Abstract

Damage to the primary visual cortex (V1) causes homonymous visual-field loss long considered intractable. Multiple studies now show that perceptual training can restore visual functions in chronic cortically-induced blindness (CB). A popular hypothesis is that training can harness residual visual functions by recruiting intact extrageniculostriate pathways. Training may also induce plastic changes within spared regions of the damaged V1. Here, we link changes in luminance detection sensitivity with retinotopic fMRI activity before and after visual discrimination training in eleven patients with chronic, stroke-induced CB. We show that spared V1 activity representing perimetrically-blind locations prior to training predicts the amount of training-induced recovery of luminance detection sensitivity. Additionally, training results in an enlargement of population receptive fields in perilesional V1, which increases blind-field coverage and may support further recovery with subsequent training. These findings uncover fundamental changes in perilesional V1 cortex underlying training-induced restoration of conscious luminance detection sensitivity in CB.

Highlights

  • Damage to the primary visual cortex (V1) causes homonymous visual-field loss long considered intractable

  • Consistent with previous results in untrained, chronic cortically-induced blindness (CB) patients[38], we found V1 population receptive field (pRF) covering blind-field regions to be significantly larger than pRFs covering solely intact-field regions at corresponding eccentricities prior to training, with this pre-training difference being attenuated with pRF eccentricity

  • We used fMRI and retinotopic mapping to examine the neural substrates of training-induced recovery of luminance detection sensitivity in CB patients with large, chronic, homonymous visual-field defects due to stroke-induced V1 damage

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Summary

Introduction

Damage to the primary visual cortex (V1) causes homonymous visual-field loss long considered intractable. Early findings generated strong interest, subsequent work identified flaws in NovaVision’s approach, which when corrected, revealed it to be relatively ineffective[14,15] Despite this initial failure, which reinforced the clinical dogma that post-stroke vision restoration is not possible, scientific teams worldwide subsequently showed that intensive training with gaze-contingent stimulus presentation inside the blind field can restore a range of visual functions at trained, blind-field locations[4,8,9,16,17,18,19,20,21,22,23,24,25,26,27]. Because blindsight is elicited by large stimuli with high-temporal and low-spatial frequency content, it is thought to rely mainly on direct geniculo-hMT+ and/or superior colliculus-pulvinar-extrastriate projections[3,7,30,31,34,35,36]

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