TY - JOUR
T1 - Limited Restoration of Contrast Sensitivity with Training after V1 Damage in Humans
AU - Yang, Jingyi
AU - Saionz, Elizabeth L.
AU - Cavanaugh, Matthew R.
AU - Fahrenthold, Berkeley K.
AU - Melnick, Michael D.
AU - Tadin, Duje
AU - Briggs, Farran
AU - Carrasco, Marisa
AU - Huxlin, Krystel R.
N1 - Publisher Copyright:
© 2024 Yang et al.
PY - 2024/3
Y1 - 2024/3
N2 - Stroke damage to the primary visual cortex (V1) causes severe visual deficits, which benefit from perceptual retraining. However, whereas training with high-contrast stimuli can locally restore orientation and motion direction discrimination abilities at trained locations, it only partially restores luminance contrast sensitivity (CS). Recent work revealed that high-contrast discrimination abilities may be preserved in the blind field of some patients early after stroke. Here, we asked if CS for orientation and direction discrimination is similarly preserved inside the blind field, to what extent, and whether it could benefit from a visual training intervention. Thirteen subacute patients (<3 months post-V1 stroke) and 12 chronic patients (>6 months post-V1 stroke) were pretested and then trained to discriminate either orientation or motion direction of Gabor patches of progressively lower contrasts as their performance improved. At baseline, more subacute than chronic participants could correctly discriminate the orientation of high-contrast Gabors in their blind field, but all failed to perform this task at lower contrasts, even when 10 Hz flicker or motion direction were added. Training improved CS in a greater portion of subacute than that of chronic participants, but no one attained normal CS, even when stimuli contained flicker or motion. We conclude that, unlike the near-complete training-induced restoration of high-contrast visual discrimination abilities, V1 damage in adulthood may severely limit the residual visual system’s ability to regain normal CS. Our results support the notion that CS involves different neural substrates and computations than those required for orientation and direction discrimination in V1-damaged visual systems.
AB - Stroke damage to the primary visual cortex (V1) causes severe visual deficits, which benefit from perceptual retraining. However, whereas training with high-contrast stimuli can locally restore orientation and motion direction discrimination abilities at trained locations, it only partially restores luminance contrast sensitivity (CS). Recent work revealed that high-contrast discrimination abilities may be preserved in the blind field of some patients early after stroke. Here, we asked if CS for orientation and direction discrimination is similarly preserved inside the blind field, to what extent, and whether it could benefit from a visual training intervention. Thirteen subacute patients (<3 months post-V1 stroke) and 12 chronic patients (>6 months post-V1 stroke) were pretested and then trained to discriminate either orientation or motion direction of Gabor patches of progressively lower contrasts as their performance improved. At baseline, more subacute than chronic participants could correctly discriminate the orientation of high-contrast Gabors in their blind field, but all failed to perform this task at lower contrasts, even when 10 Hz flicker or motion direction were added. Training improved CS in a greater portion of subacute than that of chronic participants, but no one attained normal CS, even when stimuli contained flicker or motion. We conclude that, unlike the near-complete training-induced restoration of high-contrast visual discrimination abilities, V1 damage in adulthood may severely limit the residual visual system’s ability to regain normal CS. Our results support the notion that CS involves different neural substrates and computations than those required for orientation and direction discrimination in V1-damaged visual systems.
KW - blindness
KW - direction
KW - discrimination
KW - hemianopia
KW - orientation
KW - perceptual learning
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U2 - 10.1523/ENEURO.0020-24.2024
DO - 10.1523/ENEURO.0020-24.2024
M3 - Article
C2 - 38395611
AN - SCOPUS:85187883062
SN - 2373-2822
VL - 11
JO - eNeuro
JF - eNeuro
IS - 3
M1 - ENEURO.0020-24.2024
ER -