Journal Article

Human blindsight is mediated by an intact geniculo-extrastriate pathway

Kennard, Christopher, Pestilli, Franco, Ajina, Sara, Rokem, Ariel, Bridge, Holly

2015

Overview

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. Visual information from our eyes projects to a region at the back of the brain called the primary visual cortex, which is where the information is processed to allow us to see the world around us. If a person suffers a stroke that affects this primary visual cortex, he or she can become blind on one side. However, some people can still detect images within this ‘blind’ area, even if they are not consciously aware of it. This phenomenon is known as ‘blindsight’, but it remains unclear which pathways and structures in the brain might allow this information to be detected. Ajina et al. have now examined the brains of a large group of patients with damage to the visual cortex. The results for the patients with blindsight were compared to those without, and to a group of sighted control participants. This analysis identified a pathway that seems to underlie blindsight. This pathway (which runs between an area of the brain called the lateral geniculate nucleus and another called the motion area hMT+) was present in all patients with blindsight, but was missing or disrupted in those patients without blindsight. Ajina et al. then examined other pathways that had previously been suggested to support blindsight and revealed that they were unlikely to do so. This is because the suggested connections were not identifiable in all patients with blindsight, and were often intact in those patients without blindsight. So far, this work has addressed the structure of the pathways rather than their activity. Future work will attempt to determine whether it is possible to strengthen such pathways to improve visual ability.

• Publisher: eLife Sciences Publications, Ltd,eLife Sciences Publications Ltd
• Subject: blindsight / diffusion-weighted imaging / Female / Geniculate Bodies - physiology / Hemianopsia - pathology / Humans / Neuroscience / Photic Stimulation / tractography / Vision, Ocular / Visual Cortex - injuries / Visual Pathways - physiology