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Abstract
The central tenet of the magnocellular deficit theory of dyslexia is that dyslexia is caused by a magnocellular deficit. A number of investigators have found deficiencies in visual coherent motion perception among dyslexic readers. These deficiencies have been attributed to magnocellular deficits, which means that they directly reflect the cause of dyslexia. However, similar perceptual deficiencies have been found in association with autism, Williams's syndrome, hemiplegia, and schizophrenia. These findings appear to undermine at least one of the following claims: (1) that a magnocellular deficit is the cause of dyslexia, and (2) that coherent motion is a reliable test of magnocellular sensitivity.
Notes
In the present reasoning it is assumed that the individuals with autism, Williams's syndrome, hemiplegia, and schizophrenia are not dyslexic. This may not be the case. In the unlikely case that these individuals were also dyslexic, it would be possible for coherent motion to reflect magnocellular sensitivity and magnocellular deficits to cause dyslexia. However, this would not eliminate the problem of non-dyslexic individuals with magnocellular deficits since, as pointed out elsewhere (Skoyles & Skottun, Citation2004), based on published numbers one would expect there to be a substantial number of individuals with magnocellular deficits who do not suffer from dyslexia. In fact, the estimates indicate that the majority of individuals with magnocellular deficits do not develop dyslexia.