BackgroundThree intrinsic connectivity networks in the brain, namely the central executive, salience, and default mode networks, have been identified as crucial to the understanding of higher cognitive functioning, and the functioning of these networks has been suggested to be impaired in psychopathology, including posttraumatic stress disorder (PTSD).Objective1) To describe three main large-scale networks of the human brain; 2) to discuss the functioning of these neural networks in PTSD and related symptoms; and 3) to offer hypotheses for neuroscientifically-informed interventions based on treating the abnormalities observed in these neural networks in PTSD and related disorders.MethodLiterature relevant to this commentary was reviewed.ResultsIncreasing evidence for altered functioning of the central executive, salience, and default mode networks in PTSD has been demonstrated. We suggest that each network is associated with specific clinical symptoms observed in PTSD, including cognitive dysfunction (central executive network), increased and decreased arousal/interoception (salience network), and an altered sense of self (default mode network). Specific testable neuroscientifically-informed treatments aimed to restore each of these neural networks and related clinical dysfunction are proposed.ConclusionsNeuroscientifically-informed treatment interventions will be essential to future research agendas aimed at targeting specific PTSD and related symptoms.

Our results are consistent with prior research showing intrinsic network disruptions in PTSD and imply heterogeneous connectivity patterns underlying PTSD symptom dimensions. These findings suggest possible biomarkers for PTSD and its dissociative subtype.

Exposure to psychological trauma (for example, childhood/early life adversity, exposure to violence or assault, combat exposure, accidents or natural disasters) is known to increase one's risk of developing certain chronic medical conditions. Clinical and population studies provide evidence of systemic inflammatory activity in trauma survivors with various psychiatric and nonpsychiatric conditions. This transdiagnostic meta-analysis quantitatively integrates the literature on the relationship of inflammatory biomarkers to trauma exposure and related symptomatology. We conducted random effects meta-analyses relating trauma exposure to log-transformed inflammatory biomarker concentrations, using meta-regression models to test the effects of study quality and psychiatric symptomatology on the inflammatory outcomes. Across k=36 independent samples and n=14 991 participants, trauma exposure was positively associated with C-reactive protein (CRP), interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α (mean rs =0.2455, 0.3067, 0.2890, and 0.2998, respectively). No significant relationships were noted with fibrinogen, IL-2, IL-4, IL-8, or IL-10. In meta-regression models, the presence of psychiatric symptoms was a significant predictor of increased effect sizes for IL-1β and IL-6 (β=1.0175 and 0.3568, respectively), whereas study quality assessment scores were associated with increased effect sizes for IL-6 (β=0.3812). Positive correlations between inflammation and trauma exposure across a range of sample types and diagnoses were found. Although reviewed studies spanned an array of populations, research on any one specific psychiatric diagnosis was generally limited to one or two studies. The results suggest that chronic inflammation likely represents one potential mechanism underlying risk of health problems in trauma survivors.

Key nodes of the ICNs showed altered functional connectivity in PTSD as compared to controls, and differential results characterized sub- and supraliminal processing of threat-related stimuli. These findings enhance our understanding of ICNs underlying PTSD at different levels of conscious threat perception.

Individuals with trauma histories often elevate on validity scales and forensic interviews intended to detect symptom exaggeration or “faking bad.” A widely used forensic interview designed to detect feigned psychiatric illness, the Structured Interview of Reported Symptoms (SIRS; Rogers, Bagby, & Dickens, 1992), overclassifies individuals with complex trauma, including patients with dissociative identity disorder (DID), as feigners (Brand, McNary, Loewenstein, Kolos, & Barr, 2006; Rogers, Payne, Correa, Gillard, & Ross, 2009). However, a new Trauma Index shows promise of being useful in accurately distinguishing feigned versus genuine individuals with severe trauma (Rogers et al., 2009). No studies have examined the performance of the new edition of the SIRS, the SIRS-2 (Rogers, Sewell, & Gillard, 2010), with severely traumatized or dissociative individuals. This study sought to determine the utility of the SIRS, the SIRS-2, and the Trauma Index in distinguishing genuine DID from simulated DID. A sample of 49 DID patients was compared to 77 well-coached DID simulators. The SIRS classification rules combined with the Trauma Index, as well as the Trauma Index alone, provided the best balance of sensitivity and specificity, with similar overall diagnostic power. The SIRS-2, either alone or combined with the Trauma Index, was not as sensitive as the SIRS or Trauma Index alone. However, the SIRS-2 demonstrated excellent specificity.