Fatigue is a major complaint in stroke survivors, but data focusing on intracerebral haemorrhage (ICH) survivors are scarce. In a cohort of spontaneous ICH survivors, we assessed the long-term prevalence of fatigue and its associated factors. We included consecutive 1-year ICH survivors from the prospective, observational, single-centre Prognosis of Intracerebral Haemorrhage (PITCH) study. We evaluated fatigue (defined as a score ≥ 4 in Chalder Fatigue Scale); the severity of neurological, depressive, and anxiety symptoms; and functional disability 1, 3, and 6 years after ICH. We performed univariable and multivariable models to evaluate clinical factors and brain magnetic resonance imaging (MRI) small vessel disease (SVD) markers associated with fatigue. Of 255 1-year ICH survivors, 153 (60

Les hémorragies cérébelleuses constituent environ 10 % des hémorragies cérébrales non traumatiques. Les microangiopathies retrouvées incluent la vasculopathie des artères perforantes profondes (VAPP), et plus rarement l'angiopathie amyloïde cérébrale. Décrire l'histoire naturelle des hémorragies cérébelleuses non traumatiques en fonction de leur localisation anatomique, discuter les facteurs d'orientation vers la microangiopathie sous-jacente. Nous avons recueilli les caractéristiques initiales de patients ayant présenté une hémorragie cérébelleuse diagnostiquée sur un scanner cérébral, répartis en 3 catégories anatomiques : superficielles, profondes, ou de localisation indéterminée. Nous avons comparé entre hémorragies superficielles et profondes les caractéristiques initiales, la mortalité, les récidives neurovasculaires, l'apparition d'une démence, en analyse bivariée. Les biomarqueurs de microangiopathie cérébrale ont été analysés chez les patients ayant pu bénéficier d'une IRM. Un total de 33 patients (d'âge médian 68 ans) ont été inclus : 13 hémorragies superficielles, 12 profondes, et 8 indéterminées. Les hémorragies profondes étaient plus souvent associées à une hypertension artérielle, une leucopathie et atrophie corticale sévères, marqueurs associés à la VAAP. En IRM, la présence d'une leucopathie, et de lacunes multiples semblaient également plus fréquentes. La localisation de l'hémorragie ne semblait pas influencer la mortalité à long terme (médiane de survie globale : 5 jours). Dans notre étude, les hémorragies profondes semblent associées à la VAAP, suggérant que la localisation de l'hémorragie pourrait orienter vers la microangiopathie sous-jacente. Du fait d'un faible effectif et d'une forte mortalité précoce, nous n'avons pu conclure à une différence entre les deux groupes en termes de biomarqueurs IRM de microangiopathies, de récidives vasculaires, de démence nouvellement apparue. Des études multicentriques sont en cours pour explorer le lien entre localisation de l'hémorragie et microangiopathie sous-jacente, qui influencerait le pronostic (récidives neurovasculaires) et la gestion des antithrombotiques.

OBJECTIVE:To determine the prevalence of cortical superficial siderosis (cSS), its clinical and neuroimaging associated markers, and its influence on the risk of recurrent intracerebral hemorrhage (ICH) in a prospective observational ICH cohort.METHODS:We investigated clinical and radiologic markers associated with cSS using multivariable analysis. In survival analyses, we used Cox models to identify predictors of recurrent ICH after adjusting for potential confounders.RESULTS:Of the 258 patients included in the study, 49 (19%; 95% confidence interval [CI] 14%-24%) had cSS at baseline. Clinical factors independently associated with the presence of cSS were increasing age (odds ratio [OR] 1.03 per 1-year increase, 95% CI 1.001-1.06, p = 0.044), preexisting dementia (OR 2.62, 95% CI 1.05-6.51, p = 0.039), and history of ICH (OR 4.02, 95% CI 1.24-12.95, p = 0.02). Among radiologic biomarkers, factors independently associated with the presence of cSS were ICH lobar location (OR 24.841, 95% CI 3.2-14.47, p < 0.001), severe white matter hyperintensities score (OR 5.51, 95% CI 1.17-5.78, p = 0.019), and absence of lacune (OR 4.46, 95% CI 1.06-5.22, p = 0.035). During a median follow-up of 6.4 (interquartile range 2.9-8.4) years, recurrent ICH occurred in 19 patients. Only disseminated cSS (hazard ratio 4.69, 95% CI 1.49-14.71, p = 0.008), not the presence or absence of cSS or focal cSS on baseline MRI, was associated with recurrent symptomatic ICH.CONCLUSION:In a prospective observational cohort of spontaneous ICH, clinical and radiologic markers associated with cSS suggest the implication of underlying cerebral amyloid angiopathy. Disseminated cSS may become a key prognostic neuroimaging marker of recurrent ICH that could be monitored in future clinical trials dedicated to patients with ICH.

