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作者提出构成癫痫的电释放可能是直接作用在突触处介质受体(假定是抑制性的)上的自体免疫反应的结果。根据重症肌无力产生的机理来推论,这将会减低突触传递。这种免疫学反应可由各种组织损伤时出现的抗元所激发,或为感染因子所激发。临床证据临床有关癫痫免疫学的研究极少,故谈不上支持或反对癫痫发生的免疫学基础。然而,大多数类型的癫痫伴有组织损害。Scheibel等应用高尔基染色法研究颞叶癫痫的脑组织标本,否定其病理改变是由于任何进行性血管性障碍,而赞成为一种瘢痕化
The authors suggest that the electrical release that constitutes epilepsy may be the result of an autoimmune response that acts directly on the synaptic mediator receptors (supposedly inhibitory). According to the mechanism of myasthenia gravis to infer that this will reduce the synaptic transmission. This immunological reaction can be triggered by anti-idiotingens that occur at various tissue lesions or by infectious agents. Clinical evidence Clinical research on epilepsy immunology very few, it is far from to support or oppose the immunological basis of epilepsy. However, most types of epilepsy are associated with tissue damage. Scheibel and other applications of Golgi staining of temporal lobe epilepsy brain tissue specimens, denied the pathological changes due to any progressive vascular disorders, and is in favor of a scarring