Abstract
Amblyopia results from inadequate visual experience during the critical period of visual development. Abnormal binocular interactions are believed to play a critical role in amblyopia. These binocular deficits can often be resolved, owing to the residual visual plasticity in amblyopes. In this study, we quantitatively measured the sensory eye dominance in treated anisometropic amblyopes to determine whether they had fully recovered. Fourteen treated anisometropic amblyopes with normal or corrected to normal visual acuity participated, and their sensory eye dominance was assessed by using a binocular phase combination paradigm. We found that the two eyes were unequal in binocular combination in most (11 out of 14) of our treated anisometropic amblyopes, but none of the controls. We concluded that the treated anisometropic amblyopes, even those with a normal range of visual acuity, exhibited abnormal binocular processing. Our results thus suggest that there is potential for improvement in treated anisometropic amblyopes that may further enhance their binocular visual functioning.
Highlights
Amblyopia is a common visual disorder that affects 1.6% to 3.5% of the population [1]
Because amblyopia is a neurodevelopmental disorder [8] that affects both monocular and binocular visual processing, it is unclear whether the binocular visual deficits recover in clinically treated amblyopes
We did not find any significant correlation between the degree of anisometropia and the balance point in our treated patients (p = 0 12)
Summary
Amblyopia is a common visual disorder that affects 1.6% to 3.5% of the population [1]. Amblyopia is usually treated with patching therapy, to force the patients’ brain to learn to see through the amblyopic eye [6]. This therapy, which is efficient in recovering the monocular visual acuity of the amblyopic eye [7], prevents the two eyes from working together. Because amblyopia is a neurodevelopmental disorder [8] that affects both monocular and binocular visual processing, it is unclear whether the binocular visual deficits recover in clinically treated amblyopes. Neural plasticity targeted at those remaining deficits may be required to recover visual functions
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