Functional brain abnormalities associated with comorbid anxiety in autism spectrum disorder

Anxiety disorders are common in autism spectrum disorder (ASD) and associated with social–communication impairment and repetitive behavior symptoms. The neurobiology of anxiety in ASD is unknown, but amygdala dysfunction has been implicated in both ASD and anxiety disorders. Using resting-state func...

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Bibliographic Details
Published in:Development and psychopathology 2020-10, Vol.32 (4), p.1273-1286
Main Authors: Bartolotti, James, Sweeney, John A., Mosconi, Matthew W.
Format: Article
Language:English
Subjects:
Amygdala
Amygdala - diagnostic imaging
Anxiety
Anxiety - diagnostic imaging
Anxiety disorders
Anxiety Disorders - diagnostic imaging
Autism
Autism Spectrum Disorder - diagnostic imaging
Brain - diagnostic imaging
Brain Mapping
Communication
Comorbidity
Cortex (cingulate)
Emotions
Fear & phobias
Functional magnetic resonance imaging
Humans
Magnetic Resonance Imaging
Neostriatum
Nervous system
Neural networks
Neural Pathways - diagnostic imaging
Neurobiology
Neuroimaging
Neurosciences
Prefrontal cortex
Special Section Articles
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Summary:Anxiety disorders are common in autism spectrum disorder (ASD) and associated with social–communication impairment and repetitive behavior symptoms. The neurobiology of anxiety in ASD is unknown, but amygdala dysfunction has been implicated in both ASD and anxiety disorders. Using resting-state functional magnetic resonance imaging, we compared amygdala–prefrontal and amygdala–striatal connections across three demographically matched groups studied in the Autism Brain Imaging Data Exchange (ABIDE): ASD with a comorbid anxiety disorder (N = 25; ASD + Anxiety), ASD without a comorbid disorder (N = 68; ASD-NoAnx), and typically developing controls (N = 139; TD). Relative to ASD-NoAnx and TD controls, ASD + Anxiety individuals had decreased connectivity between the amygdala and dorsal/rostral anterior cingulate cortex (dACC/rACC). The functional connectivity of these connections was not affected in ASD-NoAnx, and amygdala connectivity with ventral ACC/medial prefrontal cortex (mPFC) circuits was not different in ASD + Anxiety or ASD-NoAnx relative to TD. Decreased amygdala–dorsomedial prefrontal cortex (dmPFC)/rACC connectivity was associated with more severe social impairment in ASD + Anxiety; amygdala–striatal connectivity was associated with restricted, repetitive behavior (RRB) symptom severity in ASD-NoAnx individuals. These findings suggest comorbid anxiety in ASD is associated with disrupted emotion-monitoring processes supported by amygdala–dACC/mPFC pathways, whereas emotion regulation systems involving amygdala–ventromedial prefrontal cortex (vmPFC) are relatively spared. Our results highlight the importance of accounting for comorbid anxiety for parsing ASD neurobiological heterogeneity.
ISSN:0954-5794
1469-2198
DOI:10.1017/S0954579420000772