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1.
Brain Behav ; 12(8): e2693, 2022 08.
Artículo en Inglés | MEDLINE | ID: mdl-35816591

RESUMEN

BACKGROUND AND PURPOSE: Previous studies have revealed abnormal regional homogeneity (ReHo) in individuals with autism spectrum disorder (ASD); however, there is little consistency across the findings within these studies, partly due to small sample size and great heterogeneity among participants between studies. Additionally, few studies have explored the association between ReHo aberrance and clinical symptoms in individuals with ASD. METHODS: Forty-eight adolescents with high-functioning ASD and 63 group-matched typically developing (TD) controls received functional magnetic resonance imaging at rest. Group-level analysis was performed to detect differences in ReHo between ASD and TD. Evaluation of symptom severity in individuals with ASD was based on the Autism Behavior Checklist (ABC). Voxel-wise correlation analysis was undergone to examine the correlations between the symptom severity and ReHo map in individuals with ASD within brain areas with ReHo abnormalities. RESULTS: Compared with the TD controls, individuals with ASD exhibited increased ReHo in the bilateral anterior cingulate cortex, left caudate, right posterior cerebellum (cerebellar tonsil), and bilateral brainstem and decreased ReHo in the left precentral gyrus, left inferior parietal lobule, bilateral postcentral gyrus, and right anterior cerebellum (culmen). The correlation analysis indicated that the ReHo value in the brainstem was negatively associated with the ABC total scores and the scores of Relating factor, respectively. CONCLUSIONS: Our findings indicated that widespread ReHo abnormalities occurred in ASD, shedding light on the underlying neurobiology of pathogenesis and symptomatology of ASD.


Asunto(s)
Trastorno del Espectro Autista , Trastorno Autístico , Adolescente , Trastorno del Espectro Autista/diagnóstico por imagen , Encéfalo , Mapeo Encefálico/métodos , Humanos , Imagen por Resonancia Magnética/métodos
2.
Neuropsychiatr Dis Treat ; 18: 717-730, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35401002

RESUMEN

Background: Previous studies have indicated abnormal gray matter volume (GMV) in individuals with autism spectrum disorder (ASD); however, there is little consistency across the findings within these studies, partly due to small sample size and great heterogeneity among participants between studies. Additionally, few studies have explored the correlation between clinical symptoms and GMV abnormalities in individuals with ASD. Here, the current study examined GMV alterations in whole brain and their correlations with clinical symptoms in a relatively large and homogeneous sample of participants with ASD matched typically developing (TD) controls. Methods: Forty-eight adolescents with high-functioning ASD and 29 group-matched TD controls underwent structural magnetic resonance images. Voxel-based morphometry was applied to investigate regional GMV alterations. The participants with ASD were examined for the severity of clinical symptoms with Autism Behavior Checklist (ABC). The relationship between GMV abnormalities and clinical symptoms was explored in ASD group using voxel-wise correlation analysis within brain regions that showed significant GMV alterations in individuals with ASD compared with TD controls. Results: We found increased GMV in multiple brain regions, including the inferior frontal gyrus, medial frontal gyrus, superior frontal gyrus, superior temporal gyrus, occipital pole, anterior cingulate, cerebellum anterior lobe, cerebellum posterior lobe, and midbrain, as well as decreased GMV in cerebellum posterior lobe in individuals with ASD. The correlation analysis showed the GMV in the left fusiform was negatively associated with the scores of sensory factor, and the GMV in the right cerebellum anterior lobe was positively associated with the scores of social self-help factor. Conclusion: Our results indicated that widespread GMV abnormalities of brain regions occurred in individuals with ASD, suggesting a potential neural basis for the pathogenesis and symptomatology of ASD.

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