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BackgroundInterpersonal violence damages mental health and frequently leads to aggressive defence strategies. If survivors are subsequently blamed for the events, both consequences worsen. Stigma flourishes, especially when survivors are silenced so that details of the trauma remain unknown. Breaking the secrecy both at the individual and collective level is key to enable the healing and reconciliation of individuals and communities living under continuous threat.MethodThe NETfacts health system is a stepped care model with three components: (1) Narrative Exposure Therapy (NET), an evidence-based trauma therapy that includes survivor testimony (2) NET for Forensic Offender Rehabilitation (FORNET) acknowledges that perpetrators are frequently also victims and assists in reducing aggression and the attraction to violence, and (3) a community intervention disseminating and discussing Facts derived from NET treatment (NETfacts) to challenge the collective avoidance of atrocities and other traumatic material. The intervention was piloted in a community with 497 adult residents in Eastern Democratic Republic of Congo. The willingness of clients to consent to sharing their anonymised testimonies (with a focus on sexual violence survivors and ex-combatants) was investigated, together with other components of feasibility including security and clinical safety, extent of support of respected local authorities and participation rates. As secondary outcomes, clinical and social measures were assessed before and post NETfacts among 200 village residents of whom 160 self-enrolled and 40 had not participated in any form of treatment.ResultsImplementation was feasible with 248 clients from a partner project giving consent to use their testimonies and high support of respected local authorities and participation rates (56% of residents self-enrolled in NETfacts). Immediate beneficial effects were shown for posttraumatic stress and rejection of rape myths among NETfacts participants who experienced multiple traumatic events in their own past. Attitudes towards ex-combatants improved and the perceived lack of social acknowledgement after trauma increased independent from participation. No significant change was observed for depressive symptoms.ConclusionNETfacts is a feasible and promising approach to challenge the culture of secrecy surrounding trauma, suppression and social exclusion. Long term effectiveness requires further evaluation.

PURPOSE:Adverse childhood experiences in sensitive periods of the developing brain render the individual at a life-long risk for a broad spectrum of aberrant health outcomes. However, there is a lack of scales for the comprehensive assessment of adverse childhood experiences providing information of various types and the age of occurrence. Based on the complete, experimental version of the Maltreatment and abuse chronology of exposure (MACE-X) scale, the present study aimed to develop and psychometrically test a Norwegian version of MACE. METHODS:The 75-item MACE-X was translated from German to Norwegian and administered as a self-report measure to 90 outpatients and 145 employees at a Division of specialized mental health care in South-Eastern Norway. The outpatients also completed the Childhood trauma questionnaire (CTQ) and the Symptom checklist 90 (SCL-90) to investigate convergent and predictive validity. To investigate test-retest reliability, outpatients completed MACE once more two weeks later. RESULTS:Rasch analysis and Anderson likelihood ratio tests on the combined outpatient and employee data resulted in a 55 item version of the Norwegian MACE. In the outpatient group, test-retest reliability of the MACE-55 was excellent for total scores (ICC ≥ 0.94) and good to excellent for 10 subscale scores (ICC ≥ 0.82). Convergent validity with the CTQ was moderate to high for both total scores (0.63 ≥ r ≥ 0.86) and subscale scores (0.56 ≥ r ≥ 0.82). As compared to CTQ total scores, a MACE total score that combined severity and duration of exposure was numerically more strongly associated with overall psychiatric symptoms and each of nine symptom domains on the SCL-90. CONCLUSIONS:The newly developed Norwegian MACE comprehensively assesses past exposure to adverse childhood experiences with high psychometric properties. This scale is a useful tool for research questions addressing sensitive periods for childhood adversities and associated health phenotypes.

Exposure to traumatic stressors and subsequent trauma-related mental changes may alter a person's risk-taking behavior. It is unclear whether this relationship depends on the specific types of traumatic experiences. Moreover, the association has never been tested in displaced individuals with substantial levels of traumatic experiences. The present study assessed risk-taking behavior in 56 displaced individuals by means of the balloon analogue risk task (BART). Exposure to traumatic events, symptoms of posttraumatic stress disorder and depression were assessed by means of semi-structured interviews. Using a novel statistical approach (stochastic gradient boosting machines), we analyzed predictors of risk-taking behavior. Exposure to organized violence was associated with less risk-taking, as indicated by fewer adjusted pumps in the BART, as was the reported experience of physical abuse and neglect, emotional abuse, and peer violence in childhood. However, civil traumatic stressors, as well as other events during childhood were associated with lower risk taking. This suggests that the association between global risk-taking behavior and exposure to traumatic stress depends on the particular type of the stressors that have been experienced.

