Post-traumatic stress disorder (PTSD) includes a constellation of disabling behavioral and emotional symptoms that occur in a proportion of individuals exposed to severe psychological trauma. PTSD can be a chronic and debilitating condition in which intrusive memories, hypervigilence, heightened physiological reactivity to reminders of the traumatic event, and avoidance can lead to significant social and occupational impairment. Understanding the neurobiology of this disorder has not only served as validation of PTSD as a diagnostic entity, but may ultimately be critical to the development of more effective therapeutic interventions.

Neuroimaging studies of structural brain abnormalities in PTSD have largely emerged in the context of two principal lines of evidence in the literature. First, early animal research provided compelling evidence that exposure to severe and chronic stress, a process that may be mediated by the neurotoxic impact of elevated corticosteroids, can damage the hippocampal formation, namely, CA3 neuronal cell loss, diminished neuronal regeneration, atrophy of dendritric branching, and reduced levels of brain-derived neurotrophic factor (Gould et al., 1997; Margarinos et al., 1996; McEwen, 1995; Sapolsky et al., 1990; Smith et al., 1995; Uno et al., 1989). As a result, the initial neuroanatomical investigations of PTSD centered largely upon the morphology of the hippocampus. Second, an improved understanding in recent years of the neurocircuitry underlying conditioned fear acquisition and extinction in animals has identified a number of specific brain regions of interest (Herry et al., 2008; Maren, 2005) that are potentially relevant to an understanding of the symptomatology of PTSD (Rauch et al., 2006).