Journal of

Neurology

3. Neurol. 224, 101-109 (1980)

@ by Springer-Verlag 1980

Epilepsy in Patients with Cerebral Infarcts
J. de Reuck, N. Krahel, G. Sieben, L. Orban, W. de Coster, and H. vander Eecken
Department of Neurology, University of Ghent, Belgium

Summary. Out of series of 240 patients, with proved cerebral infarcts at
necropsy, 14 with a clinical history of epilepsy were selected. The possible
etiology of seizures was analyzed by comparing the clinical and pathological
data. It appeared from this series that epileptic spells, preceding for years the
occurrence of a stroke, were due to other causes than to cerebrovascular
insufficiency. It was also difficult to separate apoplectic seizures from those
occurring due to scar formation after a cerebral infarct, as postapoplectic
epilepsy was induced either by the occurrence of a new stroke or by
hemodynamic disturbances. Severe generalized or local hemodynamic and
metabolic disturbances were also noted in cases of convulsions resulting from a
cerebral infarct.
Key words: Epilepsy - Cerebral infarcts - Electroencephalography - Cardiac
insufficiency - Renal insufficiency - Hypertensive encephalopathy.
Zusammenfassung. Vierzehn Patienten mit der klinischen Vorgeschichte einer
Epilepsie geh6rten einer Gruppe von 240 F~llen an, bei denen zerebrale
Infarkte bei Autopsie nachgewiesen wurden. Die klinischen und pathologischen Ergebnisse wurden verglichen, um die m6gliche Atiologie der Krampfanf~ille analysieren zu k6nnen. Es zeigte sich, dab die epileptischen Anf~.lle, die
dem Auftreten eines Ictus um Jahre vorausgingen, andere Ursachen als eine
zerebrovaskul~ire Insuffizienz hatten. A u f e r d e m schien es schwierig, apoplektische Konvulsionen zu trennen von jenen Epilepsien, welche nach Narbenbildung infolge eines zerebralen Infarktes auftraten, da eine post-apoplektische
Epilepsie entweder durch das Auftreten eines neuen Ictus oder durch hemodynamische St6rungen induziert wird. Auch in F~iilen von Konvulsionen, die
mit dem Auftreten eines zerebralen Infarktes verbunden sind, wurden ernsthafte allgemeine oder lokale haemodynamische oder metabole St6rungen
festgestellt.
Offprint requests to: Dr. J. De Reuck, Kliniek voor Neurologie, Akademisch Ziekenhuis, De
Pintelaan 135, B-9000 Gent, Belgium

