In general, there are essentially two explanations of the occurrence of behavioral recovery following brain damage. One of these suggests that neural centers may be structurally reorganized following brain damage so that previously uninvolved neural centers may vicariously mediate the behaviors disrupted by the neurological insult. The other explanation espouses the proposition that the structural changes which may occur in response to brain damage are unrelated to behavioral recovery. From this latter point of view, postlesion behaviors are simply those which were spared by the neural insult. Accordingly, recovery of function is not the result of reporgrammingg structurally reorganized neural tissue but rather results from the fact that the recovery behaviors were never irreversily disrupted or lost in the first place. The present research program is designed to investigate the extent that this sort of sparing hypothesis may offer a viable alternative to vicariation as the mediating mechanism of recovery of function.