The posterior parietal cortex contributes to visuomotor processing for saccades in blindsight macaques

Patients with damage to the primary visual cortex (V1) lose visual awareness, yet retain the ability to perform visuomotor tasks, which is called "blindsight." To understand the neural mechanisms underlying this residual visuomotor function, we studied a non-human primate model of blindsight with a unilateral lesion of V1 using various oculomotor tasks. Functional brain imaging by positron emission tomography showed a significant change after V1 lesion in saccade-related visuomotor activity in the intraparietal sulcus area in the ipsi- and contralesional posterior parietal cortex. Single unit recordings in the lateral bank of the intraparietal sulcus (lbIPS) showed visual responses to targets in the contralateral visual field on both hemispheres. Injection of muscimol into the ipsi- or contralesional lbIPSs significantly impaired saccades to targets in the V1 lesion-affected visual field, differently from previous reports in intact animals. These results indicate that the bilateral lbIPSs contribute to visuomotor function in blindsight. Rikako Kato et al. use PET imaging to examine altered brain activity in blindsight macaques that lack visual awareness yet can still perform visuomotor tasks. They report that blindsight macaques exhibit a significant change in activity of the lateral bank of the intraparietal sulcus (lbIPS) bilaterally, and injection of muscimol into this region impairs visuomotor performance. These results suggest a role for the bilateral lbIPS in visuomotor function in blindsight conditions.