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Figure
Cerebral magnetic resonance images of 14 patients with cerebral infarct–related early seizures. Patients were numbered in the order they were admitted to the stroke unit. Asterisks indicate patients with watershed infarcts.

Cerebral magnetic resonance images of 14 patients with cerebral infarct–related early seizures. Patients were numbered in the order they were admitted to the stroke unit. Asterisks indicate patients with watershed infarcts.

Table 1 
Data for the 14 Patients With Stroke-Related Early-Onset Seizures
Data for the 14 Patients With Stroke-Related Early-Onset Seizures
Table 2 
Comparative Data for Patients With and Without ESs
Comparative Data for Patients With and Without ESs
1.
Giroud  MGras  PFayolle  HAndré  NSoichot  PDumas  R Early seizures after acute stroke: a study of 1,640 cases. Epilepsia 1994;35 (5) 959- 964
PubMedArticle
2.
Burn  JDennis  MBamford  JSandercock  PWade  DWarlow  C Epileptic seizures after a first stroke: the Oxfordshire Community Stroke Project. BMJ 1997;315 (7122) 1582- 1587
PubMedArticle
3.
Bladin  CFAlexandrov  AVBellavance  A  et al.  Seizures after stroke: a prospective multicenter study. Arch Neurol 2000;57 (11) 1617- 1622
PubMedArticle
4.
So  ELAnnegers  JFHauser  WAO’Brien  PCWhisnant  JP Population-based study of seizure disorders after cerebral infarction. Neurology 1996;46 (2) 350- 355
PubMedArticle
5.
Lancman  MEGolimstok  ANorscini  JGranillo  R Risk factors for developing seizures after a stroke. Epilepsia 1993;34 (1) 141- 143
PubMedArticle
6.
Berges  SMoulin  TBerger  E  et al.  Seizures and epilepsy following strokes: recurrence factors. Eur Neurol 2000;43 (1) 3- 8
PubMedArticle
7.
Labovitz  DLHauser  WASacco  RL Prevalence and predictors of early seizure and status epilepticus after first stroke. Neurology 2001;57 (2) 200- 206
PubMedArticle
8.
Ferro  JMPinto  F Poststroke epilepsy: epidemiology, pathophysiology and management. Drugs Aging 2004;21 (10) 639- 653
PubMedArticle
9.
Silverman  IERestrepo  LMathews  GC Poststroke seizures. Arch Neurol 2002;59 (2) 195- 201
PubMedArticle
10.
Camilo  OGoldstein  LB Seizures and epilepsy after ischemic stroke. Stroke 2004;35 (7) 1769- 1775
PubMedArticle
11.
Olsen  TSHøgenhaven  HThage  O Epilepsy after stroke. Neurology 1987;37 (7) 1209- 1211
PubMedArticle
12.
Kotila  MWaltimo  O Epilepsy after stroke. Epilepsia 1992;33 (3) 495- 498
PubMedArticle
13.
Paolucci  SSilvestri  GLubich  SPratesi  LTraballesi  MGigli  GL Poststroke late seizures and their role in rehabilitation of inpatients. Epilepsia 1997;38 (3) 266- 270
PubMedArticle
14.
Arboix  AGarcía-Eroles  LMassons  JBOliveres  MComes  E Predictive factors of early seizures after acute cerebrovascular disease. Stroke 1997;28 (8) 1590- 1594
PubMedArticle
15.
Lamy  CDomigo  VSemah  F  et al. Patent Foramen Ovale and Atrial Septal Aneurysm Study Group, Early and late seizures after cryptogenic ischemic stroke in young adults. Neurology 2003;60 (3) 400- 404
PubMedArticle
16.
Arboix  AComes  EGarcía-Eroles  LMassons  JBOliveres  MBalcells  M Prognostic value of very early seizures for in-hospital mortality in atherothrombotic infarction. Eur Neurol 2003;50 (2) 78- 84
PubMedArticle
17.
Cheung  CMTsoi  THAu-Yeung  MTang  AS Epileptic seizure after stroke in Chinese patients. J Neurol 2003;250 (7) 839- 843
PubMedArticle
18.
