Isolating the M(y)-cell response in dyslexia using the spatial frequency doubling illusion

Isolating the M(y)-cell response in dyslexia using the spatial frequency doubling illusion The contribution of M(y)-cell activity within a framework of a magnocellular-deficit theory of dyslexia is currently unknown. Twenty-one dyslexic readers and 19 control readers were compared on their threshold detection for the frequency doubling illusion — an index of M(y)-cell activity, coherent motion, and a visual acuity task. The dyslexic group performed more poorly on detection of the frequency doubling illusion and coherent motion compared to the control group, but both groups performed comparably on the visual acuity task. The results from this study indicate that if a magno deficit exists in dyslexia, it may originate at a retinal level at least partly mediated by M(y)-cell abnormalities. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Vision Research Elsevier

Isolating the M(y)-cell response in dyslexia using the spatial frequency doubling illusion

Vision Research, Volume 41 (16) – Jul 1, 2001

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Publisher
Elsevier
Copyright
Copyright © 2001 Elsevier Science Ltd
ISSN
0042-6989
eISSN
1878-5646
D.O.I.
10.1016/S0042-6989(01)00092-X
Publisher site
See Article on Publisher Site

Abstract

The contribution of M(y)-cell activity within a framework of a magnocellular-deficit theory of dyslexia is currently unknown. Twenty-one dyslexic readers and 19 control readers were compared on their threshold detection for the frequency doubling illusion — an index of M(y)-cell activity, coherent motion, and a visual acuity task. The dyslexic group performed more poorly on detection of the frequency doubling illusion and coherent motion compared to the control group, but both groups performed comparably on the visual acuity task. The results from this study indicate that if a magno deficit exists in dyslexia, it may originate at a retinal level at least partly mediated by M(y)-cell abnormalities.

Journal

Vision ResearchElsevier

Published: Jul 1, 2001

References

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