Katsarou Anna-Maria, Kubova Hana, Auvin Stéphane, Mantegazza Massimo, Barker-Haliski Melissa, Galanopoulou Aristea S, Reid Christopher A, Semple Bridgette D
Laboratory of Developmental Epilepsy, Saul R. Korey Department of Neurology, Albert Einstein College of Medicine, Bronx, New York, USA.
Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Epilepsia Open. 2022 Aug 11. doi: 10.1002/epi4.12641.
Epilepsy syndromes during the early years of life may be attributed to an acquired insult, such as hypoxic-ischemic injury, infection, status epilepticus, or brain trauma. These conditions are frequently modeled in experimental rodents to delineate mechanisms of epileptogenesis and investigate novel therapeutic strategies. However, heterogeneity and subsequent lack of reproducibility of such models across laboratories is an ongoing challenge to maintain scientific rigor and knowledge advancement. To address this, as part of the TASK3-WG1B Working Group of the International League Against Epilepsy/American Epilepsy Society Joint Translational Task Force, we have developed a series of case report forms (CRFs) to describe common data elements for pediatric acquired epilepsy models in rodents. The "Rodent Models of Pediatric Acquired Epilepsy" Core CRF was designed to capture cohort-general information; while two Specific CRFs encompass physical induction models and chemical induction models, respectively. This companion manuscript describes the key elements of these models and why they are important to be considered and reported consistently. Together, these CRFs provide investigators with the tools to systematically record critical information regarding their chosen model of acquired epilepsy during early life, for improved standardization and transparency across laboratories. These outcomes will support the ultimate goal of such research; that is, to understand the childhood onset-specific biology of epileptogenesis after acquired insults, and translate this knowledge into therapeutics to improve pediatric patient outcomes and minimize the lifetime burden of epilepsy.
生命早期的癫痫综合征可能归因于后天性损伤,如缺氧缺血性损伤、感染、癫痫持续状态或脑外伤。这些情况经常在实验啮齿动物中进行模拟,以阐明癫痫发生的机制并研究新的治疗策略。然而,这些模型在不同实验室之间的异质性以及随之而来的缺乏可重复性,是维持科学严谨性和知识进步的一个持续挑战。为了解决这个问题,作为国际抗癫痫联盟/美国癫痫协会联合转化任务组TASK3-WG1B工作组的一部分,我们开发了一系列病例报告表(CRF),以描述啮齿动物小儿后天性癫痫模型的常见数据元素。“小儿后天性癫痫的啮齿动物模型”核心CRF旨在获取队列一般信息;而两个特定的CRF分别涵盖物理诱导模型和化学诱导模型。这篇配套手稿描述了这些模型的关键要素以及为什么需要一致地考虑和报告它们。总之,这些CRF为研究人员提供了工具,以便系统地记录有关其选择的生命早期后天性癫痫模型的关键信息,从而提高各实验室之间的标准化和透明度。这些成果将支持此类研究的最终目标;也就是说,了解后天性损伤后儿童期癫痫发生的特定生物学机制,并将这些知识转化为治疗方法,以改善儿科患者的预后并尽量减少癫痫的终身负担。