Relocation of specific visual functions following damage of mature posterior parietal cortex

Many visual deficits have been reported following damage to specific cerebral sites within posterior parietal cortex. These deficits generally involve aspects of vision including spatial or motion perception and visuomotor control. One characteristic of many of these deficits is that they tend to attenuate over time. Presumably, other cortical regions possess adaptive neuroplastic mechanisms that allow them to accommodate functions that were previously dominated by the damaged region. This report summarizes a series of experiments that examined adaptive cortical plasticity following cerebral cortex damage sustained in maturity. Following bilateral lesions of posterior middle suprasylvian sulcal (pMSs) cortex in the cat, deficits were identified in both visual orienting and landmark discrimination tasks. However, the deficits on the visual orienting task were only profound for the first few days following the lesion and orienting abilities returned to normal levels within the first 2 weeks postlesion. In contrast, no such attenuation of the effect of the lesion was evident on the landmark discrimination task. Following recovery of function on the visual orienting task, individual cortical areas flanking the lesion were bilaterally deactivated with cooling. Reversible deactivation of anterior middle suprasylvian sulcal (aMSs) cortex, but none of the other adjacent cortices, yielded visual orienting deficits that are not found in intact animals during deactivation of aMSs cortex. Therefore, we concluded that the visual orienting functions normally mediated by pMSs cortex were able to relocate to aMSs cortex following lesion of pMSs cortex. Finally, bilateral lesion of both pMSs and aMSs cortices yielded visual orienting deficits that did not attenuate. Overall, this series of experiments demonstrates that certain visual functions may relocate to specific cortical loci following damage to discrete areas within posterior parietal cortex.