Neural mechanisms of cognitive reappraisal of negative self-beliefs in social anxiety disorder.

Department of Psychology, Stanford University, Stanford, California 94305-2130, USA.
Biological psychiatry (Impact Factor: 8.93). 09/2009; 66(12):1091-9. DOI: 10.1016/j.biopsych.2009.07.014
Source: PubMed

ABSTRACT Social anxiety disorder (SAD) is characterized by distorted negative self-beliefs (NSBs), which are thought to enhance emotional reactivity, interfere with emotion regulation, and undermine social functioning. Cognitive reappraisal is a type of emotion regulation used to alter NSBs, with the goal of modulating emotional reactivity. Despite its relevance, little is known about the neural bases and temporal features of cognitive reappraisal in patients with SAD.
Twenty-seven patients with SAD and 27 healthy control subjects (HCs) were trained to react and to implement cognitive reappraisal to downregulate negative emotional reactivity to NSBs, while undergoing functional magnetic resonance imaging and providing ratings of negative emotion experience.
Behaviorally, compared with HCs, patients with SAD reported greater negative emotion both while reacting to and reappraising NSBs. However, when cued, participants in both groups were able to use cognitive reappraisal to decrease negative emotion. Neurally, reacting to NSBs resulted in early amygdala response in both groups. Reappraising NSBs resulted in greater early cognitive control, language, and visual processing in HCs but greater late cognitive control, visceral, and visual processing in patients with SAD. Functional connectivity analysis during reappraisal identified more regulatory regions inversely related to left amygdala in HCs than in patients with SAD. Reappraisal-related brain regions that differentiated patients and control subjects were associated with negative emotion ratings and cognitive reappraisal self-efficacy.
Findings regarding cognitive reappraisal suggest neural timing, connectivity, and brain-behavioral associations specific to patients with SAD and elucidate neural mechanisms that might serve as biomarkers of interventions for SAD.

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