The scent of blood is potentially one of the most fundamental and survival-relevant olfactory cues in humans. This experiment tests the first human parameters of perceptual threshold and emotional ratings in men and women of an artificially simulated smell of fresh blood in contact with the skin. We hypothesize that this scent of blood, with its association with injury, danger, death, and nutrition will be a critical cue activating fundamental motivational systems relating to either predatory approach behavior or prey-like withdrawal behavior, or both. The results show that perceptual thresholds are unimodally distributed for both sexes, with women being more sensitive. Furthermore, both women and men's emotional responses to simulated blood scent divide strongly into positive and negative valence ratings, with negative ratings in women having a strong arousal component. For women, this split is related to the phase of their menstrual cycle and oral contraception (OC). Future research will investigate whether this split in both genders is context-dependent or trait-like.

Inconsistent findings exist for the activity of the hypothalamic-pituitary-adrenal (HPA) axis in patients with stress related disorders. Recent studies point towards early life stress as a potential modulator.We investigated the impact of childhood sexual abuse on phasic (saliva cortisol reactivity) and tonic (hair cortisol) regulation. Furthermore, we assessed predictors on cortisol accumulation in hair. Women (N = 43) with stress-related disorders underwent a standardized assessment of idiographic adverse and traumatic experiences and psychopathology, while measuring salivary cortisol and, heart rate and blood pressure.Comparing women with and without childhood sexual abuse revealed lower rates of responders and distinct levels of salivary cortisol to the interview in conjunction with a lower heart rate for the abused group. Childhood adversities, traumatic experiences, and depression contributed to higher hair cortisol levels.Our finding of lower response rate and distinct salivary cortisol pattern in individuals with childhood sexual abuse compared to individuals without early sexual abuse supports the role of environmental programming for the HPA axis. Both, childhood adversities and traumatic stress emerge as crucial factors for long-term cortisol secretion. Lower or suppressed phasic cortisol responses to trauma-related stimuli may therefore be associated with higher tonic values. Thus, early exposure to adversities may result in a biological distinct phenotype in adult patients with stress-related disorders.

Current civil wars are characterized by the increasing involvement of civilian populations and the systematic employment of child soldiers. An example of such wars was the conflict in Northern Uganda, where the war-affected population is still challenged by the reintegration of formerly abducted children and youths. A cross-sectional, population-based survey, using a multistage cluster sampling approach of 1,113 Northern Ugandans aged between 12 and 25 in camps for internally displaced persons and locally validated instruments was conducted to assess symptoms and diagnoses of Posttraumatic Stress Disorder (PTSD) and probable Depression in war-affected, as well as formerly abducted individuals. Further objectives were to determine predictors of psychopathology and to relate indicators of maladjustment (i.e., impairments in daily and community functioning, somatic complaints, suicidality, aggressiveness and discrimination) to abduction, level of exposure to violence and psychopathology. 43% of the sample reported abduction by the rebel army. Exposure to violence among this group was higher than for non-abducted youths (t = 28.05; p

BACKGROUND: Posttraumatic stress disorder (PTSD) is a serious psychiatric condition that was found to be associated with altered functioning of the hypothalamic-pituitary-adrenal (HPA) axis and changes in glucocorticoid (GC) responsiveness. The physiological actions of GCs are primarily mediated through GC receptors (GR) of which isoforms with different biological activities exist. This study aimed to investigate whether trauma-experience and/or PTSD are associated with altered expression of GR splice variants. METHODS: GRα and GRβ mRNA expression levels were determined by real-time quantitative PCR in whole blood samples of individuals with chronic and severe forms of PTSD (n = 42) as well as in ethnically matched reference subjects (non-PTSD, n = 35). RESULTS: Individuals suffering from PTSD exhibited significantly lower expression of the predominant and functionally active GRα isoform compared to non-PTSD subjects. This effect remained significant when accounting for gender, smoking, psychotropic medication or comorbid depression. Moreover, the GRα expression level was significantly negatively correlated with the number of traumatic event types experienced, both in the whole sample and within the PTSD patient group. Expression of the less abundant and non-ligand binding GRβ isoform was comparable between patient and reference groups. CONCLUSIONS: Reduced expression of the functionally active GRα isoform in peripheral blood cells of individuals with PTSD seems to be a cumulative effect of trauma burden rather than a specific feature of PTSD since non-PTSD subjects with high trauma load showed an intermediate phenotype between PTSD patients and individuals with no or few traumatic experiences.

