This review presents the current state of understanding of trauma-informed modalities in light of current research in neuroscience, analyzing which brain structures and processes are impacted by these modalities. Studies included in the present review met the inclusion criteria of 1) addressing post-traumatic stress disorder (PTSD) in a specific population, 2) treatment of PTSD using any of the evidence-based trauma-informed modalities considered in this review, and 3) presenting functional magnetic resonance imagery (fMRI) data, derived from BOLD signals and voxel-compression maps, of brain structures impacted by these trauma-informed modalities. Articles for this review were collated through PubMed and MEDLINE, using key terms in descending order, such as ‘childhood trauma’, ‘adolescent trauma’, and ‘adulthood trauma’, to ‘PTSD’, ‘fMRI’, and so on, depending on the modality in question. Based on these criteria and research methods, 37 studies remained for inclusion in the present review. Among a number of critical findings, this review demonstrates that eye movement desensitization and reprocessing (EMDR) and mindfulness therapy effectively deactivate hindbrain regions implicated in the downregulation of autonomic nervous system (ANS) hyperarousal. This review also shows that trauma-focused cognitive behavioral therapy (TF-CBT) and EMDR activate the hippocampus, anterior cingulate cortex (ACC), medial prefrontal cortex (mPFC), and orbitofrontal cortex (OFC)—areas that are implicated in crucial cognitive, affective, and behavioral processes that aid trauma survivors in navigating their challenges.

Misunderstanding, stigmatization, and fascination abound in western culture concerning the concepts of psychopathy and sociopathy. These concepts are often used interchangeably—and erroneously—to describe violent or aggressive behavior in humans. These concepts tend also to be hurled as insults at individuals assumed to exhibit a lack empathy, impulsive decision making, and violent behavior. Psychopathy and sociopathy, however, are two concepts that describe different etiologies of the same mental health condition: antisocial personality disorder. This chapter bifurcates between the neurobiological origins of psychopathy and sociopathy, contributing to the destigmatization of a broadly misunderstood mental health condition. This chapter also explores recent findings from functional magnetic resonance imagery studies that analyze neurophysiological activity germane to psychopathy and sociopathy. Using these terms, students, clinicians, and researchers have access to a language that outlines correlations in neural substrate activity between genetic antisocial personality disorder (psychopathy) and epigenetic antisocial personality disorder (sociopathy). These terms might also serve to enhance treatment outcomes, as they implicate discrete neural substrates that have the potential to be treated using psychotherapeutic and psychopharmacological interventions.

IntroductionThe present systematic review and meta-analysis explores the impacts of cognitive processing therapy (CPT), eye movement desensitization and reprocessing (EMDR), and prolonged exposure (PE) therapy on neural activity underlying the phenomenon of post-traumatic growth for adult trauma survivors.MethodsWe utilized the following databases to conduct our systematic search: Boston College Libraries, PubMed, MEDLINE, and PsycINFO. Our initial search yielded 834 studies for initial screening. We implemented seven eligibility criteria to vet articles for full-text review. Twenty-nine studies remained for full-text review after our systematic review process was completed. Studies were subjected to several levels of analysis. First, pre-and post- test post-traumatic growth inventory (PTGI) scores were collected from all studies and analyzed through a forest plot using Hedges’ g. Next, Montreal Neurological Institute (MNI) coordinates and t-scores were collected and analyzed using an Activation Likelihood Estimation (ALE) to measure brain function. T-scores and Hedges’ g values were then analyzed using Pearson correlations to determine if there were any relationships between brain function and post-traumatic growth for each modality. Lastly, all studies were subjected to a bubble plot and Egger’s test to assess risk of publication bias across the review sample.ResultsForest plot results indicated that all three interventions had a robust effect on PTGI scores. ALE meta-analysis results indicated that EMDR exhibited the largest effect on brain function, with the R thalamus (t = 4.23, p < 0.001) showing robust activation, followed closely by the R precuneus (t = 4.19, p < 0.001). Pearson correlation results showed that EMDR demonstrated the strongest correlation between increased brain function and PTGI scores (r = 0.910, p < 0.001). Qualitative review of the bubble plot indicated no obvious traces of publication bias, which was corroborated by the results of the Egger’s test (p = 0.127).DiscussionOur systematic review and meta-analysis showed that CPT, EMDR, and PE each exhibited a robust effect on PTG impacts across the course of treatment. However, when looking closer at comparative analyses of neural activity (ALE) and PTGI scores (Pearson correlation), EMDR exhibited a more robust effect on PTG impacts and brain function than CPT and PE.

This review aims to systematically assess the current literature about prenatal epigenetic markers that lead to post-traumatic stress disorder susceptibility across the lifespan. Studies included in this review met several research criteria: Studies included (1) participants with a PTSD diagnosis according to the DSM-5, (2) prenatal epigenetic marker data that could be analyzed, and (3) explicit references to postnatal PTSD susceptibility. Our study sample fit within a timeframe of 2002 (the earliest recorded studies of prenatal susceptibility to post-traumatic stress disorder in the databases used) and February 2021 when the literature search for this review was terminated. Studies for this review were collated from PubMed, MEDLINE, Science Direct, and Boston College School of Social Work Library databases. A systematic search was conducted in these databases using basic keyword terms, such as “PSTD resilience” and “PTSD vulnerability,” and then adding clarifying terms to refine specific searches, such as “epigenetics,” “genetics,” “epigenetic markers,” “haplotypes,” and “mRNA methylation.” Based on these criteria and research methods, 33 studies remained for inclusion in the review sample. This review suggests that BDNF Val66-Met, a polymorphism of FKBP5, and an altered messenger ribonucleic acid methylation marker in NR3C1 present most often in cases of PTSD. These epigenetic markers might be implicated in central neurological processes related to post-traumatic stress disorder symptomatology.