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The magnocellular ("big cell") theory of dyslexia is one of the major accounts of what may be going on in the dyslexic brain when a child fails to learn to read despite adequate opportunity and normal intelligence. This theory is built upon the deceptively simple and parsimonious idea that those who are less good at processing fast sensory inputs in general may therefore be less good at processing the specific quick visual and auditory signals that make up language.
There is now a great deal of evidence that dyslexics are on average less sensitive to certain dynamic visual stimuli than controls, especially for motion signals. The task that has most frequently been used to establish this fact is a "coherent motion task," wherein a person looks at pairs of panels of moving white dots and determines which of the pair contains the most dots that are moving together with each other. This task can be used to determine one's "motion threshold," which is the percentage of dots that have to be moving together with each other in order for the person to detect this "moving togetherness." It has consistently been found that dyslexics score on average worse than controls (i.e. they need more dots moving in synchrony before they notice that this is happening). Since miniscule motion signals are normally used by the brain to keep the eyes steady (shock absorbers of a sort), Prof. John Stein has suggested that dyslexics who are less good at perceiving motion might be also less good at keeping their eyes steady on a page. This unsteadiness may in turn contribute to their reading difficulties.
All of the papers presented in this symposium were reporting attempts to learn more about how dynamic visual processing capabilities and possible underlying magnocellular functioning may be related to reading ability and disability.
Talcott et al reported a large-scale study in normal children where it was found that motion processing ability was able to predict reading ability to a moderate degree in these children. This finding bolsters previous evidence that the relationship between reading and motion processing may be a general one, and not just one that exists among those who have the most difficulty learning to read. Cornelissen found that motion processing was related to proficiency of noticing the positioning of letters, which might support Stein's hypothesis that motion signals help keep the eyes representing a stable spatial view of what one looks at. Bradshaw found that while dyslexics had lower sensitivity to motion at normal light levels, at very low light levels there was no difference between controls and dyslexics. This finding would seem to provide data against a strictly conceived magnocellular theory, since the magnocellular system is more heavily relied upon when there is less light; however, it would be broadly consistent with previous findings of less general visual dynamic sensitivity among those with dyslexia. Finally, Pammer looked at the "frequency doubling" effect, which is supposed to tap into only a small part of the magnocellular system, in dyslexics. She found that dyslexics had on average a lower sensitivity to the frequency doubling effect, suggesting that they may have decreased functioning of this part of the visual magnocellular system.
In sum the studies presented are broadly consistent with the visual magnocellular theory of dyslexia, while raising new questions as to what specifically may be different between the visual systems of dyslexics and normal readers. It seems beyond a reasonable doubt at this point that aspects of dynamic visual processing are less sensitive an average among dyslexics than among normal readers. What remains to be teased apart is a) whether this different sensitivity is necessarily a result of differences in the visual magnocellular system, and b) what proportion of dyslexics may have an underlying visual deficit which contributes to their reading difficulties.
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