Citation

Ramage AE, Litz BT, Resick PA, Woolsey MD, Dondanville KA, Young-McCaughan S, Borah AM, Borah EV, Peterson AL, Fox PT. Soc. Cogn. Affect. Neurosci. 2015; 11(2): 234-242.

Affiliation

Department of Psychiatry and the Research Imaging Institute, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA, State Key Laboratory for Brain and Cognitive Science, Hong Kong University, Pok Fu Lam, Hong Kong.

Copyright

(Copyright © 2015, Oxford University Press)

DOI

10.1093/scan/nsv102

PMID

26373348

Abstract

Post-traumatic stress disorder (PTSD) is presumably the result of life threats and conditioned fear. However, the neurobiology of fear fails to explain the impact of traumas that do not entail threats. Neuronal function, assessed as glucose metabolism with (18)fluoro-deoxyglucose positron emission tomography, was contrasted in active duty, treatment-seeking US Army Soldiers with PTSD endorsing either danger- (n = 19) or non-danger-based (n = 26) traumas, and was compared with soldiers without PTSD (Combat Controls, n = 26) and Civilian Controls (n = 24). Prior meta-analyses of regions associated with fear or trauma script imagery in PTSD were used to compare glucose metabolism across groups. Danger-based traumas were associated with higher metabolism in the right amygdala than the control groups, while non-danger-based traumas associated with heightened precuneus metabolism relative to the danger group. In the danger group, PTSD severity was associated with higher metabolism in precuneus and dorsal anterior cingulate and lower metabolism in left amygdala (R(2 )= 0.61). In the non-danger group, PTSD symptom severity was associated with higher precuneus metabolism and lower right amygdala metabolism (R(2 )= 0.64). These findings suggest a biological basis to consider subtyping PTSD according to the nature of the traumatic context.

Language: en