Although damage to the primary visual cortex (V1) causes hemianopia, many patients retain some residual vision; known as blindsight. We show that blindsight may be facilitated by an intact white-matter pathway between the lateral geniculate nucleus and motion area hMT+. Visual psychophysics, diffusion-weighted magnetic resonance imaging and fibre tractography were applied in 17 patients with V1 damage acquired during adulthood and 9 age-matched controls. Individuals with V1 damage were subdivided into blindsight positive (preserved residual vision) and negative (no residual vision) according to psychophysical performance. All blindsight positive individuals showed intact geniculo-hMT+ pathways, while this pathway was significantly impaired or not measurable in blindsight negative individuals. Two white matter pathways previously implicated in blindsight: (i) superior colliculus to hMT+ and (ii) between hMT+ in each hemisphere were not consistently present in blindsight positive cases. Understanding the visual pathways crucial for residual vision may direct future rehabilitation strategies for hemianopia patients.DOI: http://dx.doi.org/10.7554/eLife.08935.001

It has been proposed that two major axes, dominance and trustworthiness, characterize the social dimensions of face evaluation. Whether evaluation of faces on these social dimensions is restricted to conscious appraisal or happens at a preconscious level is unknown. Here we provide behavioral evidence that such preconscious evaluations exist and that they are likely to be interpretations arising from interactions between the face stimuli and observer-specific traits. Monocularly viewed faces that varied independently along two social dimensions of trust and dominance were rendered invisible by continuous flash suppression (CFS) when a flashing pattern was presented to the other eye. Participants pressed a button as soon as they saw the face emerge from suppression to indicate whether the previously hidden face was located slightly to the left or right of central fixation. Dominant and untrustworthy faces took significantly longer time to emerge (T2E) compared with neutral faces. A control experiment showed these findings could not reflect delayed motor responses to conscious faces. Finally, we showed that participants' self-reported propensity to trust was strongly predictive of untrust avoidance (i.e., difference in T2E for untrustworthy vs neutral faces) as well as dominance avoidance (i.e., difference in T2E for dominant vs neutral faces). Dominance avoidance was also correlated with submissive behavior. We suggest that such prolongation of suppression for threatening faces may result from a passive fear response, leading to slowed visual perception.

Little is known about how non-V1 inputs influence motion area V5/MT+. Ajina et al. reveal that after V1 damage, V5/MT+ activity resembles that of early visual cortex, perhaps driven by similar subcortical inputs. While these inputs are normally overshadowed by V1 connections, acknowledging their contribution may improve neuronal models.

When the primary visual cortex (V1) is damaged, the principal visual pathway is lost, causing a loss of vision in the opposite visual field. While conscious vision is impaired, patients can still respond to certain images; this is known as ‘blindsight’. Recently, a direct anatomical connection between the lateral geniculate nucleus (LGN) and human motion area hMT+ has been implicated in blindsight. However, a functional connection between these structures has not been demonstrated. We quantified functional MRI responses to motion in 14 patients with unilateral V1 damage (with and without blindsight). Patients with blindsight showed significant activity and a preserved sensitivity to speed in motion area hMT+, which was absent in patients without blindsight. We then compared functional connectivity between motion area hMT+ and a number of structures implicated in blindsight, including the ventral pulvinar. Only patients with blindsight showed an intact functional connection with the LGN but not the other structures, supporting a specific functional role for the LGN in blindsight.