Leone  MATonini  MCBogliun  G  et al. ARES (Alcohol Related Seizures) Study Group, Risk factors for a first epileptic seizure after stroke: a case control study. J Neurol Sci 2009;277 (1-2) 138- 142
PubMedArticle
19.
Szaflarski  JPRackley  AYKleindorfer  DO  et al.  Incidence of seizures in the acute phase of stroke: a population-based study. Epilepsia 2008;49 (6) 974- 981
PubMedArticle
20.
De Reuck  JDe Groote  LVan Maele  GProot  P The cortical involvement of territorial infarcts as a risk factor for stroke-related seizures. Cerebrovasc Dis 2008;25 (1-2) 100- 106
PubMedArticle
21.
Adams  HP  JrBendixen  BHKappelle  LJ  et al.  Classification of subtype of acute ischemic stroke: definitions for use in a multicenter clinical trial: TOAST: Trial of Org 10172 in Acute Stroke Treatment. Stroke 1993;24 (1) 35- 41
PubMedArticle
22.
Bogousslavsky  JRegli  F Unilateral watershed cerebral infarcts. Neurology 1986;36 (3) 373- 377
PubMedArticle
23.
Bladin  CFChambers  BR Frequency and pathogenesis of hemodynamic stroke. Stroke 1994;25 (11) 2179- 2182
PubMedArticle
24.
Milandre  LBroca  PSambuc  RKhalil  R Epileptic crisis during and after cerebrovascular diseases: a clinical analysis of 78 cases. Rev Neurol (Paris) 1992;148 (12) 767- 772
PubMed
25.
Mohr  JPCaplan  LRMelski  JW  et al.  The Harvard Cooperative Stroke Registry: a prospective registry. Neurology 1978;28 (8) 754- 762
PubMedArticle
26.
Kilpatrick  CJDavis  SMTress  BMRossiter  SCHopper  JLVandendriesen  ML Epileptic seizures in acute stroke. Arch Neurol 1990;47 (2) 157- 160
PubMedArticle
27.
Bamford  JSandercock  PWarlow  CGray  M Why are patients with acute stroke admitted to hospital? Br Med J (Clin Res Ed) 1986;292 (6532) 1369- 1372
PubMedArticle
28.
Gupta  SRNaheedy  MHElias  DRubino  FA Postinfarction seizures: a clinical study. Stroke 1988;19 (12) 1477- 1481
PubMedArticle
29.
Hauser  WAKurland  LT The epidemiology of epilepsy in Rochester, Minnesota, 1935 through 1967. Epilepsia 1975;16 (1) 1- 66
PubMedArticle
30.
Dávalos  ACendra  EGenís  DLópez-Pousa  S The frequency, characteristics and prognosis of epileptic seizures at the onset of stroke. J Neurol Neurosurg Psychiatry 1988;51 (11) 1464
PubMedArticle
31.
Lo  YKYiu  CHHu  HHSu  MSLaeuchli  SC Frequency and characteristics of early seizures in Chinese acute stroke. Acta Neurol Scand 1994;90 (2) 83- 85
PubMedArticle
32.
Rumbach  LSablot  DBerger  ETatu  LVuillier  FMoulin  T Status epilepticus in stroke: report on a hospital-based stroke cohort. Neurology 2000;54 (2) 350- 354
PubMedArticle
33.
Gras  PGrosmaire  NSoichot  PGiroud  MDumas  R EEG periodic lateralized activities associated with ischemic cerebro-vascular strokes: physiopathologic significance and localizing value. Neurophysiol Clin 1991;21 (4) 293- 299
PubMedArticle
34.
Pohlmann-Eden  BHoch  DBCochius  JIChiappa  KH Periodic lateralized epileptiform discharges—a critical review. J Clin Neurophysiol 1996;13 (6) 519- 530
PubMedArticle
35.
Momjian-Mayor  IBaron  JC The pathophysiology of watershed infarction in internal carotid artery disease: review of cerebral perfusion studies. Stroke 2005;36 (3) 567- 577
PubMedArticle
36.
Baquis  GDPessin  MSScott  RM Limb shaking—a carotid TIA. Stroke 1985;16 (3) 444- 448
PubMedArticle
Original Contribution
October 2010

Watershed Infarctions Are More Prone Than Other Cortical Infarcts to Cause Early-Onset Seizures

