癫痫持续状态与脑损伤机制研究进展

Progress of the pathogenesis of status epilepticus and brain injury

癫痫持续状态（SE）的发病机制与脑损伤密切相关，已有试验证实钙／钙调素依赖性蛋白激酶2活性改变、氧化应激、神经免疫．内分泌网络失衡等因素不仅参与癫痫持续状态的机制，且能作为始动因素，参与神经元损伤。SE后脑组织急性缺血、缺氧，糖利用减少，神经元过度兴奋，N-甲基-D-天冬氨酸（NMDA）和非NMDA受体的活化，大量阳离子内流，除导致神经细胞急性坏死，同时还启动细胞凋亡相关基因的表达，引起细胞内的凋亡酶级联反应，导致细胞凋亡。目前研究发现死亡受体活化、线粒体损伤及内质网应激通路均介导SE后神经元凋亡信号的传导。

The pathogenesis of status epilepticus is closely associated with brain injury. Some animals experiments have proved that the activity of calcium / calmodulin-dependent protein kinase 2 （ CaM kinase Ⅱ ） , oxidative stress, and the imbalance of nervous immune-endocrine factors are not only involved in the mechanisms of status epilepticus, but also act as the initial factor in neuronal injury. The pathophysiological changes after SE, such as acute brain ischemia, hypoxia and the reduced glucose utilization, over-excited neurons, N-methyl-D- aspartate （NMDA） and non-NMDA receptor activated, a large amount of cation influx, can give rise to acute necrosis of neurons, also initiate the expression of apoptotic genes, at last leading to apoptosis by cell apoptotic enzymes cascade reaction. Studies have found that the pathway of death receptor activation, mitochondrial damage and endoplasmic reticulum stress mediated the neuronal apoptotic signal transduction after SE.