Early Seizures After Acute Stroke: A Study of 1,640 Cases

Epilepsin, 35(5):959-964, 1994 Raven Press, Ltd., New York 0 International League Against Epilepsy

Early Seizures After Acute Stroke: A Study of 1,640 Cases

M. Giroud, P. Gras, H. Fayolle, N. Andrk, P. Soichot, and R. Dumas

Registre Dijonnais des Accidents Vasculaires Cerebraux (INSERMIDGS), UniversitC de Bourgogne, Dijon, France

Summary: We evaluated prospectively the occurrence of seizures within 15 days of a first stroke or transient ischemic episode in 1,640 patients to study relation between seizures and type of stroke. Seizures occurred in 90 patients (5.4%), including 36 (4.4%) of 814 with infarct owing to atheroma, 21 (16.6%) of 126 with infarct owing to cardiogenic embolus, 3 (1%) of 273 owing to lacunar infarct, 5 (1.9%) of 259 owing to transient ischemic attack (TIA), 21 (16.2%) of 129 owing to supratentorial he-

Stroke is a common cause of seizures in adults aged 250 years (Loiseau et al., 1990; Tallis, 1990). The reported frequency of seizures with stroke var- ies from 17 to 4.4%: (17%) (Kotila and Waltimo, 1992), 13.8% (Holmes, 1980), 12.5% (Dodge et al., 1954), 10% (Black et al., 1983; Lancman; et al., 1993), 9% (Olsen et al., 1987), 8% (Richardson and Dodge, 1954); 7% (Fentz, 1971), and 4.4% (Kil- patrick et al., 1990).

Differences in frequency may be attributed to differences in study population and length of follow- up, to a mixture of early and late seizures, and to the availability of computed tomography examina- tions (CT), (Lesser et al., 1983). We evaluated the occurrence of seizures within the first 15 days of onset of a first stroke or transient ischemic episode to determine the relation between clinical features and type of stroke in a prospective series of 1,640 consecutive patients collected in a well-defined population survey from 1985 to 1992.

PATIENTS AND METHODS

Using the Stroke Registry of Dijon, established in 1985 (Giroud et al., 1989), we studied all patients living in the town of Dijon who experienced a first acute stroke during 1985 to 1992. The methods of

Received June 1993; revision accepted September 1993. Address correspondence and reprint requests to Professor M.

Giroud at Service de Neurologie, HBpital GBnCral, 3 Rue du Faubourg Raines, 21000 Dijon, France.

matoma, and 4 (16.6%) of 24 owing to subarachnoid hemorrhage. Thirteen (14.6%) of 89 subcortical infarcts were associated with seizures. Seizures were the initial sign of stroke in 80 (89%) of 90 cases and were usually single and partial. Seizure symptoms were most often motor, sensory, or visual. Key Words: Early seizures-stroke- Transient ischemic attack-Infarct-Embolism-Supra- tentorial hematoma-Subarachnoid hemorrhage- Cardiogenic embolus.

the Registry of Dijon were as follows (Giroud et al., 1991). Patients with a first stroke were either managed at the University Hospital or in one of the three private town hospitals, or at home. Each patient hospitalized at University Hospital was examined by 1 of 5 public neurologists who completed a registry chart and obtained a CT scan. Patients hospitalized at the private hospitals were examined by 1 of 5 private neurologists who completed a registry chart and obtained a CT scan. For each patient at home, the treating general practitioner sought ad- vice from either a public or private neurologist and followed the same procedures. All charts were sent to the centralized Stroke Registry at the Service of Neurology, University Hospital of Dijon.

Cerebrovascular events were classified according to the criteria of the National Institute of Neurolog- ical Disorders and Stroke (Classification, 1990). Fa- tal strokes were included. Stroke was defined as a sudden neurologic deficiency. Infarct was diagnosed by CT scan by early or late hypodensity in the territory of an artery. An infarct of the carotid artery distribution was based on clinical signs of stroke (sensorimotor deficits with or without hemianopia or aphasia) and a hypodensity on CT scan in the region of the anterior and middle cerebral artery. Cortical and subcortical distribution was assessed mainly by localization of hypodensity on the CT scan.

Lacunar infarct was assessed by clinical data (pure motor, pure sensory deficit) and a small cir- cular hypodensity in the white matter or basal gan-

959

960 M . GIROUD ET AL.

glia on CT scan. Retinal infarction was assessed by an amaurosis fugax with occlusion of some collat- eral arteries of the ophthalmic artery. Cardiac arhythmia was defined as the presence of permanent or transient but recurrent atrial fibrillation on clinical and ECG features.