Author Affiliations

Author Affiliations: Departments of Neurology (Drs Denier, Masnou, Mapoure, Guedj, Théaudin, Fagniez, Join-Lambert, Lozeron, and Adams) and Neuroradiology (Drs Souillard-Scemama and Ducreux), Centre Hospitalo–Universitaire de Bicêtre, Assistance Publique–Hôpitaux de Paris; and Unité “Epidémiologie, Démographie et Sciences Sociales,” IFR69, INED, INSERM U822 (Dr Ducot); Université Paris 11 (Drs Souillard-Scemama, Fagniez, Join-Lambert, Ducreux, and Adams); and INSERM U788 (Drs Denier, Ducreux, and Adams), le Kremlin-Bicêtre, France.

Arch Neurol. 2010;67(10):1219-1223. doi:10.1001/archneurol.2010.263
Abstract

Background  Early-onset seizures(ESs) have been reported in 2% to 6% of strokes. Most previous studies have been retrospective and did not systematically perform cerebral magnetic resonance imaging (MRI).

Objective  To determine the prevalence and determinants of ESs in a prospective cohort.

Design  Prospective cohort study.

Setting  Stroke unit in an academic hospital.

Patients  Six hundred sixty-one consecutive individuals admitted to our stroke unit during an 18-month period for suspected stroke.

Main Outcome Measures  Initial investigations systematically included cerebral MRI. Among patients with MRI-confirmed cerebral infarction, individuals with ES, defined as occurring within 14 days of stroke, were identified.

Results  Three hundred twenty-eight patients had MRI-confirmed cerebral infarcts and 178 had cortical involvement. The ESs, all initially partial seizures, occurred in 14 patients (4.3%) and at stroke onset in 5 patients. The ESs occurred exclusively in patients with cortical involvement (P <.001). With infarcts involving the cerebral cortex, there was a higher risk of ESs in watershed infarctions than in territorial strokes (6 of 26 [23.1%] vs 8 of 152 [5.3%], P = .007). Logistic regression analysis showed an almost 4-fold increased risk of ES in patients with watershed infarctions compared with other cortical infarcts (odds ratio, 4.7; 95% confidence interval, 1.5- 15.4; P = .01). Age, sex, diabetes mellitus, hypertension, smoking, National Institutes of Health Stroke Scale score, and cardioembolic origin were not significant risk factors for ES.

Conclusions  The cortical hemispheric location of ischemic strokes is associated with a higher risk of ES. Among these patients, the watershed mechanism is a strong and independent determinant of stroke-related ES.

Stroke-related seizures occur in 1.8% to 9.7% of infarcts, 2.8% to 26.1% of primary intracerebral hemorrhages, and 2.7% to 34.3% of subarachnoid hemorrhages18 (see Silverman et al9 for a review). Stroke-related seizures are classically subdivided into early-onset seizures (ESs), occurring within 2 weeks of stroke onset, and late-onset seizures (LSs), occurring later, knowing that the risk of recurrent seizures is higher in patients with LSs (vascular epilepsy).9,10 Interpretation and comparison of previous studies remain difficult because of the heterogeneity of their designs, stroke classification by computed tomography or magnetic resonance imaging (MRI), and lengths of follow-up.10

Independent risk factors for stroke-related seizures have long been recognized, including cortical location and hemorrhagic subtypes.3,6,1119 Other risk factors, such as a cardioembolic mechanism or the severity of initial deficit, remain debated (see Camilo and Goldstein10 for a review). More recently, some cortical regions have been proposed to be more prone to provoke seizures.6,20

The aim of this study was to determine the prevalence and determinants of ESs in a prospective cohort of consecutive patients with MRI-confirmed cerebral infarction admitted to a stroke unit. We herein report watershed infarcts as a new risk factor for ESs.

METHODS

This prospective stroke cohort includes 661 consecutive patients admitted for stroke or transient ischemic attack suspicion to the stroke unit (Stroke Center, Department of Neurology, Centre Hospitalo–Universitaire de Bicêtre) between June 1, 2007, and December 31, 2008. Initial diagnostic studies systematically included routine laboratory workup and cerebral MRI within 48 hours after admission (protocol: axial T1-weighted imaging, fluid-attenuated inversion recovery imaging, diffusion-weighted imaging, gradient-echo sequences, and intracranial time-of-flight and cervical vessel magnetic resonance angiography). All consecutive individuals have been explored by means of cerebral MRI except 8 (because of a pacemaker in 7 and severe claustrophobia in 1 [MRI in 98.8%]. In this cohort, 495 patients presented with various acute cerebrovascular diseases, including 328 MRI-confirmed cerebral arterial infarctions.

