4.7 Article

Cortical plasticity in central vision loss: Cortical thickness and neurite structure

Journal

HUMAN BRAIN MAPPING
Volume 44, Issue 10, Pages 4120-4135

Publisher

WILEY
DOI: 10.1002/hbm.26334

Keywords

central vision loss; cortical thickness; macular degeneration; NODDI

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Late-stage macular degeneration often impairs central vision, causing individuals to rely on peripheral vision. Patients with macular degeneration develop a preferred retinal locus to compensate for the loss of central vision. This study found that the thickness of the cortex associated with the preferred retinal locus was thinner in patients with macular degeneration compared to controls. However, there were no significant differences in cortical thickness, neurite density, or orientation dispersion between the preferred retinal locus and control regions.
Late-stage macular degeneration (MD) often causes retinal lesions depriving an individual of central vision, forcing them to learn to use peripheral vision for daily tasks. To compensate, many patients develop a preferred retinal locus (PRL), an area of peripheral vision used more often than equivalent regions of spared vision. Thus, associated portions of cortex experience increased use, while portions of cortex associated with the lesion are deprived of sensory input. Prior research has not well examined the degree to which structural plasticity depends on the amount of use across the visual field. Cortical thickness, neurite density, and orientation dispersion were measured at portions of cortex associated with the PRL, the retinal lesion, and a control region in participants with MD as well as age-matched, gender-matched, and education-matched controls. MD participants had significantly thinner cortex in both the cortical representation of the PRL (cPRL) and the control region, compared with controls, but no significant differences in thickness, neurite density, or orientation dispersion were found between the cPRL and the control region as functions of disease or onset. This decrease in thickness is driven by a subset of early-onset participants whose patterns of thickness, neurite density, and neurite orientation dispersion are distinct from matched control participants. These results suggest that people who develop MD earlier in adulthood may undergo more structural plasticity than those who develop it late in life.

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