Recent studies have suggested a protective role of physiological β-amyloid autoantibodies (Aβ-autoantibodies) in Alzheimer's disease (AD). However, the determination of both free and dissociated Aβ-autoantibodies in serum hitherto has yielded inconsistent results regarding their function and possible biomarker value. Here we report the application of a new sandwich enzyme-linked immunosorbent assay (ELISA) for the determination of antigen-bound Aβ-autoantibodies (intact Aβ-IgG immune complexes) in serum and cerebrospinal fluid (CSF) of a total number of 112 AD patients and age- and gender-matched control subjects. Both serum and CSF levels of Aβ-IgG immune complexes were found to be significantly higher in AD patients compared to control subjects. Moreover, the levels of Aβ-IgG complexes were negatively correlated with the cognitive status across the groups, increasing with declining cognitive test performance of the subjects. Our results suggest a contribution of IgG-type autoantibodies to Aβ clearance in vivo and an increased immune response in AD, which may be associated with deficient Aβ-IgG removal. These findings may contribute to elucidating the role of Aβ-autoantibodies in AD pathophysiology and their potential application in AD diagnosis.

In a previous report we showed that cognitive training fostering auditory-verbal discrimination and working memory normalized magnetoencephalographic (MEG) M50 gating ratio in schizophrenia patients. The present analysis addressed whether training effects on M50 ratio and task performance are mediated by changes in brain oscillatory activity. Such evidence should improve understanding of the role of oscillatory activity in phenomena such as M50 ratio, the role of dysfunctional oscillatory activity in processing abnormalities in schizophrenia, and mechanisms of action of cognitive training.Time-locked and non-time-locked oscillatory activity was measured together with M50 ratio in a paired-click design before and after a 4-week training of 36 patients randomly assigned to specific cognitive exercises (CE) or standard (comparison) cognitive training (CP). Patient data were compared to those of 15 healthy controls who participated in two MEG measurements 4 weeks apart without training. Training led to more time-locked gamma-band response and more non-time-locked alpha-band desynchronization, moreso after CE than after CP. Only after CE, increased alpha desynchronization was associated with normalized M50 ratio and with improved verbal memory performance. Thus, both types of cognitive training normalized gamma activity, associated with improved stimulus encoding. More targeted training of auditory-verbal discrimination and memory additionally normalized alpha desynchronization, associated with improved elaborative processing. The latter presumably contributes to improved auditory gating and cognitive function.Results suggest that dysfunctional interplay of ocillatory activity that may contribute to auditory processing disruption in schizophrenia can be modified by targeted training.

Repeated exposure to traumatic stressors such as combat results in chronic symptoms of PTSD. However, previous findings suggest that former soldiers who report combat-related aggression to be appetitive are more resilient to develop PTSD. Appetitive Aggression should therefore prevent widespread mental suffering in perpetrators of severe atrocities even after decades.To test the long-term relationship between trauma-related illness and attraction to aggression, we surveyed a sample of 51 German male World-War II veterans (age: M = 86.7, SD = 2.8). War-related appetitive aggression was assessed with the Appetitive Aggression Scale (AAS). Current- and lifetime PTSD symptoms were assessed with the PSS-I. In a linear regression analysis accounting for 31% of the variance we found that veterans that score higher on the AAS show lower PSS-I symptom severity scores across their whole post-war lifetime (β = - .31, p = .014). The effect size and power were sufficient (f(2) = 0.51, (1-β) = .99). The same was true for current PTSD (β = - .27, p = .030).Appetitive Aggression appears to be a resilience factor for negative long-term effects of combat experiences in perpetrators of violence. This result has practical relevance for preventing trauma-related mental suffering in Peace Corps and for designing adequate homecoming reception for veterans.

Physiological β-amyloid autoantibodies (Aβ-autoantibodies) are currently investigated as potential diagnostic and therapeutic tools for Alzheimer's disease (AD). In previous studies, their determination in serum and cerebrospinal fluid (CSF) using indirect ELISA has provided controversial results, which may be due to the presence of preformed Aβ antigen-antibody immune complexes. Based on the epitope specificity of the Aβ-autoantibodies, recently elucidated in our laboratory, we developed (a) a sandwich ELISA for the determination of circulating Aβ-IgG immune complexes and (b) an indirect ELISA for the determination of free Aβ-autoantibodies. This methodology was applied to the analysis of serum samples from healthy individuals within the age range of 18 to 89 years. Neuropsychological examination of the participants in this study indicated non-pathological, age-related cognitive decline, revealed especially by tests of visual memory and executive function, as well as speed-related tasks. The ELISA serum determinations showed significantly higher levels of Aβ-IgG immune complexes compared to free Aβ-autoantibodies, while no correlation with age or cognitive performance of the participants was found.

