Abstract
PURPOSE OF REVIEW: Aberrant amygdala activity is implicated in the neurobiology of social anxiety disorder (SAD) and is, therefore, a treatment target. However, the extent to which amygdala predicts clinical improvement or is impacted by treatment has not been critically examined. This review highlights recent neuroimaging findings from clinical trials and research that test links between amygdala and mechanisms of action. RECENT FINDINGS: Neuropredictor studies largely comprised psychotherapy where improvement was foretold by amygdala activity and regions beyond amygdala such as frontal structures (e.g., anterior cingulate cortex, medial prefrontal cortex) and areas involved in visual processes (e.g., occipital regions, superior temporal gyrus). Pre-treatment functional connectivity between amygdala and frontal areas was also shown to predict improvement signifying circuits that support emotion processing and regulation interact with treatment. Pre-to-post studies revealed decreases in amygdala response and altered functional connectivity in amygdala pathways regardless of treatment modality. In analogue studies of fear exposure, greater reduction in anxiety was predicted by less amygdala response to a speech challenge and amygdala activity decreased following exposures. Yet, studies have also failed to detect amygdala effects reporting instead treatment-related changes in regions and functional systems that support sensory, emotion, and regulation processes. An array of regions in the corticolimbic subcircuits and extrastriate cortex appear to be viable sites of action. The amygdala and amygdala pathways predict treatment outcome and are altered following treatment. However, further study is needed to establish the role of the amygdala and other candidate regions and brain circuits as sites of action.