J Neurol(1990) 237:166-170

Journal of

Neurology

© Springer-Verlag 1990

Epileptic seizures in thrombotic stroke C.-Y. Sung and N.-S. Chu Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan Received June 16, 1989 / Received in revised form December 7, 1989 / Accepted January 10, 1990

Summary. E p i l e p t i c seizures d u e to t h r o m b o t i c c e r e b r a l i n f a r c t i o n w e r e s t u d i e d in 118 p a t i e n t s . T h e o c c u r r e n c e o f s e i z u r e s h a d a b i m o d a l d i s t r i b u t i o n with o n e p e a k p e r i o d within 2 w e e k s a n d a n o t h e r p e a k p e r i o d f r o m 6 to 12 m o n t h s a f t e r s t r o k e . F o u r p a t i e n t s h a d seizures prec e d i n g s t r o k e , while 23 p a t i e n t s w i t h o u t a h i s t o r y of previous s t r o k e h a d "silent infarct" on the C T scan. F i f t e e n p a t i e n t s ( 1 3 % ) h a d status e p i l e p t i c u s . S i m p l e p a r t i a l seiz u r e s o c c u r r e d in 56% of p a t i e n t s , c o m p l e x p a r t i a l seiz u r e s in 24% a n d g e n e r a l i z e d tonic-clonic seizures in 4 % . E p i l e p s y d e v e l o p e d in 35% o f p a t i e n t s with e a r l y s e i z u r e s a n d in 90% o f p a t i e n t s with late seizures.

Key words:

Seizure - Epilepsy - Vascular seizure - Cere-

brovascular disease - Cerebral thrombosis

Introduction E p i l e p t i c s e i z u r e f o l l o w i n g c e r e b r o v a s c u l a r d i s e a s e is n o t u n c o m m o n [13]. C e r e b r o v a s c u l a r d i s e a s e is, i n d e e d , the m o s t f r e q u e n t cause o f s e i z u r e s in o l d e r p a t i e n t s [15, 26, 29]. A l t h o u g h t h e r e h a v e b e e n r e p o r t s o f s e i z u r e s d u e to s t r o k e [2, 11, 18, 22, 24], t h e s e studies usually h a v e b e e n o f r e l a t i v e l y small n u m b e r s o f p a t i e n t s , a n d h a v e evalua t e d seizures that o c c u r r e d o n l y d u r i n g t h e a c u t e p h a s e of s t r o k e . S u r p r i s i n g l y , o n l y the r e p o r t by L o u i s a n d M c D o w e l l [14] in 1967 specifically d e a l t with seizures d u e to t h e n o n - e m b o l i c c e r e b r a l infarction. T h a t s t u d y was c a r r i e d o u t b e f o r e c o m p u t e d t o m o g r a p h y ( C T ) b e c a m e a v a i l a b l e . It has b e e n t h e g e n e r a l c o n s e n s u s that C T is e s s e n t i a l in e s t a b l i s h i n g a diagnosis of c e r e b r a l inf a r c t i o n a n d in d i f f e r e n t i a t i n g it f r o m c e r e b r a l h a e m o r r h a g e that m a y m i m i c c e r e b r a l i n f a r c t i o n clinically. F u r t h e r m o r e , C T scan m a y r e v e a l a "silent infarct" in patients w i t h o u t a h i s t o r y of p r e v i o u s s t r o k e t h a t m a y cont r i b u t e to t h e d e v e l o p m e n t of seizures in t h o s e p a t i e n t s

[8, 25].

T h e p r e s e n t s t u d y was u n d e r t a k e n to r e - e v a l u a t e the s e i z u r e s f o l l o w i n g n o n - e m b o l i c c e r e b r a l infarction. A p Offprint requests to. Nai-Shin Chu, Department of Neurology, Chang Gung Memorial Hospital, 199 Tung Hwa North Road, Taipei, Taiwan

proximately 2000 cases of presumed

cerebral infarction

w e r e r e v i e w e d . A l l p a t i e n t s h a d at least o n e C T study. B o t h e a r l y and late seizures w e r e e v a l u a t e d in a long p e r i o d of follow-up.

