“Little Brain”, Big Role: Associations between cerebellar volume, neocortical thickness, cerebellar-neocortical covariance, and symptomatology in Autism Spectrum Disorder

Abstract

Autism Spectrum Disorder (ASD) is a developmental disability that affects social interaction and verbal and non-verbal communication. There is increasing evidence that aberrant cerebellar development and function underlies ASD symptomatology. The developmental diaschisis model hypothesizes that cerebellum injury and aberrant output affects development and function in neocortical regions. We aimed to test this hypothesis by looking at cerebellar development and its relationship with neocortical development in ASD. Using anatomical MRI scans from the Autism Brain Imaging Data Exchange II we aimed to assess cerebellar volume, regional neocortical thickness, and cerebellar-neocortical covariance differences in ASD, and how these measures relate to ASD symptomatology. While we did not find group differences in cerebellar volume, age by group effects on cerebellar volume, or age by group effects on regional neocortical thickness, we did find an age by group effect on subcortical volume. We identified group differences in left frontal eye field thickness and group differences in cerebellar-neocortical covariance. We also found various measures to be predictive of ASD symptomatology including Right Crus I volume, thickness in the pericalcarine, left cuneus, rostral middle frontal, and transverse temporal regions, and ratios of left and right dentate volume to subgenual cingulate volume and left and right dentate volume to medial superior temporal region volume. As a whole our findings show evidence that cerebellar-neocortical covariance and subcortical development differs in ASD. These findings point to future work assessing how subcortical development relates to cerebellar and neocortical development and how the covariance and subcortical differences we observed relate to ASD symptomatology. The large global burden of ASD highlights the importance of continued efforts aiming to improve our understanding of the neurological basis of the disorder. This knowledge could then be applied to develop better diagnostic methods and more individualized interventions and treatments to reduce burdensome symptomatology.