上海交通大学学报(医学版)

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癫持续状态后脑内神经元损伤的研究进展

王新林,耿 直   

  1. 上海交通大学附属第六人民医院神经内科, 上海 200233
  • 出版日期:2013-12-28 发布日期:2014-01-02
  • 通讯作者: 耿 直, 电子信箱: gengzhi1998@163.com。
  • 作者简介:王新林(1988—), 男, 硕士生; 电子信箱: 1988wangxinlin@163.com。

Advances of intracerebral neuron damage after status epilepticus

WANG Xin-lin, GENG Zhi   

  1. Department of Neurology,the Sixth People's Hospital, Shanghai Jiaotong University, Shanghai 200233
  • Online:2013-12-28 Published:2014-01-02

摘要:

癫持续状态(SE)后脑内神经元损伤的具体机制较为复杂。研究认为,SE引起脑内神经元发生一系列病理生理改变,如血脑屏障破坏、N-甲基-D-天冬氨酸(NMDA)受体活化、钙离子内流、脑内特异性酶类及炎症细胞因子释放等。这些变化可导致脑内神经元的变性、缺失和坏死。近年来,随着新技术和新理论的出现,SE后神经元损伤的机制有了一些新的研究进展,该文对其进行综述。

关键词: 癫持续状态, 血脑屏障, N-甲基-D-天冬氨酸受体, 神经元损伤

Abstract:

The specific mechanism of intracerebral neuron damage after status epilepticus was complicated. Studies suggested that status epilepticus could cause a series of physiopathologic changes in intracerebral neurons, such as the destruction of blood-brain barrier, the activation of N-methyl-D-aspartic acid (NMDA) receptors, calcium influx, brain-specific enzymes, and the release of inflammatory cytokines. These changes could lead to brain neuronal degeneration, loss and necrosis. The new studies on neurons damage after status epilepticus are reviewed in this article.

Key words: status epilepticus, blood-brain barrier, N-methyl-D-aspartic acid receptor, neuronal damage