Department of Neurology and Psychiatry, Saint Louis University School of Medicine, St. Louis, MO.
Epilepsy Curr. 2012 May;12(3):87-91. doi: 10.5698/1535-7511-12.3.87.
Text of Abstract Liability to develop posttraumatic epilepsy (PTE) correlates in a general way with trauma dose. While contusion of the brain produces an admixture of extravasated blood, edema fluid and necrotic tissue at the site of skull trauma and in regions remote from the direct force, an unpredictable cascade of shearing injury, torsion and rotation and a myriad of physiological changes occur in structures subject to the mechanical pressure wave. Animal models mimic components of injury, some more thoroughly than others. Designing a treatment that is a prophylaxis for the development of PTE awaits understanding the mechanisms of epileptogenesis initiated by trauma.
摘要
外伤性癫痫(PTE)的发病风险通常与创伤剂量相关。脑挫伤会在颅骨创伤部位和远离直接作用力的区域产生混合性的外渗血液、水肿液和坏死组织,而在受机械压力波影响的结构中,会发生一系列不可预测的剪切损伤、扭曲和旋转以及无数的生理变化。动物模型可以模拟部分损伤成分,有些则更为完整。设计一种预防外伤性癫痫发生的治疗方法,需要先了解创伤引发癫痫发生的机制。