Treatment for social anxiety disorder alters functional connectivity in emotion regulation neural circuitry

Abstract

Social anxiety disorder (SAD) is characterized at a neurobiological level by disrupted activity in emotion regulation neural circuitry. Previous work has demonstrated amygdala hyperreactivity and disrupted prefrontal responses to social cues in individuals with SAD (Kim et al., 2011). While exposure-based psychological treatments effectively reduce SAD symptoms, not all individuals respond to treatment. Better understanding of the neural mechanisms involved offers the potential to improve treatment efficacy. In this study, we investigated functional connectivity in emotion regulation neural circuitry in a randomized controlled treatment trial for SAD. Participants with SAD underwent fMRI scanning while performing an implicit emotion regulation task prior to treatment (n=62). Following 12 weeks of cognitive behavioral therapy, acceptance and commitment therapy, or wait-list, participants completed a second scan (n=42). Psychophysiological interaction analyses using amygdala seed regions demonstrated differences between SAD and healthy control participants (HC; n=16) in right amygdala-vmPFC connectivity. SAD participants demonstrated more negative amygdala-to-vmPFC connectivity, compared to HC participants, an effect that was correlated with SAD symptom severity. Post-treatment symptom reduction was correlated with altered amygdala-to-vm/vlPFC connectivity, independent of treatment type. Greater symptom reduction was associated with more negative amygdala-to-vm/vlPFC connectivity. These findings suggest that effective psychological treatment for SAD enhances amygdala-prefrontal functional connectivity.

Amygdalar expression of the microRNA miR‐101a and its target Ezh2 contribute to rodent anxiety‐like behaviour

“…Dysregulation of amygdalar activity has been implicated in numerous anxiety disorders (Rauch et al ., ). Hyperactivity in the amygdala in response to stressful or fear‐inducing stimuli has been shown in patients with generalized anxiety disorder (Fonzo et al ., ; Mochcovitch et al ., ), social anxiety disorder (Kim et al ., ; Young et al ., ) and post‐traumatic stress disorder (Nuss, ; Patel et al ., ). We recently found that low‐anxiety HR rats display reduced c‐Fos activation in multiple amygdalar subnuclei following electric shock stress compared to LRs.…”

Preliminary Evidence That CD38 Moderates the Association of Neuroticism on Amygdala-Subgenual Cingulate Connectivity

“…No genotype could be determined for three participants and six participants' fMRI data were removed due to high levels of motion-induced noise (>10% of images had a global signal intensity >2.5 SD of mean, or were affected by motion of >2.5 mm in any direction; Young et al, 2017). This resulted in 72 participants (39 male; 33 female; Mean age = 27.56; Age range = 18-43).…”

Multivoxel Neural Reinforcement Changes Resting-State Functional Connectivity Within the Threat Regulation Network

“…With respect to the regulatory regions, both the vmPFC and vlPFC had many different definitions in the previous literature depending on the tasks (Buhle et al, 2014;Diekhof et al, 2011;Frank et al, 2014;Kalisch, 2009;Kohn et al, 2014;Messina et al, 2015) and populations studied (Dodhia et al, 2014;Etkin & Wager, 2007;Kircher et al, 2013;Klumpp et al, 2014;Sylvester et al, 2012;Young et al, 2017) . Here the regions of interest were determined using previous meta-analyses (Fullana et al, 2016;Ipser et al, 2013) and the parcelation established by the Brainnetome atlas.…”