Blümcke I, Beck H, Lie A A, Wiestler O D
Department of Neuropathology, University of Bonn Medical Center, Germany.
Epilepsy Res. 1999 Sep;36(2-3):205-23. doi: 10.1016/s0920-1211(99)00052-2.
With the recent progress in surgical treatment modalities, human brain tissue from patients with intractable focal epilepsies will increasingly become available for studies on the molecular pathology, electrophysiological changes and pathogenesis of human focal epilepsies. An inherent problem for studies on human temporal lobe epilepsy (TLE) is the lack of suitable controls. Strategies to alleviate this obstacle include the use of human post mortem samples, hippocampus from experimental animals and, in particular, the comparative analysis of surgical specimens from patients with Ammon's horn sclerosis (AHS) and with focal temporal lesions but anatomically preserved hippocampal structures. In this review we focus on selected aspects of the molecular neuropathology of TLE: (1) the potential impact of persisting calretinin-immunoreactive neurons with Cajal-Retzius cell morphology, (2) astrocytic tenascin-C induction and redistribution as potential regulator of aberrant axonal sprouting and (3) alterations of Ca2+ -mediated hippocampal signalling pathways. The diverse and complex changes described so far in human TLE specimens require a systematic interdisciplinary approach to distinguish primary, epileptogenic alterations and secondary, compensatory mechanisms in the pathogenesis of human temporal lobe epilepsies.
随着外科治疗方式的最新进展，来自难治性局灶性癫痫患者的人脑组织将越来越多地用于人类局灶性癫痫的分子病理学、电生理变化及发病机制的研究。人类颞叶癫痫（TLE）研究中一个固有的问题是缺乏合适的对照。缓解这一障碍的策略包括使用人类尸检样本、实验动物的海马体，特别是对患有海马硬化（AHS）和局灶性颞叶病变但海马结构在解剖学上保存完好的患者的手术标本进行比较分析。在这篇综述中，我们聚焦于TLE分子神经病理学的某些方面：（1）具有 Cajal-Retzius 细胞形态的持续钙视网膜蛋白免疫反应性神经元的潜在影响；（2）星形细胞腱生蛋白-C 的诱导和重新分布作为异常轴突发芽的潜在调节因子；（3）Ca2+ 介导的海马信号通路的改变。迄今为止，在人类 TLE 标本中描述的多样而复杂的变化需要一种系统的跨学科方法，以区分人类颞叶癫痫发病机制中的原发性致痫改变和继发性代偿机制。