Patients with ischemic events underwent etiologic investigations, including systematic cervical and transcranial Doppler, echocardiography, and electrocardiographic monitoring for at least 48 hours. Additional explorations were performed if necessary (complementary biological tests, lumbar puncture, transesophageal echocardiography, and cerebral angiography). Based on the results of diagnostic studies, causes were classified according to the TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification.21 Cerebral infarctions were also classified according to vascular territories determined by cerebral MRI in (1) total middle cerebral artery (MCA) infarction (cortical and subcortical ischemia due to an occlusion of the main stem of the MCA or of the internal carotid artery, (2) partial anterior circulation infarction (ischemia due to occlusion of a branch of the MCA, anterior choroidal artery, or anterior cerebral artery), (3) posterior circulation infarction (ischemia in the posterior cerebral artery [PCA] territory), (4) deep hemispheric infarcts (mainly lacunar strokes due to small vessel disease), (5) brainstem or cerebellar infarction, (6) multifocal infarctions, and (7) hemispheric watershed infarcts. Two types of hemispheric watershed infarcts associated with cortical involvement were considered in this study on diffusion-weighted MRI patterns: the border zone area between the superficial territories of the MCA and the anterior cerebral artery and between the superficial territories of the MCA and the PCA.22,23

All ESs were defined as occurring within 14 days of stroke in a paradigm comparable with posttraumatic epilepsy in which an arbitrary cutoff point of 2 weeks was considered to distinguish ESs and LSs.9,10 The exclusion criteria were a history of seizures before stroke, severe metabolic abnormalities, and a history of substance abuse, particularly alcohol.

Patient characteristics, including age, sex, history of hypertension, diabetes mellitus, current tobacco use, stroke severity based on National Institutes of Health Stroke Scale score, involved vascular territories, categories of etiologies of stroke, and ES occurrence, were routinely entered into the database. Different groups were compared using χ2 or Fisher exact tests for categorical variables and the Kruskal-Wallis test for quantitative variables. Among patients with cortical infarctions, relations between ES occurrence and several risk factors were first evaluated in univariate analysis using Fisher exact or Kruskal-Wallis tests (age, sex, presence or absence of diabetes, hypertension, tobacco use, hypercholesterolemia, cardioembolic origin, stroke disability [National Institutes of Health Stroke Scale score], and presence of watershed vs territorial cerebral infarctions). Then, variables related to ESs in univariate analysis with P < .15 were introduced into a multivariate logistic regression model to determine the independent factors of ES occurrence. The significance level was set at α = .05.

RESULTS
COHORT CHARACTERISTICS

Of 328 consecutive patients with MRI-confirmed cerebral infarctions included in this study (200 males and 128 females; mean age, 63.6 years; age range, 17-99 years), 31 had total MCA infarction, 88 had partial anterior circulation infarction (due to occlusion of a branch of the MCA [n = 70], anterior choroidal artery [n = 11], or anterior cerebral artery [n = 7]), 26 had partial posterior circulation infarction (due to occlusion of a branch of the PCA), 70 had deep hemispheric infarcts (mainly lacunar stroke), 26 had hemispheric watershed infarcts, 62 had brainstem or cerebellar infarctions, and 25 had multifocal infarctions (Table 1 and Table 2). Age, sex, history of hypertension, diabetes mellitus, hypercholesterolemia, and current tobacco use did not significantly differ between these groups (data not shown).

ES OCCURRENCE

Seizures within 14 days of stroke occurred in 14 of the 328 patients with cerebral infarctions (4.3%; mean age, 63.1 years; age range, 43-77 years; 8 men) (Tables 1 and 2). The ESs were initially partial seizures in all 14 patients, followed by secondary generalization in 9 and complicated by status epilepticus in 3. The ESs occurred at stroke onset in 5 patients (36%), after stroke onset but within the first 24 hours in 3 (21%), and between 24 hours and 14 days in 6 (43%) (Table 1).

