Cendes F, Andermann F, Carpenter S, Zatorre R J, Cashman N R
Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada.
Ann Neurol. 1995 Jan;37(1):123-6. doi: 10.1002/ana.410370125.
We describe the development of temporal lobe epilepsy in an 84-year-old man who had suffered domoic acid intoxication. Following intoxication he had nausea, vomiting, confusion, and coma. Generalized convulsions and complex partial status epilepticus progressively developed. After 3 weeks he improved and was seizure free with severe residual memory deficit. Electroencephalograms initially showed periodic epileptiform discharges, later evolving to epileptic abnormalities over frontotemporal regions with diffuse slow waves. Eight months after the intoxication the electroencephalogram was normal. One year after the acute episode, complex partial seizures developed. Electroencephalograms showed epileptic discharges independently over both temporal lobes, with left-sided predominance. Magnetic resonance imaging revealed a hyperintense T2-weighted signal and atrophy of both hippocampi; a positron emission tomographic scan showed bitemporal decreased glucose metabolism. Pneumonia developed and the patient died 3 1/4 years after the intoxication. Autopsy disclosed severe bilateral hippocampal sclerosis. The seizures following acute domoic acid intoxication, the postmortem pathology, and the fact that temporal lobe epilepsy developed 1 year after intoxication indicate that the human hippocampus is also vulnerable to kainate receptor excitotoxicity, and provide strong evidence supporting the role of excitotoxic injury in epileptogenesis. This report provides a unique human parallel to, and validates the animal model of, kainate-induced epilepsy as an important tool for studying temporal lobe epilepsy.
我们描述了一名84岁男性在遭受软骨藻酸中毒后发生颞叶癫痫的情况。中毒后，他出现恶心、呕吐、意识模糊和昏迷。全身性惊厥和复杂部分性癫痫持续状态逐渐发展。3周后他有所好转，不再发作，但仍有严重的残余记忆缺陷。脑电图最初显示周期性癫痫样放电，后来发展为额颞叶区域的癫痫异常伴弥漫性慢波。中毒8个月后脑电图恢复正常。急性发作1年后，出现复杂部分性发作。脑电图显示双侧颞叶独立出现癫痫放电，左侧更为明显。磁共振成像显示双侧海马体T2加权信号增强和萎缩；正电子发射断层扫描显示双侧颞叶葡萄糖代谢降低。患者发生肺炎，在中毒3年零3个月后死亡。尸检发现严重的双侧海马硬化。急性软骨藻酸中毒后的癫痫发作、死后病理学检查，以及中毒1年后发生颞叶癫痫这一事实表明，人类海马体也易受海人藻酸受体兴奋性毒性的影响，并为兴奋性毒性损伤在癫痫发生中的作用提供了有力证据。本报告提供了一个独特的人类病例，与海人藻酸诱导的癫痫动物模型相似，并验证了该模型作为研究颞叶癫痫的重要工具的有效性。