Brain infarction due to atherothrombotic carotid artery disease was based on acute or subacute onset, neurologic deficiency in the perisylvian area with incomplete sensorimotor deficiency, Broca’s aphasia, CT scan hypodensity in the perisylvian area, or atheroma on cervical artery ultrasound examination. Brain infarction due to a cardiogenic mechanism was based on sudden onset, neurologic deficiency in frontal or posterior cerebral regions with motor aphasia or motor crural deficiency, Wernicke’s aphasia, sensory deficiency, or hemianopia. On CT scan, hypodensity in the frontal or posterior cerebral area, with or without secondary hemorrhage, and a dense sylvian artery (an indica- tor of embolism) and cardiac arhythmia on ECG were suggestive of infarction of probable cardiogenic origin.

Diagnosis .of vertebrobasilar brain infarction was based on clinical symptoms (visual, cerebellar, or thalamic symptoms, cranial nerve palsy) and on a CT scan hypodensity in the occipital area, cerebellar lobes, thalamus or brain stem.

Cases with no evidence for a cardiogenic etiology or atheroma were classified as uncertain. Hemor- rhagic lesions ‘were diagnosed by clinical symptoms (acute neurologic deficit, cephalalgia, vomiting, altered consciousness) and on CT scan hyperdensity supratentorially (cerebral lobes or deep area) or in- fratentorially (cerebellar lobes, brainstem). Sub- arachnoid hemorrhage was diagnosed by clinical signs (acute cephalalgia, vomiting, and meningeal signs) with CT scan hyperdensity in the subarachnoid spaces or red cerebrospinal fluid after lumbar puncture.

A transient ischemic attack (TIA) was diagnosed by a neurologic deficit of <24-h duration, with no CT-scan lesion. Carotid or vertebrobasilar distribution lesions were assessed solely by clipical signs.

Seizures at stroke onset were defined as those occurring within the first 15 days of the stroke, as was done in the studies of Shinton et al. (1988), DBvalos et al. (1988), and Kilpatrick et al. (1990). Most seizures at stroke onset occur in the first 15 days. After the first month, different mechanisms are believed to give rise to the seizures. Seizures were classified according to the International League Against Epilepsy (ILAE) (Commission, 1981). An EEG was performed in all seizure patients.

Chi-square test was used to compare mean val- ues, with Yates’ correction when necessary, and Fisher’s test was used for statistical analysis. To determine the independent predictive value of clinical data on incidence of early seizures, variables related to seizures in univariate analysis were studied in a multiple-regression analysis with the LOGIST procedure for SAS.

RESULTS

Dijon has a population of approximately 150,000. From 1985 to the end of 1992, 1,722 first cerebrovascular events were recorded with a frequency of 210 * 8 cases per year, and an annual incidence of 133 per 100,000. In 82 cases, CT scan was not performed, leaving 1,640 cases eligible for study. The 869 men (53%) and 771 women (47%) had a mean age of 73 * 15 years. Ultrasound examination of the cervical arteries was performed in 90.1% of patients, EEG was recorded in all patients and echo- cardiography in 65%. Plasma glucose, hematocrit, and cholesterol levels were determined in all patients. CT scan diagnosis (Table l) was hemorrhage 168, infarct 940, lacuna 273, and TIA 259 (Table 2). Infarcts with atheroma were diagnosed in 814 cases (49.6% of all patients), with carotid distribution in 640 cases (78.6% of infarcts with atheroma) and vertebrobasilar distribution in 174 cases (21.4% of infarcts with atheroma).

Infarct due to cardiogenic embolus was diagnosed in 126 cases (7.6% of all patients) with carotid distribution in 91 cases (74% of infarcts from cardiogenic embolus) and vertebrobasilar distribution in 35 cases (26% of infarcts with cardiogenic embolism). There was no significant difference in distribution of stroke between cardiogenic cerebral infarct and noncardiogenic cerebral infarct. Lacunar infarct was diagnosed in 273 cases (16.6% of all cases), and TIA was diagnosed in 259 (15.7% of all cases). Hemorrhagic stroke (Table 3) was observed in 168 cases (10.2% of all cases), with 24 subarachnoid hemorrhages (14.2% of all hemorrhages), 88 lobar hemorrhages (52.3% of all hemorrhages), and 41 deep hemorrhages (37.5% of all hemorrhages).

