One of the most consistent findings in the epidemiology of posttraumatic stress disorder (PTSD) is the higher risk of this disorder in women. Explanations reviewed within a psychobiological model of PTSD suggest that women's higher PTSD risk may be due to the type of trauma they experience, their younger age at the time of trauma exposure, their stronger perceptions of threat and loss of control, higher levels of peri-traumatic dissociation, insufficient social support resources, and greater use of alcohol to manage trauma-related symptoms like intrusive memories and dissociation, as well as gender-specific acute psychobiological reactions to trauma. This review demonstrates the need for additional research of the gender differences in posttraumatic stress. Recommendations are made for clinical practice.

BackgroundInterpersonal trauma exposure and trauma-related disorders in people with severe mental illness (SMI) are often not recognized in clinical practice.ObjectiveTo substantiate the prevalence of interpersonal trauma exposure and trauma-related disorders in people with SMI.MethodsWe conducted a systematic review of four databases (1980–2010) and then described and analysed 33 studies in terms of primary diagnosis and instruments used to measure trauma exposure and trauma-related disorders.ResultsPopulation-weighted mean prevalence rates in SMI were physical abuse 47% (range 25–72%), sexual abuse 37% (range 24–49%), and posttraumatic stress disorder (PTSD) 30% (range 20–47%). Compared to men, women showed a higher prevalence of sexual abuse in schizophrenia spectrum disorder, bipolar disorder, and mixed diagnosis groups labelled as having SMI.ConclusionsPrevalence rates of interpersonal trauma and trauma-related disorders were significantly higher in SMI than in the general population. Emotional abuse and neglect, physical neglect, complex PTSD, and dissociative disorders have been scarcely examined in SMI.

Post-traumatic stress disorder (PTSD) is associated with impaired memory performance coupled with functional changes in brain areas involved in declarative memory and emotion regulation. It is not yet clear how symptom severity and comorbidity affect neurocognitive functioning in PTSD. We performed a functional magnetic resonance imaging (fMRI) study with an emotional declarative memory task in 28 Complex PTSD patients with comorbid depressive and personality disorders, and 21 healthy non-trauma-exposed controls. In Complex PTSD patients--compared to controls--encoding of later remembered negative words vs baseline was associated with increased blood oxygenation level dependent (BOLD) response in the left ventral anterior cingulate cortex (ACC) and dorsal ACC extending to the dorsomedial prefrontal cortex (dmPFC) together with a trend for increased left hippocampus activation. Patients tended to commit more False Alarms to negative words compared to controls, which was associated with enhanced left ventrolateral prefrontal and orbitofrontal cortex (vlPFC/OFC) responses. Severity of child abuse was positively correlated with left ventral ACC activity and severity of depression with (para) hippocampal and ventral ACC activity. Presented results demonstrate functional abnormalities in Complex PTSD in the frontolimbic brain circuit also implicated in fear conditioning models, but generally in the opposite direction, which may be explained by severity of the trauma and severity of comorbid depression in Complex PTSD.

Smaller hippocampal volume has been reported in individuals with posttraumatic stress disorder (PTSD) and dissociative identity disorder (DID), but the regional specificity of hippocampal volume reductions and the association with severity of dissociative symptoms and/or childhood traumatization are still unclear. Brain structural MRI scans were analyzed for 33 outpatients (17 with DID and 16 with PTSD only) and 28 healthy controls (HC), all matched for age, sex, and education. DID patients met criteria for PTSD (PTSD-DID). Hippocampal global and subfield volumes and shape measurements were extracted. We found that global hippocampal volume was significantly smaller in all 33 patients (left: 6.75%; right: 8.33%) compared to HC. PTSD-DID (left: 10.19%; right: 11.37%) and PTSD-only with a history of childhood traumatization (left: 7.11%; right: 7.31%) had significantly smaller global hippocampal volume relative to HC. PTSD-DID had abnormal shape and significantly smaller volume in the CA2-3, CA4-DG and (pre)subiculum compared to HC. In the patient groups, smaller global and subfield hippocampal volumes significantly correlated with higher severity of childhood traumatization and dissociative symptoms. These findings support a childhood trauma-related etiology for abnormal hippocampal morphology in both PTSD and DID and can further the understanding of neurobiological mechanisms involved in these disorders.