This is a review article of neuroimaging studies in post-traumatic stress disorder (PTSD). Findings from structural, biochemical, and functional studies are summarized. Magnetic resonance imaging (MRI) volumetric studies have consistently reported decreased hippocampal volumes in PTSD. Proton magnetic resonance spectroscopy studies report decreased N-acetyl aspartate (NAA) ratios and absolute concentrations in the medial temporal lobe. Although still controversial, these findings from volumetric and spectroscopic studies are thought to represent decreased neuronal density of the hippocampus. Functional imaging studies document different patterns of limbic and paralimbic structure activation in PTSD compared with controls. Of theoretical importance are findings of failure to activate the anterior cingulate as well as amygdala activation during symptom provocation studies. Also, increased amygdala activation was found with a behavioral task targeted to this structure. A neurobiological model is presented that takes into account findings from neuroimaging studies in PTSD as well as animal studies of fear conditioning. This model proposes that central to symptom mediation is a dysfunction of the anterior cingulate, with a failure to inhibit amygdala activation and/or an intrinsic lower threshold of amygdala response to fearful stimuli. The model further proposes that hippocampal atrophy is a result of the chronic hyperarousal symptoms mediated by amygdala activation.
Copyright 2001 Copyright by W.B. Saunders Company.