Ninety patients (5.5% of all patients) had epileptic seizures during the first 15 days after stroke onset. Seizures were classified as simple partial seizures (SPS: motor, autonomic, somatosensory or psychic) in 55 cases (61%), secondarily generalized partial in 25 cases (28%) and generalized tonic- clonic from onset in 10 cases (11%). No complex partial seizures (CPS) were observed in the early stage. Seizures were the presenting sign of the cerebrovascular event in 80 cases (89%) and appeared

Epilepsia, Vol. 35, No. 5 , 1994

EARLY SEIZURES AFTER ACUTE STROKE 961

Table 1. Distribution of types of stroke according to CT scan features

82 Ct scan not performed Eligible

168 r 1640P 940 273 2.59

Hemorrhage

1 2.5

Cortical infarct

1 57

Lacunar infarct

1 3

Tr 5

14.8% with seizures 6.00% 1 .00% 2.00% I I 1

With seizures

Ct, computed tomography; TIA, transient ischemic attack.

in the first 15 days onset in 10 cases (11%). All EEGs were abnormal, with nonspecific focal slow waves in 43 cases, bilateral slow waves in 18, focal periodic lateralized epileptiform discharges (PLEDS) in 15, paroxysmal features in 10, and elec- trical partial status epilepticus (SE) in 4.

Demographic variables and age were similar in the two groups with and without seizures (Table 4). Seizures were more frequent in males (p < 0.05) and when altered consciousness (p < 0.001), headache (p < 0.001) or posterior cerebral deficits (hemianopia + sensory deficiency) (p < 0.001) ex- isted (Table 4). There was no relation between age and seizures in males and females (Table 5) . Five variables (loss of consciousness, male predominance, age, headache, and sensory and visual deficiency) were analyzed by stepwise logistic regression to determine independent and significant risk factors for early seizures. Two significant risk factors for early seizures were identified: loss of consciousness and male predominance (Table 6). Based on the etiology of the ischemic stroke (Table 2), seizures were noted in 32 of 640 infarcts with atheroma in the carotid distribution (5%) versus 19 of 91 infarcts in the carotid distribution owing to cardiogenic embolus (20.8%) (p < 0.01), in 4 of 174 infarcts with atheroma in the vertebrobasilar distribution (2.2%) versus 2 of 35 infarcts owing to cardiogenic embolus in the vertebrobasilar distribution (5.7%) (NS after Yates correction), in 3 of 273 lacunar infarcts (l%), and in 5 of 259 TIA (2%).

In hemorrhagic stroke (Table 3), seizures were observed in 20 of 88 lobar hemorrhages (22.7%) ver-

TABLE 2. Seizures and ischemic stroke and TIA

Patients with

Type of stroke seizures

All patients

n (%)

Infarcts with atheroma Carotid distribution

Cortical Subcortical Retinal Uncertain Total

Brainstem Occipital Cerebellar Thalamus Uncertain Total

Vertebrobasilar distribution

Total

Infarcts with cardiogenic embolus Carotid distribution

Cortical Subcortical Retinal Uncertain Total

Brainstem Occipital Cerebellar Thalamus Uncertain Total

Total

Lacunar infarct TIA

Vertebrobasilar distribution

Carotid distribution Vertebrobasilar distribution Total

21 11 0 0

32

0 4 0 0 0 4

36

17 2 0 0

19

0 2 0 0 0 2

21

3

5 0 5

488 89 9

54 640 (5)

22 34 39 35 44

174 (2.2) 814 (4.4)

70 15 2 4

91 (20.8)

5 19 5 2 4

35 (5.7) 126 (16)

273 ( I )

20 1 58

2.59 (2)

TIA, transient ischemic attack.

Epilepsia, Vol. 35, No. 5, 1994


TABLE 3. Seizures and hemorrhagic stroke TABLE 5. Age-specific incidence by gender

Patients with All patients Type of stroke seizures n (%I

Hemorrhage Supratentorial

Lobar 20 88 (22.7) Deep 1 41 (2.4) Subarachnoid 4 24 (16.4)

Cerebellar 0 10 Brainstem 0 5

Infratentorial

Total 25 168 (10)

sus 1 of 41 deep hemorrhage (2.49%) (p < 0.01 after Yates correction) and in 4 of 24 subarachnoid hemorrhage (16.6%) cases. We did not observe seizures in brainstem, cerebellar, thalamic or retinal infarctions or in infratentorial hemorrhage.

