Social anxiety disorder (SAD) is one of the most frequent anxiety disorders. The landmark meta-analysis of functional neuroimaging studies by Etkin and Wager (2007) revealed primarily the typical fear circuit as overactive in SAD. Since then, new methodological developments such as functional connectivity and more standardized structural analyses of grey and white matter have been developed. We provide a comprehensive update and a meta-analysis of neuroimaging studies in SAD since 2007 and present a new model of the neurobiology of SAD. We confirmed the hyperactivation of the fear circuit (amygdala, insula, anterior cingulate and prefrontal cortex) in SAD. In addition, task-related functional studies revealed hyperactivation of medial parietal and occipital regions (posterior cingulate, precuneus, cuneus) in SAD and a reduced connectivity between parietal and limbic and executive network regions. Based on the result of this meta-analysis and review, we present an updated model of SAD adopting a network-based perspective. The disconnection of the medial parietal hub in SAD extends current frameworks for future research in anxiety disorders.

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Social anxiety disorder (SAD) is the second leading anxiety disorder. On the functional neurobiological level, specific brain regions involved in the processing of anxiety-laden stimuli and in emotion regulation have been shown to be hyperactive and hyper-responsive in SAD such as amygdala, insula and orbito- and prefrontal cortex. On the level of brain structure, prior studies on anatomical differences in SAD resulted in mixed and partially contradictory findings. Based on previous functional and anatomical models of SAD, this study examined cortical thickness in structural magnetic resonance imaging data of 46 patients with SAD without comorbidities (except for depressed episode in one patient) compared with 46 matched healthy controls in a region of interest-analysis and in whole-brain. In a theory-driven ROI-analysis, cortical thickness was increased in SAD in left insula, right anterior cingulate and right temporal pole. Furthermore, the whole-brain analysis revealed increased thickness in right dorsolateral prefrontal and right parietal cortex. This study detected no regions of decreased cortical thickness or brain volume in SAD. From the perspective of brain networks, these findings are in line with prior functional differences in salience networks and frontoparietal networks associated with executive-controlling and attentional functions.

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In conclusion, continued treatment with cinacalcet is required to maintain long-term normocalcaemia and to suppress the enhanced PTH production in renal transplant recipients with persistent hyperparathyroidism.