Pitkänen Asla, Immonen Riikka
Epilepsy Research Laboratory, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, PO Box 1627, FIN-70211, Kuopio, Finland,
Neurotherapeutics. 2014 Apr;11(2):286-96. doi: 10.1007/s13311-014-0260-7.
Post-traumatic epilepsy accounts for 10-20% of symptomatic epilepsy in the general population and 5% of all epilepsy. During the last decade, an increasing number of laboratories have investigated the molecular and cellular mechanisms of post-traumatic epileptogenesis in experimental models. However, identification of critical molecular, cellular, and network mechanisms that would be specific for post-traumatic epileptogenesis remains a challenge. Despite of that, 7 of 9 proof-of-concept antiepileptogenesis studies have demonstrated some effect on seizure susceptibility after experimental traumatic brain injury, even though none of them has progressed to clinic. Moreover, there has been some promise that new clinically translatable imaging approaches can identify biomarkers for post-traumatic epileptogenesis. Even though the progress in combating post-traumatic epileptogenesis happens in small steps, recent discoveries kindle hope for identification of treatment strategies to prevent post-traumatic epilepsy in at-risk patients.
创伤后癫痫在普通人群的症状性癫痫中占10%-20%,在所有癫痫中占5%。在过去十年中,越来越多的实验室在实验模型中研究了创伤后癫痫发生的分子和细胞机制。然而,确定创伤后癫痫发生所特有的关键分子、细胞和网络机制仍然是一项挑战。尽管如此,9项概念验证性抗癫痫发生研究中有7项已证明对实验性创伤性脑损伤后的癫痫易感性有一定影响,尽管它们都尚未进入临床阶段。此外,有迹象表明新的可临床转化的成像方法能够识别创伤后癫痫发生的生物标志物。尽管在对抗创伤后癫痫发生方面进展缓慢,但最近的发现为确定预防高危患者创伤后癫痫的治疗策略带来了希望。