Richard A. Bryant

Association of Torture and Other Potentially Traumatic Events With Mental Health Outcomes Among Populations Exposed to Mass Conflict and Displacement: A Systematic Review and Meta-analysis

CONTEXT Uncertainties continue about the roles that methodological factors and key risk factors, particularly torture and other potentially traumatic events (PTEs), play in the variation of reported prevalence rates of posttraumatic stress disorder (PTSD) and depression across epidemiologic surveys among postconflict populations worldwide. OBJECTIVE To undertake a systematic review and meta-regression of the prevalence rates of PTSD and depression in the refugee and postconflict mental health field. DATA SOURCES An initial pool of 5904 articles, identified through MEDLINE, PsycINFO and PILOTS, of surveys involving refugee, conflict-affected populations, or both, published in English-language journals between 1980 and May 2009. STUDY SELECTION Surveys were limited to those of adult populations (n > or = 50) reporting PTSD prevalence, depression prevalence, or both. Excluded surveys comprised patients, war veterans, and civilian populations (nonrefugees/asylum seekers) from high-income countries exposed to terrorist attacks or involved in distal conflicts (> or = 25 years). DATA EXTRACTION Methodological factors (response rate, sample size and design, diagnostic method) and substantive factors (sociodemographics, place of survey, torture and other PTEs, Political Terror Scale score, residency status, time since conflict). DATA SYNTHESIS A total of 161 articles reporting results of 181 surveys comprising 81,866 refugees and other conflict-affected persons from 40 countries were identified. Rates of reported PTSD and depression showed large intersurvey variability (0%-99% and 3%-85.5%, respectively). The unadjusted weighted prevalence rate reported across all surveys for PTSD was 30.6% (95% CI, 26.3%-35.2%) and for depression was 30.8% (95% CI, 26.3%-35.6%). Methodological factors accounted for 12.9% and 27.7% PTSD and depression, respectively. Nonrandom sampling, small sample sizes, and self-report questionnaires were associated with higher rates of mental disorder. Adjusting for methodological factors, reported torture (Delta total R(2) between base methodological model and base model + substantive factor [DeltaR(2)] = 23.6%; OR, 2.01; 95% CI, 1.52-2.65) emerged as the strongest factor associated with PTSD, followed by cumulative exposure to PTEs (DeltaR(2) = 10.8%; OR, 1.52; 95% CI, 1.21-1.91), time since conflict (DeltaR(2) = 10%; OR, 0.77; 95% CI, 0.66-0.91), and assessed level of political terror (DeltaR(2) = 3.5%; OR, 1.60; 95% CI, 1.03-2.50). For depression, significant factors were number of PTEs (DeltaR(2) = 22.0%; OR, 1.64; 95% CI, 1.39-1.93), time since conflict (DeltaR(2) = 21.9%; OR, 0.80; 95% CI, 0.69-0.93), reported torture (DeltaR(2) = 11.4%; OR, 1.48; 95% CI, 1.07-2.04), and residency status (DeltaR(2) = 5.0%; OR, 1.30; 95% CI, 1.07-1.57). CONCLUSION Methodological factors and substantive population risk factors, such as exposure to torture and other PTEs, after adjusting for methodological factors account for higher rates of reported prevalence of PTSD and depression.

Five essential elements of immediate and mid-term mass trauma intervention: empirical evidence

Abstract Given the devastation caused by disasters and mass violence, it is critical that intervention policy be based on the most updated research findings. However, to date, no evidence–based consensus has been reached supporting a clear set of recommendations for intervention during the immediate and the mid–term post mass trauma phases. Because it is unlikely that there will be evidence in the near or mid–term future from clinical trials that cover the diversity of disaster and mass violence circumstances, we assembled a worldwide panel of experts on the study and treatment of those exposed to disaster and mass violence to extrapolate from related fields of research, and to gain consensus on intervention principles. We identified five empirically supported intervention principles that should be used to guide and inform intervention and prevention efforts at the early to mid–term stages. These are promoting: 1) a sense of safety, 2) calming, 3) a sense of self– and community efficacy, 4) connectedness, and 5) hope.

