慢性电刺激诱发大鼠癫痫模型中核磁共振检测信号异常的非对称性与特征性行为发作的关系

本文旨在探讨内嗅皮质（EC）－海马环路在颞叶癫痫发生中的作用,慢性强直电刺激大鼠石背海马（DH－PC）或右中部颞叶新皮质（MTNC）,每日一次（60Hz,2s,0.4-0.6mA),加续7－10d,刺激DHPC（57.4%,8/14只）或MTNC（71．42％,10／14只）均能引起电极对侧出现非对称性脑区核磁共振（T2－WI）信号增强,组织学切片证实与扩大的侧脑室吻合,可能涉及脑帝质结构的损伤,DHPC刺激组大鼠对侧脑扣内务 伴有高频原发性湿狗样抖（WEDS）,MTNC刺激组大鼠对侧脑损伤伴有低频原发性WEDS,后者在第2个刺激日开始出现,持续到第10天以后,所有假电极组无脑区T2-WI稚号和行为改变,我们推测,刺激HPC或MTNC所致癫痫性早期脑损伤具有同一种机制,涉及EC－HPC环路,刺激MTNC时,可能由于EC潜在门控作用,削弱了进出EC－HPC环路通往新皮质的信息流,致使脑损伤明显时行为发作频度低,另外,非对称非脑扣内务 提示了颞叶癫痫的致痫灶的对侧易感特征。

Characteristic behavioral seizures and abnormal signal asymmetry of magnetic resonance imaging in an electrogenic rat model of chronic epilepsy

Chronic tetani (60 Hz, 2 s, 0.4-0.6 mA) were administered to the dorsal hippocampua (DHPC) or the medial temporal lobe neocortex (MTNC) of rats, to study the role of the entorhinal cortex (EC)-hippocampal loop in temporal lobe epilepto-genesis. This was repeated once a day for 7 or 10 days. Magnification of hyper-intensity was induced by tetanization of the HPC or the MTNC, as detected by contralateral T2 weighted magnetic resonance imaging (T2-WI). The effects were associated with an en-larged volume of the lateral ventricle (LV), which was verified histologically. T2-WI hyper-intensities, contralateral to the tetanized hemispheres, were observed with high frequency primary wet dog shakes (WEDS) in the DHPC-stimulated rats and with low fre-quency WEDS in the MTNC-stimulated rats. It seems likely that the same neural mechanisms are shared by chronic tetanization of the tight HPC and the tight MTNC, involving the closed EC-HPC loop. Poor correelation between contralateral T2-WI hyper-intensi-ties and light primary behavioral seizures in the MTNC-stimulated rats might be attributed to a controlled information flow into or out of this loop because of potential EC gating In addition, asymmetric T2-WI hyper-intensities in the LV area reflected a hemispheric dependence, contralateral to the electrogenic focus in our model of rat epilepsy.