Findings from electroencephalography within the first 24 hours after seizures were normal in 4 patients, showed asymmetrical background activities in 5, and had focal slow waves in 5. Periodic lateralized epileptiform discharges were not observed in any patients.

RISK FACTORS FOR STROKE-RELATED ESs

Of 328 patients with cerebral infarctions, cortical involvement was present in 178 (including 108 anterior and 26 posterior circulation infarcts, 26 watershed infarcts, and 18 of the 25 multifocal infarcts). All ESs occurred in this group (14 of 178 vs 0 of 150; Fisher exact test, P < .001). No difference between the groups with and without ESs was observed concerning age, sex, history of hypertension, diabetes, hypercholesterolemia, current tobacco use, stroke severity (initial National Institutes of Health Stroke Scale score), or cardioembolic origin (Table 2). Although a history of symptomatic stroke or transient ischemic attacks was not systematically entered into the database, only 1 of the 14 patients with ES previously had symptomatic cerebrovascular disease (PCA infarction 2 years earlier) (patient 27).

Among infarcts with cortical hemispheric involvement, ESs occurred more frequently in patients with watershed infarcts (6 of 26 [23.1%]) than in patients with territorial infarcts (8 of 152 [5.3%]) (Fisher exact test, P = .007). Logistic regression analysis showed that there was an almost 4-fold increased risk of ESs in patients with watershed infarcts compared with other cortical infarcts (multivariate logistic regression: odds ratio, 4.7; 95% confidence interval, 1.5-15.4; P = .01). Other variables between these 2 groups did not differ (age, sex, diabetes, hypertension, hypercholesterolemia, tobacco use, and stroke severity) (data not shown).

COMMENT

Stroke-related ESs occurred in 4.3% of patients with cerebral infarcts, within the range (1.4%-6.0%) in most recent series.17,14,15,2428 The classic association between ESs and cortical localization is confirmed in the present study.15,15,26,2932 The new finding is the association between ESs and watershed infarcts. This association has been previously reported in 1 article in different conditions24: the authors studied ESs and LSs occurring after cerebral hematomas and infarctions explored by means of computed tomography (including two-thirds of patients with seizures occurring more than 1 month after stroke).24

While LSs are thought to be caused by permanent changes, such as gliosis and meningocerebral scars, stroke-related ESs are thought to result from cellular biochemical dysfunctions leading to electrically irritable tissue (see Camilo and Goldstein10 for a review). Acute ischemia is known to lead to increased extracellular concentrations of glutamate, an excitatory neurotransmitter, and intracellular calcium and sodium, which result in depolarization of the transmembrane potential and other calcium-mediated effects. Neuronal discharges can also occur from surviving neurons exposed to glutamate facilitated by local ionic shifts that lower the seizure threshold. While LSs are independent high-risk factors for the subsequent development of recurrent epilepsy, ESs may, according to recent experimental data, increase infarct size and hamper later recovery. Moreover, antiepileptic drug therapy may also impair recovery after stroke (see Camilo and Goldstein10 for a review).

Although electroencephalographic recordings showing periodic lateralized epileptiform discharges have been previously reported to be associated with watershed infarcts33 and might reflect a key pattern for focal hyperexcitability in the penumbra zone of ischemic stroke,34 periodic lateralized epileptiform discharges were not identified in any of the present patients.

Two distinct etiopathologic hypotheses—hemodynamic compromise and microembolism—have been proposed for hemispheric watershed infarcts.35 Both could promote seizures via focal hypoperfusion or distal artery-to-artery embolism. In the present patients, low flow existed because we observed severe carotid stenosis or occlusion in 19 of 26 patients with watershed infarcts (Figure and Table 1, [data not shown]). Future explorations, including brain diffusion-weighted and perfusion imaging and ultrasound detection of microembolic signals, should help us better understand the physiopathologic features of these infarcts and their association with ESs.35

Although limb shakings have been described in association with high-grade stenosis or occlusion of the internal carotid artery,36 we did not observe any limb-shaking episodes in the present series. Some of these episodes could have been mistaken as seizures. The fact that most of the ES episodes generalized in this population suggests that these, indeed, were seizure disorders.