The Psychiatric Sequelae of Traumatic Injury

OBJECTIVE Traumatic injury affects millions of people each year. There is little understanding of the extent of psychiatric illness that develops after traumatic injury or of the impact of mild traumatic brain injury (TBI) on psychiatric illness. The authors sought to determine the range of new psychiatric disorders occurring after traumatic injury and the influence of mild TBI on psychiatric status. METHOD In this prospective cohort study, patients were drawn from recent admissions to four major trauma hospitals across Australia. A total of 1,084 traumatically injured patients were initially assessed during hospital admission and followed up 3 months (N=932, 86%) and 12 months (N=817, 75%) after injury. Lifetime psychiatric diagnoses were assessed in hospital. The prevalence of psychiatric disorders, levels of quality of life, and mental health service use were assessed at the follow-ups. The main outcome measures were 3- and 12-month prevalence of axis I psychiatric disorders, levels of quality of life, and mental health service use and lifetime axis I psychiatric disorders. RESULTS Twelve months after injury, 31% of patients reported a psychiatric disorder, and 22% developed a psychiatric disorder that they had never experienced before. The most common new psychiatric disorders were depression (9%), generalized anxiety disorder (9%), posttraumatic stress disorder (6%), and agoraphobia (6%). Patients were more likely to develop posttraumatic stress disorder (odds ratio=1.92, 95% CI=1.08-3.40), panic disorder (odds ratio=2.01, 95% CI=1.03-4.14), social phobia (odds ratio=2.07, 95% CI=1.03-4.16), and agoraphobia (odds ratio=1.94, 95% CI=1.11-3.39) if they had sustained a mild TBI. Functional impairment, rather than mild TBI, was associated with psychiatric illness. CONCLUSIONS A significant range of psychiatric disorders occur after traumatic injury. The identification and treatment of a range of psychiatric disorders are important for optimal adaptation after traumatic injury.

The relationship between acute stress disorder and posttraumatic stress disorder : A prospective evaluation of motor vehicle accident survivors

Motor vehicle accident survivors (n = 92) were assessed for acute stress disorder (ASD) within 1 month of the trauma and reassessed (n = 71) for posttraumatic stress disorder (PTSD) 6 months posttrauma. ASD was diagnosed in 13% of participants, and a further 21% had subclinical levels of ASD. At follow-up, 78% of ASD participants and 60% of subclinical ASD participants met criteria for PTSD. The strong predictive power of acute numbing, depersonalization, a sense of relieving the trauma, and motor restlessness, in contrast to the low to moderate predictive power of other symptoms, indicates that only a subset of ASD symptoms is strongly related to the development of chronic PTSD. Although these findings support the use of the ASD diagnosis, they suggest that the dissociative and arousal clusters may require revision.

Interactions between BDNF Val66Met polymorphism and early life stress predict brain and arousal pathways to syndromal depression and anxiety

Individual risk markers for depression and anxiety disorders have been identified but the explicit pathways that link genes and environment to these markers remain unknown. Here we examined the explicit interactions between the brain-derived neurotrophic factor (BDNF) Val66Met gene and early life stress (ELS) exposure in brain (amygdala–hippocampal–prefrontal gray matter volume), body (heart rate), temperament and cognition in 374 healthy European volunteers assessed for depression and anxiety symptoms. Brain imaging data were based on a subset of 89 participants. Multiple regression analysis revealed main effects of ELS for body arousal (resting heart rate, P=0.005) and symptoms (depression and anxiety, P<0.001) in the absence of main effects for BDNF. In addition, significant BDNF–ELS interactions indicated that BDNF Met carriers exposed to greater ELS have smaller hippocampal and amygdala volumes (P=0.013), heart rate elevations (P=0.0002) and a decline in working memory (P=0.022). Structural equation path modeling was used to determine if this interaction predicts anxiety and depression by mediating effects on the brain, body and cognitive measures. The combination of Met carrier status and exposure to ELS predicted reduced gray matter in hippocampus (P<0.001), and associated lateral prefrontal cortex (P<0.001) and, in turn, higher depression (P=0.005). Higher depression was associated with poorer working memory (P=0.005), and slowed response speed. The BDNF Met–ELS interaction also predicted elevated neuroticism and higher depression and anxiety by elevations in body arousal (P<0.001). In contrast, the combination of BDNF V/V genotype and ELS predicted increases in gray matter of the amygdala (P=0.003) and associated medial prefrontal cortex (P<0.001), which in turn predicted startle-elicited heart rate variability (P=0.026) and higher anxiety (P=0.026). Higher anxiety was linked to verbal memory, and to impulsivity. These effects were specific to the BDNF gene and were not evident for the related 5HTT-LPR polymorphism. Overall, these findings are consistent with the correlation of depression and anxiety, yet suggest that partially differentiated gene–brain cognition pathways to these syndromes can be identified, even in a nonclinical sample. Such findings may aid establishing an evidence base for more tailored intervention strategies.

Treatment of acute stress disorder: a comparison of cognitive-behavioral therapy and supportive counseling.

Acute stress disorder (ASD) is a precursor of chronic posttraumatic stress disorder (PTSD). Twenty-four participants with ASD following civilian trauma were given 5 sessions of either cognitive-behavioral therapy (CBT) or supportive counseling (SC) within 2 weeks of their trauma. Fewer participants in CBT (8%) than in SC (83%) met criteria for PTSD at posttreatment. There were also fewer cases of PTSD in the CBT condition (17%) than in the SC condition (67%) 6 months posttrauma. There were greater statistically and clinically significant reductions in intrusive, avoidance, and depressive symptomatology among the CBT participants than among the SC participants. This study represents the 1st demonstration of successful treatment of ASD with CBT and its efficacy in preventing chronic PTSD.