Patients and methods We reviewed the medical records of patients who were admitted to our hospital between 1982 and 1986 because of seizures or cerebral infarction. The diagnosis of cerebral thrombosis was based primarily on the criteria used by Mohr et al. [18]. To rule out the possibility of embolic stroke, we eliminated patients with cardiac arrhythmias, recent myocardial infarction, cardiomyopathy with congestive heart failure, valvular heart disease, bacterial endocarditis, or a significant abnormality in the region of the carotid bifurcation on Doppler and/or angiographic examination. Patients with a previous history of seizure disorder, intracerebral haemorrhage, subarachnoid haemorrhage, arteriovenous malformation, severe head trauma or brain surgery were excluded. Also excluded from the study were patients with dural sinus thrombosis, malignant hypertension with encephalopathy, or toxic-metabolic disturbances at the time when seizures occurred. The possibility of mistaking Todd's paralysis as cerebral infarction was excluded by negative CT findings and by recovery of paralysis usually within 48 h after the seizure. The cerebral infarcts were divided into three major categories according to size and location: watershed infarct, lacunar infarct and other infarcts. Watershed infarct occurred in the border zones between two main artery territories and was further divided into (1) anterior watershed infarct located between the superficial territories of the anterior and middle cerebral arteries, (2) posterior watershed infarct located between the superficial territories of the middle and posterior cerebral arteries, and (3) subcortical watershed infarct located between the deep and superficial territories of the middle cerebral artery [4, 32, 33]. The diagnosis of lacunar infarction was made in patients who presented clinically with certain lacunar syndromes [12, 17] and whose CT scans showed either no visible infarcts or small infarcts in the deep structures such as the thalamus, basal ganglia, internal capsule and corona radiata area. All patients underwent routine laboratory studies, including complete blood count, urinalysis, serum electrolytes, blood chemistry, chest radiography and ECG. One hundred and twelve patients had EEGs and 11 patients had cerebral angiography. At least one CT scan was obtained in every patient and reviewed by the authors. The seizure was considered to be related to the thrombotic stroke if it occurred at the onset of or following the cerebral infarction and other possible causes for the seizure were excluded. Seizures were classified according to the 1981 proposal of the Interna-

168 Table 3. Clinical and radiotogical summary of four patients with seizures preceding the stroke

Epilepsy

Patient

Age (years)/ sex

Seizure type

No. of seizures

Status epilepticus

Interval

Neurological findings

CT lesion site

Angiography

1

31/F

L focal motor

1

-

A few hours

L hemiparesis

R frontal border zone

R 1CA occlusion with collateral circulation

2

50/F

Many

-

2 days

L hemiparesis

R frontal

+

3

69/F

L Jacksonian motor GTC

5

+

A few hours

R striatum

+

4

65/M

GTC

1

-

2-3 days

L hemiparesis L hemiparesis

Large L MCA infarct

GTC = Generalized tonic-clonie seizure: ICA = internal carotid artery; MCA = middle cerebral artery; + = present, - = absent, L = left, R = right

Location of the infarction

25

2O +3 oo +~

15

Z

z

12

18

l

24

}0

Interval (months)

Fig. 1. Temporal relationship between thrombotic stroke and seizure. Forty-two patients with uncertain intervals were excluded

Table 4. Location of cerebral infarcts in patients with seizures and status epilepticus

F P T O F-P P-T P-O T-O F-P-T P-T-O Multiple infarcts Lacunar stroke Borderzone infarct

T h e sites of the cerebral infarcts are s u m m a r i z e d in T a b l e 4. W h e n patients with m u l t i p l e infarcts, l a c u n a r stroke a n d b o r d e r zone infarction were excluded, the infarct was located within a single lobe in 40 patients and involved m o r e than one lobe in 42 patients. A m o n g those 82 patients, the frontal lobe was solely or partially involved in 48 patients (58%), the t e m p o r a l lobe in 48 ( 5 8 % ) , the parietal lobe in 35 (43%) a n d the occipital lobe in 16 (20%). H o w e v e r , the infarct was seen in the frontal lobe in half of the cases w h e n only a single lobe was involved. A m o n g 11 patients who had a c e r e b r a l a n g i o g r a p h i c study, 4 had occlusion of the i n t e r n a l carotid artery b u t their C T scans showed only small infarcts in the b o r d e r zone area. T h r e e of those 4 patients had seizures occurring before or shortly after the onset of h e m i p a r e s i s , and 2 p a t i e n t s d e v e l o p e d epilepsy.