Most epileptic seizures were related to lesion localization. Seizures occurred in 38 of 558 cortical infarcts (6.8%) with atheroma (488 cases) or with cardiogenic embolus (70 cases) versus 13 of 104 subcortical infarcts (14.6%) with atheroma (89 cases) or with cardiogenic embolus (15 cases) (p < 0.05).

Considering only superficial lesions, whatever the mechanism, we observed seizures in 69 of 847 (8%) versus 17 deep lesions of 455 (3.7%) (p < 0.001). In stroke with cortical involvement, seizures were more frequent with lobe hemorrhage (22.7%) than with cortical infarction (6.8%) (p < 0.001). Six of 53 occipital infarcts (1 1.3%) had seizures, and 43 of 759 extraoccipital cortical infarcts (5.6%) had seizure (NS).

TABLE 4. Demographic variables und neurological symptoms at stroke onset

Stroke Stroke with without

Seizures Seizures n = 90 n = 1,550

Parameter (%I (%) p-Value

Mean age (yrs) Male Tobacco abuse

Alcohol abuse (>60 g/day) Arterial hypertension Diabetes High cholesterol levels Ischemic cardiac disease Heart failure Atrial fibrillation Headache Loss of consciousness Nausea plus vomiting Aphasia Hemianopia plus

Motor deficit

(>lo cigarettedday)

sensory deficits

71 70 (77)

21 (24) 17 (19) 59 (66) 1 1 (12) 13 (15) 1 1 (12)

25 (28) 28 (31) 42 (47)

8 (9) 46 (51)

37 (41) 68 (76)

74 806 (52)

341 (22) 279 (18)

1069 (69) 201 (13) 279 ( I 8) 170 (1 1 ) 62 (4)

403 (26) 124 (8) 186 (12) 108 (79) 759 (49)

186 (12) 1100 (71)

NS <0.05

NS NS NS NS NS NS NS NS

<0.001 <0.001

NS NS

<0.001 NS

M ________

F

All Stroke with All Stroke with stroke seizures, stroke seizures,

Age (yrs) (n) n (9%) (n) n (%)

50-59 101 3 (2.9) 125 10 (8.0) 60-69 I99 4 (2.0) 228 18 (7.8) 70-79 23 1 7 (3.0) 235 17 (7.2) 80-90 240 6 (2.5) 28 1 25 (8.8) Total 77 1 20 (2.5) 869 70 (8.0)

DISCUSSION

We observed 5.5% of early epileptic seizures (within the first 15 days) in this prospective population-based study. There was no bias in our patient sampling technique because we collected first- stroke patients hospitalized at University Hospital, in private hospitals, or followed at home. Distribu- tion of cardiogenic cerebral infarct, noncardiogenic infarct, lacunar infarct, TIA, and hemorrhage was similar to that observed in other population-based studies of stroke (Bamford et al., 1990). We observed more vertebrobasilar infarcts in cardiogenic cerebral infarct than in noncardiogenic cerebral infarcts, but the difference was not significant. The small number of subarachnoid hemorrhages (1.5% of all strokes, 14% of all cerebral hemorrhage) is a well-defined characteristic in European populations (Bamford et al., 1990). Our incidence is similar to that in other published population-based studies (Shinton et al., 1988; Davalos et al., 1988, 1992; Kilpatrick et al., 1990). Our numbers were lower than those of hospital-based studies [Black et al., 1983 (12.5%); Olsen et al., 1987 (10%); Lancman et al., 1993 (lo%)]. In these studies, data included both early and late poststroke seizures. Our per- centage is not underestimated because all cases are collected inclusively by the health care systems. Our data give a true picture of epilepsy at stroke onset, whatever the mechanism and severity grade. There were no seizures in the 82 cases with no CT scan.

We studied epileptic seizures occurring only in the first 15 days after stroke onset, and not later.

TABLE 6. Multiple regression analysis with seizure incidence as dependent variable

Clinical symptoms and demographic variables p-Value

Loss of consciousness <0.001 M C0.05 Age NS Headache NS Sensory plus visual deficit NS


EARLY SEIZURES AFTER ACUTE STROKE 963

Almost 57% of the seizures occur in the first 4 weeks after stroke (Black et al., 1983; Lancman et al., 1993). Important differences exist between the early and later poststroke seizures, both clinically and etiologically and according to outcome, justify- ing separate analysis (Gupta et al., 1988; Davalos et al., 1992). Therefore, we focused only on patients with early seizures.

