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C. E. Stewart, A. R. Fielder, M. J. Moseley, A. B. Morland, K. L. MacRae; Neural Deficit of Human Amblyopia. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2592. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Primate models of amblyopia have repeatedly shown the primary visual cortex (area V1) to be dysfunctional. Most functional imaging studies confirm this in humans with the suggestion of additional deficits within higher cortical areas. This study aims to examine how the visual cortex is topographically mapped in human amblyopia and identify specific areas of neural dysfunction.
Participants were 6 adults (mean age = 20 ± 2 years) with amblyopia; associated with anisometropia (n=2); both anisometropia and strabismus (n=4) and 3 adult normal observers (mean age = 31 ± 4 years). Cortical activation for each eye individually was measured using functional magnetic resonance imaging (fMRI) and psychophysical methods. Stimuli included four attributes of spatial vision known to be deficient in individuals with amblyopia and capable of isolating striate and exstrastriate cortical responses: visual resolution, contrast sensitivity, vernier acuity and global motion. In each subject, retinotopic mapping experiments were also be performed to establish locations of different visual areas, to act as regions of interest and determine whether intrinsic properties of the retinotopic maps, such as cortical magnification vary between fellow and amblyopic inputs. All paradigms used a block
All participants with amblyopia had residual amblyopia following treatment as a child. Mean logMAR visual acuity was 0.24 (sd 0.06) and -0.08 (sd 0.06) for amblyopic and fellow eyes respectively. Mean visual acuity for the normals was -0.06 (sd 0.06). Global motion was reduced significantly in the amblyopic (p=0.04) and fellow eyes (p=0.05) of observers compared to normal observers. Mean global orientation coherence (SD); amblyopic eye: 54% (25%); fellow eye: 41% (16%); normals: 25% (7%).
Amblyopic observers show significant deficits of global motion for amblyopic and fellow eye stimulation. This is suggestive of extrastriatal deficits of amblyopia in addition those well documented in V1.
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