In conclusion, ESs are rare, occurring in 4.3% of patients with cerebral infarcts; all ESs occurred in cortical infarcts; and ESs are 4 times more frequent in watershed infarcts than in territorial infarcts.

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Article Information

Correspondence: Christian Denier, MD, PhD, Department of Neurology, Centre Hospitalo–Universitaire de Bicêtre, 78 rue du Général Leclerc, 94275 Le Kremlin-Bicêtre Cedex, France (christian.denier@bct.aphp.fr).

Accepted for Publication: March 15, 2010.

Author Contributions:Study concept and design: Denier, Masnou, and Adams. Acquisition of data: Denier, Masnou, Souillard-Scemama, Guedj, Théaudin, Fagniez, Join-Lambert, Lozeron, and Ducreux. Analysis and interpretation of data: Denier, Masnou, Mapoure, Souillard-Scemama, Ducot, and Adams. Drafting of the manuscript: Denier. Critical revision of the manuscript for important intellectual content: Masnou, Mapoure, Souillard-Scemama, Guedj, Théaudin, Fagniez, Join-Lambert, Lozeron, Ducot, Ducreux, and Adams. Statistical analysis: Denier and Ducot. Administrative, technical, and material support: Denier, Masnou, Souillard-Scemama, and Ducreux. Study supervision: Denier and Adams.

Financial Disclosure: None reported.

Additional Contributions: M.-G. Bousser, MD, provided helpful discussions and excellent critical reading of the manuscript.