0340-5354/80/0224/0101/$01.80

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Introduction
Epilepsy, arising in elderly patients, is not u n c o m m o n (Niedermeyer 1958;
Schwade 1960; L a n d a - C a n n o n a n d Jauregui 1967; B e a u m a n o i r and De Souza
1970). No cause o f the fits can be f o u n d in the m a j o r i t y o f cases (Serafetinides a n d
D o m i n i a n 1963). A lesion can be d e m o n s t r a t e d in only 10 to 30%, a n d m a y be
t u m o r , c e r e b r o v a s c u l a r insult, h e a d injury, vascular m a l f o r m a t i o n , abscess or
severe t o x i c - m e t a b o l i c or h e m o d y n a m i c d i s t u r b a n c e s (Seifer and Ignacio 1972;
Stevens a n d A m m e r m a n 1972; Wallace 1974). The association o f a p o p l e x y a n d
epilepsy has been stressed by different a u t h o r s during the previous century
( C o p l a n d 1850; J a c k s o n 1881). G o w e r s (1888) p o i n t e d out that recurring epileptic
fits were m o r e frequent after cerebral softening than after h e m o r r h a g e a n d that the
cerebral cortex h a d to be involved. The latter has been c o n f i r m e d by more recent
studies ( R i c h a r d s o n a n d D o d g e 1954; Barolin a n d Reinisch 1972). The concept of
vascular epilepsy is n o w widely accepted ( D o d g e et al. 1954; Wild 1965; A n g a n d
U t t e r b a c k 1967; H u t c h i n s o n a n d Acheson 1975); m i n o r a n d generalized epileptic
spells, as weil as focal, J a c k s o n i a n a n d uncinate seizures m a y occur (Brain a n d
W a l t o n 1969). A c c o r d i n g to Barolin et al. (1975) the epileptic insult can precede or
a c c o m p a n y the onset o f a stroke or can occur with a free interval after scar
f o r m a t i o n . C e r e b r o v a s c u l a r disease is s u p p o s e d to be the most frequent cause o f
epileptic d i s o r d e r s in elderly patients (White et al. 1953). A c c o r d i n g to Fischer
(1959) it occurs m o s t frequently in the early d e v e l o p m e n t of cerelsral a r t e r i o sclerosis. A convulsive episode d u r i n g the occurrence of a stroke is infrequent
(Barolin et al. 1962; Merritt 1967), except in cases of hypertensive e n c e p h a l o p a t h y
(Alpers a n d M a n c a l l 1971) or e m b o l i c cortical infarcts ( A d a m s a n d Victor 1977). It
is generally a c c e p t e d t h a t a t h r o m b o t i c infarct can be responsible for epilepsy as a
sequel o f a stroke (Fine 1967; Louis a n d M c D o w e l l 1967), and that the incidence o f
seizures increases with the survival rate of the p a t i e n t ( M o s k o w i t z et al. 1972). In
the p r e s e n t study the occurrence o f e p i l e p s y and the relation to the stroke episode is
a n a l y z e d in a series of a u t o p s i e d patients with p r o v e n cerebral infarcts, in o r d e r to
d e t e r m i n e the responsible factors.

Material and Methods
During the last decade 4287 necropsies were performed in the University of Ghent and the brain
was examined in 2975 cases. Cerebral infarcts were found in 240 patients. The clinical files of these
patients were reviewed and in 19 a convulsive disorder was noted. Five cases were excluded from
this study because, in addition to the infarcts, large hemorrhages were also observed in four and a
recent subdural hematomas in one. One patient had uncinate fits, while generalized convulsions,
lasting a few minutes to several hours and days were noted in the others. In 8 patients the
convulsions had a focal onset or were more pronounced on one side. EEGs were available in 12 of
the 14 patients. A general necropsy had been performed in 12 cases. Only the relevant features, in
relation to the stroke and the convulsive disorder, will be mentioned.

Results
Case 1

A 55-year-old w o m a n was a d m i t t e d with a p r o n o u n c e d form of Lyell's disease.
F r o m the age of 22 she suffered from r e p e a t e d generalized convulsions a n d was

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103

treated with several antiepileptic drugs. She developed a syndrome of progressively increasing mental deterioration 2 years before her final admission and the
epileptic fits were more frequent. She died from septic shock. EEGs taken at
different times during her life had shown only diffuse slowing and on one
occasion bitemporal spikes, more pronounced on the right side. The brain
contained several lacunar infarcts in the putamina, the periventricular white
matter and left thalamus. An old cystic cortico-subcortical infarct was present in
the left temporal lobe and a small arteriovenous malformation was found in the
centrum semiovale of the right frontal lobe.
Case 2

A 62-year-old man was admitted with a left frontal syndrome and leit facial
paresis. The E E G showed bifrontal delta waves without epileptic elements. The
prior history included longstanding alcohol abuse and uncinate fits for 20 years.
The patient suffered from cardiac insufficiency for 3 months and he had hypertension. The brain contained several lacunes in the left caudate nucleus, the
putamina and internai capsules.
Case 3

A 68-year-old woman was admitted because of sudden aphasia and confusion.
The next day she developed convulsions on the right side and became comatose.
The E E G revealed periodic spike-wave complexes in the left temporo-occipital
region, with secondary generalization. The patient became progressively anuric
and died on the ninth hospital day. Postmortem examination revealed a recent
cortico-subcortical infarct in the left temporal lobe.
Case 4

