Discriminating neural abnormalities into the causes versus consequences of psychopathology would enhance the translation of neuroimaging findings into clinical practice. By regarding the traumatic encounter as a reference point for disease onset, neuroimaging studies of post-traumatic stress disorder (PTSD) can potentially allocate PTSD neural abnormalities to either predisposing (pre-exposure) or acquired (post-exposure) factors. Based on novel research strategies in PTSD neuroimaging, including genetic, environmental, twin, and prospective studies, we provide a causal model that accounts for neural abnormalities in PTSD, and outline its clinical implications. Current data suggest that abnormalities within the amygdala and dorsal anterior cingulate cortex represent predisposing risk factors for developing PTSD, whereas dysfunctional hippocampal-ventromedial prefrontal cortex (vmPFC) interactions may become evident only after having developed the disorder.
Bibliographical noteFunding Information:
This work was supported by a grant from the U.S. Department of Defense (DoD) award number W81XWH-11-2-0008; Israel-Centers of Excellence (I-CORE) Program of the Planning and Budgeting Committee, and the Israel Science Foundation (grant no. 51/11); and Adams Super Center for Brain Studies, Tel Aviv University. We would like to thank: Dr David Papo for his fruitful comments on earlier versions; Dr Gadi Lubin and Dr Eyal Fructer from the Israel Defense Forces medical corps for their support of this work; and Mr Matan Shalita for graphical assistance.
- Fear extinction
- Functional connectivity
- Prefrontal cortex
- Risk factor
ASJC Scopus subject areas
- Neuropsychology and Physiological Psychology
- Experimental and Cognitive Psychology
- Cognitive Neuroscience