ACUTE AND CHRONIC CEREBRAL WHITE-MATTER DAMAGE IN NEONATAL HYDROCEPHALUS

The neonatal cat model of kaolin-induced hydrocephalus is associated w ith progressive and severe ventriculomegaly. In this experiment we stu died the evolution of the histopathological changes in hydrocephalic ( n = 23) cats from 5-168 days after the induction of hydrocephalus alon g with age-matched controls (n = 10). In the periventricular white mat ter, extracellular edema and axonal damage were present within days of the onset of hydrocephalus. This was followed by reactive gliosis, wh ite matter atrophy, and in some animals gross cavitation of the white matter. Even in the chronic, apparently compensated state there was on going glial cell death. Six cats were shunted an average of 23.6 +/- 6 .5 days after the induction of hydrocephalus because they were no long er able to feed independently. In spite of clinical improvement the wh ite matter changes persisted. Overt cortical changes were minimal exce pt where areas of white matter destruction encroached upon the deep la yers. The white matter changes are very similar to those seen in periv entricular leukomalacia and suggest that ischemia plays a role in neon atal brain injury caused by hydrocephalus.