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1 or system adjust to a loss of foveal vision (central scotoma)?
2 us of fixation, with marked reduction of the central scotoma.
3 ces in subjects with and without a simulated central scotoma.
4 gulation because this would cause a blinding central scotoma.
5 ned of loss of vision in the left eye with a central scotoma.
6 ch with fixation sparing and supero-temporal central scotoma.
9 had equal to or more than a doubling of the central scotoma area in response to a II2e test stimulus
10 ow that a new foveated ideal observer with a central scotoma correctly predicts that the human optima
11 with no visual impairment confronted with a central scotoma develop a preferred retinal locus to rep
12 severity of Stargardt disease, likelihood of central scotoma expansion, and visual acuity deteriorati
14 olled in this study: 30 patients affected by central scotoma, group 1, and 30 affected by peripheral
15 ht volunteers (80%) successfully simulated a central scotoma in the first field and all 10 (100%) did
17 egions of the visual cortex corresponding to central scotomas in subjects with macular degeneration (
20 al acuity and contrast sensitivity loss, the central scotoma per se delayed hazard detection even tho
21 pic B-wave amplitudes) a higher mean rate of central scotoma progression compared with those patients
22 al visual field data, 8 patients with faster central scotoma progression rates had significantly wors
23 t was found that some patients with relative central scotomas reliably used two different preferred r
25 tion; from full kinetic fields with relative central scotomas to remnant peripheral islands; from red
27 uals presented with declining visual acuity, central scotomas, waxy disc pallor, attenuated vasculatu
29 Microperimetry revealed a reduction in the central scotoma with three patients recovering normal fo
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