Changes in Cortical Processing Following Unilateral Visual Cortex Deafferentation

After the loss of inputs, cells in visual cortex adapt and begin representing space beyond their classical receptive fields. This ability for functional reorganization is a phenomenon known as neuroplasticity. Homonymous hemianopia is a unique case of this scenario that results from hemispheric deafferentation, or when all visual inputs in to one hemisphere of the brain are lost. This condition occurs due to unilateral damage of the post-chiasmatic geniculo-striate pathway, the network that carries visual information from one side of visual space to the visual cortex for processing. Damage to this pathway causes perceptual blindness in the side of space that it represents. In two experiments, this dissertation investigates the changes in neural response properties immediately following hemispheric deafferentation using event-related potentials (ERPs) and psychophysics. Hemianopia was simulated in healthy adults with the use of an eye-tracker to produce a gaze-contingent display on a computer screen. Results of the ERP study indicate a significant difference in the state of cortical excitability after deafferentation. The complementary psychophysics experiment demonstrated a significant reduction in contrast thresholds for the deafferented hemisphere. These results are consistent with a model of short-term neuroplasticity known as disinhibition and extend our understanding of neuroplasticity to cases of hemispheric deafferentation