Objective To determine the prevalence of cortical superficial siderosis (cSS), its clinical and neuroimaging associated markers, and its influence on the risk of recurrent intracerebral hemorrhage (ICH) in a prospective observational ICH cohort. Methods We investigated clinical and radiologic markers associated with cSS using multivariable analysis. In survival analyses, we used Cox models to identify predictors of recurrent ICH after adjusting for potential confounders. Results Of the 258 patients included in the study, 49 (19%; 95% confidence interval [CI] 14%–24%) had cSS at baseline. Clinical factors independently associated with the presence of cSS were increasing age (odds ratio [OR] 1.03 per 1-year increase, 95% CI 1.001–1.06, p = 0.044), preexisting dementia (OR 2.62, 95% CI 1.05–6.51, p = 0.039), and history of ICH (OR 4.02, 95% CI 1.24–12.95, p = 0.02). Among radiologic biomarkers, factors independently associated with the presence of cSS were ICH lobar location (OR 24.841, 95% CI 3.2–14.47, p < 0.001), severe white matter hyperintensities score (OR 5.51, 95% CI 1.17–5.78, p = 0.019), and absence of lacune (OR 4.46, 95% CI 1.06–5.22, p = 0.035). During a median follow-up of 6.4 (interquartile range 2.9–8.4) years, recurrent ICH occurred in 19 patients. Only disseminated cSS (hazard ratio 4.69, 95% CI 1.49–14.71, p = 0.008), not the presence or absence of cSS or focal cSS on baseline MRI, was associated with recurrent symptomatic ICH. Conclusion In a prospective observational cohort of spontaneous ICH, clinical and radiologic markers associated with cSS suggest the implication of underlying cerebral amyloid angiopathy. Disseminated cSS may become a key prognostic neuroimaging marker of recurrent ICH that could be monitored in future clinical trials dedicated to patients with ICH.

AIM:In patients with cerebral ischemia, intravenous (i.v.) recombinant tissue plasminogen activator (rt-PA) increases survival without handicap or dependency despite an increased risk of bleeding. This study evaluated whether the results of randomized controlled trials are reproduced in clinical practice. METHOD:Data from a registry of consecutive patients treated by rt-PA at Lille University Hospital were retrospectively analyzed for outcomes, using modified Rankin Scale (mRS) scores, at 3 months. The observed outcomes were then compared with the probability of good (mRS 0-1) and of catastrophic (mRS 5-6) outcomes, as predicted by the stroke-thrombolytic predictive instrument (STPI). RESULTS:Of the 1000 consecutive patients (469 male, median age 74 years, median baseline National Institutes of Health Stroke Scale 11, median onset-to-needle time 143min), 438 (43.8%) had a good outcome, 565 (56.5%) had an mRS score 0-2 or similar to their pre-stroke mRS, 155 (15.5%) died within 3 months and 74 (7.4%) developed symptomatic intracerebral hemorrhage according to ECASS-II (Second European-Australasian Acute Stroke Study) criteria. Of the 613 patients (61.3%) eligible for evaluation by the s-TPI, the observed rate of good outcomes was 41.3% (95% CI: 37.5-45.3%), while expected rates with and without rt-PA were 48.8% (95% CI: 44.8-52.7%) and 32.5% (95% CI: 28.8-36.2%), respectively; the observed rate of catastrophic outcomes was 17.0% (95% CI: 14.0-19.9%), while the expected rate was 19.2% (95% CI: 16.1-22.4%) with or without rt-PA. CONCLUSION:In clinical practice, the rate of good outcomes is slightly lower than expected, according to the s-TPI, except for the most severe cases, whereas the rate of catastrophic outcomes is roughly similar. However, the rate of good outcomes is higher than predicted without treatment. This finding suggests that rt-PA is effective for improving outcomes in clinical practice.

