Thompson, BDanesh-Meyer, HBlack, JBorges, Victor2016-03-0920152015http://hdl.handle.net/2292/28415Background: A fundamental question in neuroscience is whether the adult cortex is able to exhibit plastic changes in order to adapt to or recover from a loss of sensory input. The visual system is a powerful model for investigating cortical plasticity and evidence from both animal and human studies suggests that there is the potential for functional and structural cortical reorganisation to occur when visual input is compromised. However, there is controversy regarding the nature and extent of this reorganisation. This study used unilateral optic neuropathy as a model to shed light on the structural and functional changes that occur in the adult human visual cortex in response to a loss of visual input. Aims: The overall aim was to use functional magnetic resonance imaging (fMRI) to investigate the response of the adult visual cortex to unilateral vision loss caused by primary open-angle glaucoma (POAG), non-arteritic anterior ischemic optic neuropathy (NAION) and compressive optic neuropathy (CON). The specific aims were: 1) to investigate whether the functional responses to the non-affected fellow eye differed between the lesion projection zone (LPZ) and a control region of cortex with intact visual input and, 2) to assess whether unilateral optic neuropathy causes localized structural changes within the visual cortex. Methods: Participants with unilateral paracentral visual field defects from POAG, NAION or CON participated in two fMRI sessions. Session 1 involved monocular retinotopic mapping of the visual cortex to define affected (LPZ) and control regions of cortex. Session 2 involved monocular viewing of counterphasing (8Hz) checkerboards presented to the central visual field (16 degrees) at 5%, 25% and 80% contrast. General linear modelling and event-related averaging were used to assess the functional response of the LPZ and control regions to these checkerboards when driven by each eye. Cortical thickness analysis was used to measure grey matter thickness within the LPZ and control regions of cortex in V1 and V2. Results: We found no evidence for an increased response to the fellow eye within the LPZ; however, there was a pronounced loss of activation in localised regions of V1 and V2, when participants viewed through their affected eye. Despite the reduced activation, visual cortex responses were still evident in V1 and V2 for affected eye viewing. The eccentricity mapping of these responses did not differ between the fellow eye and the affected eye indicating a lack reorganisation of function in the visual cortex. Our results showed no significant loss of grey matter thickness within V1 and V2. Conclusion: The results suggest a remarkable level of stability within the adult primary and extrastriate visual cortex in response to vision loss from unilateral optic neuropathy.Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher.https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htmhttp://creativecommons.org/licenses/by-nc-sa/3.0/nz/ThesisCopyright: The Authorhttp://purl.org/eprint/accessRights/OpenAccessQ111963432