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Striatal Activation to Social Reward Anticipation Predicts Symptoms of Social Anxiety Disorder in At-Risk Girls

Thu, March 21, 9:30 to 11:00am, Baltimore Convention Center, Floor: Level 3, Room 322

Integrative Statement

Introduction: Social anxiety disorder (SAD) is characterized by impairing fear of social situations, such as being negatively evaluated by others. SAD typically onsets during early adolescence and there is evidence suggesting that shyness represents a risk factor for SAD, particularly among girls (Tsui et al., 2017). Recent studies have reported striatal hyperactivation to reward anticipation in youth at-risk for (Guyer et al., 2006) and diagnosed with SAD (Guyer et al., 2012). Here, we examined neural activation to social reward cues in girls at risk for anxiety disorders and tested whether such activation predicted levels of SAD symptoms at follow-up.
Methods: Adolescent girls (n=59; Mage=12.6 (SD=.95) were recruited varying in level of risk for anxiety disorders (41 high; 18 low) based on scores being 0.75 SD above or below the mean on the Fearfulness and Shyness subscales of the Early Adolescent Temperament Questionnaire-Revised. Participants completed a modified version of the fMRI Social Incentive Delay (SID) task (Spreckelmeyer et al., 2009). This task was adapted to examine neural activation to anticipation and receipt of social feedback from a virtual peer (i.e., virtual peer facial expression) based on the participants’ task performance. An ROI mask was constructed by combining meta-analytic maps for the terms social (z>3.30, FDR p<.05), reward (z>8.84, FDR p<.05), and punishment (z>4.45, FDR p<.05) from Neurosynth.org. Four separate voxelwise analyses were conducted for the following contrasts: reward anticipation vs. neutral anticipation; punishment anticipation vs. neutral anticipation, reward outcome vs. neutral outcome, punishment outcome vs. neutral outcome contrasts. Analyses were conducted using AFNI’s 3dttest with the -Clustsim option, which uses a nonparametic approach to cluster-size thresholding with a cluster forming threshold of p<.001, extent threshold of 23 voxels. Linear regression analyses focused on neural activation to social reward anticipation and SAD symptoms, measured using the SAD subscale of the SCARED at 12 and 18 months following the scan and controlling for age and baseline SAD symptoms.
Results: Analyses focusing on task-related activation indicated greater activation in the caudate and medial frontal gyrus (MFG) to reward (vs neutral) anticipation. There was greater activation in a number of subcortical (amygdala, striatum), prefrontal cortical (e.g., VMPFC, VLPFC) regions, and the superior temporal gyrus (STG) to reward (vs. neutral) outcome. Similar regions were activated to punishment (vs. neutral) outcome in addition to activation in posterior cingulate gyrus (PCG). Regression analyses revealed that greater caudate activation to social reward anticipation predicted higher levels of SAD symptoms at 18 months, (R2=.48, Beta=.63, t=3.18, p=.008).
Discussion: Findings suggest that the adapted version of the SID task recruited expected regions implicated in processing social (e.g., STG, PCG), reward (e.g., caudate, putamen, VMPFC), and punishment (e.g., amygdala) information. Our findings of greater caudate activation to social reward anticipation predicting later symptoms of SAD is consistent with previous findings in behaviorally inhibited youth (Guyer et al., 2014) and suggest that altered processing of social reward cues may escalate the risk for SAD at a time when increased sensitivity to rewarding experiences such as peer acceptance typically occurs (Caouette and Guyer, 2014).

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