There are now replicated findings that posttraumatic stress disorder (PTSD) symptoms related to the September 11, 2001, attacks occurred in large numbers of persons who did not fit the traditional definition of exposure to a traumatic event. These data are not explained by traditional epidemiologic "bull's eye" disaster models, which assume the psychological effects are narrowly, geographically circumscribed, or by existing models of PTSD onset. In this article, the authors develop a researchable model to explain these and other terrorism-related phenomena by synthesizing research and concepts from the cognitive science, risk appraisal, traumatic stress, and anxiety disorders literatures. They propose the new term relative risk appraisal to capture the psychological function that is the missing link between the event and subjective response in these and other terrorism-related studies to date. Relative risk appraisal highlights the core notion from cognitive science that human perception is an active, multidimensional process, such that for unpredictable societal threats, proximity to the event is only one of several factors that influence behavioral responses. Addressing distortions in relative risk appraisal effectively could reduce individual and societal vulnerability to a wide range of adverse economic and ethnopolitical consequences to terrorist attacks. The authors present ways in which these concepts and related techniques can be helpful in treating persons with September 11- or terrorism-related distress or psychopathology.

Predicting suicide is difficult due to its low base-rate and the limited specificity of clinical predictors. Prospective biological studies suggest that dysfunctions in the serotonergic system and hypothalamic-pituitary-adrenal axis have some predictive power for completed suicide in mood disorders. A prediction model that incorporates biological testing to increase specificity and sensitivity of prediction of suicide is of potential clinical value. Meta-analyses of prospective biological studies of suicide and cerebrospinal fluid 5-hydroxyindoleacetic acid (CSF 5-HIAA) and suicide and the dexamethasone suppression test (DST) in mood disorders using the penalized quasi-likelihood (PQL) and bootstrap method yield odds ratios for prediction of suicide of 4.48 and 4.65 respectively. Two combinatory prediction models, the first requiring positive results on more than one test, and the second requiring a positive result on either one of two tests, were tested to assess their sensitivity, specificity, and predictive power using biological data from published and unpublished studies. The prediction model that requires both DST and CSF 5-HIAA tests to be positive results in 37.5% sensitivity, 88% specificity, and has a positive predictive value of 23%. The prediction model that requires either DST or CSF 5-HIAA tests to be positive results in 87.5% sensitivity, 28% specificity, and has a positive predictive value of 10%. Thus, models attempting to predict a lethal outcome that is uncommon perform very differently making model choice of major importance. Further work on refining biological predictors and integration with clinical predictors is needed to optimize a model to predict suicide in the clinic.

Objective Selective serotonin reuptake inhibitors are often recommended in combination with established cognitive behavioral therapies for posttraumatic stress disorder (PTSD), but combined initial treatment of PTSD has not been studied under controlled conditions. There are also few studies of either treatment in PTSD related to terrorism. This study compared combined prolonged exposure (a cognitive behavioral therapy) plus paroxetine (a selective serotonin reuptake inhibitor) to prolonged exposure plus placebo in the treatment of terrorism-related PTSD. Method Adult survivors of the World Trade Center attacks of September 11, 2001 with PTSD were randomized to 10 weeks of treatment with combined prolonged exposure (10 sessions) plus paroxetine (N=19) versus prolonged exposure plus placebo (N=18). After week 10, patients discontinued prolonged exposure and were offered 12 additional weeks of continued randomized treatment. Results Patients treated with prolonged exposure plus paroxetine experienced significantly greater improvement in PTSD symptoms (incidence rate ratio=0.50; 95% CI=0.30–0.85; p=.013) and remission status (odds ratio=12.6; 95% CI=1.23–129; p=.034) during 10 weeks of combined treatment than patients treated with prolonged exposure plus placebo. Response rate and quality of life also improved significantly more with combined treatment. The subset of patients who continued randomized treatment for 12 more weeks showed no group differences. Conclusions Initial treatment with combined paroxetine plus prolonged exposure was more efficacious than prolonged exposure plus placebo for PTSD related to the World Trade Center attacks. Combined medication and prolonged exposure treatment deserves further study in larger samples with diverse forms of PTSD, and over longer periods of follow-up.

Scientifically robust symptom profiles that reflect severe but largely untreated mental health problems were identified. Used as "action signs," these profiles might help increase public awareness about children's mental health needs, facilitate communication and referral for specific children in need of evaluation, and narrow the child mental health services gap.

Purpose The major purpose of this study was to detect the changes in gut microbiota composition and inflammatory cytokines production associated with acute and chronic insomnia. This study also evaluated the relationship between gut microbiota changes and increased inflammatory cytokines in insomnia patients. Patients and Methods Outpatients with acute and chronic insomnia (aged 26–55 years; n=20 and 38, respectively) and age/gender-matched healthy controls (n=38) were recruited from a southern China region. Participants’ gut microbiome, plasma cytokines, and self-reported sleep quality and psychopathological symptoms were measured. Results The gut microbiomes of insomnia patients compared with healthy controls were characterized by lower microbial richness and diversity, depletion of anaerobes, and short-chain fatty acid (SCFA)-producing bacteria, and an expansion of potential pathobionts. Lachnospira and Bacteroides were signature bacteria for distinguishing acute insomnia patients from healthy controls, while Faecalibacterium and Blautia were signature bacteria for distinguishing chronic insomnia patients from healthy controls. Acute/chronic insomnia-related signature bacteria also showed correlations with these patients’ self-reported sleep quality and plasma IL-1β. Conclusion These findings suggest that insomnia symptomology, gut microbiota, and inflammation may be interrelated in complex ways. Gut microbiota may serve as an important indicator for auxiliary diagnosis of insomnia and provide possible new therapeutic targets in the field of sleep disorders.