The magnocellular deficit hypothesis in dyslexia: a review of reported evidence

Abstract

Many reports suggest that the majority of dyslexic children have a measurable disorder of the fast processing pathway of the visual system. This pathway is believed to extend from the retina to the occipital and parietal areas of the brain, and is referred to as the magnocellular (M) or transient pathway. Evidence in support of the magnocellular deficit theory comes from several sources, but is not totally consistent. Histological studies have revealed shrinkage and disorganisation of M cells in the lateral geniculate nucleus of dyslexic subjects. Psychophysical investigations of visual persistence, contrast sensitivity to moving sine wave gratings and flicker sensitivity, report atypical results in dyslexic children, reflecting an apparent deficiency in the transient system, although not all psychophysical studies have demonstrated such a deficiency. Visual evoked potential responses to a wide range of stimuli have been reported to be deficient in dyslexic subjects, but again there are dissenting papers. These reports have been subject to critical review and analysis, new techniques specifically to stimulate the magnocellular pathway are described, and the relevance of this research to tinted lens therapies and clinical reading problems is discussed.