Cindy S. Ho

Deficient motion perception in the fellow eye of amblyopic children

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.

Abnormal spatial selection and tracking in children with amblyopia

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.

Deficient maximum motion displacement in amblyopia

Direction discrimination thresholds for maximum motion displacement (Dmax) are not fixed, but are stimulus dependent. Dmax increases with reduced dot probability or increased dot size. We previously reported abnormal Dmax in the fellow eyes of amblyopic children for dense patterns of small dots. To determine how deficits of Dmax in amblyopic eyes compare to those in fellow eyes, thresholds were obtained in both eyes of 9 children with unilateral amblyopia and 9 control children. The expected increase in Dmax was observed for reduced dot probability and increased dot size conditions relative to baseline in both control and amblyopic groups. Both eyes of the amblyopic group demonstrated significant deficits. Our findings implicate abnormal binocular motion processing, which may involve both low-level and high-level motion mechanisms, in the neural deficit underlying amblyopia.

Neural correlates of the multiple-object tracking deficit in amblyopia

Deficits in multiple-object tracking have previously been reported in both the amblyopic and the clinically unaffected fellow eye of patients with amblyopia. We examined the neural correlates of this deficit using functional MRI. Attentive tracking of 1, 2 or 4 moving targets was compared to passive viewing and to baseline fixation in an amblyopic group and an age-matched control group in six regions of interest: V1, middle temporal complex (MT+), superior parietal lobule (SPL), frontal eye fields (FEF), anterior intraparietal sulcus (IPS), and posterior IPS. Activation in all regions of interest, except V1, increased with attentional load in both groups. MT+ was less active in both eyes of the amblyopic group relative to controls for passive viewing and each of the tracking conditions. Anterior IPS and FEF were less active with amblyopic eye viewing when tracking four targets. These results implicate both the low-level passive and high-level active motion systems in the multiple-object tracking deficit in amblyopia.

Stereopsis-dependent deficits in maximum motion displacement in strabismic and anisometropic amblyopia

Direction discrimination thresholds for maximum motion displacement (D(max)) have been previously reported to be abnormal in amblyopic children [Ho, C. S., Giaschi, D. E., Boden, C., Dougherty, R., Cline, R., & Lyons, C. (2005). Deficient motion perception in the fellow eye of amblyopic children. Vision Research, 45, 1615-1627; Ho, C. S., & Giaschi, D. E. (2006). Deficient maximum motion displacement in amblyopia. Vision Research, 46, 4595-4603]. We looked at D(max) thresholds for random dot kinematograms (RDKs) biased toward low- or high-level motion mechanisms. D(max) is thought to be limited, for high-level motion mechanisms, by the efficiency of object feature tracking and probability of false matches. To reduce the influence of low-level mechanisms, we determined thresholds also for a high-pass filtered version of the RDKs. Performance did not significantly differ between strabismic and anisometropic groups with amblyopia, although both groups performed significantly worse than the age-matched control group. D(max) thresholds were higher for children with poor stereoacuity. This was significant in both anisometropic and strabismic groups, and more robust for high-pass filtered RDKs than for unfiltered RDKs. The results imply that impairment of the extra-striate dorsal stream is a likely part of the neural deficit underlying both strabismic and anisometropic amblyopia. This deficit appears to be more dependent on extent of binocularity than etiology. Our findings suggest a possible relationship between fine stereopsis, coarse stereopsis, and motion correspondence mechanisms.

Low- and high-level first-order random-dot kinematograms: evidence from fMRI.

Maximum motion displacement (Dmax) represents the largest dot displacement in a random-dot kinematogram (RDK) at which direction of motion can be discriminated. Direction discrimination thresholds for maximum motion displacement (Dmax) are not fixed but are stimulus dependent. For first-order RDKs, Dmax is larger as dot size increases and/or dot density decreases. Dmax may be limited by the receptive field size of low-level motion detectors when the dots comprising the RDK are small and densely spaced. With RDKs of increased dot size/decreased dot density, however, Dmax exceeds the spatial limits of these detectors and is likely determined by high-level feature-matching mechanisms. Using functional MRI, we obtained greater activation in posterior occipital areas for low-level RDKs and greater activation in extra-striate occipital and parietal areas for high-level RDKs. This is the first reported neuroimaging evidence supporting proposed low-level and high-level models of motion processing for first-order random-dot stimuli.