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 »  Introduction
 »  Material and methods
 »  Results
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Year : 2001  |  Volume : 49  |  Issue : 1  |  Page : 33-6

Seizures after stroke : a prospective clinical study.

Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226014, India.

Correspondence Address:
Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226014, India.

  »  Abstract

Stroke is one of the most common causes of epilepsy in elderly. However, there have been very few prospective studies to define the incidence, pattern and outcome of seizures in stroke. Most studies are based on retrospective analysis of hospital records. Hence, we planned this prospective study to see the clinical, radiological and electroencephalographic characteristics of seizures in stroke and their outcome, from a north Indian tertiary care centre. Over a span of approximately 6 years, 269 consecutive patients with stroke were studied and followed up. Thirty-five (13%) of these developed seizures, primarily related to stroke, during mean follow up period of 15.9 months. Twenty of these had infarctions while 15 had haemorrhages. Involvement of the cortical region was seen in most of the patients with seizures. In these patients, 86% of the lesions involved cortical areas exclusively or in addition to subcortical areas on CT scan of the brain. Twenty-seven (77%) developed early seizures, two third of them had immediate post-stroke seizures. None of the patients with early onset seizures developed recurrent seizures or epilepsy, while 50% of late onset seizures developed epilepsy. No specific EEG pattern was found in those who later developed epilepsy. In the present study, early onset seizures after stroke were rather common and did not affect outcome and did not recur even when not treated with anti-epileptics. Late onset seizures were less common but were associated with recurrent seizures.

How to cite this article:
Dhanuka A K, Misra U K, Kalita J. Seizures after stroke : a prospective clinical study. Neurol India 2001;49:33

How to cite this URL:
Dhanuka A K, Misra U K, Kalita J. Seizures after stroke : a prospective clinical study. Neurol India [serial online] 2001 [cited 2023 Mar 21];49:33. Available from: https://www.neurologyindia.com/text.asp?2001/49/1/33/1284

   »   Introduction Top

The relation between seizures and stroke was
recognized more than a century ago by John Hughling
Jackson.1 As on today, stroke (cerebral infarction and
haemorrhage) has been considered as one of the most
important causes of epilepsy in the elderly.[2],[3]
However, there have been very few prospective
studies to define the incidence of seizures in stroke,
their clinical pattern, response to therapy and
outcome. Incidence of seizures has been reported to
vary from 7.7% to 42.8%.[4],[5],[6],[7] Louis and McDowell
studied non-embolic cerebral infarction and found an
incidence of 7.7%.4 Other studies included both
cerebral infarctions and haemorrhages and the
reported incidences was 12.5% and 10% respectively.[5],[6] Meyer et al reported higher incidence
of seizures (42.8%) in embolic cerebral infarctions.[7]
The incidence of seizures in intracerebral haemorrhage
has been reported to be 4.6%.[8] The present
study was conducted prospectively to define the
clinical features, CT findings, EEG correlation,
response to therapy and prognosis of post-stroke
seizures in consecutive patients of stroke.

   »   Material and methods Top

Thirty five consecutive patients, admitted under
department of Neurology at the Sanjay Gandhi
Postgraduate Institute of Medical Sciences, Lucknow,
India, with the diagnosis of post-stroke seizures
between January 1990 to March 1996, were studied.
Post-stroke seizures were defined as those either at the
beginning of or after stroke in a patient without prior
history of seizure disorder. All patients with history of
previous seizures, previous brain surgery, head
trauma, subarachnoid haemorrhage, aneurysmal /
tumour, AVM related bleed, significant metabolic
abnormality (hypoglycaemia, severe hyperglycaemia,
hypo-natraemia, uraemia, alcohol intoxication etc.)
and septicaemia were excluded from the study. Thus,
out of 269 cases of stroke admitted during this period,
35 met these criteria. There were 20 male and 15
female patients. Mean age was 45.41 years (range-5
months to 76 years of age). Date of stroke, symptoms
and signs of stroke and duration of follow-up were
recorded in all patients and an attempt was made to
establish the likely aetiology of stroke.
Seizures were classified as generalised, localisation
related (focal, with or without secondary generalisation)
or unclassified.[9] Presence or absence of status
epilepticus, the timing of occurrence after stroke, and
frequency and recurrence were carefully noted. The
seizures were considered 'early' if the initial seizure
(the first seizure after stroke) occurred within two
weeks of stroke, and 'late' if initial seizure occurred
after two weeks of stroke. Early onset seizures were
further classified as 'immediate' if seizure occurred
within 24 hours of stroke. 'Recurrent' seizures were
defined as those occurring at least two weeks after the
onset of the initial seizure. We considered 2 or > 2
seizures as multiple.
CT scan of head and EEG were performed in all the
patients. These investigations were repeated as and
when indicated. Other relevant investigations were
performed to establish the likely aetiology (e.g.
embolic infarction) and any provoking factor for
seizures. CT findings were categorised as infarction
and haematoma. Infarctions were further classified as
cortical, subcortical and cortical-subcortical. The
greatest diameter on that CT slice showing the largest
area involved, was used to determine the size of the
infarct as small (< 5 cms) or large (> 5 cms).
Haematomas were noted for their location and
volume. Haematomas were classified as small (0-29
ml) and large (30 ml or more). EEG findings were
categorised as - (i) normal, (ii) diffuse slowing,
(iii) focal slowing, with or without diffuse slowing
and (iv) epileptiform discharges. An attempt was
made to avoid medication for prevention of further
seizure and to use only single medicine (phenytoin or
carbamazepine or phenobarbitone) if required.

