Damage to the visuoparietal cortex located in the banks of the middle suprasylvian gyrus of the cat has been shown to produce a deficit in the detection and localization of moving visual cues presented in the contralesional visual hemifield. There is evidence from reversible cooling deactivation studies that the integrity of this orienting function is not completely dependent on the VP cortex and that under the right circumstances, other brain regions may come online and completely take over the processing that subserves this behavior. We examined the recovery of orienting behavior after unilateral damage to the VP cortex. We found that consistent with previous data, VP damage produced an impairment in the capacity to detect and orient to moving visual stimuli in the contralesional visual field. Over a span of days, spontaneous recovery fully occurred. The ability to detect and localize static visual stimuli was tested as a fiducial measure of parietal cortex function, and this function did not recover. We conclude that the detection and localization of moving visual stimuli is not a function that requires VP cortex and argue for the existence of a parallel and redundant subcortical-cortical brain network that serves as the substrate for recovery of function.