Division of Fundamental Neurobiology, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada M5T 2S8.
Cereb Cortex. 2011 Dec;21(12):2863-75. doi: 10.1093/cercor/bhr080. Epub 2011 Apr 29.
Postischemic seizures are associated with worsened outcome following stroke, but the underlying pathophysiology is poorly understood. Here we examined acute seizures in adult mice following hypoxia-ischemia (HI) via combined behavioral, electrophysiological, and histological assessments. C57BL/6 mice aged 4-9 months received a permanent occlusion of the right common carotid artery and then underwent a systemic hypoxic episode. Generalized motor seizures were observed within 72 h following HI. These seizures occurred nearly exclusively in animals with extensive brain injury in the hemisphere ipsilateral to the carotid occlusion, but their generation was not associated with electroencephalographic discharges in bilateral hippocampal and neocortical recordings. Animals exhibiting these seizures had a high rate of mortality, and post-HI treatments with diazepam and phenytoin greatly suppressed these behavioral seizures and improved post-HI animal survival. Based on these data, we conclude that these seizures are a consequence of HI brain injury, contribute to worsened outcome following HI, and that they originate from deep subcortical structures.
缺血后发作与中风后预后恶化有关，但发病的病理生理学机制尚不清楚。在这里，我们通过行为学、电生理学和组织学评估，研究了成年小鼠缺氧缺血（HI）后的急性发作。4-9 月龄的 C57BL/6 小鼠接受右侧颈总动脉永久性闭塞，然后进行全身缺氧发作。HI 后 72 小时内观察到全身性运动性发作。这些发作几乎仅发生在与颈动脉闭塞同侧半球有广泛脑损伤的动物中，但它们的产生与双侧海马和新皮层记录中的脑电图放电无关。出现这些发作的动物死亡率很高，HI 后用地西泮和苯妥英钠治疗可显著抑制这些行为性发作，并提高 HI 后动物的存活率。基于这些数据，我们得出结论，这些发作是 HI 脑损伤的结果，会加重 HI 后的不良预后，并且它们起源于深部皮质下结构。