   »   Results Top

Thirty five patients (20 males and 15 females) in age
range of 5 months to 76 years (Mean 45.41 years)
from 269 consecutive patients of stroke, fulfilled the
selection criteria. Twenty patients had infarction and
15 had haemorrhage. Five of 20 patients with
infarction had an embolic stroke from cardiac source
(valvular disease, atrial fibrillation and myocardial
infarctions). Seventeen out of 20 patients of infarction
involved cortical areas, with or without subcortical
regions. Only 3 patients had pure subcortical lesions
on cranial CT. Five haematomas were in the cerebral
cortex while 10 were primarily located to ganglionic
region (Table I). However, 8 of these ganglionic
haematomas were large, with extension of haematoma
and/or surroundings oedema to the cortical regions.
Twenty-seven (77%) patients had early seizures
including 17 who had immediate seizures (i.e. within
24 hrs of stroke) and 8 (23%) had late onset seizures.
Fourteen (40%) initial seizures were single while 21
(60%) had multiple seizures. Eleven (78.6%) of single
initial seizures were focal while 3 (21.4%) were
generalised. Fifteen (71.4%) of 21 initial multiple
seizures were focal including one focal status, while 6
(28.6%) were generalised. Recurrent seizures
developed in 4 patients (focal-3, generalised-1) all of
whom had late onset seizures (onset ranged from 20
days to 12 months). None of the early onset seizures
developed epilepsy or recurrent seizure, during mean
follow-up period of 15.9 months (range 3 to 60
months) (Table II). EEG recordings were normal in 12
(34.28%), showed diffuse slowing in 9 (25.71%),
focal slowing or significant asymmetry in 8 (22.86%)
and epileptiform discharges in 6 (17.14%). One of the
4 patients with recurrent seizures had focal slowing,
one had focal spikes, while other two (50%) had
normal EEG. Thus, no specific EEG pattern was seen
with early versus late seizures and recurrent versus
non-recurrent seizures. Presence of epileptiform
activity on EEG was not correlated with multiple or
recurrent seizures.
Nine patients out of 14 with early single seizures did
not receive antiepileptics, while 5 received
antiepileptics. None in the either group developed
recurrence. 10 out of 13 patients with early multiple
seizures were given antiepileptics while 3 did not
receive the same. None developed chronic
epilepsy/recurrent seizures. All 8 patients with late
onset seizures, were given antiepileptics including 4
cases, who developed recurrent seizures. In all cases,
monotherapy with carbamazepine, phenytoin or
phenobarbitone was sufficient to control seizures.
There were only 4 deaths in the follow up period. 17
patients had good recovery while 14 had poor
recovery. Of the 4 deaths, 2 patients had ganglionic
haemorrhages while the other two had MCA territory
infarction. Two of them had developed seizures at
onset of stroke while remaining two within next two

   »   Discussion Top

35 out of 269 patients (13%) had seizures following
stroke. 27 cases (77%) had early onset seizures of
which 2/3rd had immediate post-stroke seizures. Out
of 97 patients in five series, who had experienced
seizures in the post-stroke period, seizures occurred in
55 at the onset of stroke.[4],[10],[11],[12],[13] We had similar
findings. However, in a recent series of 72 patients,
where only post-ischaemic strokes were considered,
only 24% initial seizures were of early onset.[14] In
intracerebral haemorrhage, incidence of early seizures
tends to be higher than the late onset seizures.[8] Focal
motor seizures, with or without secondary
generalisation, were the predominant types of seizures
both in early onset (74%) and late onset (75%) group.
Rest of the patients had generalised seizures. Complex
partial seizures were not observed. Similar findings
have been reported by other authors as well.[12],[13],[15]
However, in series of Susanna et al, early onset
seizures were more likely to be generalised.[14]
Complex partial or unclassified seizures were rare.
We found recurrent seizures only in cases of late onset
seizures. Susanna et al[14] had also reported recurrent
seizures mainly in late onset seizures group though
few previous studies disagree.[16],[17] All our patients
had undergone EEG. Periodic lateralised epileptiform
discharges were not recorded while diffuse slowing
(25.71%) and focal slowing with or without diffuse
slowing (22.86%) were seen in approximately equal
number of cases. There was no specific pattern of
EEG correlating to recurrence. However, the total
number of cases of recurrent seizures (n=4) is too
small for any conclusion. Recurrent seizures in 100%
of the four patients with periodic lateralised
epileptiform discharges and in 75% of the eight
patients with diffuse slowing, have been reported.[18] In
our patient, late onset of initial seizure was related to
recurrence rather than pattern of EEG abnormality.
The involvement of cerebral cortex has been
emphasised in the pathogenesis of epilepsy caused by
stroke.[12],[14] Some authors have given more stress on
the size of cerebral infarction.[18] Incidence of seizures
in lobar haemorrhage has been reported to be 32%,
while it is 2% in putaminal, thalamic and pontine
haemorrhages.[8] In present study, 85% of infarctions
leading to seizure involved cerebral cortex with or
without involvement of subcortical region. 33% of
haematomas were localised exclusively to the cortical
region while 80% of ganglionic haematomas were
large with extension of haematoma/oedema to the
cortical area. Thus, collectively only 14.28% of
lesions (infarcts or haematoma) were localised to
subcortical regions. However, MRI studies were not
done in present series, hence possibility of cortical
involvement still cannot be ruled out, in these cases of
'pure subcortical' involvement as seen on CT scan.
Early seizures, whether treated with antiepileptics or
not, did not lead to chronic epilepsy. Even recurrent
seizures were easily controlled with one anti epileptic
drug. Thus, inspite of presence of structural lesion,
post-stroke seizures did not present as therapeutic
challenge. Similar conclusion has been reached by
earlier authors as well.[15],[18] All four patients who died,
had early onset seizures. Late onset seizures probably
correlated with recurrent seizures (chronic epilepsy),
thus enhancing morbidity. They are however, not
significantly correlated with mortality.