In our series, partial seizures predominated, in agreement with results of other studies (Gupta et al., 1988; Kilpatrick et al., 1990; Milandre et al., 1992; Lancman et al., 1993). We included somatosensory or psychic seizures, seizures that are not emphasized in the literature. We observed no CPS in the first 15 days after stroke. PLEDS occurred frequently in the EEG in relation to cortical infarcts. Other EEG abnormalities were similar to those reported by Milandre et al. (1992). In almost 89% of patient, the seizure was the initial event, in agreement with results reported in the literature (Kilpatrick et al., 1990). Male predominance was reported by Davalos et al. (1992) but not by Kil- patrick et al. (1992). Most epileptic seizures occurred in strokes with cortical involvement (8%) , but in 13 cases we observed only basal ganglia lesions.

Data concerning the relation between epileptic seizures and type of stroke are conflicting. As did previous investigators; we noted a higher incidence of seizures in cerebral hemorrhage (Mohr et al., 1978; Faught et al., 1989; Kilpatrick et al., 1990) and in cerebral infarct of embolic origin (Mohr et al., 1978; Lesser et al., 1985). Others have reported similar numbers in thrombotic and embolic cerebral infarcts (DBvalos et al., 1988; Shinton et al., 1988; Hornig et al., 1990; Kilpatrick et al., 1990; Milandre et al., 1992). Conflicting data may be attributed to the difficulty in distinguishing embolic from thrombotic stroke, to the small number of patients in most series, to the biases of collection in hospital-based studies, and to the fact that localization and size of stroke on CT scan have not been always consid- ered.

The incidence of seizures in cortical ischemic infarcts was higher when origin was embolic. We have observed a high susceptibility of the occipital lobe to epileptic seizures, although this finding re- quires confirmation (DBvalos et al., 1992; Milandre et al., 1992). The acuteness of stroke onset when secondary to a cardiac embolus may explain the frequent occurrence of the seizures. On the other hand, hemodynamic-type infarcts are usually related to seizures and PLEDS on EEG (Gras et al., 1991).

Even if the association of seizures with TIA re-

mains uncertain, we found only 5 seizures in 201 TIA cases, as compared to 10% by Davalos et al. (1992), and 3.7% by Kilpatrick et al. (1990). More- over, SPS may represent a clinical sign due to TIA (Cocito and Lerb, 1989).

We observed 1% of seizures related to lacuna infarctions. Kilpatrick et al. (1990) reported no relation between lacunae and epilepsy, whereas Olsen et al. (1987) reported an association in 2% of their cases. Most epileptic seizures are produced by lesions affecting the cortex, but subcortical lesions may induce epileptic seizures (Faught et al., 1989; Kilpatrick et al., 1990), either because an adjacent cortical lesion is not apparent on CT scan, or because lesions (such as in the head of caudate nu- cleus) may produce seizures (Faught et al., 1989). The incidence of seizures in all hemorrhages was similar to that in the studies of Mohr et al. (1978) and Kilpatrick et al. (1990).

We examined the clinical profile of patients within the first 15 days of a stroke and, as reported by DBvalos et al. (1992), noted that male gender, headache, and alteration of consciousness correlated with risk of early seizure. We also noted that cerebral posterior symptoms (hemianopia plus sensory symptoms) are correlated to a cardiogenic source.

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a S U M E

Nous avons CvaluC de faCon prospective la frCquence des crises Cpileptiques chez 1,640 patients recensC de faCon prospective a l’occasion de la survenue d’un premier accident vasculaire cerCbral ou d’un accident ischkmique transitoire pour rechercher la relation entres les crises, et le type et les mkanismes de I’accident vasculaire cCrCbral. Les crises sont apparues chez 90 patients (5.4%), incluant 36 patients (4.4%) sur 814 prksentant un infarctus cCrebral par athCrome, 21 patients (16.6%) sur 126 prC- sentant un infarctus ctrCbral cardioembolique, 3 patients (1%) sur 273 prksentant un infarctus lacunaire, 5 patients (1.9%) sur 259 presentant un accident ischCmique transitoire, 21 patients (16.2%) sur 129 prksentant un hCmatome supratentoriel, et 4 patients (16.6%) sur 24 presentant une hCmorragie mCningCe. Treize patients (14%) sur les 89 ayant eu un infarctus sous- cortical ont present6 des crises prCcoces. Les crises kpileptiques ont rCvClC I’accident vasculaire cCrCbral dans 80 cas sur 90 (89%). I1 s’agissait le plus souvent de crises partielles, simples, motrices, sensitives on visuelles.

(Translation supplied by authors)


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Early Seizures After Acute Stroke: A Study of 1,640 Cases