Del Campo Martin, Abdelmalik Peter A, Wu Chi Ping, Carlen Peter L, Zhang Liang
Department of Neurology, Toronto Western Hospital, Toronto, Ontario, Canada.
Epilepsy Res. 2009 Feb;83(2-3):243-8. doi: 10.1016/j.eplepsyres.2008.11.012. Epub 2009 Jan 10.
The neuropathology of hypoglycemia and its mechanisms have been well studied. However, the physiopathogenesis of hypoglycemia-related seizures has escaped elucidation. Various animal models reportedly show "seizures" when rendered hypoglycemic, however, correlation with the electroencephalogram (EEG) is inconsistent. In order to characterize the role of the hippocampus and frontal neocortex in the generation of hypoglycemic seizures, this study was undertaken.
Adult rats were implanted stereotaxically with electrodes in the left hippocampus and right frontal cortex. After 1 week, they were fasted 18-24h, then injected intraperitoneally with insulin, 35 IU/kg. Simultaneous EEG/video monitoring was conducted.
Interpretable EEG recordings were obtained in 8/12 animals. Two showed poor association of seizure-like behaviour (neck extension, vocalizations, tonic extension of the tail, digging or running limb movements) with ictal EEG patterns. Four animals exhibited such behaviours during periods of high amplitude polymorphic slow wave activity, burst-suppression patterns or non-rhythmic spiking. Two others were encephalopathic (behaviourally and electroencephalographically) until death.
Not all animals develop seizure-like behaviour when hypoglycemic. If these are seizures, they may originate from subcortical structures, or the "convulsive" behaviours observed may simply be flight/fight reflexes released during profound encephalopathy. Spike activity in the EEG may be a manifestation of this state. Recording EEG from rat cortex and hippocampus during seizure-like activity brought on by hypoglycemia correlates poorly with seizure-like behaviours suggesting that the relevant electrophysiological correlates, if present, are generated from deeper brain structures.
低血糖的神经病理学及其机制已得到充分研究。然而，低血糖相关癫痫发作的生理发病机制仍未阐明。据报道，各种动物模型在出现低血糖时会表现出“癫痫发作”，但其与脑电图（EEG）的相关性并不一致。为了明确海马体和额叶新皮质在低血糖性癫痫发作产生中的作用，开展了本研究。
成年大鼠通过立体定位在左侧海马体和右侧额叶皮质植入电极。1周后，禁食18 - 24小时，然后腹腔注射胰岛素，剂量为35 IU/kg。同时进行脑电图/视频监测。
12只动物中有8只获得了可解释的脑电图记录。其中2只动物的癫痫样行为（颈部伸展、发声、尾巴强直性伸展、挖掘或奔跑肢体运动）与发作期脑电图模式的关联性较差。4只动物在高振幅多形性慢波活动、爆发抑制模式或非节律性棘波期间出现此类行为。另外2只动物直至死亡时均存在脑病表现（行为和脑电图方面）。
并非所有动物在低血糖时都会出现癫痫样行为。如果这些是癫痫发作，它们可能起源于皮质下结构，或者观察到的“惊厥”行为可能仅仅是在严重脑病期间释放的逃跑/战斗反射。脑电图中的棘波活动可能是这种状态的一种表现。在低血糖引发的癫痫样活动期间记录大鼠皮质和海马体的脑电图，与癫痫样行为的相关性较差，这表明相关的电生理相关性（如果存在的话）是由更深层的脑结构产生的。
