炎症过程、热性惊厥及随后的癫痫发生。
Inflammatory processes, febrile seizures, and subsequent epileptogenesis.
作者信息
Choy ManKin, Dubé Céline M, Ehrengruber Markus, Baram Tallie Z
机构信息
Department of Pediatrics, University of California-Irvine, Irvine, CA.
Department of Pediatrics, University of California-Irvine, Irvine, CA ; Department of Anatomy/Neurobiology, University of California-Irvine, Irvine, CA.
出版信息
Epilepsy Curr. 2014 Jan;14(1 Suppl):15-22. doi: 10.5698/1535-7511-14.s2.15.
Febrile seizures (FS) are the most common type of seizures in infants and preschool children. Inflammatory mediators, which are known triggers of fever, have also been implicated as contributors to the onset of these seizures. Evidence that inflammation is present following FS and during established epilepsy suggests that it could also influence epileptogenesis. However, the potential involvement of inflammatory mediators to the epileptogenic process that may follow prolonged FS has yet to be fully determined. This article reviews the current state of our knowledge and major gaps that remain by focusing on four questions: Does inflammation contribute to the generation of FS? Does prolonged FS or febrile status epilepticus (SE) cause temporal lobe epilepsy in the absence of predisposing factors? Does inflammation contribute to the process by which febrile SE causes limbic epilepsy? And finally, can inflammation be a foundation for biomarkers and therapy for FS-induced epileptogenesis?
热性惊厥（FS）是婴幼儿和学龄前儿童最常见的惊厥类型。炎症介质是已知的发热诱因，也被认为是这些惊厥发作的促成因素。热性惊厥发作后以及癫痫确立过程中存在炎症的证据表明，炎症也可能影响癫痫发生。然而，炎症介质在长时间热性惊厥后可能参与的致痫过程尚未完全明确。本文通过关注四个问题回顾了我们目前的知识状况以及仍然存在的主要差距：炎症是否促成热性惊厥的发生？在没有易感因素的情况下，长时间热性惊厥或热性癫痫持续状态（SE）是否会导致颞叶癫痫？炎症是否促成热性癫痫持续状态导致边缘叶癫痫的过程？最后，炎症能否成为热性惊厥诱导的癫痫发生的生物标志物和治疗基础？
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