Purpose: Dyslexia is a common language disorder affecting up to 10% of the population. While thought to have a biologic basis, the exact neurological mechanisms responsible for the observed abnormalities remain unclarified. Several researchers have suggested that dyslexia results from of an underlying visual and/or auditory sensory processing abnormality. We believe that dyslexia is a manifestation of abnormal interactions between the auditory and visual cortices, and we designed an fMRI experiment to test this hypothesis.
Methods and Materials: 22 dyslexic patients, diagnosed on the basis of standardized neuropsychological testing, and 22 normal controls underwent fMRI on a 1.5T MR scanner while performing an auditory phoneme matching paradigm. Standard echoplanar fMRI imaging using blood oxygen level dependent (BOLD) contrast was performed. In addition, anatomical T1-weighted volumetric images were acquired in all patients using an inversion recovery-prepared, 3DSPGR sequence. All data was processed using SPM99 (Welcome Department of Cognitive Neurology, London, UK). Briefly, the fMRI images were motion corrected, normalized to stereotaxic space, smoothed, and analyzed using the General Linear Model within SPM. Contrast images (con) for each subject were generated to identify the main effect of auditory stimulation. Using a random effects model, brain activity was compared between groups while performing this auditory matching task. The resulting activation maps were thresholded at P < 0.005.
Results: When comparing dyslexics with normal readers while performing the auditory matching language task, the dyslexics showed increased activity in the ventral visual pathway. Just looking at the main effect in each group alone, the dyslexics activated this ventral visual region, and the normal controls did not activate this region. In fact, the controls actually deactivated the ventral visual area, as is often seen during an auditory task.
Conclusion: Using fMRI, we showed that dyslexics use neuronal ensembles in the ventral visual pathway to perform an auditory matching language task unlike normal readers who do not use this region. These findings support our hypothesis that dyslexics exhibit altered auditory/visual interactions, and these altered interactions may contribute to the deficits seen in dyslexia. Thus, remediation strategies based on improving auditory and visual sensory interactions may help those suffering from this prevalent disorder. (J.B. is a GERRAF fellow and receives salary support from General Electric.)
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