Status Epilepticus‐induced Neuronal Injury and Network Reorganization
Status Epilepticus‐induced Neuronal Injury and Network Reorganization
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DOI：
10.1111/j.1528-1157.1999.tb00876.x
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发表时间：
1999-01
期刊：
影响因子：
5.6
通讯作者：
R. S. Sloviter
中科院分区：
文献类型：
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作者：
R. S. Sloviter
现在很明显，儿童时期的长时间热性惊厥或任何年龄的癫痫持续状态发作都会产生海马细胞丢失和萎缩的高度特征性模式，这种模式在患者以后发展为颞叶癫痫时会出现。癫痫引起的病理学可能是兴奋性毒性病理，包括神经元丢失、反应性神经胶质增生、存活细胞的异常突触重组以及可能改变细胞外空间并影响离子稳态的海马组织收缩。长时间兴奋的这些病理效应是否在最终导致自发性无热惊厥的致痫过程中发挥因果作用仍然是人们强烈关注的主题。有人提出了两种假设来解释癫痫发作引起的神经元丢失如何引发癫痫过程。一种假设表明，正常的抑制和兴奋性是由脆弱的非主细胞维持的，它们的丧失会使抑制性神经元失活，导致主细胞去抑制和过度兴奋。另一种假设认为，最初的损失是对通常不连接的主细胞的刺激，以形成异常的周期性兴奋性连接。其他影响无疑包括逐渐克服多突触抑制的“点燃”过程，以及可能促进突触和突触去极化的细胞外空间变化。癫痫发生的可疑基质的鉴定将刺激未来的进展，并为新的实验设计提供方向。
It is now evident that prolonged febrile seizures in childhood, or an episode of status epilepticus at any age, can produce the highly characteristic pattern of hippocampal cell loss and shrinkage that is seen later in life, when patients develop temporal lobe epilepsy. Seizure‐induced and presumably excitotoxic pathology includes neuronal loss, reactive gliosis, aberrant synaptic reorganization of surviving cells, and hippocampal tissue shrinkage that may alter extracellular space and affect ionic homeostasis. Whether any of these pathological effects of prolonged excitation play a causal role in the epileptogenic process that ultimately leads to spontaneous afebrile seizures remains a subject of intense interest. Two hypotheses have been suggested to explain how seizure‐induced neuronal loss might initiate the epileptogenic process. One hypothesis suggests that normal inhibition and excitability is maintained by vulnerable non‐principal cells, and that their loss deactivates inhibitory neurons, rendering principal cells disinhibited and hyperexcitable. The other hypothesis regards the initial loss as a stimulus for normally unconnected principal cells to form aberrant recurrent excitatory connections. Additional influences undoubtedly include a “kindling” process that gradually overcomes polysynaptic inhibition, and changes in extracellular space that may facilitate synaptic and ephaptic depolarization. Identification of the suspected substrates of epileptogenesis will serve as a stimulus for future progress and provide direction for new experimental designs.