  »   References Top

1.Jackson JH : Epileptiform convulsions from cerebral disease In : Selected writings of John Hughlings Jackson on Epilepsy and epileptiform convulsion, Taylor J, Homes G, Walshe FMR (Eds); Hodder and Stoughton Ltd., London, 193I; 1 :330-340.  Back to cited text no. 1    
2.Gilmore PC, Brenner RP : Correlation of EEG, CT and clinical findings - study of 100 patients with focal delta activity. Arch Neurol 1981; 38 : 371-372.  Back to cited text no. 2    
3.Luhdorf K, Jensen LK, Plesner AM : Etiology of seizures in the elderly. Epilepsia 1986; 27 : 458-463.  Back to cited text no. 3    
4.Louis S, McDowell F : Epileptic seizures in non-embolic cerebral infarction. Arch Neurol 1967; 17 : 414-418.  Back to cited text no. 4    
5.Dodge PR, Richardson EP, Victor M : Recurrent convulsive seizures as a sequel to cerebral infarction: a clinical and pathological study. Brain1954; 77 : 610-638.  Back to cited text no. 5    
6.Black SE, Norris JW, Hachinski VC : Post-stroke seizures (Abstract). Stroke1983; 14 : 134.  Back to cited text no. 6    
7.Meyer JS, Chamey JZ, Rivera VM et al : Cerebral embolisation prospective clinical analysis of 42 cases. Stroke 1971; 2 : 541-554.  Back to cited text no. 7    
8.Chung-Yang Sung, Nai Shin Chu : Epileptic seizures in intracerebral haemorrhages. J Neurol Neurosurg Psychiatry 1989; 52 : 1273-1276.  Back to cited text no. 8    
9.Proposal for revised classifications of epilepsies and epileptic syndrome. Epilepsia 1989; 30 : 389-399.  Back to cited text no. 9    
10.Richardson EP, Dodge PR : Epilepsy in cerebral vascular disease. A study of the incidence and nature of seizures in 104 consecutive autopsy proven cases of cerebral infarction and haemorrhage. Epilepsia 1954; 3 : 49-65.  Back to cited text no. 10    
11.Homes GL : The electroencephalogram as a predictor of seizures following cerebral infarction. Clin Electroencephalogr 1980; 11 : 83-86.  Back to cited text no. 11    
12.Cocito L, Favale F, Rani L : Epileptic seizures in cerebral arterial occlusive disease. Stroke 1982; 13 : 189-195.  Back to cited text no. 12    
13.Frank G : Border zone (Watershed area) cerebral ischaemia. Electroencephalogr Clin Neurophysiol 1982; 35 : 297-306.  Back to cited text no. 13    
14.Susanna H, Xiu-Shi Ni, Margret D et al : EEG, CT and neurosonographic findings in patient with post-ischaemic seizures. J Neurol Sci l995; 132 : 57-60.  Back to cited text no. 14    
15.Fish DR, Miller DH, Roberts RC et al : The natural history of late onset epilepsy secondary to vascular disease. Acta Neurol Scand 1989; 80 : 524-526.  Back to cited text no. 15    
16.Hauser WA, Ramirez-Lasepas M, Rosenstein R : Risk for seizures and epilepsy following cerebro-vascular insults. Epilepsia1984; 25 : 666.  Back to cited text no. 16    
17.Kilpatrick CJ, Davis SM, Hopper JL et al : Early seizures after acute stroke. Archives of Neurology Sciences 1992; 49 :509-511.  Back to cited text no. 17    
18.Gupta SR, Naheedy MH, Elias D et al : Postinfarctioin seizures. A clinical study. Stroke 1988; 19 : 1477-1481.  Back to cited text no. 18    


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