There is evolving evidence that developmental dyslexia is associated with anomalous cerebral morphology in the bilateral frontal and left temporoparietal regions. This study examined the morphology of the corpus callosum, as possible deviations in other important structures are poorly understood in this behaviorally diagnosed syndrome.
Magnetic resonance imaging scans were obtained from children with developmental dyslexia and from matched control children. Morphometric measurements were examined to determine if regional differences existed in the corpus callosum between these two groups of children.
Magnetic resonance imaging studies were completed at Athens (Ga) Magnetic Imaging.
Patients and Other Participants:
Sixteen developmental dyslexic children (mean age, 9.7 years) and a matched sample of children who were diagnosed as being normal were examined by using a reliable comprehensive diagnostic process.
Main Outcome Measures:
Using a midsagittal magnetic resonance imaging scan, corpus callosum morphology was evaluated by segmenting the corpus callosum into five regions of interest.
Analysis of the corpus callosum revealed that the anterior region of interest (the genu) was significantly smaller in the dyslexic children. Significant correlations existed between reading achievement and the region-of-interest measurements for the genu and splenium. Measured intelligence, chronologic age, and gender were not related to region-of-interest measurements of the corpus callosum. Consistent with previous studies, the dyslexic individuals were characterized by significant psychiatric comorbidity, particularly attentiondeficit disorder with and without hyperactivity. Reported familial left-handedness also distinguished the dyslexic children.
Subtle neurodevelopmental variation in the morphology of the corpus callosum may be associated with the difficulty that dyslexic children experience in reading and on tasks involving interhemispheric transfer.
Hynd GW, Hall J, Novey ES, et al. Dyslexia and Corpus Callosum Morphology. Arch Neurol. 1995;52(1):32–38. doi:https://doi.org/10.1001/archneur.1995.00540250036010
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