Russian
public.
Discussion
Various sources support the assumption that Lenin
suffered and died of syphilis. The official efforts to
conceal Lenin’s infliction with a stigmatized venereal
disorder were impressive but even more significant were
the attempts to completely hide Lenin’s illness. These
succeeded, in part, due to the lack of English language
scientific publications regarding involvement of syphilis
Figure 1 The last year of Lenin’s life.
374 V. Lerner et al.
2004 EFNS European Journal of Neurology 11, 371–376
in Lenin’s illness and death. Kaplan and Petrikovsky’s
paper (the only relevant paper in English) appeared in
1992 before the collapse of USSR and the opening of
secret archives, relied heavily on Osipov’s memories
from 1930 and ignored significant sources in the Russian
language that had already appeared outside the
USSR (e.g. Flerov, 1987). They did not discuss the
differential diagnosis and chose to ignore significant
clinical data that could indicated an alternative diagnosis
(Kaplan and Petrikovsky, 1992). This case could
serve as a good demonstration of non-purposeful misdiagnosis
or even of conceptual misdiagnosis – when all
the data is available but conclusions are misleading
under the spell of a misconception (Witztum et al.,
1996). The possibility of this diagnosis has been discussed
in several German and Russian popular newspapers
and books (Henschen, 1974; Strumpell and
Klapheck, 1974; Flerov, 1987; Lopukhin, 1997; Roslyakov,
1997; Hesse, 1998; Arutyunov, 1999; Danilov,
2000).
The detailed stages of Lenin’s illness correlate highly
with the clinical course of neurosyphilis. The clinical
correlates of middle cerebral artery involvement including
hemiparesis and aphasia are typical in neurosyphilis,
as are the autopsy findings of complete
obliteration of large-, medium- and small-sized blood
vessels.
The tremendous fees offered to foreign experts for
consultation (Fo¨ rster and Klemperer received 50 000
rubles in gold each, and Henschen received 25 000
Swedish Krone) suggest payment for silence (Volkogonov,
1994).
It is possible that future DNA technology applied to
preserved Lenin’s brain material (Spivak, 2001) ultimately
could establish or disprove neurosyphilis as the
primary cause of Lenin’s death.
The concealment of Lenin’s incapacity during his
lengthy terminal disease enabled the consequent
usurpation of Soviet leadership by Stalin and this
demonstrates clearly the horrid consequences of
deliberate disinformation regarding the health of
political leaders, a lesson that is just as relevant today.
Lenin chronic illness and his death at an young age
cleared the way and created a political vacuum and
administrative decontrol. These were fully exploited
by the usurper Stalin who took over both the Communist
party and the Soviet Union for the next three
decades.
Acknowledgements
The authors would like to thank Jacob T. Buchbinder
PhD, Anne Marie Petrov PhD for helping in preparing
the paper and constructive comments.
References
Arutyunov A (1999). Lenin’s Record without Retouch. Veche,
Moscow.
Danilov E (2000). [The Enigma of the Russian Sphinx]. Pravo
i Zakon, Moscow.
Flerov V (1987). [Lenin’s illness and death]. Grani issue no.:
146 145–174.
Freeman H (1991). The human brain and political behaviour.
Br J Psychiatry 159:19–32.
Henschen F (1974). Noch einmal: Das Sterben Lenins. Frankfurter
Allgemeine Zeitung, Frankfurt.
Hesse H (1998). [V.I. Lenin] (translated by the author).
Independent Psychiatric J 3:83–84.
Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci
AS, Kasper DL (eds). (1994). Harrison’s Principles of
Internal Medicine, Vol. 1, 13th edn. McGraw-Hill, Inc,
NewYork.
Kaplan GP, Petrikovsky BM (1992). Advanced cerebrovascular
disease and the death of Vladimir Ilyich Lenin.
Neurology 42:241–245.
Krupskaya NK (1925). [Recollections about Lenin (1901–
1902)]. Krasnaya Nov:176–185.
Krupskaya N (1989). [Recollections]. Politizdat, Moscow.
Lenin VI (1970). [The Whole Works]. Politizdat, Moscow.
Lishman WA (1987). Organic Psychiatry. The Psychological
Consequences of Cerebral Disorder. Blackwell Scientific
Publications, Oxford.
Lopukhin YM (1997). [The Illness, Death and V.I. Lenin’s
Embalming. The Truth and the Myths]. Respublika, Moscow.
Lukehart SA, Holmes KK (1994). Syphilis. In: Isselbacher KJ,
Braunwald E, Wilson JD, Martin J, Fauci AS, Kasper DL,
eds. Harrison’s Principles of Internal Medicine. McGraw-
Hill, Inc, NewYork, pp. 726–737.
Nikiforov AS (1986). Bekhterev. Molodaya gvardiya,
Moscow.
Osipov V (1990). [V.I. Lenin’s illness and death]. Ogonyek:
6–8. |