Seizure type

No. of patients with seizure

No. of patients with status

20 9 3 8 8 6 2 3 20 3 22 5 9

2 1

T a b l e 5 shows that simple partial seizure (SPS) with or w i t h o u t s e c o n d a r y g e n e r a l i z a t i o n occurred in 66 p a t i e n t s ( 5 6 % ) , c o m p l e x partial seizure (CPS) with or w i t h o u t s e c o n d a r y g e n e r a l i z a t i o n in 28 patients ( 2 4 % ) , a n d generalized tonic-clonic seizure in 5 p a t i e n t s ( 4 % ) . Seizures

1

Table 5. Seizure type in patients with thrombotic infarction

118

No. of patients

3 1 4 2 1

15

F = Frontal: P = parietal; T = temporal; O = occipital

Simple partial seizure Simple partial seizure with secondary generalization Complex partial seizure Complex partial seizure with secondary generalization Generalized tonic-clonic seizure Others Undetermined

28 (24%) 38 (32%) 21 (18%) 7 (6%) 5 (4%) 9 (8%) l0 (8%) 118 000%)

167 tional League Against Epilepsy [7]. The seizure was considered to be an early seizure if it occurred within 2 weeks after infarction and to be a late seizure if it occurred more than 2 weeks after infarction. This definition was in accordance with the criteria adopted for post-traumatic seizures [1, 31]. Epilepsy was considered in patients whose seizures occurred more than once and beyond the acute phase of infarction (2 weeks). Status epilepticus was defined as a seizure that was repeated frequently enough to produce a fixed and enduring neurological condition lasting at least 30 min, or as a series of more than two convulsions without recovery of consciousness between them [5, 21]. We obtained the follow-up data through the outpatient clinic or by telephone inquiry.

Results

Out of approximately 2000 cases of presumed cerebral infarction, 118 patients had fulfilled our criteria of selection. There were 72 males and 46 females. Their ages ranged from 29 to 93 years, with a mean age of 63 years. The duration of the follow-up is shown in Table 1. If the patients who expired within 3 months after the stroke were excluded, the mean duration of the follow-up was 20 months and 22 months respectively for the early and late seizures. Table 1. Duration of follow-up in patients with thrombotic infarction and seizuresa

Duration of follow-up

No. of patients with early seizures

No. of patients with late seizures

Expired within 3 months < 3 months 4- 6 months 7-12 months 13-18 months 19-24 months 25-48 months > 48 months

5 1 1 2 3 1 3 1

2 2 16 10 5 10 10 4

17

59

a Forty-two patients with uncertain intervals between stroke and seizure were excluded Table 2. Interval between thrombotic infarction and seizures

Interval between infarction and seizure occurrence The interval could not be determined in 42 patients, including 19 patients with recurrent infarction, 16 patients with a single "silent infarct" on the CT scan and 7 patients with multiple "silent infarcts". If those 42 patients were excluded, 5% of patients developed seizures before the infarction, 28% within 1 month after the infarction, 68% within 1 year, and 86% within 2 years (Table 2). The clinical and radiological findings of 4 patients with seizures preceding the stroke are presented in Table 3. There were 17 patients with early seizures and 59 patients with late seizures. There appeared to be two peak periods in which the seizures occurred. The early peak period was within 2 weeks after the stroke and the late peak period was 6 months to 1 year after the stroke (Fig. 1). If the 42 patients with undetermined intervals were excluded, epilepsy developed in 6 (35%) out of 17 patients with early seizure and in 53 (90%) out of 59 patients with late seizure.

Border zone infarction and seizure Nine patients had border zone infarction. Four patients had a history of previous stroke, while 3 patients did not have such a history and the seizure was the only manifestation of the stroke. In the remaining 2 patients, seizures occurred around the onset of hemiparesis and their cerebral angiograms showed occlusion of the contralateral internal carotid artery with partial collateral circulation. Eight of these 9 patients developed chronic recurrent seizures. The infarcts were located in the anterior watershed area in 5 patients, in the posterior watershed area in 3, and in the subcortical watershed area in 1.

