Changes in Anterior Cingulate and Amygdala After Cognitive Behavior Therapy of Posttraumatic Stress Disorder

Abstract

Posttraumatic stress disorder (PTSD) may develop from impaired extinction of conditioned fear responses. Exposure-based treatment of PTSD is thought to facilitate extinction learning (Charney, 2004). Fear extinction is mediated by inhibitory control of the ventromedial prefrontal cortex (vmPFC) over amygdala-based fear processes (Phelps, Delgado, Nearing, & LeDoux, 2004; Quirk, Russo, Barron, & LeBron, 2000). Most neuroimaging studies of PTSD reveal reduced vmPFC activity (particularly in rostral anterior cingulate cortex, or rACC; Lanius et al., 2001; Shin et al., 2005), and some find increased amygdala activity during threat processing (Shin et al., 2005). In addition, increased amygdala activity during fear conditioning and reduced vmPFC activity during extinction have been reported in PTSD (Bremner et al., 2005). Although PTSD patients show increased orbitofrontal and medial prefrontal activity following treatment with serotonin reuptake inhibitors (SSRIs; Fernandez et al., 2001; Seedat et al., 2004), no studies have investigated neural networks before and after exposure-based treatment of PTSD. We report the first such study. We hypothesized that symptom reduction would be associated with increased rACC activity and reduced amygdala activity during fear processing.