A 60-year-old man, with a previous history of hypertension and angor, developed
flaccid right hemiplegia and aphasia. He developed signs of temporal lobe
herniation 6 days later and was immediately treated with high doses of steroids
and mannitol. The signs of intracranial hypertension regressed, but on the 1 lth
day after the apoplexy he had two generalized convulsions and coma. The E E G
showed generalized slowing with a more pronounced disorganization in the left
hemisphere. The patient died 15 days later from lung emboli, as shown by postmortem examination. An extensive lytic infarct was found in the territory of the
left middle cerebral artery of the brain. These was only moderate brain edema
(Fig. 1).
Case 5

A 69-year-old woman was admitted in coma with generalized convulsions, more
pronounced on the left side, and a left Babinski sign. The blood pressure was
250/120. The previous history included cardiac insufficiency, hypertension, renal
insufficiency and mental deterioration, attributed to cerebral arteriosclerosis. The

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Fig. 1. Coronal sections of cerebral hemispheres of Case 4, revealinglarge lytic infarct in territory
of teft middle cerebrat artery. There is only moderate brain edema

patient remained in coma with continuous convulsions until death, although
hypertensive and anticonvulsive medication had been given. Repeated EEG
showed periodic delta waves in the frontal regions, more pronounced on the left.
Postmortem examination revealed several recent hemorrhagic infarcts in the right
cerebral hemisphere, brain edema, right temporal herniation and brainstem
compression.
Case 6

A 47-year-old woman developed generalized convulsions and coma. She died 20 h
later. She had been admitted 3 days before because of lung edema, pleuritis and
pericarditis. The previous history included hypertension and renal insufficiency,
due to phenacetine abuse. The brain contained a large, recent cortico-subcortical
infarct in the territory of the left middle cerebral artery, with brain edema,
temporal lobe herniation and secondary brainstem compression (Fig. 2).
Case 7

An 84-year-old man was admitted because of left sudden faciobracial myoclonus.
The convulsions lasted a few hours and afterwards the patient was found to have
a left hemiparesis. The EEG showed diffuse slowing with a more pronounced
disorganization in the right cerebral hemisphere. The patient died from massive
lung emboli and bronchopneumonia. Large areas of demyelination with several

Epilepsy in Patients with Cerebral Infarcts

105

Fig. 2. Horizontal section of mesencephalon of Case 6 showing secondary hemorrhages and
elongation of left oculomotor nerve, due to left temporal lobe herniation by recent cerebral
infarct and brain edema
small cystic infarcts were found in the periventricular white matter of the centra
semiovalia on both sides. Small cystic infarcts were also present in both thalami.
Case 8

A 12-year-old boy was admitted because of sudden coma and myoclonus on the
left side, following a period of hypotension and shock, due to anuria, after a right
nephrectomy for a renal Staphylococcus abces. Although renal dialysis was
immediately performed the patient remained in coma with continuous myoclonus
on the left. EEGs taken on several occasions showed generalized disorganization
with intermittent spikes and sharp waves in the right cerebral hemisphere. The
brain contained a cortico-subcortical watershed infarct in the right cerebral
hemisphere, the age of which corresponded to the beginning of the convulsive
disorder (Fig. 3).
Case 9

A 66-year-old woman with a history of hypertension, bronchopneumonia, and
renal insufficiency with severe electrolytic disturbances, became comatose during
treatment with renal dialysis. She had a blood pressure of 210/85 and generalized
convulsions. The convulsions stopped after a few minutes, but the patient

Fig. 3. Watershed infarcts in left occipital lobe on coronal sections of cerebral hemisphere of
Case 7

Fig. 4. Small watershed infarcts in convex surface of the left cerebral hemisphere of Case 10

Epilepsy in Patients with Cerebral Infarcts

107

remained comatose. The neurological examination revealed a mild right hemisyndrome. EEGS taken on several occasions in the following days, revealed
moderate generalized slowing and, on one occasion, slightly more pronounced
disorganization in the left cerebral hemisphere. The brain revealed several small
lacunar infarcts in the lenticular nuclei, caudate nuclei and thalami. A small
recent hemorrhagic infarct was observed in the pons.
Case 10

