The neurobiology of posttraumatic stress disorder: Dysfunction in the prefrontal-amygdala circuit?

Abstract

Posttraumatic stress disorder (PTSD) is an anxiety disorder that can develop following exposure to a traumatic event, including terrifying or life-threatening situations such as sexual assault or natural disasters. The disorder is characterized by a reaction of intense fear, helplessness, or horror when the individual experiences, testifes about, or is faced with one or more events that involve death, severe wounds, or a threat to one's own or another's physical integrity. One of the most important symptoms of PTSD is the revival of the traumatic event, which has been interpreted as an inability to downregulate negative emotions. Neuroimaging studies that probed the ability to regulate emotions in healthy volunteers have found a pattern characterized by activation of the prefrontal cortex associated with a reduction in amygdala activity. This suggests an inhibitory prefrontal cortex-amygdala circuit that underlies emotional regulation. The hypothesis that increased amygdala activation associated with PTSD results from dysfunction in the inhibitory mechanism exerted by the prefrontal cortex has been the topic of debate. The present review investigates the validity of dysfunction in the prefrontal-amygdala pathway in PTSD. The studies provide evidence that the amygdala and prefrontal cortex exhibit distinct activation patterns in PTSD, thus supporting the model of a dysfunctional circuit. Inconsistencies in the literature may be attributable to distinct PTSD subgroups, different experimental approaches, different contrasts employed in neuroimaging studies, and small sample sizes.