From the Department of Neurology (T.T., M.I., K.F.), National Cerebral and Cardiovascular Center, Osaka, Japan; Department of Neurology (N.K.M.), Yale University School of Medicine, New Haven, CT; Department of Clinical & Experimental Epilepsy (M.J.K.), UCL Queen Square Institute of Neurology, London, United Kingdom; Moscow Research and Clinical Center for Neuropsychiatry (A.G.), Pirogov Russian National Research Medical University, Russia; and Department of Epilepsy, Movement Disorders and Physiology (A.I.), Kyoto University Graduate School of Medicine, Japan.
Neurology. 2024 Jun 11;102(11):e209450. doi: 10.1212/WNL.0000000000209450. Epub 2024 May 17.
Poststroke epilepsy (PSE) is associated with higher mortality and poor functional and cognitive outcomes in patients with stroke. With the remarkable development of acute stroke treatment, there is a growing number of survivors with PSE. Although approximately 10% of patients with stroke develop PSE, given the significant burden of stroke worldwide, PSE is a significant problem in stroke survivors. Therefore, the attention of health policymakers and significant funding are required to promote PSE prevention research. The current PSE definition includes unprovoked seizures occurring more than 7 days after stroke onset, given the high recurrence risks of seizures. However, the pathologic cascade of stroke is not uniform, indicating the need for a tissue-based approach rather than a time-based one to distinguish early seizures from late seizures. EEG is a commonly used tool in the diagnostic work-up of PSE. EEG findings during the acute phase of stroke can potentially stratify the risk of subsequent seizures and predict the development of poststroke epileptogenesis. Recent reports suggest that cortical superficial siderosis, which may be involved in epileptogenesis, is a promising marker for PSE. By incorporating such markers, future risk-scoring models could guide treatment strategies, particularly for the primary prophylaxis of PSE. To date, drugs that prevent poststroke epileptogenesis are lacking. The primary challenge involves the substantial cost burden due to the difficulty of reliably enrolling patients who develop PSE. There is, therefore, a critical need to determine reliable biomarkers for PSE. The goal is to be able to use them for trial enrichment and as a surrogate outcome measure for epileptogenesis. Moreover, seizure prophylaxis is essential to prevent functional and cognitive decline in stroke survivors. Further elucidation of factors that contribute to poststroke epileptogenesis is eagerly awaited. Meanwhile, the regimen of antiseizure medications should be based on individual cardiovascular risk, psychosomatic comorbidities, and concomitant medications. This review summarizes the current understanding of poststroke epileptogenesis, its risks, prognostic models, prophylaxis, and strategies for secondary prevention of seizures and suggests strategies to advance research on PSE.
卒中后癫痫(PSE)与卒中患者的死亡率升高和功能及认知结局较差相关。随着急性卒中治疗的显著发展,越来越多的 PSE 幸存者出现。尽管约 10%的卒中患者发生 PSE,但鉴于全球卒中负担巨大,PSE 是卒中幸存者面临的重大问题。因此,需要卫生政策制定者关注并提供大量资金,以促进 PSE 预防研究。目前的 PSE 定义包括卒中发作后 7 天以上发生的无诱因发作,这是由于癫痫发作的复发风险较高。然而,卒中的病理级联反应并不一致,这表明需要采用基于组织而非基于时间的方法来区分早期发作和晚期发作。脑电图是 PSE 诊断中的常用工具。卒中急性期的脑电图发现可能有助于分层随后发生癫痫的风险,并预测卒中后癫痫发生的发展。最近的报告表明,可能参与癫痫发生的皮质表浅铁沉积是 PSE 的一个有前途的标志物。通过纳入这些标志物,未来的风险评分模型可以指导治疗策略,特别是用于 PSE 的一级预防。迄今为止,尚无预防卒中后癫痫发生的药物。主要挑战在于由于难以可靠地招募发生 PSE 的患者,因此存在巨大的成本负担。因此,迫切需要确定 PSE 的可靠生物标志物。目标是能够将其用于试验富集,并作为癫痫发生的替代结局测量指标。此外,预防癫痫发作对于预防卒中幸存者的功能和认知下降至关重要。迫切需要进一步阐明导致卒中后癫痫发生的因素。与此同时,抗癫痫药物的治疗方案应基于个体的心血管风险、心身共病和伴随用药。本综述总结了目前对卒中后癫痫发生、风险、预后模型、预防以及预防癫痫发作的二级预防策略的理解,并提出了推进 PSE 研究的策略。