Lacunar stroke and seizure Four of 5 patients with lacunar stroke developed chronic recurrent seizures several months after the stroke, while the remaining patient had only one seizures 4 days after the stroke. All their seizures involved the previously or currently hemiparetic limbs. CT scans at the onset of weakness and several days later revealed no visible infarcts.

No. of patients Preceding stroke 1-14 days 15-30 days 2- 6 months 7-12 months 13-18 months 19-24 months > 24 months Unknown

4 13 4 6 25 9 4 11 42 118

Silent infarction and seizure Twenty-three patients had no history of previous stroke, and the seizure was their sole neurological manifestation. Neurological work-up revealed no other possible causes for their seizures except for the "silent infarct" on the CT scan. Twenty patients developed recurrent seizures. The "silent infarcts" were usually small and located in the frontal lobe in 8 patients, occipital lobe in 3, and temporal lobe in 1. Four patients had single infarcts involving more than one lobe, while 7 patients had multiple infarcts.

169 could not be classified in 10 patients (8%) mainly because of the inadequate description of the seizures. Other types of seizures include 4 cases of SPS evolving into CPS, 1 case of generalized tonic seizure, 1 case of myoclonic seizure, and 3 cases of both CPS and SPS that occurred independently. The CT scans of the latter showed multiple infarcts.

Status epiIepticus Status epilepticus occurred in 15 patients (13%) if cases of status due to antiepileptic drug withdrawal were excluded. The status was the initial manifestation of the stroke in 1 patient, and it occurred in the acute phase of the stroke in 3 patients. The remaining 9 patients had late seizures. Five patients had elementary partial status, 9 patients generalized tonic-clonic status, and 1 patient complex partial status. Frontal predilection for the status was not seen (Table 4).

Discussion

Although an effort was made to exclude patients with embolic stroke in the present study, the distinction between thrombotic and embolic strokes may not be always possible by clinical, radiological and pathological examinations [10, 18, 19, 20, 23, 24]. However, such a distinction is important because previous reports have emphasized a higher incidence of seizures at the onset of or shortly after an embolic stroke [9, 16]. In patients with "silent infarct" on the CT scan, especially those with multiple "silent infarcts", there remains the possibility that some of them might have had an embolic stroke. The present retrospective study also poses certain methodological shortcomings. The length of follow-up of patients with seizures varied considerably and some patients with early seizure might later develop recurrent seizures. The follow-up of patients with thrombotic stroke but without seizures was not attempted. Thus, the incidence of seizures and epilepsy after thrombotic stroke is not known. Furthermore, the causal relationship between stroke and seizure might not be sufficiently clear, as it relied mainly on a temporal association between stroke and seizure and exclusion of other possible aetiologies. The majority of previous reports on seizures due to thrombotic infarction have usually been limited to relatively small numbers of patients and evaluation of seizures that occurred in the acute phase of the stroke [2, 11, 18, 22, 24]. The only study that seemed to be comparable to ours was conducted by Louis and McDowell [14] in 1967, who reviewed the medical records of 1000 patients with presumed thrombotic infarction, mainly diagnosed by the clinical criteria, and analysed both early and late seizures for an average follow-up period of 27 months. Because CT scanning was not available at that time, it would be difficult for them to include patients who had no history of previous stroke but had ' silent infarct" or to exclude some patients with intra-

