Department of Pharmacology, Toxicology and Pharmacy, University of Veterinary Medicine, Bünteweg 17, Hannover, Germany.
Pharmacol Rev. 2010 Dec;62(4):668-700. doi: 10.1124/pr.110.003046.
Diverse brain insults, including traumatic brain injury, stroke, infections, tumors, neurodegenerative diseases, and prolonged acute symptomatic seizures, such as complex febrile seizures or status epilepticus (SE), can induce "epileptogenesis," a process by which normal brain tissue is transformed into tissue capable of generating spontaneous recurrent seizures. Furthermore, epileptogenesis operates in cryptogenic causes of epilepsy. In view of the accumulating information about cellular and molecular mechanisms of epileptogenesis, it should be possible to intervene in this process before the onset of seizures and thereby either prevent the development of epilepsy in patients at risk or increase the potential for better long-term outcome, which constitutes a major clinical need. For identifying pharmacological interventions that prevent, interrupt or reverse the epileptogenic process in people at risk, two groups of animal models, kindling and SE-induced recurrent seizures, have been recommended as potentially useful tools. Furthermore, genetic rodent models of epileptogenesis are increasingly used in assessing antiepileptogenic treatments. Two approaches have been used in these different model categories: screening of clinically established antiepileptic drugs (AEDs) for antiepileptogenic or disease-modifying potential, and targeting the key causal mechanisms that underlie epileptogenesis. The first approach indicated that among various AEDs, topiramate, levetiracetam, carisbamate, and valproate may be the most promising. On the basis of these experimental findings, two ongoing clinical trials will address the antiepileptogenic potential of topiramate and levetiracetam in patients with traumatic brain injury, hopefully translating laboratory discoveries into successful therapies. The second approach has highlighted neurodegeneration, inflammation and up-regulation of immune responses, and neuronal hyperexcitability as potential targets for antiepileptogenesis or disease modification. This article reviews these areas of progress and discusses the challenges associated with discovery of antiepileptogenic therapies.
多种脑部损伤,包括创伤性脑损伤、中风、感染、肿瘤、神经退行性疾病和持续性急性症状性癫痫发作,如复杂热性惊厥或癫痫持续状态(SE),可诱导“癫痫发生”,即正常脑组织转变为能够产生自发性反复发作的组织的过程。此外,癫痫发生也存在于隐源性癫痫的病因中。鉴于关于癫痫发生的细胞和分子机制的信息不断积累,应该有可能在癫痫发作发作之前干预这一过程,从而防止处于风险中的患者发生癫痫,或提高更好的长期预后的潜力,这构成了主要的临床需求。为了确定预防、中断或逆转有风险的人群中的癫痫发生过程的药物干预措施,已推荐两种动物模型组,即点燃和 SE 诱导的复发性癫痫发作,作为潜在有用的工具。此外,癫痫发生的遗传啮齿动物模型越来越多地用于评估抗癫痫发生治疗。这两种方法已用于不同的模型类别:筛选临床上已确立的抗癫痫药物(AEDs)的抗癫痫发生或疾病修饰潜力,以及针对癫痫发生的关键因果机制。第一种方法表明,在各种 AEDs 中,托吡酯、左乙拉西坦、卡马西平和丙戊酸可能最有希望。基于这些实验发现,两项正在进行的临床试验将研究托吡酯和左乙拉西坦在创伤性脑损伤患者中的抗癫痫发生潜力,希望将实验室发现转化为成功的治疗方法。第二种方法强调了神经退行性变、炎症和免疫反应上调以及神经元过度兴奋作为抗癫痫发生或疾病修饰的潜在靶点。本文综述了这些领域的进展,并讨论了发现抗癫痫发生治疗方法所面临的挑战。