A causal model of post-traumatic stress disorder: Disentangling predisposed from acquired neural abnormalities

Roee Admon*, Mohammed R. Milad, Talma Hendler

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)337-347
Number of pages11
JournalTrends in Cognitive Sciences
Volume17
Issue number7
DOIs
StatePublished - Jul 2013

Funding

FundersFunder number
Israel-Centers of Excellence
U.S. Department of DefenseW81XWH-11-2-0008
Israel Science Foundation51/11
Tel Aviv University
Israeli Centers for Research Excellence

    Keywords

    • Amygdala
    • Fear extinction
    • Functional connectivity
    • Hippocampus
    • Neuroimaging
    • PTSD
    • Prefrontal cortex
    • Risk factor
    • Stress

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