Parcellation Analysis of Language Areas of the Brain and Its Clinical Association in Children with Autism Spectrum Disorder
Introduction Children with autism spectrum disorder (ASD) are reported to have atypical symmetry patterns and volumes of language-related brain areas. There is a dearth of evaluation of the significance of this finding clinically for children with ASD in India. Objective Perform brain morphometric analysis in children with ASD and evaluate the left–right asymmetry of primary and association areas of language and its clinical implications. Methodology Drug-naïve children with ASD who visited developmental paediatrics, aged 3–12 years, were recruited for the study after informed consent. The diagnosis was by a multidisciplinary team. All children underwent assessments and MRI brain scan. Postprocessing included cortical reconstruction and volumetric segmentation of unimodal and higher order association areas related to language. The quantitative neuroimaging results were analysed with respect to both autism severity and ability test scores. Results Analysis included 10 children (8 males and 2 females) aged 36–99 months. Autism severity score ranged from 30.5 to 40 on CARS. The unimodal association areas of pars opercularis and planum temporale indicated left asymmetry, and in the higher association areas, supramarginal gyrus had left asymmetry, while pars triangularis displayed right asymmetry. The supramarginal gyrus indicated a left asymmetry in males, while it showed right asymmetry in females. Children who had higher autism symptoms had significantly lower left frontal opercular volume compared to those with lower autism symptom severity. Conclusion Asymmetry patterns of language areas of brain in children with ASD and low left frontal opercular volumes in children with higher autism symptomatology indicate anomalous fronto-temporal grey matter development.
KeywordsAutism spectrum disorder Asymmetry Language association cortex
Funding for this study was provided by the Indian Council of Medical Research to BK (Autism/57/2011-NCD-1).
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