Predicting cognitive behavioral therapy response in social anxiety disorder with anterior cingulate cortex and amygdala during emotion regulation

Background Cognitive Behavioral Therapy (CBT) for social anxiety disorder (SAD) and other internalizing conditions attempts to improve emotion regulation. Accumulating data indicate anterior cingulate cortex (ACC), and to a lesser extent amygdala, activation in various tasks predicts treatment outcome. However, little is known about ACC and amygdala activation to emotion regulation in predicting clinical improvement following CBT in SAD. Methods Before treatment, 38 SAD patients completed implicit and explicit emotion regulation paradigms during fMRI. Implicit regulation involved attentional control over negative distractors. Explicit regulation comprised cognitive reappraisal to negative images. Pre-CBT brain activity was circumscribed to anatomical-based ACC sub-regions (rostral, dorsal) and amygdala masks, which were submitted to ROC curves to examine predictive validity as well as correlational analysis to evaluate prognostic change in symptom severity. Results More rostral (rACC) activity in implicit regulation and less rACC activity during explicit regulation distinguished responders (34%) from non-responders. Greater amygdala response in implicit regulation also foretold responder status. Baseline rACC and amygdala activity during attentional control correlated with pre-to-post CBT change in symptom severity such that more activation was related to greater decline in symptoms. No significant correlations were observed for explicit regulation. Conclusions Across forms of regulation, rACC activity predicted responder status whereas amygdala as a neuromarker was limited to implicit regulation. While the direction of effects (enhanced vs. reduced) in rACC activity was task-dependent, results suggest SAD patients with deficient regulation benefited more from CBT. Findings support previous studies involving patients with depression and suggest the rACC may be a viable marker of clinical improvement in SAD.