References
1.
Giroud  MGras  PFayolle  HAndré  NSoichot  PDumas  R Early seizures after acute stroke: a study of 1,640 cases. Epilepsia 1994;35 (5) 959- 964
PubMedArticle
2.
Burn  JDennis  MBamford  JSandercock  PWade  DWarlow  C Epileptic seizures after a first stroke: the Oxfordshire Community Stroke Project. BMJ 1997;315 (7122) 1582- 1587
PubMedArticle
3.
Bladin  CFAlexandrov  AVBellavance  A  et al.  Seizures after stroke: a prospective multicenter study. Arch Neurol 2000;57 (11) 1617- 1622
PubMedArticle
4.
So  ELAnnegers  JFHauser  WAO’Brien  PCWhisnant  JP Population-based study of seizure disorders after cerebral infarction. Neurology 1996;46 (2) 350- 355
PubMedArticle
5.
Lancman  MEGolimstok  ANorscini  JGranillo  R Risk factors for developing seizures after a stroke. Epilepsia 1993;34 (1) 141- 143
PubMedArticle
6.
Berges  SMoulin  TBerger  E  et al.  Seizures and epilepsy following strokes: recurrence factors. Eur Neurol 2000;43 (1) 3- 8
PubMedArticle
7.
Labovitz  DLHauser  WASacco  RL Prevalence and predictors of early seizure and status epilepticus after first stroke. Neurology 2001;57 (2) 200- 206
PubMedArticle
8.
Ferro  JMPinto  F Poststroke epilepsy: epidemiology, pathophysiology and management. Drugs Aging 2004;21 (10) 639- 653
PubMedArticle
9.
Silverman  IERestrepo  LMathews  GC Poststroke seizures. Arch Neurol 2002;59 (2) 195- 201
PubMedArticle
10.
Camilo  OGoldstein  LB Seizures and epilepsy after ischemic stroke. Stroke 2004;35 (7) 1769- 1775
PubMedArticle
11.
Olsen  TSHøgenhaven  HThage  O Epilepsy after stroke. Neurology 1987;37 (7) 1209- 1211
PubMedArticle
12.
Kotila  MWaltimo  O Epilepsy after stroke. Epilepsia 1992;33 (3) 495- 498
PubMedArticle
13.
Paolucci  SSilvestri  GLubich  SPratesi  LTraballesi  MGigli  GL Poststroke late seizures and their role in rehabilitation of inpatients. Epilepsia 1997;38 (3) 266- 270
PubMedArticle
14.
Arboix  AGarcía-Eroles  LMassons  JBOliveres  MComes  E Predictive factors of early seizures after acute cerebrovascular disease. Stroke 1997;28 (8) 1590- 1594
PubMedArticle
15.
Lamy  CDomigo  VSemah  F  et al. Patent Foramen Ovale and Atrial Septal Aneurysm Study Group, Early and late seizures after cryptogenic ischemic stroke in young adults. Neurology 2003;60 (3) 400- 404
PubMedArticle
16.
Arboix  AComes  EGarcía-Eroles  LMassons  JBOliveres  MBalcells  M Prognostic value of very early seizures for in-hospital mortality in atherothrombotic infarction. Eur Neurol 2003;50 (2) 78- 84
PubMedArticle
17.
Cheung  CMTsoi  THAu-Yeung  MTang  AS Epileptic seizure after stroke in Chinese patients. J Neurol 2003;250 (7) 839- 843
PubMedArticle
18.
Leone  MATonini  MCBogliun  G  et al. ARES (Alcohol Related Seizures) Study Group, Risk factors for a first epileptic seizure after stroke: a case control study. J Neurol Sci 2009;277 (1-2) 138- 142
PubMedArticle
19.
Szaflarski  JPRackley  AYKleindorfer  DO  et al.  Incidence of seizures in the acute phase of stroke: a population-based study. Epilepsia 2008;49 (6) 974- 981
PubMedArticle
20.
De Reuck  JDe Groote  LVan Maele  GProot  P The cortical involvement of territorial infarcts as a risk factor for stroke-related seizures. Cerebrovasc Dis 2008;25 (1-2) 100- 106
PubMedArticle
21.
Adams  HP  JrBendixen  BHKappelle  LJ  et al.  Classification of subtype of acute ischemic stroke: definitions for use in a multicenter clinical trial: TOAST: Trial of Org 10172 in Acute Stroke Treatment. Stroke 1993;24 (1) 35- 41
PubMedArticle
22.
Bogousslavsky  JRegli  F Unilateral watershed cerebral infarcts. Neurology 1986;36 (3) 373- 377
PubMedArticle
23.
Bladin  CFChambers  BR Frequency and pathogenesis of hemodynamic stroke. Stroke 1994;25 (11) 2179- 2182
PubMedArticle
24.
Milandre  LBroca  PSambuc  RKhalil  R Epileptic crisis during and after cerebrovascular diseases: a clinical analysis of 78 cases. Rev Neurol (Paris) 1992;148 (12) 767- 772
PubMed
25.
Mohr  JPCaplan  LRMelski  JW  et al.  The Harvard Cooperative Stroke Registry: a prospective registry. Neurology 1978;28 (8) 754- 762
PubMedArticle
26.
Kilpatrick  CJDavis  SMTress  BMRossiter  SCHopper  JLVandendriesen  ML Epileptic seizures in acute stroke. Arch Neurol 1990;47 (2) 157- 160
PubMedArticle
27.
Bamford  JSandercock  PWarlow  CGray  M Why are patients with acute stroke admitted to hospital? Br Med J (Clin Res Ed) 1986;292 (6532) 1369- 1372
PubMedArticle
28.
Gupta  SRNaheedy  MHElias  DRubino  FA Postinfarction seizures: a clinical study. Stroke 1988;19 (12) 1477- 1481
PubMedArticle
29.
Hauser  WAKurland  LT The epidemiology of epilepsy in Rochester, Minnesota, 1935 through 1967. Epilepsia 1975;16 (1) 1- 66
PubMedArticle
30.
Dávalos  ACendra  EGenís  DLópez-Pousa  S The frequency, characteristics and prognosis of epileptic seizures at the onset of stroke. J Neurol Neurosurg Psychiatry 1988;51 (11) 1464
PubMedArticle
31.
Lo  YKYiu  CHHu  HHSu  MSLaeuchli  SC Frequency and characteristics of early seizures in Chinese acute stroke. Acta Neurol Scand 1994;90 (2) 83- 85
PubMedArticle
32.
Rumbach  LSablot  DBerger  ETatu  LVuillier  FMoulin  T Status epilepticus in stroke: report on a hospital-based stroke cohort. Neurology 2000;54 (2) 350- 354
PubMedArticle
33.
Gras  PGrosmaire  NSoichot  PGiroud  MDumas  R EEG periodic lateralized activities associated with ischemic cerebro-vascular strokes: physiopathologic significance and localizing value. Neurophysiol Clin 1991;21 (4) 293- 299
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