Sarnat H B
Department of Pediatrics, University of Washington School of Medicine, Seattle.
J Neuropathol Exp Neurol. 1995 Jan;54(1):1-15. doi: 10.1097/00005072-199501000-00001.
The ependyma reacts to injury with a few stereotypical responses and does not regenerate at any age. Non-neoplastic ependymal cells do not undergo mitotic proliferation and do not re-express fetal cytoskeletal or secretory proteins. Atrophy of ependymal cells accompanies generalized cerebral atrophy. The ependyma may be damaged by stretching during ventricular dilatation, by infarcts of the ventricular wall or by infection and inflammation. Tearing of the epithelium leaves discontinuities that become filled with processes of subventricular astrocytes. In some cases reactive gliosis is minimal, but in most it is extensive and gliotic nodules form beneath intact ependyma and within gaps between ependymal islands. Ependymal rosettes may form in several ways: sequestration of diverticuli from the surface; curling of a torn edge or penetration of an edge into the parenchyma; reactive gliosis overgrowing an ependymal edge; in situ differentiation of ependymal cells from deep neuroepithelial cells. Migration and metaplasia are unlikely mechanisms. Bacterial and fungal ependymitis are highly destructive. Several viruses, especially mumps, selectively infect ependymal cells and are an important cause of acquired aqueductal stenosis without inflammation. Damaged ependyma may not be able to perform its function in the regulation of transport of fluid, ions and small molecules between cerebral parenchyma and ventricular fluid and thus may contribute to hydrocephalus. Damage to the fetal ependyma may result in secondary focal dysplasias of the developing brain.
室管膜对损伤的反应具有一些典型特征，且在任何年龄都不会再生。非肿瘤性室管膜细胞不会进行有丝分裂增殖，也不会重新表达胎儿期的细胞骨架蛋白或分泌蛋白。室管膜细胞萎缩伴随广泛性脑萎缩。室管膜可能因脑室扩张时的牵拉、室壁梗死或感染及炎症而受损。上皮的撕裂会留下间断处，这些间断处会被室管膜下星形胶质细胞的突起填充。在某些情况下，反应性胶质增生很轻微，但在大多数情况下则很广泛，并且在完整的室管膜下方和室管膜岛之间的间隙内会形成胶质结节。室管膜玫瑰花结可能通过几种方式形成：从表面隔离憩室；撕裂边缘卷曲或边缘向实质内穿透；反应性胶质增生使室管膜边缘过度生长；室管膜细胞从深部神经上皮细胞原位分化。迁移和化生不太可能是其形成机制。细菌性和真菌性室管膜炎具有高度破坏性。几种病毒，尤其是腮腺炎病毒，可选择性感染室管膜细胞，是导致后天性导水管狭窄且无炎症的重要原因。受损的室管膜可能无法在调节脑实质与脑室液之间的液体、离子和小分子运输中发挥其功能，因此可能导致脑积水。胎儿室管膜受损可能导致发育中的大脑继发性局灶性发育异常。
