Takano T, Uno M, Yamano T, Shimada M
Department of Pediatrics, Shiga University of Medical Science, Ohtsu, Japan.
Acta Neuropathol. 1994;87(2):168-73. doi: 10.1007/BF00296187.
We sought to elucidate the pathogenesis of Chiari type I malformation using an experimental model of hydrocephalus produced by inoculating hamsters with mumps virus. Dilatation of the lateral ventricules was detected in all brains inoculated at 2, 10, and 25 days of age. The cerebellum in hamsters inoculated at 2 and 10 days of age showed elongation and flattening of the vermis and protrusion or notching of the uvula. All layers, i.e., the molecular, Purkinje cell, and granular layers, and the white matter were preserved, but had become narrow. Purkinje cells remained normal. Hamsters inoculated at 25 days of age did not develop the cerebellar deformity. Mumps virus antigen was detected in all ependymal cells and in some epithelial cells of the choroid plexus in all hamsters that had been inoculated at 2, 10, or 25 days of age. Results suggest that Chiari type I malformation is caused by two main factors occurring simultaneously, i.e., increasing intracranial pressure and rapid histogenesis of the cerebellar cortex.
我们试图通过给仓鼠接种腮腺炎病毒制造脑积水的实验模型来阐明 Chiari I 型畸形的发病机制。在 2 日龄、10 日龄和 25 日龄接种的所有仓鼠脑中均检测到侧脑室扩张。2 日龄和 10 日龄接种的仓鼠小脑显示蚓部伸长变平，蚓垂突出或有切迹。所有层，即分子层、浦肯野细胞层、颗粒层和白质均得以保留，但变窄了。浦肯野细胞保持正常。25 日龄接种的仓鼠未出现小脑畸形。在 2 日龄、10 日龄或 25 日龄接种的所有仓鼠中，在所有室管膜细胞和脉络丛的一些上皮细胞中均检测到腮腺炎病毒抗原。结果表明，Chiari I 型畸形由两个同时出现的主要因素引起，即颅内压升高和小脑皮质快速组织发生。
