Abstract

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.

Highlights

  • Following damage to the primary visual cortex (V1) patients experience homonymous hemianopia, in which vision on one side of the visual field is lost

  • 12 were classified as ‘blindsight positive’ and this relatively sensitive binary measure allowed us to be confident that patients labelled as ‘blindsight negative’ (n = 5) showed no residual visual function

  • The first algorithm was k-nearest-neighbours: it classified participants based on the labels (‘blindsight positive’ or ‘blindsight negative’) assigned to the majority of the 5 participants with behavior most similar to theirs, based only on the performance of these 5 participants at 100% contrast

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Summary

Introduction

Following damage to the primary visual cortex (V1) patients experience homonymous hemianopia, in which vision on one side of the visual field is lost. In spite of this cortical blindness, some patients are still able to ascertain information about visual stimulation within the blind area; this is called blindsight. The method provides a unique approach to investigate how white matter properties relate to visual behaviour in blindsight. Using dMRI in a number of individual patients, intact ipsilateral white matter connecting lateral geniculate nucleus (LGN) and extrastriate cortex, area hMT+, has been proposed as a candidate circuit that could support blindsight (de Gelder et al, 2008; Bridge et al, 2010). Two alternative proposals suggest blindsight results either from visual plasticity, for example to strengthen interhemispheric white matter in humans

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