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Sheila Crewther, Robin Laycock, David Crewther; Both abrupt and ramped onset of contrast reversing phantom contours reveals a magnocellular impairment in dyslexia.. Journal of Vision 2012;12(9):527. doi: 10.1167/12.9.527.
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© ARVO (1962-2015); The Authors (2016-present)
Despite thirty years of experimentation controversy still exists over whether there is a magnocellular deficit associated with developmental dyslexia and where it might operate. Thus we designed a purely magnocellular phantom contour stimuli defined by contrast reversals at high temporal frequency (58.5Hz), with the aim of comparing contrast thresholds for a 4 alternative choice orientation discrimination in a group of children (9-14 years) with dyslexia and an age- and nonverbal intelligence- matched control group. Stimuli were either abruptly presented for 4 refresh frames (34 ms), or in two reduced transience conditions via stimuli that were progressively ramped on and off over either 4 frames or 10 frames (86 ms). Children in the dyslexia group showed much higher contrast thresholds than the control group in all three conditions, thus demonstrating strong evidence for a magnocellular deficit in dyslexia. A similar relative difference in contrast threshold and similar relative difference in size of the first contrast step needed for conscious orientation discrimination was also shown by dyslexics and controls under both abrupt and ramped conditions. Furthermore although the absolute size of the differences in threshold scores between the controls and dyslexic group increased dramatically between the abrupt and the 4 and 10 frame ramped onset stimuli, a similar effect size was seen across all task conditions, suggesting a single mechanism affecting performance underlies both abrupt and ramped onset conditions. If this is true then the abrupt condition with its high transience that indicates a dorsal stream deficit in the dyslexic group gives credence to the suggestion that even when the stimuli are ramped, it is the relative ease of dorsal stream activation that limits fluency in dyslexic readers.
Meeting abstract presented at VSS 2012
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