Assessing the structure and function of the posterior visual pathway in eye disease

This thesis examines the consequences of partial vision loss, namely macular disease (MD), on both the structure and function of the posterior visual pathway. Using both cross-sectional and longitudinal analyses we explored how the anatomy of MD patients may change differently than in those aging naturally. The patient group showed reduced cortical thickness, which appears to largely impact the anatomical representation of central vision. However, they also showed reduced fractional anisotropy of the underlying white matter; but both the fiber bundles projecting to central and peripheral representations in early visual cortex were affected, suggesting broader deficits emerge in visual white matter. Our longitudinal assessments identified continued decline in cortical thickness and myelin density, even in long-standing vision loss, but individual case studies indicate the greatest changes in cortex likely emerge early in the disease following functional vision loss. We next assessed how partial vision loss may impact functional connectivity between striate and extrastriate cortex and found a selective reduction in functional connectivity between striate and the fusiform face area patients with central field loss. Finally, we used transient retinal lesions to test for responses in a ‘simulated lesion projection zone’ (sLPZ) in sighted participants, providing some evidence that peripheral visual stimulation can produce ‘patient-like’ responses in central representations in some individual controls while performing a task. This suggests LPZ responses - often deemed the ‘signature of reorganization of visual processing’ - may be driven by unmasked top-down feedback. Collectively, our findings add to growing evidence for atrophy in the posterior visual pathway in MD. Given that the viability of the visual brain may limit the success of visual restoration, development of neuroprotective strategies will benefit from a better understanding of the time scale and magnitude of changes observed in the brain following MD.