Baldy-Moulinier M, Crespel A
Service explorations neurologiques et épileptologie, hôpital Gui-de-Chauliac, 34295 Montpellier, France.
Ann Fr Anesth Reanim. 2001 Feb;20(2):97-107. doi: 10.1016/s0750-7658(00)00280-x.
Primary and secondary epileptogenesis involves multiple genetic and acquired factors. Epileptogenesis is a complex result of combined factors including membrane factors, neurotransmitter and environmental factors. Ion channel-related diseases, GABA and glutamate dysfunction, and glial reaction intervene in different epileptic conditions. The understanding of the mechanisms which emphasize initiation and maintenance of status epilepticus (SE) are in progress. Prognosis of SE is related to the duration of epileptic activity and to the acute cerebral and systemic consequences. Delayed cellular and molecular alterations after SE are responsible for secondary epileptogenesis. Glutamate receptor activation is the main key point leading to an excessive intraneuronal accumulation of ionic calcium by which a cascade of reactions is induced. Apoptotic neuronal death, glial reaction axonal sprouting and neurogenesis contribute to a state of hyperexcitability and hypersynchrony. A better understanding of underlying mechanisms of epileptogenesis may serve the development of new drugs with both anticonvulsant and antiepileptic (prevention or neuroprotection) actions.
原发性和继发性癫痫发生涉及多种遗传和后天因素。癫痫发生是包括膜因素、神经递质和环境因素在内的多种因素共同作用的复杂结果。离子通道相关疾病、γ-氨基丁酸（GABA）和谷氨酸功能障碍以及胶质细胞反应会干预不同的癫痫状况。目前正在深入了解强调癫痫持续状态（SE）起始和维持的机制。SE的预后与癫痫活动持续时间以及急性脑和全身后果有关。SE后延迟出现的细胞和分子改变是继发性癫痫发生的原因。谷氨酸受体激活是导致细胞内离子钙过度蓄积的主要关键点，由此引发一系列反应。凋亡性神经元死亡、胶质细胞反应、轴突发芽和神经发生导致了过度兴奋和高度同步化状态。更好地理解癫痫发生的潜在机制可能有助于开发具有抗惊厥和抗癫痫（预防或神经保护）作用的新药。
