Department of Neurology, Acibadem University School of Medicine, Istanbul, Turkey.
Epileptic Disord. 2011 Dec;13(4):446-51. doi: 10.1684/epd.2011.0472.
Prolonged status epilepticus may directly cause selective neuronal necrosis due to excitotoxic mechanisms, as observed in experimental models and described in case reports. A 36-year-old woman presented with right hemiplegia and aphasia following a generalised tonic-clonic status epilepticus of two hours duration. Accompanying serial MRI with advanced imaging techniques, EEG and histopathology of the cortical tissue of the patient were all compatible with excitotoxic neuronal necrosis. In this histopathologically-proven rare case of status epilepticus-induced excitotoxic neuronal injury, the observation of delayed cortical laminar necrosis on MRI, together with paroxysmal lateralised epileptiform discharges on the EEG, suggests that these changes may be an early sign of impending and ongoing excitotoxic neuronal injury and delayed cell death caused by glutamate release due to excessive neuronal firing in status epilepticus.
持续性癫痫持续状态可能通过兴奋性毒性机制直接导致选择性神经元坏死，这在实验模型中观察到，并在病例报告中描述。一位 36 岁女性在全身性强直-阵挛性癫痫持续状态持续两小时后出现右侧偏瘫和失语。伴随连续的 MRI 和高级成像技术、患者皮质组织的 EEG 和组织病理学均与兴奋性毒性神经元坏死相符。在这个经组织病理学证实的罕见癫痫持续状态引起的兴奋性毒性神经元损伤病例中，MRI 上观察到皮质层状坏死延迟，EEG 上出现阵发性偏侧癫痫样放电，提示这些变化可能是癫痫持续状态中过度神经元放电导致谷氨酸释放引起的即将发生和正在进行的兴奋性毒性神经元损伤和延迟性细胞死亡的早期征象。
