Hydrocephalus-induced damage is dependent on the rate and magnitude of vent
ricular dilatation, the proximity to the ventricle, and the developmental s
tage at which the disturbance occurs. It is mediated through a combination
of mechanical, ischemic, and metabolic-toxic disturbances. Developmental pr
ocesses, including myelin production, can be impaired. Periventricular axon
s 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.