OBJECTIVE:To determine whether the ratio single chain (sc)/(sc + 2 chain [tc]) recombinant tissue plasminogen activator (rtPA) influences outcomes in patients with cerebral ischemia.METHODS:We prospectively included consecutive patients treated with IV rtPA for cerebral ischemia in 13 stroke centers and determined the sc/(sc + tc) ratio in the treatment administered to each patient. We evaluated the outcome with the modified Rankin Scale (mRS) at 3 months (prespecified analysis) and occurrence of epileptic seizures (post hoc analysis). We registered Outcome of Patients Treated by IV Rt-PA for Cerebral Ischaemia According to the Ratio Sc-tPA/Tc-tPA (OPHELIE) under ClinicalTrials.gov identifier no. NCT01614080.RESULTS:We recruited 1,004 patients (515 men, median age 75 years, median onset-to-needle time 170 minutes, median NIH Stroke Scale score 10). We found no statistical association between sc/(sc + tc) ratios and handicap (mRS > 1), dependency (mRS > 2), or death at 3 months. Patients with symptomatic intracerebral hemorrhages had lower ratios (median 69% vs 72%, adjusted p = 0.003). The sc/(sc + tc) rtPA ratio did not differ between patients with and without seizures, but patients with early seizures were more likely to have received a sc/(sc + tc) rtPA ratio >80.5% (odds ratio 3.61; 95% confidence interval 1.26-10.34).CONCLUSIONS:The sc/(sc + tc) rtPA ratio does not influence outcomes in patients with cerebral ischemia. The capacity of rtPA to modulate NMDA receptor signaling might be associated with early seizures, but we observed this effect only in patients with a ratio of sc/(sc + tc) rtPA >80.5% in a post hoc analysis.

Background and Purpose— We aimed to identify prognostic and associated factors of incident cerebral microbleeds (CMBs) in intracerebral hemorrhage (ICH) survivors. Methods— Observational prospective cohort of 168 ICH survivors who underwent 1.5T magnetic resonance imaging at ICH onset and during follow-up (median scan interval, 3.4; interquartile range, 1.4–4.7) years. We used logistic regression adjusted for age, sex, and scan interval. Analyses were stratified according to the index ICH location (58 lobar ICH, 103 nonlobar ICH, excluding patients with multiple or unclassifiable ICH). Results— Eighty-nine (53%) patients had CMBs at ICH onset, and 80 (48%) exhibited incident CMBs during follow-up. Predictors of incident CMBs at ICH onset were ≥1 CMBs (adjusted odds ratio [aOR], 2.27; 95% confidence interval [CI], 1.18–4.35), old radiological macrohemorrhage (aOR, 6.78; 95% CI, 2.76–16.68), and CMBs in mixed location (aOR, 3.73; 95% CI, 1.67–8.31). When stratifying by ICH location, incident CMBs were associated in nonlobar ICH with incident lacunes (aOR, 2.86; 95% CI, 1.04–7.85) and with the use of antiplatelet agents (aOR, 2.89; 95% CI, 1.14–7.32). In lobar ICH, incident CMBs were associated with incident radiological macrohemorrhage (aOR, 9.76; 95% CI, 1.07–88.77). Conclusions— Prognostic and associated factors of incident CMBs differed according to the index ICH location. Whereas in lobar ICH, incident CMBs were associated with hemorrhagic biomarkers, in nonlobar ICH, ischemic burden also increased. CMBs may be interesting biomarkers to monitor in randomized trials on restarting antithrombotic drugs after ICH.

