| Literature DB >> 32276238 |
Christina F Sandman1, Katherine S Young2, Lisa J Burklund1, Darby E Saxbe3, Matthew D Lieberman4, Michelle G Craske5.
Abstract
Approximately half of individuals with Social Anxiety Disorder (SAD) treated with psychological intervention do not achieve clinically significant improvement or retain long-term gains. Neurobiological models of SAD propose that disruptions in functioning of amygdala-prefrontal circuitry is implicated in short-term treatment response. However, whether treatment-related changes in functional connectivity predict long-term well-being after psychotherapy is unknown. Patients with SAD completed an incidental emotion regulation task during fMRI before and after treatment with cognitive behavioral therapy or acceptance and commitment therapy (n = 23, collapsed across groups). Psychophysiological interaction analyses using amygdala seed regions were conducted to assess changes in functional connectivity from pre-to post-treatment that predicted symptom change from 6 to 12-month follow-up. Negative change (i.e., greater inverse/weaker positive) in amygdala connectivity with the dorsomedial prefrontal cortex (dmPFC) and dorsal anterior cingulate cortex (dACC) predicted greater symptom reduction during follow-up. Positive change in amygdala connectivity with the cerebellum, fusiform gyrus, and pre-central and post-central gyri predicted less symptom reduction (e.g., no change or worsening). Results suggest that strengthened amygdala connectivity with regulatory regions may promote better long-term outcomes, whereas changes with visual and sensorimotor regions may represent sensitization to emotion-related cues, conferring poorer outcomes. Clinical implications for treatment personalization are discussed, should effects replicate in larger samples.Entities:
Keywords: Amygdala; Emotion regulation; Long-term treatment response; Prefrontal cortex; fMRI
Year: 2020 PMID: 32276238 PMCID: PMC7329578 DOI: 10.1016/j.brat.2020.103612
Source DB: PubMed Journal: Behav Res Ther ISSN: 0005-7967