Dudek F E, Spitz M
Department of Anatomy and Neurobiology, Colorado State University, Fort Collins 80523, USA.
J Clin Neurophysiol. 1997 Mar;14(2):90-101. doi: 10.1097/00004691-199703000-00002.
This review article evaluates the hypothetical cellular mechanisms responsible for chronic lesion-induced epilepsy. Emphasis is given to particular clinical characteristics of secondary epileptogenesis: (a) a temporal latency, (b) the involvement of distant but related sites, and (c) irreversibility. Although loss of GABAergic inhibitory interneurons or increased excitatory input to these interneurons may contribute to epileptogenesis, several studies have provided evidence that inhibition is not depressed in epileptogenic regions and may actually be enhanced. Axonal sprouting, synaptic reorganization, and formation of new recurrent excitatory circuits have been proposed to account for the increased seizure susceptibility of temporal lobe epilepsy. Recent data support the hypothesis that local inhibitory circuits mask the multisynaptic excitatory interactions that are associated with mossy fiber sprouting in the dentate gyrus and that physiological mechanisms that reduce inhibition or increase excitability unmask the new recurrent excitatory circuits responsible for seizures. A hypothesis based on axonal sprouting and synaptic reorganization can account for the essential clinical characteristics of secondary epileptogenesis and may have widespread applicability to the general phenomenon of lesion-induced epilepsy.
这篇综述文章评估了导致慢性损伤性癫痫的假设性细胞机制。重点关注继发性癫痫发生的特定临床特征：(a) 时间潜伏期，(b) 远处但相关部位的累及，以及 (c) 不可逆性。虽然GABA能抑制性中间神经元的丧失或这些中间神经元兴奋性输入的增加可能导致癫痫发生，但多项研究已提供证据表明，癫痫发生区域的抑制作用并未降低，实际上可能增强。轴突发芽、突触重组以及新的反复性兴奋性回路的形成已被提出用于解释颞叶癫痫发作易感性的增加。最近的数据支持这样一种假设，即局部抑制性回路掩盖了与齿状回苔藓纤维发芽相关的多突触兴奋性相互作用，并且降低抑制或增加兴奋性的生理机制会揭示出导致癫痫发作的新的反复性兴奋性回路。基于轴突发芽和突触重组的假设可以解释继发性癫痫发生的基本临床特征，并且可能广泛适用于损伤性癫痫的一般现象。
