Babb T L, Brown W J
Adv Neurol. 1986;44:949-66.
Partial complex seizures are known to arise from abnormal firing of neurons in cortex that has histologic abnormalities associated with tumors, infarcts, or neuron loss. The latter pathology of sclerosis is most frequently found in the hippocampus, and partial seizures from this region are focalized by direct electrical recordings and treated by anterior temporal lobectomy. Although we can link this hippocampal sclerosis to nearby hyperexcitability, the synaptic mechanisms involved in hippocampal seizure genesis are not yet known. We have used in vivo microelectrode recordings from hippocampal neurons and found rare instances of anomalous bursting patterns as well as coupled firing. Postinhibitory "rebound excitation" has also been recorded, supporting the concept that synchronized hippocampal outputs are important for seizure genesis. Immunocytochemistry of GAD-positive inhibitory interneurons indicates no significant loss in inhibition in the sclerotic hippocampus and a normal number of inhibitory interneurons in its output target, the presubiculum. The presubiculum, with its multi-layered cortex, may amplify and propagate seizures to other cortices. Golgi and electron microscopy of epileptic neurons have shown pre- and postsynaptic alterations that may contribute to seizure genesis. Finally, ultrastructural analysis of capillaries in sclerotic hippocampus indicates deficient plasma-tissue transport that may contribute to cell loss or may alter neuronal excitability.
已知部分性癫痫发作源于皮质中神经元的异常放电，该皮质存在与肿瘤、梗死或神经元丢失相关的组织学异常。后者的硬化病理最常见于海马体，来自该区域的部分性癫痫发作可通过直接电记录定位，并通过前颞叶切除术进行治疗。尽管我们可以将这种海马硬化与附近的过度兴奋联系起来，但海马癫痫发作发生的突触机制尚不清楚。我们使用海马神经元的体内微电极记录，发现了罕见的异常爆发模式以及耦合放电的情况。还记录到了抑制后“反弹兴奋”，支持了同步海马输出对癫痫发作发生很重要的概念。GAD阳性抑制性中间神经元的免疫细胞化学表明，硬化海马体中的抑制没有明显丧失，其输出靶点前下托中的抑制性中间神经元数量正常。具有多层皮质的前下托可能会将癫痫发作放大并传播到其他皮质。癫痫神经元的高尔基染色和电子显微镜检查显示了突触前和突触后的改变，这些改变可能有助于癫痫发作的发生。最后，硬化海马体中毛细血管的超微结构分析表明血浆-组织转运不足，这可能导致细胞丢失或改变神经元兴奋性。
