Abstract

A characterizing symptom of social anxiety disorder (SAD) is increased emotional reactivity towards potential social threat in combination with impaired emotion and stress regulation. While several neuroimaging studies have linked SAD with hyperreactivity in limbic brain regions when exposed to emotional faces, little is known about habituation in both the amygdala and neocortical regulation areas. 15 untreated SAD patients and 15 age- and gender-matched healthy controls underwent functional magnetic resonance imaging during repeated blocks of facial emotion () and object discrimination tasks (). Emotion processing networks were defined by a task-related contrast (). Linear regression was employed for assessing habituation effects in these regions. In both groups, the employed paradigm robustly activated the emotion processing and regulation network, including the amygdalae and orbitofrontal cortex (OFC). Statistically significant habituation effects were found in the amygdalae, OFC, and pulvinar thalamus of SAD patients. No such habituation was found in healthy controls. Concurrent habituation in the medial OFC and the amygdalae of SAD patients as shown in this study suggests intact functional integrity and successful short-term down-regulation of neural activation in brain areas responsible for emotion processing. Initial hyperactivation may be explained by an insufficient habituation to new stimuli during the first seconds of exposure. In addition, our results highlight the relevance of the orbitofrontal cortex in social anxiety disorders.

Highlights

  • According to recently published epidemiological data, social anxiety disorder (SAD) has a 12-month prevalence rate of 2:3% in Europe [1], 2:8{7:1% in the USA [2], and 0:8% in Japan [3]

  • Task-related (EDTwODT) activations were observed in both right and left amygdalae, and in left and right dorsolateral prefrontal cortex, which have been linked to voluntary cognitive control and performance monitoring

  • Activation was found within the medial orbitofrontal cortex, which is a critical area for modulating fear [65,66]

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Summary

Introduction

According to recently published epidemiological data, social anxiety disorder (SAD) has a 12-month prevalence rate of 2:3% in Europe [1], 2:8{7:1% in the USA [2], and 0:8% in Japan [3] (for data on other regions refer to [4]). SAD is a disabling condition impairing normal social life as patients tend to limit or remove themselves from social situations where they may be subject to evaluation by other people. This avoidance behavior is based on the fear to display anxiety symptoms (e.g., blushing) or act in a way (e.g., stuttering) that will be humiliating or embarrassing and potentially lower their social status and acceptance. Patients commonly recognize their fear as excessive or unreasonable, their behavior has devastating consequences for their social relationships, career opportunities, family life, and partner relations. SAD entails personal hardships for patients and their families and, as a consequence, enormous economic and social burden. SAD might be considered a risk factor for major depression, given the commonly earlier onset of SAD in co-morbid patients [7]

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