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Cindy S. Ho, Deborah E. Giaschi; Low-level and high-level maximum motion displacement deficits in amblyopic children. Journal of Vision 2005;5(8):292. doi: 10.1167/5.8.292.
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Direction discrimination thresholds for maximum motion displacement (Dmax) are not fixed values but are highly dependent on stimulus parameters. Dmax increases with reduced dot probability (Boulton & Baker, 1993; Ramachandran & Anstis, 1983) or increased dot size (Cavanagh et al., 1985; Morgan, 1992). It has been theorized that the increase in Dmax under these conditions might reflect a switch in processing from low-level to high-level motion mechanisms in normal observers (Nishida & Sato, 1995; Sato, 1998). The proposed low-level process is reliant on spatial-frequency-tuned motion detectors and the high-level process is mediated by feature matching mechanisms. To determine whether this “switch” in motion mechanisms is observed in amblyopic individuals, thresholds were obtained in both eyes of 9 children with unilateral amblyopia and 9 controls. Each subject performed the task under three random dot display parameters: 20 min size at 5% density (baseline condition), 20 min size at 0.5% density (reduced probability condition), and 1 deg size at 5% density (increased dot size condition). A significant increase in Dmax was observed for displays with reduced dot probability and increased dot size relative to baseline in both groups. However, on the baseline and reduced dot probability conditions, Dmax was significantly lower in both eyes of the amblyopic group compared to the control group. For the increased dot size condition, Dmax was significantly lower in the amblyopic eye but significantly higher in the fellow eye compared to the control group. Extent of binocularity and subtype of amblyopia were not predictive of abnormal performance in this small sample. The results suggest that amblyopic children show the expected shift from low- to high-level motion mechanisms, but both mechanisms appear to be deficient. Our findings implicate abnormal binocular motion processing mechanisms in the neural deficit underlying amblyopia.
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