Neural Bases of Social Anxiety Disorder

Abstract

Context Social anxiety disorder is thought to involve emotional hyper-reactivity, cognitive distortions, and ineffective emotion regulation. While the neural bases of emotional reactivity to social stimuli have been described, the neural bases of emotional reactivity and cognitive regulation during social and physical threat, and their relationship to social anxiety symptom severity, have yet to be investigated. Objective This study investigated behavioral and neural correlates of emotional reactivity and cognitive regulation in patients and controls during processing of social and physical threat stimuli. Design Participants were trained to implement cognitive-linguistic regulation of emotional reactivity induced by social (harsh facial expressions) and physical (violent scenes) threat while undergoing functional magnetic resonance imaging and providing behavioral ratings of negative emotion experience. Setting Academic psychology department. Participants 15 adults with social anxiety disorder and 17 demographically-matched healthy controls. Main Outcome Measures Blood oxygen level dependent signal and negative emotion ratings. Results Behaviorally, patients reported greater negative emotion than controls during social and physical threat, but showed equivalent reduction in negative emotion following cognitive regulation. Neurally, viewing social threat resulted in greater emotion-related neural responses in patients than controls, with social anxiety symptom severity related to activity in a network of emotion and attention processing regions in patients only. Viewing physical threat produced no between-group differences. Regulation during social threat resulted in greater cognitive and attention regulation-related brain activation in controls compared to patients. Regulation during physical threat produced greater cognitive control-related response (i.e., right DLPFC) in patients compared to controls. Conclusions Compared to controls, patients demonstrated exaggerated negative emotion reactivity and reduced cognitive regulation related neural activation, specifically for social threat stimuli. These findings help to elucidate potential neural mechanisms of emotion regulation that might serve as biomarkers for interventions for social anxiety disorder.

Social anxiety and emotion regulation flexibility: considering emotion intensity and type as contextual factors

“…Socially anxious individuals and individuals with SAD have been found to use more experiential avoidance and expressive suppression both at the trait level and on a daily basis (e.g., Blalock, Kashdan, & Farmer, 2016;Goldin et al, 2014;Kashdan & Rottenberg, 2010;O'Toole, Jensen, Fentz, Zachariae, & Hougaard, 2014;Werner, Goldin, Ball, Heimberg, & Gross, 2011). These individuals may also use less reappraisal or feel less selfefficacious in the employment of this strategy (e.g., Goldin, Manber, Hakimi, Canli, & Gross, 2009;O'Toole et al, 2014;Werner et al, 2011).…”

Hjärnan formas av psykologisk behandling

“…This suggests that the amygdala and the fear circuitry may be major players in processing emotional facial expressions, but still, the amygdala works collaboratively, and these studies suggest that amygdala couplings may also differentiate individuals with SAD from healthy controls. Interestingly, hyper-responsiveness to emotional faces differentiates SAD from other anxiety disorders (Blair et al, 2008b), and it has repeatedly been shown that social anxiety symptom severity predicts amygdala responsivity (Evans et al, 2008;Goldin, Manber, Hakimi, Canli, & Gross, 2009a;Phan, Fitzgerald, Nathan, & Tancer, 2006). Furthermore, Goldin et al (2009a) found that the differences between SAD and controls were specific to social threats (i.e., emotional faces) and that the SAD hyper-responsiveness was located in in the parahippocampal gyrus.…”

“…Interestingly, hyper-responsiveness to emotional faces differentiates SAD from other anxiety disorders (Blair et al, 2008b), and it has repeatedly been shown that social anxiety symptom severity predicts amygdala responsivity (Evans et al, 2008;Goldin, Manber, Hakimi, Canli, & Gross, 2009a;Phan, Fitzgerald, Nathan, & Tancer, 2006). Furthermore, Goldin et al (2009a) found that the differences between SAD and controls were specific to social threats (i.e., emotional faces) and that the SAD hyper-responsiveness was located in in the parahippocampal gyrus. Interestingly, they did not find any evidence of between-group differences on instant reactivity to stimuli of nonsocial violent scenarios, suggesting that heightened reactivity in the fear-circuitry frequently reported in SAD may be specific to social threats.…”

“…Goldin et al, found that the medial orbitofrontal cortex (mOFC) and the subgenual ACC were hyper-responsive in SAD while viewing emotional faces (Goldin et al, 2009a). Moreover, a previously mentioned study on unintentional social transgressions found that SAD individuals showed elevated responsivity in the vmPFC and the dorsomedial prefrontal cortex (dmPFC) (Blair et al, 2010).…”

“…A previously mentioned study by Goldin et al, (2009a) evaluated instant reactions as well as extended actions in a single study, i.e., the authors instructed participants to both passively view neutral and violent scenarios, and negative faces, and also to actively reappraise the content. The authors found that, while reappraising negative stimulus, the dmPFC activity was stronger in healthy controls, relative to SAD individuals.…”