Background: Stroke and dementia are closely related but no prospective study ever focused on dementia in patients with intracerebral hemorrhage (ICH). Objective: To determine incidence, prognostic factors and possible mechanisms of post-ICH dementia in a large population of non-demented ICH patients over a long period of follow-up. Methods: Prospective cohort of consecutive adults with spontaneous ICH. Patients free of dementia and alive at 6 months were included. We studied clinical and neuroradiological (MRI) biomarkers with a prespecified subgroup analysis according to ICH location. Age-adjusted analyses were used to select variables (p<0.1) included in multivariable models that took into account death as competing risk. Results: In a cohort of 218 ICH patients (108 males; median age 67.5, interquartile range (IQR) 55-76), 63 patients developed new onset dementia during a median follow-up of 5.4 years (IQR, 4.2-5.8). At 1 year after ICH, the overall incidence of dementia was 20% (95% CI 15-25). It differed between lobar ICH (n=77, 30% 95% CI 20-40) and non lobar ICH (n=141, 16% 95% CI 10-22). Prognostic factors of new onset dementia were lobar Iocation (Hazard Ratio (HR): 2.21; 95% CI 1.30-3.79), older age (HR: 1.06 per year; 95% CI 1.03-1.09), history of previous stroke or transient ischemic attack (HR: 2.56; 95% CI 1.42-4.61), higher NIHSS (HR: 1.03 per year; 95% CI 1.01-1.06), severe leucoaraïosis (HR: 2.87; 95% CI 1.63-5.07) and recurrent stroke during follow-up (HR: 3.22; 95% CI 1.27-8.15). Prognostic neuroradiological biomarkers were increasing cortical atrophy (HR: 2.7; 95% CI 1.7-4.3), presence of disseminated superficial siderosis (HR: 7.10; 95% CI 3.93-12.83), higher number of lobar cerebral microbleeds (HR: 3.40; 95%CI 1.87-6.18). Among lobar ICH, superficial siderosis was a strong predictor (HR: 6.74; 95% CI 3.32-13.68). Conclusion: The incidence of new onset dementia is high after ICH with a strong influence of lobar location. Among patients with lobar ICH, prognostic factors suggested a strong implication of underlying cerebral amyloid angiopathy that might predict future risk of dementia. Results of our study suggest that all prognostic factors of dementia are already present before the ICH occurs.

Background: Histological analysis of thromboemboli obtained from acute ischemic stroke patients and evaluation of clinico-histological correlation could provide informations regarding response to therapy, complications and outcome. Methods: Thromboemboli were retrieved by endovascular mechanical thrombectomy from major arteries of the circle of Willis of patients with acute ischemic stroke. Total thrombus area and percentage of fibrin were calculated. Results: Three patterns of thrombus histology were identified based on fibrin architecture in 28 specimens: serpentine (15/28), layered (11/28) and red clot (2/28). No differences in stroke etiology were found between different patterns. Comparing serpentine and layered, the latter showed a significantly higher percentage of fibrin (70.5 vs 40.3, p=0.03), significantly higher pre-treatment National Institute of Health Stroke Scale score (21 vs 17.7, p=0.02), a significantly shorter onset to recanalization time (286 min vs 356 min, p=0.02). Thrombus area showed to be higher in cases with multiple vessels involvement (p=0.04), with symptomatic intracranial hemorrhage (p=0.02), with worst 3 months outcome (p=0.04) and higher mortality (p=0.02). Conclusion: Histological analysis of thromboemboli proved useful in the identification of specific patterns and their behaviour in terms of response to endovascular treatment and clinical outcome.

