Brain - Hydrocephalus

Hydrocephalus may be communicating or noncommunicating; that is, the former has no apparent obstructive process, whereas the latter has an obstructive cause somewhere in the ventricular connections. Most commonly, communicating hydrocephalus is considered to result from an idiopathic increase in cerebrospinal fluid production or deceased resorption. However, most examples are not clearly investigated. Figure 1 is an example of noncommunicating, obstructive hydrocephalus of the lateral ventricles (arrows) secondary to a pituitary neoplasm (arrowhead) obstructing the ventral aspect of the third ventricle. Figure 2 depicts the flattened attenuation of normally cuboidal ependymal cells (arrow). This is due to obstructive hydrocephalic ventricular expansion associated with incidental pituitary cysts. In this example, the effects of increased intraventricular pressure in hydrocephalus are evident on ependymal cells. The normally cuboidal ependymal cells are stretched to cover the increased ventricular surface area. There is some edematous separation of the epithelium from underlying brain and mild vacuolation of subjacent neuropil.

Ependymal cells have been generally considered by pathologists to be poorly responsive to insults, simply undergoing degeneration and necrosis. However, in investigations of controlled spinal injury of rats, ependymal cells and closely associated subjacent cells appear to be quite responsive, at least to trauma. Nestin and GAP-43, immunohistochemical indicators of immature neural stem cells, and glial fibrillary acid protein were detected posttrauma in in vivo cells identified as ependymal, suggesting dedifferentiation of ependymal cells to neural stem cells and glia and their potential role in spinal injury repair.