Blindsight : Saccadic Eye Movement Control Mechanisms Without Visual Awareness in Primary Visual Cortex Lesions

<p>　Damage to the primary visual cortex (V1) impairs visual awareness. However, some patients with damaged V1 have the visuomotor ability to locate a visual target in the affected visual field using their rapid eye movements (saccades), despite impaired visual awareness. This phenomenon is known as blindsight. In other words, after a V1 lesion, there are neural pathways that do not drive visual awareness but convert visual information into saccadic movements. We used unilateral V1 lesion monkeys as animal models of blindsight and neurophysiological techniques, positron emission tomography (PET), and technique for pathway-selective blockade using viral vectors to elucidate the visuomotor pathways after V1 lesion. The retino-tectal-pulvinar pathway, via the superior colliculus as a relay point, was important for transmitting visual information to the brain after V1 lesion. In the cortex, the role of LIP in parietal-association cortex increased after the lesion. The LIP receives input from MT/MST areas to which the pulvinar projects strongly, suggesting that this series of pathways is important in saccadic movements to locate a visual target in the affected visual field after V1 lesion. It was found that visual signal through these pathways could not only drive saccades to the visual target, but could also act as a secondary reinforcer in reinforcement learning.</p><p>　These studies identified the pathways from the retina to the cortex that are essential for visually guided saccades to a target in the affected visual field by the V1 lesion. It was also shown that this neural pathway not only drives reflexive movements, but also acquires novel behaviors in coordination with the neural mechanisms of reinforcement learning.</p>