Abstract
Hydrocephalus-induced damage is dependent on the rate and magnitude of ventricular dilatation, the proximity to the ventricle, and the developmental stage at which the disturbance occurs. It is mediated through a combination of mechanical, ischemic, and metabolic-toxic disturbances. Developmental processes, including myelin production, can be impaired. Periventricular axons are the primary target, however. The potential for reversal of damage by shunting diminishes as the duration and severity of hydrocephalus increases. Ancillary pharmacologic means for preventing hydrocephalus-induced brain damage are worth pursuing.
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