1990 Volume 30 Issue 4 Pages 229-233
To investigate the mechanism of cystic cavity formation in the cerebral white matter of the HTX rat, a strain with inherited hydrocephalus, the authors carried out a histopathological study of the brain in pups from birth to postnatal day (P) 26. Cystic cavities were formed in the cerebral white matter on the lateral side of the basal ganglia of all HTX rats with moderate to severe ventricular dilatation and, additionally, in the white matter beneath the paramedian cortex in advanced cases at P 10-26. In the initial stage of cyst formation, disarrangement of the ependymal cell layer and spongy alteration of the white matter took place in pups between P 1 and P7. The ependymal disarrangement involved disruption and flattening of the ependymal cells, which were often devoid of microvilli, cilia and intercellular junctional complexes. The spongy state was due to expansion of the extracellular space and multiple microcyst formation with fluid accumulation in the early stage, and large cystic cavities in the advanced stage. The cerebrospinal fluid (CSF) in the ventricle communicated with the fluid in the cystic cavities via the disarranged ependymal cell layer. The ependymal damage was more prominent at the lateral wall of the posterior horn than at the anterior horn of the lateral ventricles. These cavities were demarcated by reactive glial cells in the advanced stage. However, the cavities enlarged in accordance with progressive dilatation of the lateral ventricles during postnatal development. These findings indicate that the initial change responsible for cyst formation is induced by infusion of CSF from the ventricle to the developing white matter as interstitial edema via the disarranged ependymal cell laver, subsequently forming large cystic cavities in the white matter.
