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The Journal of Neuroscience, April 1, 2009, 29(13):3981-3991; doi:10.1523/JNEUROSCI.4882-08.2009

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Behavioral/Systems/Cognitive
Perceptual Relearning of Complex Visual Motion after V1 Damage in Humans

Krystel R. Huxlin,¹ Tim Martin,¹ Kristin Kelly,¹ Meghan Riley,¹ Deborah I. Friedman,^1,2 W. Scott Burgin,² and Mary Hayhoe³

¹University of Rochester Eye Institute and ²Department of Neurology, University of Rochester, Rochester, New York 14642, and ³Department of Psychology, University of Texas at Austin, Austin, Texas 78712-01871

Correspondence should be addressed to Dr. Krystel R. Huxlin, University of Rochester Eye Institute, 601 Elmwood Avenue, Box 314, Rochester, NY 14642. Email: huxlin{at}cvs.rochester.edu

Damage to the adult, primary visual cortex (V1) causes severe visual impairment that was previously thought to be permanent, yet several visual pathways survive V1 damage, mediating residual, often unconscious functions known as "blindsight." Because some of these pathways normally mediate complex visual motion perception, we asked whether specific training in the blind field could improve not just simple but also complex visual motion discriminations in humans with long-standing V1 damage. Global direction discrimination training was administered to the blind field of five adults with unilateral cortical blindness. Training returned direction integration thresholds to normal at the trained locations. Although retinotopically localized to trained locations, training effects transferred to multiple stimulus and task conditions, improving the detection of luminance increments, contrast sensitivity for drifting gratings, and the extraction of motion signal from noise. Thus, perceptual relearning of complex visual motion processing is possible without an intact V1 but only when specific training is administered in the blind field. These findings indicate a much greater capacity for adult visual plasticity after V1 damage than previously thought. Most likely, basic mechanisms of visual learning must operate quite effectively in extrastriate visual cortex, providing new hope and direction for the development of principled rehabilitation strategies to treat visual deficits resulting from permanent visual cortical damage.

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Received Oct. 9, 2008; revised Jan. 6, 2009; accepted Jan. 28, 2009.

Correspondence should be addressed to Dr. Krystel R. Huxlin, University of Rochester Eye Institute, 601 Elmwood Avenue, Box 314, Rochester, NY 14642. Email: huxlin{at}cvs.rochester.edu

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