Considering PTSD for DSM‐5

This is a review of the relevant empirical literature concerning the DSM‐IV‐TR diagnostic criteria for PTSD. Most of this work has focused on Criteria A1 and A2, the two components of the A (Stressor) Criterion. With regard to A1, the review considers: (a) whether A1 is etiologically or temporally related to the PTSD symptoms; (b) whether it is possible to distinguish “traumatic” from “non‐traumatic” stressors; and (c) whether A1 should be eliminated from DSM‐5. Empirical literature regarding the utility of the A2 criterion indicates that there is little support for keeping the A2 criterion in DSM‐5. The B (reexperiencing), C (avoidance/numbing) and D (hyperarousal) criteria are also reviewed. Confirmatory factor analyses suggest that the latent structure of PTSD appears to consist of four distinct symptom clusters rather than the three‐cluster structure found in DSM‐IV. It has also been shown that in addition to the fear‐based symptoms emphasized in DSM‐IV, traumatic exposure is also followed by dysphoric, anhedonic symptoms, aggressive/externalizing symptoms, guilt/shame symptoms, dissociative symptoms, and negative appraisals about oneself and the world. A new set of diagnostic criteria is proposed for DSM‐5 that: (a) attempts to sharpen the A1 criterion; (b) eliminates the A2 criterion; (c) proposes four rather than three symptom clusters; and (d) expands the scope of the B–E criteria beyond a fear‐based context. The final sections of this review consider: (a) partial/subsyndromal PTSD; (b) disorders of extreme stress not otherwise specified (DESNOS)/complex PTSD; (c) cross‐ cultural factors; (d) developmental factors; and (e) subtypes of PTSD. Depression and Anxiety, 2011.

Posttraumatic stress disorder following cancer. A conceptual and empirical review.

Life-threatening illness has recently been recognized as a stressor that can precipitate posttraumatic stress disorder (PTSD). This development has raised questions over the extent to which the PTSD diagnosis is applicable to the psychological reaction to being diagnosed with cancer. This paper identifies the core conceptual issues pertaining to cancer-related PTSD, critically reviews the empirical literature on PTSD following cancer, and considers the possible mechanisms and course of PTSD following a diagnosis of cancer. Specific issues that need to be considered in the assessment and treatment of cancer-related PTSD are reviewed. This review highlights that there is a need for stronger empirical base to guide clinical management of PTSD in cancer patients.

Posttraumatic stress disorder in children: The influence of developmental factors

Despite the prevalence of childhood trauma, there are currently no developmentally oriented cognitive theories of posttraumatic stress disorder (PTSD). This paper outlines the definitional issues of PTSD in children, reviews the incidence of PTSD in children, and compares PTSD profiles in children and adults. We propose that a cognitive theory of childhood PTSD needs to accommodate developmental factors, including knowledge, language development, memory, emotion regulation, and social cognition, in addition to contextual factors such as family interactions. Implications of these developmental factors for assessment and treatment of traumatized children are discussed.

Trauma modulates amygdala and medial prefrontal responses to consciously attended fear.

Effective fear processing relies on the amygdala and medial prefrontal cortex (MPFC). Post-trauma reactions provide a compelling model for examining how the heightened experience of fear impacts these systems. Post-traumatic stress disorder (PTSD) has been associated with excessive amygdala and a lack of MPFC activity in response to nonconscious facial signals of fear, but responses to consciously processed facial fear stimuli have not been examined. We used functional MRI to elucidate the effect of trauma reactions on amygdala-MPFC function during an overt fear perception task. Subjects with PTSD (n = 13) and matched non-traumatized healthy subjects (n = 13) viewed 15 blocks of eight fearful face stimuli alternating pseudorandomly with 15 blocks of neutral faces (stimulus duration 500 ms; ISI 767 ms). We used random effects analyses in SPM2 to examine within- and between-group differences in the MPFC and amygdala search regions of interest. Time series data were used to examine amygdala-MPFC associations and changes across the first (Early) versus second (Late) phases of the experiment. Relative to non-traumatized subjects, PTSD subjects showed a marked bilateral reduction in MPFC activity (in particular, right anterior cingulate cortex, ACC), which showed a different Early-Late pattern to non-traumatized subjects and was more pronounced with greater trauma impact and symptomatology. PTSD subjects also showed a small but significant enhancement in left amygdala activity, most apparent during the Late phase, but reduction in Early right amygdala response. Over the time course, trauma was related to a distinct pattern of ACC and amygdala connections. The findings suggest that major life trauma may disrupt the normal pattern of medial prefrontal and amygdala regulation.