Article

Admon R, Milad MR, Hendle T (2013). A causal model of post-traumatic stress disorder: disentangling predisposed from acquired neural abnormalities

Center for Depression, Anxiety and Stress Research, McLean Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: .
Trends in Cognitive Sciences (Impact Factor: 21.97). 06/2013; 17(7). DOI: 10.1016/j.tics.2013.05.005
Source: PubMed

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.

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    • "Under such circumstances, it may become adaptive to be highly attentive to threat cues (LeDoux, 1995; Öhman, 1993). Shedding further light on the neural and behavioral mechanisms affected by acute stress (Admon et al., 2013; Lin et al., 2015; McEwen and Sapolsky, 1995) and the neuro-functional changes resulting from ABM and other forms of cognitive training (Britton et al., 2014; Browning et al., 2010; Cohen et al., 2016; Eldar and Bar-Haim, 2010; Sari et al., 2015), could considerably impact the development of more efficacious prevention protocols (Bar-Haim and Pine, 2013). "
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    • "Neurocircuitry models from this work suggest that PTSD is characterized by increased amygdala (and other limbic) activation and reduced ventromedial prefrontal cortex activation (Rauch et al. 1998, 2006). A recent model by Admon et al. (2013) suggested that abnormalities in the amygdala and dorsal anterior cingulate cortex are predisposing, while abnormal interactions between the hippocampus and ventromedial prefrontal cortex arise after developing PTSD (Admon et al. 2013). However, patient studies can tell us little about how intrusive memories are formed since they cannot examine the original encoding of the trauma. "
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    • "We hypothesized that soldiers with danger-based traumas would manifest greater resting neuronal activity in brain regions involved in heightened fear or hyperarousal (amygdalae), possibly indicating nascent defensive states, whereas non-danger-based traumas would be associated with brain regions involved in emotion regulation (rostral or dorsal anterior cingulate cortex— dACC; cf. Admon et al., 2013). We tested our hypotheses using a priori region of interest (ROI) analyses of brain regions most commonly active under fear-based conditions or uniquely implicated in PTSD during trauma script imagery. "
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