Damage to the adult primary visual cortex (V1) causes a loss of conscious vision over the same part of the visual field in both eyes (cortical blindness - CB). This increasingly common cause of permanent disability in older, adult humans is still considered untreatable. Our long-term objective is to define a new paradigm for understanding visual recovery after permanent visual cortex damage. Our goal is to characterize the properties of and signal processing mechanisms that enable visual relearning and recovery in CB. Knowing what mechanisms and brain pathways mediate recovery will allow us to predict the extent to which vision can be recovered, as well as the quality and modality of recovered vision that can be attained in a given individual. We will meet our objective and goal by testing the primary hypothesis that after V1 damage, training-induced relearning in CB fields depends on motion processing for its initiation. This is based on our preliminary findings that motion training in CB fields transfers to static orientation discriminations not normally perceivable in blindsight. However, without the initial motion training, these static discriminations cannot be relearned. While training could work via a variety of mechanisms, our preliminary findings suggest the following alternatives, to be tested here: 1) training stimulates the motion processing complex hMT+ to more effectively process visual information from CB fields, including that needed for static orientation discriminations, 2) training stimulates the motion pathway to reactivate other visual areas (incl. parts of V1, V2, V3, V4, V01) and their pre-existing processing abilities, or 3) training alters readout of information from hMT+/other areas.
Aim 1 will use visual psychophysics to test the hypothesis that static orientation relearning depends on learning in the motion pathway, and to measure specificity of learning for trained directions/orientations.
Aim 2 will use the perceptual template model (PTM) and psychophysical tests of spatial suppression to test the hypothesis that relearning in CB fields occurs via 1) changes in tuning of basic orientation or direction channels, possibly via changes in spatial suppression within these channels, or 2) that training improves the readout of these channels.
Aim 3 will use functional MRI (fMRI) to measure changes in functional anatomy associated with relearning in CB fields. We will test the hypothesis that visual training: 1) alters the blind field's retinotopic representation either in just hMT+ or both in hMT+ and other visual areas (V1, V2, V3, V4, V01);2) increases direction and/or orientation specificity in just hMT+ or both in hMT+ and V1, V2, V3, V4, V01 or 3) none of the above. Our results will provide critical information about brain pathways and signal processing mechanisms stimulated by training to evoke visual relearning in CB fields. This knowledge is essential theoretically to better understand the type and degree of plasticity possible in damaged, adult visual systems, and to improve our treatment strategies for humans suffering from the disability induced by permanent visual cortical damage.
Damage to the primary visual cortex of humans causes permanent cortical blindness and debilitation to almost 1% of our aging population. The proposed experiments are intended to provide new information about the brain areas and processing mechanisms that underlie training-induced visual recovery in cortical blindness. This knowledge will be instrumental in allowing us to design more effective visual rehabilitative strategies to treat this underserved patient group.
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