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Posterior parietal cortex and developmental dyslexia

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Dyslexia is defined as a specific reading disorder despite normal intelligence and conventional teaching. One of the most influential theories attempting to explain problems suffered by dyslexics assumes that dyslexia is caused by deficits of the magnocellular system. This system, generally responsible for processing fast sensory information, projects mostly to the parietal cortex. Consistent with this theory, dyslexics should have problems with tasks which specifically involve parietal cortex. In the article, we review data and show that, indeed, dyslexics have problems with fast attention shifts, show some symptoms of mild unilateral neglect syndrome and have abnormal saccadic and pursuit eye movements. Little is known about visuo-motor coordination and mental rotation, the tasks in which the parietal cortex is thought to play important roles.
EN
Lesions of the medial prefrontal cortex strongly impaired rats delayed alternation behaviour in a T-maze, both when the lesion was inflicted after the initial acquisition of the task and when the lesion was added after criterion performance had been reattained following an of the parietal cortex. Lesions of the parietal cortex did not impair this behaviour, either when the parietal lesion was inflicted after the initial acquisition of the task or when it was added to a prefrontal lesion after criterion performance had beed reattained. Combined, one stage, parietal and prefrontal lesions did not have a stronger effect on delayed alternation than did prefrontal lesions alone. These results indicate that in spite of the strong anatomical connectivity between the prefrontal and parietal "association" cortex the latter is not necessary for the recovery of delayed alternation after prefrontal lesions. In comparison with the parietal cortex, the prefrontal cortex seems to be uniquely involved in mediation of delayed alternation.
EN
Automatic multimodal spatial attention was studied in 12 dyslexic children (SRD), 18 chronological age matched (CA) and 9 reading level matched (RL) normally reading children by measuring reaction times (RTs) to lateralized visual and auditory stimuli in cued detection tasks. The results show a slower time course of focused multimodal attention (FMA) in SRD children than in both CA and RL controls. Specifically, no cueing effect (i.e., RTs difference between cued?uncued) was found in SRD children at 100 ms cue-target delay, while it was present at 250 ms cue-target delay. In contrast, in both CA and RL controls, a cueing effect was found at the shorter cue-target delay but it disappeared at the longer cue-target delay, as predicted by theories of automatic capture of attention. Our results suggest that FMA may be crucial for learning to read, and we propose a possible causal explanation of how a FMA deficit leads to specific reading disability, suggesting that sluggish FMA in dyslexic children could be caused by a specific parietal dysfunction.
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