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作 者:王桂松[1] 张佳梦[1] 郭辉[1] 徐纪文[1] 罗其中[1]
出 处:《功能性和立体定向神经外科杂志》1998年第3期17-18,共2页
摘 要:目的:研究损伤性窒息致癫痫(EP)发生的神经细胞形态学改变,以探索EP发生的机制。方法:通过损伤性窒息EP的动物模型建立,观察损伤后EP发生率,神经细胞超微结构变化,海马神经元密度等分析与EP发作有关的神经细胞形态学改变及相互关系。结果:损伤性窒息后24小时后EP发生率为46.2%(P<0.05)。发作形式:主要为狂奔、全身性痉挛及局限性痉挛。神经细胞超微结构改变显示,除线粒体肿胀外,还有细胞固缩,胞浆浓缩,胞膜内陷,染色体呈块状集聚,细胞泡状改变及凋亡小体形成等凋亡特征。损伤后有EP发作比无EP发作者改变更为多见。海马CA1区神经元细胞密度分析显示,损伤性窒息可导致海马CA1区神经元密度减少(P<0.05)。结论:损伤性窒息引起脑损伤可诱发EP,而EP反复发作又加重神经细胞损害的程度和范围,两者互为因果,提示中断初始的EP发作。The purpose of the study is to research the mechanism of epilepsy after traumatic asphyxia. Methods: The epilepsy was induced by traumatic asphyxia. The rate of epilepsy was counted, the neuronal ultramicrostructure was observed by electronic microscopy and the neuronal densities was analyzed by computer. Results: The rate of epilepsy after 24hr post asphyxia was 46.2% ( P<0.05 ). The electronic microscopy observation showed characteristic as followed: chromatin densation and marginizationl cell shrinkage, nuclear framentation. apoptotic bodies formation etc. The neuronal densities analysis showed that ND decreased in asphyxia with epilepsy ( P<0.05 ). Conclusion: These results indicated that asphyxia induced epilepsy and epilepsy increased the neuronal deficits.
分 类 号:R742.102[医药卫生—神经病学与精神病学]
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