The genetic basis of phenotypic variation can be partially explained by the presence of copy-number variations (CNVs). Currently available methods for CNV assessment include high-density single-nucleotide polymorphism (SNP) microarrays that have become an indispensable tool in genome-wide association studies (GWAS). However, insufficient concordance rates between different CNV assessment methods call for cautious interpretation of results from CNV-based genetic association studies. Here we provide a cross-population, microarray-based map of copy-number variant regions (CNVRs) to enable reliable interpretation of CNV association findings. We used the Affymetrix Genome-Wide Human SNP Array 6.0 to scan the genomes of 1167 individuals from two ethnically distinct populations (Europe, N=717; Rwanda, N=450). Three different CNV-finding algorithms were tested and compared for sensitivity, specificity, and feasibility. Two algorithms were subsequently used to construct CNVR maps, which were also validated by processing subsamples with additional microarray platforms (Illumina 1M-Duo BeadChip, Nimblegen 385K aCGH array) and by comparing our data with publicly available information. Both algorithms detected a total of 42669 CNVs, 74% of which clustered in 385 CNVRs of a cross-population map. These CNVRs overlap with 862 annotated genes and account for approximately 3.3% of the haploid human genome.We created comprehensive cross-populational CNVR-maps. They represent an extendable framework that can leverage the detection of common CNVs and additionally assist in interpreting CNV-based association studies.

BACKGROUND: T. J. Crow suggested that the genetic variance associated with the evolution in Homo sapiens of hemispheric dominance for language carries with it the hazard of the symptoms of schizophrenia. Individuals lacking the typical left hemisphere advantage for language, in particular for phonological components, would be at increased risk of the typical symptoms such as auditory hallucinations and delusions. METHODOLOGY/PRINCIPAL FINDINGS: Twelve schizophrenic patients treated with low levels of neuroleptics and twelve matched healthy controls participated in an event-related potential experiment. Subjects matched word-pairs in three tasks: rhyming/phonological, semantic judgment and word recognition. Slow evoked potentials were recorded from 26 scalp electrodes, and a laterality index was computed for anterior and posterior regions during the inter stimulus interval. During phonological processing individuals with schizophrenia failed to achieve the left hemispheric dominance consistently observed in healthy controls. The effect involved anterior (fronto-temporal) brain regions and was specific for the Phonological task; group differences were small or absent when subjects processed the same stimulus material in a Semantic task or during Word Recognition, i.e. during tasks that typically activate more widespread areas in both hemispheres. CONCLUSIONS/SIGNIFICANCE: We show for the first time how the deficit of lateralization in the schizophrenic brain is specific for the phonological component of language. This loss of hemispheric dominance would explain typical symptoms, e.g. when an individual's own thoughts are perceived as an external intruding voice. The change can be interpreted as a consequence of "hemispheric indecision", a failure to segregate phonological engrams in one hemisphere.

BackgroundTinnitus is an auditory phantom perception that is most likely generated in the central nervous system. Most of the tinnitus research has concentrated on the auditory system. However, it was suggested recently that also non-auditory structures are involved in a global network that encodes subjective tinnitus. We tested this assumption using auditory steady state responses to entrain the tinnitus network and investigated long-range functional connectivity across various non-auditory brain regions.Methods and findingsUsing whole-head magnetoencephalography we investigated cortical connectivity by means of phase synchronization in tinnitus subjects and healthy controls. We found evidence for a deviating pattern of long-range functional connectivity in tinnitus that was strongly correlated with individual ratings of the tinnitus percept. Phase couplings between the anterior cingulum and the right frontal lobe and phase couplings between the anterior cingulum and the right parietal lobe showed significant condition x group interactions and were correlated with the individual tinnitus distress ratings only in the tinnitus condition and not in the control conditions.ConclusionsTo the best of our knowledge this is the first study that demonstrates existence of a global tinnitus network of long-range cortical connections outside the central auditory system. This result extends the current knowledge of how tinnitus is generated in the brain. We propose that this global extend of the tinnitus network is crucial for the continuos perception of the tinnitus tone and a therapeutical intervention that is able to change this network should result in relief of tinnitus.