Neuronal mechanisms of motion detection underlying blindsight assessed by functional magnetic resonance imaging...

Brain imaging offers a valuable tool to observe functional brain plasticity by showing how sensory inputs reshape cortical activations after a visual impairment. Following a unilateral post-chiasmatic lesion affecting the visual cortex, patients may suffer a contralateral visual loss referred to homonymous hemianopia. Nevertheless, these patients preserve the ability to unconsciously detect, localize and discriminate visual stimuli presented in their impaired visual field. To investigate this paradox, known as blindsight, we conducted a study using functional magnetic resonance imaging (fMRI) to evaluate the structural and functional impact of such lesion in a 33-year old patient (ML), who suffers a complete right hemianopia without macular sparing and showing strong evidences of blindsight. We thus performed whole brain and sliced thalamic fMRI scan sequences during an event-related motion detection task. We provided evidence of the neuronal fingerprint of blindsight by acquiring and associating neural correlates, specific structures and functional networks of the midbrain during blindsight performances which may help to better understand this condition. Accurate performance demonstrated the presence of residual vision and the ability to unconsciously perceive motion presented in the blind hemifield, although her reaction time was significantly higher in her blind-field. When the normal hemifield was stimulated, we observed significant contralateral activations in primary and secondary visual areas as well as motion specific areas, such as the supramarginal gyrus and middle temporal area. We also demonstrated sub-thalamic activations within the superior colliculi (SC) and the pulvinar. These results suggest a role of secondary subcortical structures in normal spontaneous motion detection. In a similar way, when the lesioned hemifield was stimulated, we observed contralateral activity in extrastriate areas with no activation of the primary lesioned visual cortex. Moreover, we observed activations within the SC when the blind hemifield was stimulated. However, we observed unexpected ipsilateral activations within the same motion specific areas, as well as bilateral frontal activations. These results highlight the importance of abnormal secondary pathways bypassing the primary visual area (V1) in residual vision. This reorganization in the structure and function of the visual pathways correlates with behavioral changes, thus offering a plausible explanation for the blindsight phenomenon. Our results may potentially impact the development of rehabilitation strategies to target subcortical pathways.