Masters C, Alpers M, Kakulas B
Arch Neurol. 1977 Jan;34(1):18-28. doi: 10.1001/archneur.1977.00500130038008.
The pathogenesis of hydrocephalus following reovirus type 1 inoculation of neonatal mice has been examined by light microscopy, radiology, immunofluorescence, and electron microscopy. The reovirus infection causes an acute ependymitis and leptomeningitis, followed by a fibrous arachnoiditis and arachnoid villitis. Hydrocephalus develops in proportion to the degree of inflammatory/fibrotic changes within the cerebrospinal fluid pathways. With the beginning of hydrocephalus there is radiographic evidence of basal cistern blockage. As the hydrocephalic state progresses, axial herniation and compression of the midbrain result in the appearance of aqueduct stenosis. We demonstrate that the stenosis of the aqueduct is a secondary phenomenon, not causally related to the pathogenesis of hydrocephalus, and discuss the significance of this finding to human aqueduct stenosis.
通过光学显微镜、放射学、免疫荧光和电子显微镜对1型呼肠孤病毒接种新生小鼠后发生脑积水的发病机制进行了研究。呼肠孤病毒感染引起急性室管膜炎和软脑膜炎，随后是纤维性蛛网膜炎和蛛网膜绒毛炎。脑积水的发展与脑脊液通路内炎症/纤维化变化的程度成正比。随着脑积水的开始，有影像学证据表明基底池阻塞。随着脑积水状态的进展，中脑的轴向疝和受压导致导水管狭窄的出现。我们证明导水管狭窄是一种继发现象，与脑积水的发病机制无因果关系，并讨论了这一发现对人类导水管狭窄的意义。
