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- W2189833931 abstract "The neural basis of amblyopia is a matter of debate. The following possibilities have been suggested: loss of foveal cells, reduced cortical magnification, loss of spatial resolution of foveal cells, and topographical disarray in the cellular map. To resolve this we undertook a population receptive field (pRF) functional magnetic resonance imaging analysis in the central field in humans with moderate-to-severe amblyopia. We measured the relationship between averaged pRF size and retinal eccentricity in retinotopic visual areas. Results showed that cortical magnification is normal in the foveal field of strabismic amblyopes. However, the pRF sizes are enlarged for the amblyopic eye. We speculate that the pRF enlargement reflects loss of cellular resolution or an increased cellular positional disarray within the representation of the amblyopic eye. SIGNIFICANCE STATEMENT The neural basis of amblyopia, a visual deficit affecting 3% of the human population, remains a matter of debate. We undertook the first population receptive field functional magnetic resonance imaging analysis in participants with amblyopia and compared the projections from the amblyopic and fellow normal eye in the visual cortex. The projection from the amblyopic eye was found to have a normal cortical magnification factor, enlarged population receptive field sizes, and topographic disorganization in all early visual areas. This is consistent with an explanation of amblyopia as an immature system with a normal complement of cells whose spatial resolution is reduced and whose topographical map is disordered. This bears upon a number of competing theories for the psychophysical defect and affects future treatment therapies." @default.
- W2189833931 created "2016-06-24" @default.
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- W2189833931 date "2015-11-04" @default.
- W2189833931 modified "2023-10-14" @default.
- W2189833931 title "Is the Cortical Deficit in Amblyopia Due to Reduced Cortical Magnification, Loss of Neural Resolution, or Neural Disorganization?" @default.
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- W2189833931 doi "https://doi.org/10.1523/jneurosci.1101-15.2015" @default.
- W2189833931 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6605231" @default.
- W2189833931 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26538646" @default.
- W2189833931 hasPublicationYear "2015" @default.
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