Kumada S, Hayashi M, Umitsu R, Arai N, Nagata J, Kurata K, Morimatsu Y
Department of Pediatrics, Musashino Red Cross Hospital, Tokyo, Japan.
Acta Neuropathol. 1997 Jul;94(1):36-41. doi: 10.1007/s004010050669.
The dentate nucleus was examined histologically and immunohistochemically in 47 cases of nonprogressive developmental disorders. Neuronal loss and/or atrophy was observed in 13 cases, while mild neuronal lesions, characterized by dendritic swelling and/or the appearance of eosinophilic materials around the neurons, were exhibited in 20 cases. The former change was accompanied by diffuse central nervous system involvement, and the etiology was perinatal hypoxic ischemic encephalopathy, acute encephalopathy, and meningoencephalitis in most cases. On the other hand, most of the patients with kernicterus showed the latter change. Immunohistochemically, the mild neuronal lesions mimicking grumose, degeneration, described in some neurodegenerative diseases, seemed to reflect the changes of Purkinje cell terminals. It is suggested that secondary structural alteration of the dentate neurons in the absence of severe atrophy can occur in nonprogressive developmental disorders.
对47例非进行性发育障碍患者的齿状核进行了组织学和免疫组织化学检查。13例观察到神经元丢失和/或萎缩,20例表现为轻度神经元病变,其特征为树突肿胀和/或神经元周围出现嗜酸性物质。前一种变化伴有弥漫性中枢神经系统受累,大多数病例的病因是围产期缺氧缺血性脑病、急性脑病和脑膜脑炎。另一方面,大多数核黄疸患者表现出后一种变化。免疫组织化学显示,模仿某些神经退行性疾病中描述的颗粒状变性的轻度神经元病变,似乎反映了浦肯野细胞终末的变化。提示在非进行性发育障碍中,在无严重萎缩的情况下齿状神经元可发生继发性结构改变。