We investigated global motion processing in a group of adult amblyopes using a method that allows us to factor out any influence of the known contrast sensitivity deficit. We show that there are independent global motion processing deficits in human amblyopia that are unrelated to the contrast sensitivity deficit, and that are more extensive for contrast-defined than for luminance-defined stimuli. We speculate that the site of these deficits must include the extra-striate cortex and in particular the dorsal pathway.

The dichoptic-based perceptual learning therapy employed in the present study improved both the monocular VA of the AE and stereofunction, verifying the feasibility of a binocular approach in the treatment of childhood amblyopia.

Do amblyopes demonstrate general irregularities in processes of global image integration? Or are these anomalies stimulus specific? To address these questions we employed directly analogous global-orientation and global-motion stimuli using a method that allows us to factor out any influence of the low-level visibility loss [Simmers, A. J., Ledgeway, T., Hess, R. F., & McGraw, P. V. (2003). Deficits to global motion processing in human amblyopia. Vision Research 43, pp. 729-738]. The combination of orientation and motion coherence thresholds reported here provides comparable psychophysical measures of global processing by spatial-sensitive and motion-sensitive mechanisms in the amblyopic visual system. The results show deficits in both global-orientation and global-motion processing in amblyopia, which appear independent of any low-level visibility loss, but with the most severe deficit affecting the extraction of global motion. This provides evidence for the existence of a dominant temporal processing deficit in amblyopia.

Previously, we have shown that humans with amblyopia exhibit deficits for global motion discrimination that cannot be simply ascribed to a reduction in visibility or contrast sensitivity. Deficits exist in the processing of global motion in the fronto-parallel plane that suggest reduced extra-striate function (i.e., MT) in amblyopia. Here, we ask whether such a deficit also exists for rotation and radial components of optic flow that are first processed at higher sites along the dorsal pathway (i.e., MSTd). We show that similar motion processing deficits occur in our amblyopic group as a whole for translation, rotation, and radial components of optic flow and that none of these can be solely accounted for by the reduced visibility of the stimuli. Furthermore, on a subject-by-subject basis there is no significant correlation between the motion deficits for radial and rotational motion and those for translation, consistent with independent deficits in dorsal pathway function up to and including MSTd.