UBC Theses and Dissertations
Low- and high-level motion deficits in amblyopia: studies of maximum motion displacement Ho, Cindy
The human visual system comprises two neural pathways, the magnocellular/M and parvocellular/P pathways that process aspects of motion and form perception, respectively. Amblyopia is a developmental condition which may affect an otherwise healthy eye if it experiences abnormal visual stimulation due to ocular misalignment (strabismus), unequal refractive errors (anisometropia), or both. Amblyopia has been associated with deficits in both form and motion perception. Random-dot kinematograms (RDKs) which are created by shifting a computer-generated dot display in one direction by a given displacement can be used to assess motion processing. Maximum motion displacement (Dmax) is the largest dot displacement at which the direction of motion for a RDK can be correctly discriminated. Strabismic and anisometropic amblyopia represent two distinct subtypes of amblyopia and have been proposed to have different neural substrates. They have also been reported to have different Dmax deficits (Ho et al., 2005). The intentions of this thesis were: 1) to characterize deficits in Dmax for direction discrimination in the fellow and amblyopic eyes of participants with anisometropic and strabismic amblyopia using psychophysical methods; and 2) to investigate the relationship between psychophysical Dmax deficits and dysfunction in motion-sensitive extrastriate cortex of the M pathway using functional MRI techniques. The psychophysical results showed that Dmax thresholds are smaller in both amblyopic and fellow eyes for both subtypes of amblyopia relative to controls, although the deficits were greatest for strabismic amblyopia. Functional MRI results revealed decreased extrastriate cortical activation in both the strabismic and anisometropic groups relative to the control group when either eye viewed the RDK stimulus, although the lack of cortical activation was greatest for strabismic amblyopia. Taken together, this evidence suggests that dysfunctional binocular motion processing mechanisms in extrastriate cortex are part of the neural deficit underlying anisometropic and strabismic amblyopia and implies that strabismic amblyopia may be affected to a greater degree. For both amblyopic groups, there was a robust correlation between depth perception (stereoacuity) and Dmax thresholds. Specifically, direction discrimination was better when stereoacuity was worse. Abnormal binocular integration may have a significant role in predicting motion deficits in both anisometropic and strabismic amblyopia.
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