cerebral haemorrhage, dural sinus thrombosis or brain tumour that might mimic thrombotic stroke by the clinical criteria. This may be one reason for a higher incidence of early seizures in their study. The present data show that the occurrence of seizures due to thrombotic infarction had two peak periods, one within 2 weeks and another between 6 months and i year after the stroke. In 76 patients with known intervals between stroke and seizure, early seizure occurred in 17 patients (22%) and late seizure in 59 (78%). The figures are different from those of Louis and McDowell [14], who observed 33 patients (55%) with early seizures and 27 patients (45%) with late seizures. While the incidence of developing epilepsy in patients with late seizures was similar between these two studies (90% vs 81%), the prognosis for early seizures was different. The incidence of epilepsy for early seizures was 35% in ours, but only 3% in theirs. It has been proposed that the pathogeneses for early and late seizures are different. Early seizures may result from acute brain insult such as neuronal ischaemic reaction, oedema and accumulation of cytotoxic substances or metabolites, while late seizures are primarily due to the scar formation [13, 14]. Such a view seems to be supported by our data, showing a bimodal distribution of peak periods for the occurrence of seizures. Previous reports on the seizure type in thrombotic infarction have shown that simple partial seizure with motor manifestations was the most common type, followed by generalized tonic-clonic seizure in about onethird of cases, while complex partial seizure was rare [6, 13, 14]. Our data are slightly different from previous ones in showing a low incidence of generalized tonic-clonic seizure (4%) and a relatively high incidence of complex partial seizure (24%). Since frontal and temporal lobes were frequently affected in the present study, complex partial seizure following thrombotic infarction may not be as uncommon as previously thought [6, 13, 14]. Status epilepticus following thrombotic infarction has not been evaluated in detail before. Previous reports have shown that the majority of attacks of status epilepticus appeared to occur in the acute phase of stroke [14]. This is quite different from our finding that the majority (80%) of our patients had the status occurring after the acute phase of stroke. In contrast, our previous study has shown that status epilepticus due to intracerebral haemorrhage tended to occur during the acute phase of stroke [30]. In the present study, 23 patients (19%) who had no history of previous stroke and who presented with seizures as the only neurological disorder were found to have previous silent stroke on the CT scan. Similar cases have been reported recently [8, 25], and the seizures were thought to be causally related to the "silent infarct". Seizures occurred prior to the onset of stroke in 4 of our patients. Epileptic seizure preceding stroke has been reported and termed "vascular precursor epilepsy" [6, 11, 14, 23]. Louis and McDowell [14] reported that the seizures of 13 patients (22%) preceded stroke, but the intervals between seizures and stroke were not men-

170 t i o n e d . T h e study by Cocito et al. [6] has i m p l i e d that seizures m a y p r e c e d e the stroke by a few hours to a few years in s o m e p a t i e n t s with occlusive carotid artery disease. S h i n t o n et al. [27] i n v e s t i g a t e d the f r e q u e n c y of epilepsy p r e c e d i n g stroke in a c a s e - c o n t r o l study of 230 p a t i e n t s a n d f o u n d that 4,5% of p a t i e n t s with first stroke h a d a p r e v i o u s history of epilepsy, c o m p a r e d with 0.6% in the m a t c h e d controls. T h e s e studies seem to suggest that clinically a s y m p t o m a t i c c e r e b r o v a s c u l a r occlusive disease m a y p r e s e n t with seizures as its first clinical m a n ifestation. It is possible that the seizure m a y arise from a small clinically u n d e t e c t a b l e area of i n f a r c t i o n as has b e e n s h o w n at n e c r o p s y [9] a n d o n C T scan [25]. F i n a l l y , a l t h o u g h it has b e e n t h o u g h t that l a c u n a r infarction is rarely associated with seizure [12], 5 p a t i e n t s with l a c u n a r stroke d e v e l o p e d seizures in the p r e s e n t study. T h e association of l a c u n a r i n f a r c t i o n with lateo n s e t epilepsy was r e p o r t e d by de la Sayette et al. [8] a n d A v r a h a m i et al. [3]. I n a case c o n t r o l study, patients with l a t e - o n s e t epilepsy b u t w i t h o u t a history of p r e v i o u s stroke have a higher i n c i d e n c e of l a c u n a r infarcts o n the C T scan t h a n the c o n t r o l group, a n d it was suggested that those l a c u n a r infarcts were indicative of a m o r e w i d e s p r e a d c e r e b r o v a s c u l a r disease r a t h e r t h a n that they were directly r e s p o n s i b l e for the epilepsy [17, 28]. I n c o n c l u s i o n , o u r data show that epileptic seizures after t h r o m b o t i c stroke had a b i m o d a l t e m p o r a l distribution a n d that epilepsy d e v e l o p e d in 35% of patients with early seizure a n d in 90% of p a t i e n t s with late seizure. I n c o n t r a s t to e m b o l i c stroke a n d i n t r a c e r e b r a l h a e m o r rhage [16, 19, 30], seizures m a y p r e c e d e the o n s e t of n e u r o l o g i c a l deficits of t h r o m b o t i c stroke.

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Epileptic seizures in thrombotic stroke.

Epileptic seizures due to thrombotic cerebral infarction were studied in 118 patients. The occurrence of seizures had a bimodal distribution with one ...
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