Park S H, Becker-Catania S, Gatti R A, Crandall B F, Emelin J K, Vinters H V
Department of Pathology and Laboratory Medicine, UCLA Medical Center, Los Angeles, CA 90095-1732, USA.
Acta Neuropathol. 1998 Oct;96(4):315-21. doi: 10.1007/s004010050900.
We report two sisters with congenital olivopontocerebellar atrophy, including immunohistochemical studies of autopsy brain tissue. Both cases showed microcephaly with disproportionately marked hypoplasia of the posterior fossa structures including pons, inferior olivary nuclei, and cerebellum. Microscopically, the pons was atrophic with near total loss of pontine nuclei and transverse pontocerebellar tracts (inferior and middle cerebellar peduncles). The medulla showed absent inferior olivary and arcuate nuclei. The cerebellum showed hypoplasia with rudimentary dentate nuclei, profound loss of Purkinje cells and external granule cell layer, a sparse internal granule cell layer of the entire dorsal vermis and the dorsal portions of the lateral folia, as well as markedly reduced underlying axon fibers in the white matter with marked astrogliosis. These features were highlighted by immunohistochemical study using antibodies against Purkinje cell epitopes, synaptophysin, neurofilament, glial fibrillary acidic protein, and tuberin. The cerebral hemispheres were unremarkable. Our cases are characterized by a pattern of diffuse posterior cerebellar involvement that has rarely been described in previous reports. An autosomal recessive pattern of inheritance is suggested. The abnormalities may result from antenatal degeneration or atrophy of neurons in the involved sites rather than hypoplasia or developmental arrest starting in the second and third month of late embryonic life.
我们报告了两例患有先天性橄榄脑桥小脑萎缩的姐妹病例,包括对尸检脑组织的免疫组织化学研究。两例均表现为小头畸形,后颅窝结构包括脑桥、下橄榄核和小脑发育不全,程度不成比例且较为明显。显微镜下,脑桥萎缩,脑桥核和脑桥横纤维束(小脑下脚和中脚)几乎完全缺失。延髓显示下橄榄核和弓状核缺如。小脑发育不全,齿状核发育不全,浦肯野细胞和外颗粒细胞层严重缺失,整个小脑蚓部背侧和外侧叶背侧的内颗粒细胞层稀疏,白质中潜在的轴突纤维明显减少,伴有明显的星形胶质细胞增生。使用针对浦肯野细胞表位、突触素、神经丝、胶质纤维酸性蛋白和结节性硬化蛋白的抗体进行免疫组织化学研究突出了这些特征。大脑半球无明显异常。我们的病例特征是弥漫性小脑后部受累模式,此前报道中很少描述。提示为常染色体隐性遗传模式。这些异常可能是由于受累部位神经元的产前变性或萎缩,而非胚胎晚期第二个和第三个月开始的发育不全或发育停滞所致。