sleep time, REM sleep time, and REM-period duration (Taylor et al. 2007). See Chapter 6 for more discussion of PTSD and sleep disturbance.
Neuroimaging studies have been used to identify the neural circuits that may be involved in the development of PTSD. Neuroimaging studies, using magnetic resonance imaging (MRI), of people with PTSD have focused primarily on the amygdala, the hippocampus, the medial prefrontal cortex, and the anterior cingulate cortex. Reduced hippocampal volume has been reported in a diverse population of adults with PTSD, both those with a history of childhood trauma and those who suffered trauma as adults. A recent neuroimaging study of identical twin children of veterans who had PTSD and reduced hippocampal volume found that the twin children also had reduced hippocampal volume despite having had no exposure to combat and no history of PTSD (Gilbertson et al. 2002). In some people, smaller hippocampal volumes may predate their trauma exposure and PTSD and be a risk factor for PTSD rather than a consequence of it.
However, not all studies report smaller hippocampal findings in subjects with PTSD (Bonne et al. 2001), and the literature is ambiguous about whether PTSD is associated with reduced hippocampal volume in children (De Bellis et al. 2001). Recent studies suggest that traumatic stress in early development may have diffuse effects on total brain volume rather than only effects on hippocampal volume (De Bellis et al. 2002a,b). Possible explanations for discrepant findings on hippocampal volume in PTSD include variability in intensity and duration of trauma exposure, the presence of comorbid psychiatric disorders, differences in imaging methods (Vythilingam et al. 2005), and the lack of an effect of PTSD on hippocampal volume.
Functional MRI studies that measure regional cerebral blood flow (rCBF) using cognitive activation models, script-driven imagery, or other methods that provoke PTSD re-experiencing symptoms have generally found exaggerated activation of the amygdala or reduced activation of the prefrontal cortex. The overactive amygdala may be receiving insufficient negative feedback from the anterior cingulate gyrus and the medial prefrontal cortex.
Although most functional imaging studies have examined responses to threat- or trauma-relevant stimuli, it is also important to sort out how neural networks function in PTSD in the absence of threat-related stimuli. One study explored PTSD responses to a selective attention task that engages anterior cingulate cortex networks but in response to a nonthreatening stimulus. Bryant and Guthrie (2005) investigated whether anterior cingulate-amygdala dysregulation in PTSD was specific to processing threat-related stimuli or generalized to more generic, nonthreatening stimuli. They believe that their findings of enhanced anterior cingulate responses, and activation in the left amygdala and posterior parietal networks in response to nonthreatening stimuli, may reflect generalized hypervigilance. The nature and anatomic bases of attention and working-memory deficits in PTSD are also being studied with functional neuroimaging. With proton-emission tomography, working-memory deficits in PTSD have been found to be associated with reduced left dorsolateral prefrontal cortical activity (Clark et al. 2003).
In summary, many structural MRI studies have found that decreased hippocampal volume is associated with PTSD in adults. In general, functional neuroimaging studies in trauma survivors with PTSD have reported exaggerated rCBF in the amygdala and other paralimbic regions and relative decreases in prefrontal cortical rCBF. Increased stress-induced activation of the amygdala in combination with reduced inhibition by the prefrontal cortex might leave a