Lewis Darrell V
Duke University Medical Center, Durham, North Carolina 27710, USA.
Epilepsia. 2005;46 Suppl 7:39-44. doi: 10.1111/j.1528-1167.2005.00306.x.
Mesial temporal sclerosis (MTS) is found in about two-thirds of patients with refractory temporal lobe epilepsy (TLE), and surgical removal of the sclerotic structures eliminates seizures in the majority of cases undergoing surgical resection. Although multiple factors have been implicated in the genesis of MTS, it is still unclear why some individuals are more likely to develop hippocampal sclerosis than others. Epileptologists have proposed that there must be at least two factors involved-an initial precipitating injury (IPI), such as a prolonged febrile seizure, CNS infection, or head trauma, and a second factor that increases vulnerability to neuronal injury. This has been termed the "two-hit hypothesis." Three of the many factors that could possibly heighten susceptibility to neuronal injury and MTS are discussed here. These are microdysgenesis, hippocampal dysgenesis, prior seizures, and genetic predisposition. We conclude that there is currently no compelling evidence to support a role for microdysgenesis in MTS. Hippocampal dysgenesis, on the other hand, may account for febrile seizures and possibly MTS in a small subpopulation of patients with TLE. Additional larger studies are needed to confirm these findings. Experimental evidence indicates that an epileptogenic hippocampus can result from prolonged febrile seizures in infant rats, even though these seizures do not cause MTS in the rat. It is not known if this pathophysiological sequence occurs in humans. Lastly, there appears to be a strong genetic component that predisposes some individuals to MTS, regardless of whether they experience an IPI.
内侧颞叶硬化（MTS）见于约三分之二的难治性颞叶癫痫（TLE）患者，手术切除硬化结构可使大多数接受手术切除的病例癫痫发作消失。尽管多种因素与MTS的发生有关，但仍不清楚为何有些人比其他人更容易发生海马硬化。癫痫学家提出，至少必须涉及两个因素——初始促发损伤（IPI），如长时间发热性惊厥、中枢神经系统感染或头部外伤，以及增加神经元损伤易感性的第二个因素。这被称为“两次打击假说”。这里讨论了众多可能增加神经元损伤易感性和MTS易感性的因素中的三个。这些因素是微小发育异常、海马发育异常、既往癫痫发作和遗传易感性。我们得出结论，目前没有令人信服的证据支持微小发育异常在MTS中起作用。另一方面，海马发育异常可能是一小部分TLE患者发热性惊厥以及可能的MTS的原因。需要更多更大规模的研究来证实这些发现。实验证据表明，即使长时间发热性惊厥不会在大鼠中导致MTS，但在幼鼠中可导致致痫性海马形成。尚不清楚这种病理生理过程是否发生在人类身上。最后，似乎存在强大的遗传因素，使一些个体易患MTS，无论他们是否经历过IPI。
