Neurology Division, University Hospital of Geneva, Geneva, Switzerland.
EEG & Epilepsy Unit, Neurology Division, Department of Clinical Neurosciences, Faculty of Medicine, University Hospital, University of Geneva, 4, Rue Gabrielle-Perret-Gentil, CH-1211, Geneva, Switzerland.
J Neurol. 2022 Nov;269(11):5934-5939. doi: 10.1007/s00415-022-11254-0. Epub 2022 Jul 7.
Hippocampal sclerosis (HS) is a prominent biomarker of epilepsy. If acquired later in life, it usually occurs in the context of degenerative or acute inflammatory-infectious disease. Conversely, acute symptomatic seizures (ASS) are considered a risk factor for developing post-stroke epilepsy, but other factors remain unrecognized. Here, we hypothesize that silent hippocampal injury contributes to the development of post-stroke epilepsy.
We performed a retrospective observational study of patients hospitalized between 1/2007 and 12/2018 with an acute stroke in the Stroke Center of the Geneva University Hospital. Patients were included if they had a documented normal hippocampal complex at onset and a control MRI at ≥ 2 year interval without new lesion in the meantime.
162 patients fulfilled our inclusion criteria. ASS during the first week (p < 0.0001) and epileptiform abnormalities in electroencephalography (EEG; p = 0.02) were more frequently associated with the development of epilepsy. Hemorrhagic stroke was strongly associated to both ASS and future focal epilepsy (p = 0.00097). Three patients (1.8%) developed hippocampal sclerosis ipsilateral to the cerebrovascular event between 2 and 5 years, all with ASS and hemorrhagic stroke.
ASS and epileptiform EEG abnormalities are strong predictors of post-stroke epilepsy. HS develops in a minority of patients after hemorrhagic lesions, leading to focal epilepsy. Prospective studies are required, including follow-up with EEG and if characterized by epileptiform discharges, with MRI, to determine the true frequency of HS and to better understand predictors of post-stroke epilepsy (AAS, stroke type, and HS), and their impact on stroke recovery.
海马硬化（HS）是癫痫的重要生物标志物。如果在生命后期获得，则通常发生在退行性或急性炎症性感染性疾病的背景下。相反，急性症状性发作（ASS）被认为是中风后癫痫发生的危险因素，但其他因素仍未被识别。在这里，我们假设沉默性海马损伤有助于中风后癫痫的发展。
我们对 2007 年 1 月至 2018 年 12 月期间在日内瓦大学医院中风中心住院的急性中风患者进行了回顾性观察研究。如果患者在发病时存在记录的正常海马复合体，并且在同时没有新病变的情况下在≥2 年内进行了对照 MRI，则将其纳入研究。
162 名患者符合纳入标准。发病后第一周 ASS（p<0.0001）和脑电图（EEG）中的癫痫样异常（p=0.02）更频繁地与癫痫的发展相关。出血性中风与 ASS 和未来局灶性癫痫均有强烈相关性（p=0.00097）。3 名患者（1.8%）在中风后 2 至 5 年内同侧发展为海马硬化，均有 ASS 和出血性中风。
ASS 和癫痫样 EEG 异常是中风后癫痫的强烈预测因子。HS 在少数出血性病变患者中发展，导致局灶性癫痫。需要进行前瞻性研究，包括 EEG 随访，如果有癫痫样放电，则需要 MRI 随访，以确定 HS 的真实频率，并更好地了解中风后癫痫的预测因子（AAS、中风类型和 HS），以及它们对中风恢复的影响。
