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。

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.