A 47-year-old woman was admitted because of sudden coma with generalized
convulsions, which had started in the left arm and leg, following complaints of
headache and vertigo. The prior history included periods of headache and vertigo
for 7 years, due to arterial hypertension. For 2 years the patient had developed
progressively increasing renal insufficiency, due to phenacetine abuse. The E E G
during her final admission revealed only diffuse slowing and disorganization. She
remained comatose with a blood pressure of approximately 200/105. The brain
contained recent watershed infarcts in both cerebral hemispheres (Fig. 4), and an
old cystic watershed infarct in the right occipital lobe.
Case 11

A 77-year-old man was admitted becausc of coma and generalized convulsions,
which had started in the right arm and leg. The convulsions lasted 4 days
although several anticonvulsant drugs had been given. The EEGs once showed
bilateral spike-wave complexes, starting in the left hemisphere and on the
following occasions continuous delta waves in the left cerebral hemisphere. The
patient died from bronchopneumonia. The brain contained an old cystic infarct
in the convex surface of the left frontal lobe and a recent cortico-subcortical
infarct in the territory of the right middle cerebral artery. In addition a left
putaminal lacuna and a small cystic infarct in the left cerebellar hemisphere were
found.
Case 12

A 46-year-old man had developed a left posterior heart infarct with irregular
heart rate, followed by sudden right hemiplegia and aphasia 2 years ago. During
the last 6 months he had several attacks of Jacksonian epilepsy starting in the
right hand, followed by generalized convulsions and loss of consciousness. The
brain revealed an old cystic infarct of the left insular cortex. More recent infarcts
were found in the more distal irrigation fields of the left middle cerebral artery.
Case 13

A 70-year-old man was admitted in coma with myoclonus in the right arm and in
right side of the face. The E E G revealed only generalized slowing. The patient
had developed a right hemiplegia 5 years before, from which he had partially
recovered. The general necropsy revealed lung edema, right ventricular heart

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dilatation, and an old posterior-inferior infarct. The brain contained an old cystic
cortico-subcortical infarct involving the whole territory of the left middle cerebral
artery and also part of the putamen.
Case 14

A 66-year-old man was admitted with generalized convulsions and coma. He died
12h later. He had developed a moderate paresis of the left arm and leg with
hypertension 4 years before. EEGs performed at that time revealed only minor
non-specific changes. The general necropsy showed a recent left ventricular
cardiac infarct. Only a few lacunar infarcts of the putamina and of the periventricular white matter were f o u n d in the brain.
Discussion

A convulsive disorder was noted in 7.9% of patients with cerebral infarcts in our
series. Only 7 patients had a typical history of a stroke. If the clinical history is
c o m p a r e d with the pathological findings, a classification of vascular epilepsy into
pre-apoplectic, apoplectic and post-apoplectic is rather difficult. In the two cases
of so-called pre-apoplectic type, it is clearly shown that there is a coincident
association of infarcts and epilepsy. As to the case of a convulsive disorder
a c c o m p a n i n g the establishment of a stroke an intimate relation is not clear and
the associated disturbances, such as the renal insufficiency, severe arterial hypertension, brain edema and intracranial hypertension, could have been the cause of
the seizures. In some cases it appears from the correlation of the clinical
description of the spells and the p o s t m o r t e m brain findings, that the occurrence
of a recent cerebral infarct had triggered convulsions, starting in an old one,
making these cases examples of apoplectic as weil as of post-apoplectic epilepsy.
Exogenous causes for the occurrence of spells were also found in other patients
with post-apoplectic epilepsy, such as acute lung edema, a recent cardiac infarct,
or new embolic cerebral infarcts.
So finally one can question if epilepsy, occurring in a patient with a stroke,
can be explained by the cerebral infarct alone. H e m o d y n a m i c disturbances have
already been suggested by different authors (Chatrian 1961; Naquet et al. 1961;
Barolin et al. 1962) to be important in the genesis of vascular epilepsy. They can
p r o b a b l y induce the seizures by activating some cells in the infarcted area or in
the surrounding tissue, either neurons (Meldrum and Brierley t973) or astrocytes
(Brotchi 1979).

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Received April 14, 1980