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Impaired neuronal timing in developmental dyslexia—the magnocellular hypothesis

Impaired neuronal timing in developmental dyslexia—the magnocellular hypothesis Developmental dyslexia is not just a literacy problem. Dyslexics' reading and spelling difficulties are but two of a much larger number of differences between dyslexic and normal readers. The condition is a wide‐ranging, genetically based, neurodevelopmental syndrome. Reading requires fast and accurate processing of transient visual and auditory stimuli, functions for which large neurones, known as magnocellular, are specialized. We review the evidence that many dyslexics have impaired function of the visual magnocellular system, which correlates with their reading impairment, whereas good readers have high magnocellular sensitivity. We discuss possible mechanisms for this relationship. Although there is no such clearly defined magnocellular pathway in the auditory system as there is for vision, there is an analogous set of large auditory neurones which are specialized for following changes in the frequency or amplitude of sounds. We review evidence that the sensitivity of this auditory transient system is reduced in many dyslexics and that this reduction correlates with, hence may cause, their impaired phonological ability. As for the visual magnocellular system we show that auditory transient sensitivity predicts phonological and reading ability not only in dyslexics but also in good readers. Thus the magnocellular hypothesis postulates that dyslexics have lower sensitivity to dynamic visual and auditory stimuli as a result of slightly impaired development of large neurones and that this may explain not only their visual problems when attempting to read, but also their phonological deficit. Copyright © 1999 John Wiley & Sons, Ltd. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Dyslexia Wiley

Impaired neuronal timing in developmental dyslexia—the magnocellular hypothesis

Stein, John; Talcott, Joel
Dyslexia , Volume 5 (2) – Jun 1, 1999
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References (112)

Publisher
Wiley
Copyright
Copyright © 1999 John Wiley & Sons, Ltd.
ISSN
1076-9242
eISSN
1099-0909
DOI
10.1002/(SICI)1099-0909(199906)5:2<59::AID-DYS134>3.0.CO;2-F
Publisher site
See Article on Publisher Site

Abstract

Developmental dyslexia is not just a literacy problem. Dyslexics' reading and spelling difficulties are but two of a much larger number of differences between dyslexic and normal readers. The condition is a wide‐ranging, genetically based, neurodevelopmental syndrome. Reading requires fast and accurate processing of transient visual and auditory stimuli, functions for which large neurones, known as magnocellular, are specialized. We review the evidence that many dyslexics have impaired function of the visual magnocellular system, which correlates with their reading impairment, whereas good readers have high magnocellular sensitivity. We discuss possible mechanisms for this relationship. Although there is no such clearly defined magnocellular pathway in the auditory system as there is for vision, there is an analogous set of large auditory neurones which are specialized for following changes in the frequency or amplitude of sounds. We review evidence that the sensitivity of this auditory transient system is reduced in many dyslexics and that this reduction correlates with, hence may cause, their impaired phonological ability. As for the visual magnocellular system we show that auditory transient sensitivity predicts phonological and reading ability not only in dyslexics but also in good readers. Thus the magnocellular hypothesis postulates that dyslexics have lower sensitivity to dynamic visual and auditory stimuli as a result of slightly impaired development of large neurones and that this may explain not only their visual problems when attempting to read, but also their phonological deficit. Copyright © 1999 John Wiley & Sons, Ltd.

Journal

Dyslexia – Wiley

Published: Jun 1, 1999

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