Les accidents vasculaires cérébraux et la démence sont étroitement liés. Cependant, les données concernant le pronostic cognitif des patients ayant présenté une hémorragie intracérébrale (HIC) sont rares. Déterminer l’incidence, les facteurs prédictifs et les mécanismes possibles sous-tendant la démence post-HIC dans une large cohorte de patients non déments à l’admission, sur une longue période de suivi. Cohorte prospective observationnelle (suivi médian : 6 ans) de patients présentant une HIC spontanée admis au CHU de Lille. Les patients n’ayant pas de démence préexistante et vivants à 6 mois ont été inclus. Nous avons étudié des marqueurs cliniques et neuroradiologiques (IRM). Des analyses multivariées ont été réalisées et répétées dans un sous-groupe prédéfini par la localisation de l’HIC. Le décès a été considéré comme un évènement compétitif. Parmi 218 patients (âge médian : 67,5 ans), 63 ont développé une démence soit un taux d’incidence cumulée de 28,8 % (95 %IC 22,9–35,0) à 4.5 ans. Les facteurs prédictifs de démence étaient la localisation lobaire [SubHazard Ratio (SHR : 2,21 ; 95 %IC 1,30–3,79)], la sidérose superficielle disséminée (SHR : 7,45 ; 95 %IC 4,27–12,99), le score d’atrophie corticale (SHR pour 1-point d’augmentation 2,61 ; 95 %IC 1,70–4,01), et un nombre plus élevé de microhémorragies cérébrales (SHR pour >5 MBC 2,33 ; 95 %IC 1,38–3,94). Il s’agit de la première étude prospective sur la démence post-HIC. La survenue d’une démence après une HIC est fréquente et les patients avec HIC lobaire semblent plus exposés que ceux avec HIC non lobaire. Les facteurs prédictifs de démence post-HIC mis en évidence suggèrent une implication forte des marqueurs de l’angiopathie amyloïde cérébrale. Ces résultats permettront de mieux organiser le suivi cognitif des patients ayant eu une HIC et soulignent l’importance d’intégrer un critère de jugement cognitif dans les études neurovasculaires.

Background Dementia occurs in at least 10% of patients within 1 year after stroke. However, the risk of dementia after spontaneous intracerebral haemorrhage that accounts for about 15% of all strokes has not been investigated in prospective studies. We aimed to determine the incidence of dementia and risk factors after an intracerebral haemorrhage.Methods We did a prospective observational cohort study in patients with spontaneous intracerebral haemorrhage from the Prognosis of Intracerebral Haemorrhage (PITCH) cohort who were admitted to Lille University Hospital, Lille, France. We included patients aged 18 years and older with parenchymal haemorrhage on the first CT scan. Exclusion criteria were pure intraventricular haemorrhage; intracerebral haemorrhage resulting from intracranial vascular malformation, intracranial venous thrombosis, head trauma, or tumour; haemorrhagic transformation within an infarct; and referral from other hospitals. Median follow-up was 6 years. We studied risk factors (clinical and neuroradiological [MRI] biomarkers) of new-onset dementia as per a prespecified subgroup analysis, according to intracerebral haemorrhage location. Dementia diagnosis was based on the National Institute on Aging-Alzheimer's Association criteria for all-cause dementia. We did multivariable analyses using competing risk analyses, with death during follow-up as a competing event.Findings From the 560 patients with spontaneous intracerebral haemorrhage enrolled in the PITCH cohort between Nov 3, 2004 and March 29, 2009, we included 218 patients (median age 67.5 years) without pre-existing dementia who were alive at 6 months follow-up. 63 patients developed new-onset dementia leading to an incidence rate of 14.2% (95% CI 10.0-19.3) at 1 year after intracerebral haemorrhage, and incidence reached 28.3% (22.4-34.5) at 4 years. The incidence of new-onset dementia was more than two times higher in patients with lobar intracerebral haemorrhage (incidence at 1 year 23.4%, 14.6-33.3) than for patients with non-lobar intracerebral haemorrhage (incidence at 1 year 9.2%, 5.1-14.7). Disseminated superficial siderosis (subhazard ratio [SHR] 7.45, 95% CI 4.27-12.99), cortical atrophy score (SHR per 1-point increase 2.61, 1.70-4.01), a higher number of cerebral microbleeds (SHR for >5 cerebral microbleeds 2.33, 1.38-3.94), and older age (SHR per 10-year increase 1.34, 1.00-1.79) were risk factors of new-onset dementia.Interpretation There is a substantial risk of incident dementia in dementia-free survivors of spontaneous intracerebral haemorrhage; our results suggest that underlying cerebral amyloid angiopathy is a contributing factor to the occurrence of new-onset dementia. Future clinical trials including patients with intracerebral haemorrhage should assess cognitive endpoints.Funding French Ministry of Education, Research, and Technology, Adrinord, Inserm U1171.

