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Teri Lawton, Garrison Cottrell; Magnocellular Deficits in Dyslexia Provide Evidence Against Noise Exclusion Hypothesis. Journal of Vision 2010;10(7):454. doi: https://doi.org/10.1167/10.7.454.
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There is significant controversy about the mechanism underlying dyslexia. Sperling et al. (2005;2006), for example, hypothesize that the underlying mechanism is an inability to ignore noise in visual stimuli (the noise exclusion hypothesis), and that this inability is not due to a magnocellular deficit, as it shows up in both parvocellular-oriented (static, high frequency gabor filters) and magnocellular-oriented (counterphase flicker low frequency gabors) stimuli in their experiments. Dyslexics are differentially impaired in discriminating these stimuli in noise. However, the noise used in their experiments is a flashed white noise stimulus, which can activate the magnocellular system, a system that has been implicated in figure-ground discrimination. If there is a magnocellular deficit, this would impact both the parvo- and magno-oriented decisions because of poor figure/ground discrimination. Several studies by the first author using sinusoidal test and background patterns that optimally activate magnocellular neurons have shown that dyslexics have reduced contrast sensitivity to direction discrimination. These studies showed that with equal test and background spatial frequencies, dyslexics were initially least sensitive to the direction of movement, but that following training on left-right movement discrimination twice weekly for 12-15 weeks, dyslexics were most sensitive to the direction of movement with equal test and background frequencies. Equal test and background spatial frequencies provide the greatest amount of noise, since test and background patterns are analyzed by neural channels tuned to the same spatial frequencies. Since training rapidly removes this deficit, these data suggest that the deficit in noise exclusion is due to the relatively sluggish magnocellular pathway in dyslexics. Furthermore, this training dramatically improves reading speed in the subjects. Our results are consistent with the view that dyslexia is due to sluggish magnocellular neurons, but not with the view that a noise exclusion deficit, without a concomitant magnocellular deficit, underlies dyslexia
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