Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by early-onset impairments in socialization, communication, repetitive behaviors, and restricted interests. ASD exhibits considerable heterogeneity, with clinical presentations varying across individuals and age groups. The pathophysiology of ASD is hypothesized to be due to abnormal brain development influenced by a combination of genetic and environmental factors. One of the most consistent morphological parameters for assessing the abnormal brain structures in patients with ASD is cortical thickness. Studies have shown changes in the cortical thickness within the frontal, temporal, parietal, and occipital lobes of individuals with ASD. These changes in cortical thickness often correspond to specific clinical features observed in individuals with ASD. Furthermore, the aberrant brain anatomical features and cortical thickness alterations may lead to abnormal brain connectivity and synaptic structure. Additionally, ASD is associated with cortical hyperplasia in early childhood, followed by a cortical plateau and subsequent decline in later stages of development. However, research in this area has yielded contradictory findings regarding the cortical thickness across various brain regions in ASD.
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