Background and purpose: Stroke and dementia are closely related, but no prospective study ever focused on post-stroke cognitive decline in patients with intracerebral haemorrhage (ICH). We aimed to determine prognostic factors for cognitive decline in ICH patients. Methods: We prospectively included 167 consecutive ICH survivors without pre-existing dementia from the Prognosis of InTra-Cerebral Haemorrhage (PITCH) cohort. Median follow-up was 4 years (interquartile range [IQR]:2.3-5.4). We explored factors associated with cognitive decline using linear mixed models. Cognitive decline was determined based on repeated mini-mental state examination (MMSE). We investigated each prognostic factor separately in univariate models. Next, we constructed clinical and radiological multivariable models. In a sensitivity analysis we excluded patients with pre-existing cognitive impairment. Results: Median age was 64 (IQR: 53-75) years, 69 (41%) patients were female and median MMSE at 6 months was 27 (IQR: 23-29). Overall, 37% of the patients declined during follow-up. Factors associated with cognitive decline in univariate analyses were: previous stroke or TIA, pre-existing cognitive impairment, microbleed presence, severity of white matter hyperintensities, and severity of cortical atrophy. In multivariable analyses, previous stroke or TIA (β [SE]-0.55[0.23], p<0.05), pre-existing cognitive impairment (β [SE]-0.56[0.25], p<0.01), and severity of cortical atrophy (β [SE]-0.50[0.19], p<0.01) remained independent prognostic factors. In patients without pre-existing cognitive impairment (n=139), severity of cortical atrophy (β [SE]-0.38[0.17], p<0.05) was the only prognostic factor for future cognitive decline. Conclusions: Prognostic factors for cognitive decline after ICH are already present when ICH occurs, suggesting a process of ongoing cognitive impairment instead of new-onset decline induced by the ICH itself.

BACKGROUND AND PURPOSE:Stroke and dementia are closely related, but no prospective study ever focused on poststroke cognitive decline in patients with intracerebral hemorrhage (ICH). We aimed to determine prognostic factors for cognitive decline in patients with ICH. METHODS:We prospectively included 167 consecutive ICH survivors without preexisting dementia from the Prognosis of Intra-Cerebral Hemorrhage (PITCH) cohort. Median follow-up was 4 years (interquartile range, 2.3-5.4). We explored factors associated with cognitive decline using linear mixed models. Cognitive decline was determined based on repeated mini-mental state examination. We investigated each prognostic factor separately in univariate models. Next, we constructed clinical and radiological multivariable models. In a sensitivity analysis, we excluded patients with preexisting cognitive impairment. RESULTS:Median age was 64 (interquartile range, 53-75) years, 69 (41%) patients were women, and median mini-mental state examination at 6 months was 27 (interquartile range, 23-29). Overall, 37% of the patients declined during follow-up. Factors associated with cognitive decline in univariate analyses were previous stroke or transient ischemic attack, preexisting cognitive impairment, microbleed presence, severity of white matter hyperintensities, and severity of cortical atrophy. In multivariable analyses, previous stroke or transient ischemic attack (β [SE], -0.55 [0.23]; P<0.05), preexisting cognitive impairment (β [SE], -0.56 [0.25]; P<0.01), and severity of cortical atrophy (β [SE], -0.50 [0.19]; P<0.01) remained independent prognostic factors. In patients without preexisting cognitive impairment (n=139), severity of cortical atrophy (β [SE], -0.38 [0.17]; P<0.05) was the only prognostic factor for future cognitive decline. CONCLUSIONS:Prognostic factors for cognitive decline after ICH are already present when ICH occurs, suggesting a process of ongoing cognitive impairment instead of new-onset decline induced by the ICH itself.

