A test of the magnocellular deficit theory of dyslexia in an adult sample

Geoffrey W. Stuart*, Ken I. McAnally, Adam McKay, Michael Johnston, Anne Castles

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

16 Citations (Scopus)


An influential theory of dyslexia is based on the premise that individuals with the disorder have impaired sensitivity to rapidly changing stimuli in the visual and auditory modalities, due to a dysfunction in the magnocellular channel of the visual system and its analogue in the auditory pathway. The deficit in the auditory system is thought to cause difficulties in the segmentation of speech and the formation of accurate phonological representations, leading to problems in making the grapheme-phoneme correspondences necessary for reading. In a sample of 13 adults with a history of severe reading difficulty and 18 controls, visual contrast thresholds were measured in response to an 8-Hz flickering Gaussian blob as well as a slowly modulated 8 cycles/deg Gaussian windowed grating. Auditory thresholds were measured in response to a 4-s burst of white noise, the 2nd or 3rd second of which was amplitude modulated at 100 Hz or 1 Hz. The adult reading difficulty group exhibited normal thresholds to rapidly changing stimuli in both modalities and to the slowly modulated visual stimulus, but some showed reduced sensitivity to the 1-Hz amplitude-modulated auditory stimulus. Sensitivity to amplitude modulation at slower rates has been shown to be important for segmentation of the speech stream and so may be implicated in the reading difficulty of the affected individuals. A magnocellular deficit cannot explain this impaired sensitivity, which may be the result of a reduced echoic memory span.

Original languageEnglish
Pages (from-to)1215-1229
Number of pages15
JournalCognitive Neuropsychology
Issue number8
Publication statusPublished - Dec 2006
Externally publishedYes


Dive into the research topics of 'A test of the magnocellular deficit theory of dyslexia in an adult sample'. Together they form a unique fingerprint.

Cite this