23919
Common and Distinct Patterns of Functional and Structural Activity in Resting State Brain Networks in Autism and Social Anxiety
Individuals with Autism Spectrum Disorder (ASD) also commonly have Social Anxiety Disorder (SAD), with up to 42-84% of those with ASD also meeting diagnostic criteria for SAD in their lifetime (de Bruin et al., 2007; Muris et al., 1998; Simonoff et al., 2008). Examination of possible disruption in the default mode network (DMN), which is active in the absence of task demands and involved in normative aspects of social cognition, may offer an opportunity to identify basic mechanisms responsible for heightened risk for social anxiety. Disruptions in the function of DMN would be expected in disorders characterized by alterations in social function. Consistent with this notion, both ASD and SAD are associated with altered activation of several core regions of the DMN. Despite emergent evidence for alterations within the same brain systems in SAD and ASD, as well as a behavioral continuum of social impairments, no study to date has examined the unique and common underlying brain systems within these disorders.
Objectives:
The primary aim of the current study is to characterize brain connectivity using a multimodal approach (e.g., functional and structural analyses) within the DMN in SAD, ASD, and controls.
Methods:
Forty-five individuals (15 per group; mean age = 23.92) participated in this study. Functional connectivity analyses were conducted by using resting-state fMRI data to identify intrinsic connectivity via independent components analysis (ICA). The ICA approach is based on FSL’s MELODIC (Beckmann et al., 2005).
To evaluate the structural connectivity of the DMN, we examined diffusion tensors via AFNI’s FATCAT (Taylor & Saad, 2013). We selected regions of interest (ROIs) based on the DMN (Left and Right Parietal Region, Posterior Cingulate Cortex (PCC), Anterior Cingulate Cortex (ACC)) to examine the structural integrity between these regions.
Results:
Functional analyses revealed increased coactivation of the dorsomedial prefrontal cortex in ASD and SAD compared to controls, p < .05.
Structural analyses revealed both over and under white matter fiber connectivity in ASD compared to both controls and the SAD group. Specifically, there were significant differences between the ASD and control group for the Right Parietal Region <--> ACC connectivity contrast, p = 0.0387, and the ASD and SAD groups, p = 0.039. This difference was not found between the SAD and control groups, p = 1. In the Left Parietal Region <--> PCC connectivity contrast, we found a significant difference between the ASD group and control group, p = 0.20, and ASD and SAD group, p = 0.019, but not between the SAD and control, p = 0.667.
Conclusions:
These results may hold significance for clinical treatment of ASD with comorbid SAD. Treatment of ASD often targets specific symptoms and ranges from speech to social and cognitive skills without insight into the neural structures subserving the mechanisms of social deficits (Reichow & Wolery, 2009; Dawson & Bernier, 2013). Knowledge of potentially common neural and physiological processes subserving social deficits could aid identification of treatment informed by the underlying mechanisms.