摘要
目的:癫痫能导致神经元的损伤,并增加其后癫痫发作的危险性。分析癫痫发作后神经元损伤的可能机制,以期为预防及减轻癫痫发作后脑损伤提供理论依据。资料来源:应用计算机检索PubMed数据库1995／2004-06相关文章,检索词为“epilepsy”“neuron damage”“necrosis”和“apoptosis”,分别组合进行检索,限定语言种类为英文。资料选择:对资料进行初审,选取包括癫痫及其发作后神经元损伤的有关人类及动物实验的文献,筛除其他非相关资料,对剩余的文献开始查找全文。资料提炼:共收集到14篇有关癫痫发作后神经元损伤的随机对照实验,4篇有关中枢神经元兴奋毒性损伤的非随机对照实验,另有3篇关于神经元损伤的相关文献。共21篇文献,全部符合入选标准。资料综合:14个随机对照实验均选用化学点燃或电点燃的方法诱导癫痫模型,观测指标包括神经元及细胞器超微结构的改变及凋亡相关因子的表达变化。4篇非随机对照实验采用中枢神经元其他缺血缺氧模型,用电镜直接观察不同损伤形式的神经元中不同凋亡因子的表达,为中枢神经元的兴奋毒性损伤的机制提供直接依据。另3篇相关文献介绍了神经元损伤的途径和损伤相关因子的表达。结论:癫痫发作后神经元的死亡形式与损伤的强度和线粒体的功能状态有关,线粒体构成了神经元存亡的控制中心。细胞色素C的释放和半胱氨酸天冬氨酸蛋白酶的激活是神经元损伤的最后共同通路。
OBJECTIVE： Epileptic attack can cause neuronal damage and increase the risk of potential seizure. Analysis of the possible mechanism of neuronal damage following epileptic seizure may provide evidences for implementing preventive measures against brain damage due to epileptic seizures.DATA SOURCES： A computer-based search of the related publications in PubMed database between June 1995 and June 2004 with different combinations of the key words of “epilepsy”, “neuron damage”, “necrosis”and “apoptosis”, limiting the results to the language of English.STUDY SELECTION： The retrieved articles were examined at first to select reports of experimental study on human and animals related to epilepsy and the subsequent neuronal damages, and their full-text publications were obtained with the other unrelated articles excluded.DATA EXTRACTION： Eighteen articles documenting randomized controlled experiment immediately related to neuronal damage after epilepsy seizure, 4 reporting non-randomized controlled experiments related to central neuronal excitatory toxic damage, and 3 concerning neuronal damage were collected for this review.DATA SYNTHESIS： In the 14 randomized controlled experiments, chemical or electric methods were used to induce epilepsy in the animal models in which the ultrastructural changes of the neurons and cell organelles were observed and the expression of apoptosis-related factors determined.In the 4 non-randomized controlled experiments, central neuronal ischemic and hypoxic models were adopted for observing the expression of various apoptotic factors in the neurons due to different damages with the assistance of electron microscope, to provide direct evidences for the mechanism of central neuronal excitatory toxic damage. The other three related literatures introduced the pathways of neuronal damages and the expression of the related factors.CONCLUSION： Neuronal death after epileptic seizure is correlated with the severity of the damage and mitochondrial functional status, and the mitochondria constitute the control center for neuronal survival. The release of cytochrome C and the activation of caspases are the final common pathway of neuronal damage.
出处
《中国临床康复》
CSCD
北大核心
2005年第41期187-189,共3页
Chinese Journal of Clinical Rehabilitation
