No abstract

The extent of motion processing deficits and M/dorsal pathway involvement in amblyopia is unclear. Fellow eye performance was assessed in amblyopic children for motion-defined (MD) form, global motion, and maximum displacement (Dmax) tasks. Group performance on MD form was significantly worse in amblyopic children than in control children. Global motion deficits were significantly related to residual binocular function. Abnormally elevated Dmax thresholds were most prevalent in children with anisometropia. Our findings from these three uncorrelated tasks implicate involvement of binocular motion-sensitive mechanisms in the neural deficits of amblyopic children with strabismic, anisometropic, and aniso-strabismic etiologies.

We assessed 18 children with unilateral amblyopia and 30 age-matched controls on one low-level and three high-level motion tasks. Children with amblyopia showed similar performance to controls in both amblyopic and fellow eyes on a low-level global motion task and on a high-level 2-dot apparent motion task. Performance on both single-object and multiple-object attentive tracking tasks was significantly depressed in both amblyopic and fellow eyes relative to controls. These findings suggest that binocular regions of posterior parietal cortex likely contribute to a deficit in voluntary, spatial attention that is a component of amblyopia.