a1 Department of Psychiatry, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
a2 Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
a3 Institute of Psychological Medicine and Clinical Neurosciences, Cardiff University School of Medicine, Heath Park, Cardiff, UK
a4 St Catharine's College, Cambridge, UK
a5 Computer Laboratory, University of Cambridge, UK
Background Prior studies of adult post-traumatic stress disorder (PTSD) suggest abnormal functioning of prefrontal and limbic regions. Cumulative childhood and adult trauma exposures are major risk factors for developing adult PTSD, yet their contribution to neural dysfunction in PTSD remains poorly understood. This study aimed to examine the neural correlates of childhood and adult trauma exposure and post-traumatic stress symptoms (PTSS) within a single model.
Method Medication-free male combat veterans (n = 28, average age 26.6 years) with a wide range of PTSS were recruited from the community between 2010 and 2011. Subjects completed an emotional face-morphing task while undergoing functional magnetic resonance imaging (fMRI). Clinical ratings included the Clinician-Administered PTSD Scale (CAPS), Childhood Trauma Questionnaire (CTQ) and Combat Exposure Scale (CES). A priori regions were examined through multivariate voxelwise regression in SPM8, using depressive symptoms and IQ as covariates.
Results In the angry condition, CAPS scores correlated positively with activation in the medial prefrontal cortex [mPFC; Brodmann area (BA) 10, z = 3.51], hippocampus (z = 3.47), insula (z = 3.62) and, in earlier blocks, the amygdala. CES and CTQ correlated positively with activation in adjacent areas of the dorsal anterior cingulate cortex (dACC; BA 32, z = 3.70 and BA 24, z = 3.88 respectively). In the happy condition, CAPS, CTQ and CES were not correlated significantly with activation patterns.
Conclusions dACC activation observed in prior studies of PTSD may be attributable to the cumulative effects of childhood and adult trauma exposure. By contrast, insula, hippocampus and amygdala activation may be specific to PTSS. The specificity of these results to threat stimuli, but not to positive stimuli, is consistent with abnormalities in threat processing associated with PTSS.
(Received April 24 2012)
(Revised September 03 2012)
(Accepted September 06 2012)
(Online publication October 18 2012)
c1 Address for correspondence: R. J. Herringa, M.D., Ph.D., Department of Psychiatry, University of Wisconsin School of Medicine and Public Health, 6001 Research Park Blvd, Madison, WI 53719, USA. (Email: firstname.lastname@example.org)