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


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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    ABSTRACT: Combat deployment enhances risk for posttraumatic stress symptoms. We assessed whether attention bias modification training (ABMT), delivered immediately prior to combat, attenuates the association between combat exposure and stress-related symptoms. 99 male soldiers preparing for combat were randomized to receive either an ABMT condition designed to enhance vigilance toward threat or an attention control training (ACT) designed to balance attention deployment between neutral and threat words. Frequency of combat events, and symptoms of PTSD and depression were measured prior to deployment and at a two-month follow-up.
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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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    ABSTRACT: Background: A hallmark symptom after psychological trauma is the presence of intrusive memories. It is unclear why only some moments of trauma become intrusive, and how these memories involuntarily return to mind. Understanding the neural mechanisms involved in the encoding and involuntary recall of intrusive memories may elucidate these questions. Method: Participants (n = 35) underwent functional magnetic resonance imaging (fMRI) while being exposed to traumatic film footage. After film viewing, participants indicated within the scanner, while undergoing fMRI, if they experienced an intrusive memory of the film. Further intrusive memories in daily life were recorded for 7 days. After 7 days, participants completed a recognition memory test. Intrusive memory encoding was captured by comparing activity at the time of viewing 'Intrusive scenes' (scenes recalled involuntarily), 'Control scenes' (scenes never recalled involuntarily) and 'Potential scenes' (scenes recalled involuntarily by others but not that individual). Signal change associated with intrusive memory involuntary recall was modelled using finite impulse response basis functions. Results: We found a widespread pattern of increased activation for Intrusive v. both Potential and Control scenes at encoding. The left inferior frontal gyrus and middle temporal gyrus showed increased activity in Intrusive scenes compared with Potential scenes, but not in Intrusive scenes compared with Control scenes. This pattern of activation persisted when taking recognition memory performance into account. Intrusive memory involuntary recall was characterized by activity in frontal regions, notably the left inferior frontal gyrus. Conclusions: The left inferior frontal gyrus may be implicated in both the encoding and involuntary recall of intrusive memories.
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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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