Intracerebral hemorrhage (ICH) is a devastating condition with multiple possible underlying causes. Early diagnosis of ICH associated with a precise diagnostic work-up is mandatory. Clinical signs may give clues to diagnosis but are not reliable enough and imaging remains the cornerstone of management. Noncontrast computed tomography and magnetic resonance imaging (MRI) are highly sensitive for ICH identification. Additionally, MRI may disclose brain parenchymal biomarkers that can contribute to the etiologic diagnosis. Vessel examination should be carried out whenever there is a clinical suspicion of underlying structural lesions, such as vascular malformations or tumors. To date, conventional angiography remains the gold standard to detect intracranial vascular malformations in patients with ICH.

Spontaneous intracerebral haemorrhage (ICH) is defined as a collection of blood in the cerebral parenchyma that is not caused by trauma. ICH is the second most frequent cause of stroke, accounting for 10–15 % of all cases in high-income countries and about 20 % in low- to middle-income countries. Despite an apparent stability of incidence over the past decades, the profile of ICH has changed: there are fewer deep ICHs associated with pre-stroke hypertension, whereas the increasing age of the population associated with a more extensive use of antithrombotic drugs leads to an increase of lobar ICH. Deep perforating vasculopathy remains the most important cause of ICH, followed by cerebral amyloid angiopathy, these two aetiologies account for nearly 70 % of all ICH cases. Recent scientific evidence has highlighted new aspects of the pathophysiology of such disorders; nevertheless, the morbidity and mortality of ICH remain extremely high. In the present article, the different causes of ICH will be reviewed.

Background and Purpose— Seizures are a common complication of intracerebral hemorrhage (ICH). We developed a novel tool to quantify this risk in individual patients. Methods— Retrospective analysis of the observational Helsinki ICH Study (n=993; median follow-up, 2.7 years) and the Lille Prognosis of InTra-Cerebral Hemorrhage (n=325; 2.2 years) cohorts of consecutive ICH patients admitted between 2004 and 2010. Helsinki ICH Study patients’ province-wide electronic records were evaluated for early seizures occurring within 7 days of ICH and among 7-day survivors (n=764) for late seizures (LSs) occurring >7 days from ICH. A Cox regression model estimating risk of LSs was used to derive a prognostic score, validated in the Prognosis of InTra-Cerebral Hemorrhage cohort. Results— Of the Helsinki ICH Study patients, 109 (11.0%) had early seizures within 7 days of ICH. Among the 7-day survivors, 70 (9.2%) patients developed LSs. The cumulative risk of LSs was 7.1%, 10.0%, 10.2%, 11.0%, and 11.8% at 1 to 5 years after ICH, respectively. We created the CAVE score (0–4 points) to estimate the risk of LSs, with 1 point for each of cortical involvement, age <65 years, volume >10 mL, and early seizures within 7 days of ICH. The risk of LSs was 0.6%, 3.6%, 9.8%, 34.8%, and 46.2% for CAVE scores 0 to 4, respectively. The c-statistic was 0.81 (0.76–0.86) and 0.69 (0.59–0.78) in the validation cohort. Conclusions— One in 10 patients will develop seizures after ICH. The risk of this adverse outcome can be estimated by a simple score based on baseline variables.