Visual search performance in dyslexia

According to the magnocellular theory of dyslexia, otherwise intelligent children may fail to learn to read because of abnormalities in the magnocellular layers of the lateral geniculate nucleus (mLGN). If this were the case, one would predict that dyslexic subjects who show a deficit on low-level psychophysical tasks which tax the magnocellular system would also have deficits on higher-level visual tasks which do not rely on the properties of mLGN cells but depend upon the functioning of areas whose main inputs originate in the mLGN. In other words, magnocellular deficits should be traceable at later stages of visual processing. One area where such later processing is thought to occur is the posterior parietal cortex, damage to which impairs function on some classes of visual search. To test this hypothesis, we tested two groups of dyslexic subjects and a group of non-dyslexic controls on a range of visual search tasks. One group of dyslexic subjects had elevated motion coherence thresholds, a sign of deficits at the early levels (e.g. mLGN) of visual processing, and the other group had normal motion coherence thresholds. If the magnocellular deficits extended to the parietal cortex, it follows that the subjects with elevated motion coherence thresholds should have deficit in visual search, whereas those with normal motion coherence thresholds should not. The dyslexics with a motion coherence deficit were also impaired on serial visual search tasks but not on a parallel search. The dyslexics with normal motion coherence performance were unimpaired on visual search. The deficit was expressed as an elevation in reaction times, but there was no difference between the groups either in error rates or in the way the tasks were ranked according to difficulty. The results suggest that those dyslexics who have visual problems related to magnocellular functions also have visual-attentional problems related to the functions of areas such as the parietal cortex, which are dominated by inputs originating in the magnocellular LGN.