Barlow R M
Vet Pathol. 1981 Mar;18(2):151-62. doi: 10.1177/030098588101800202.
Cerebellar lesions develop in a heritable disorder characterized by recurrent episodic seizures in newborn and young calves and by ataxia in survivors of several bouts of convulsions. Earliest changes were altered patterns of phosphatase reaction products in Purkinje cells. Purkinje cells axons in the outer half of the granular layer developed fusiform or spheroidal argyrophilic swellings. Early lesions were restricted to the lingula and uvula, but cases with more persistent clinical disease involved other parts of the vermis. In ataxic calves these lesions were also in the cerebellar hemispheres. The axonal swellings showed proliferation of tubulovesicular endoplasmic reticulum, neurofibrils and mitochondria. In other swellings axoplasm was degenerate, and in some it resembled Purkinje cell cytoplasm. In some clinically normal adult transmitters of the disorder, light microscopy showed some similar swellings, but most calves that recovered had no lesions.
小脑病变发生于一种遗传性疾病,其特征为新生和幼年犊牛反复出现发作性癫痫,以及经历多次惊厥发作的存活者出现共济失调。最早的变化是浦肯野细胞中磷酸酶反应产物的模式改变。颗粒层外半部的浦肯野细胞轴突出现梭形或球形嗜银性肿胀。早期病变局限于舌叶和蚓垂,但临床疾病持续时间较长的病例涉及蚓部的其他部位。在共济失调的犊牛中,这些病变也见于小脑半球。轴突肿胀显示出管状小泡内质网、神经原纤维和线粒体的增殖。在其他肿胀中,轴浆发生退化,在一些情况下类似于浦肯野细胞的细胞质。在该疾病的一些临床正常的成年传播者中,光学显微镜检查显示出一些类似的肿胀,但大多数恢复的犊牛没有病变。