Subcortical pathways to extrastriate visual cortex underlie residual vision following bilateral damage to V1.

Residual vision, or blindsight, following damage to the primary visual cortex (V1) has been investigated for almost half a century. While there have been many studies of patients with unilateral damage to V1, far fewer have examined bilateral damage, mainly due to the rarity of such patients. Here we re-examine the residual visual function and underlying pathways of previously studied patient SBR who, as a young adult, suffered bilateral damage restricted to V1 which rendered him cortically blind. While earlier work compared his visual cortex to healthy, sighted participants, here we consider how his visual responses and connections compare to patients with unilateral damage to V1 in addition to sighted participants. Detection of drifting Gabor patches of different contrasts (1%, 5%, 10%, 50% and 100%) was tested in SBR and a group of eight patients with unilateral damage to V1. Performance was compared to the neural activation in motion area hMT+ measured using functional magnetic resonance imaging. Diffusion tractography was also used to determine the white matter microstructure of the visual pathways in all participants. Like the patients with unilateral damage, patient SBR showed increased % BOLD signal change to the high contrast stimuli that he could detect compared to the lower contrast stimuli that were not detectable. Diffusion tractography suggests this information is conveyed by a direct pathway between the lateral geniculate nucleus (LGN) and hMT+ since this pathway had microstructure that was comparable to the healthy control group. In contrast, the pathway between LGN and V1 had reduced integrity compared to controls. A further finding of note was that, unlike control participants, SBR showed similar patterns of contralateral and ipsilateral activity in hMT+, in addition to healthy white matter microstructure in the tract connecting hMT+ between the two hemispheres. This raises the possibility of increased connectivity between the two hemispheres in the absence of V1 input. In conclusion, the pattern of visual function and anatomy in bilateral cortical damage is comparable to that seen in a group of patients with unilateral damage. Thus, while the intact hemisphere may play a role in residual vision in patients with unilateral damage, its influence is not evident with the methodology employed here.