Anxiety and depression are common following traumatic brain injury (TBI), often co-occurring. This study evaluated the efficacy of a 9-week cognitive behavioral therapy (CBT) program in reducing anxiety and depression and whether a three-session motivational interviewing (MI) preparatory intervention increased treatment response.

A randomized parallel three-group design was employed. Following diagnosis of anxiety and/or depression using the Structured Clinical Interview for DSM-IV, 75 participants with mild-severe TBI (mean age 42.2 years, mean post-traumatic amnesia 22 days) were randomly assigned to an Adapted CBT group: (1) MI + CBT (n = 26), or (2) non-directive counseling (NDC) + CBT (n = 26); or a (3) waitlist control (WC, n = 23) group. Groups did not differ in baseline demographics, injury severity, anxiety or depression. MI and CBT interventions were guided by manuals adapted for individuals with TBI. Three CBT booster sessions were provided at week 21 to intervention groups.

Using intention-to-treat analyses, random-effects regressions controlling for baseline scores revealed that Adapted CBT groups (MI + CBT and NDC + CBT) showed significantly greater reduction in anxiety on the Hospital Anxiety and Depression Scale [95% confidence interval (CI) −2.07 to −0.06] and depression on the Depression Anxiety and Stress Scale (95% CI −5.61 to −0.12) (primary outcomes), and greater gains in psychosocial functioning on Sydney Psychosocial Reintegration Scale (95% CI 0.04–3.69) (secondary outcome) over 30 weeks post-baseline relative to WC. The group receiving MI + CBT did not show greater gains than the group receiving NDC + CBT.

Findings suggest that modified CBT with booster sessions over extended periods may alleviate anxiety and depression following TBI.

Individual-level measures of acculturation (e.g. age of immigration) have a complex relationship with psychiatric disorders. Fine-grained analyses that tap various acculturation dimensions and population subgroups are needed to generate hypotheses regarding the mechanisms of action for the association between acculturation and mental health.

Study participants were US Latinos (N = 6359) from Wave 2 of the 2004–2005 National Epidemiologic Survey of Alcohol and Related Conditions (N = 34 653). We used linear χ2 tests and logistic regression models to analyze the association between five acculturation dimensions and presence of 12-month DSM-IV mood/anxiety disorders across Latino subgroups (Mexican, Puerto Rican, Cuban, ‘Other Latinos’).

Acculturation dimensions associated linearly with past-year presence of mood/anxiety disorders among Mexicans were: (1) younger age of immigration (linear χ21 = 11.04, p < 0.001), (2) longer time in the United States (linear χ21 = 10.52, p < 0.01), (3) greater English-language orientation (linear χ21 = 14.57, p < 0.001), (4) lower Latino composition of social network (linear χ21 = 15.03, p < 0.001), and (5) lower Latino ethnic identification (linear χ21 = 7.29, p < 0.01). However, the associations were less consistent among Cubans and Other Latinos, and no associations with acculturation were found among Puerto Ricans.

The relationship between different acculturation dimensions and 12-month mood/anxiety disorder varies across ethnic subgroups characterized by cultural and historical differences. The association between acculturation measures and disorder may depend on the extent to which they index protective or pathogenic adaptation pathways (e.g. loss of family support) across population subgroups preceding and/or following immigration. Future research should incorporate direct measures of maladaptive pathways and their relationship to various acculturation dimensions.

A structural neuroanatomical change indicating a reduction in brain tissue is a notable feature of schizophrenia. Several pathophysiological processes such as aberrant cortical maturation, progressive tissue loss and compensatory tissue increase could contribute to the structural changes seen in schizophrenia.

We studied cortical thickness using surface-based morphometry in 98 clinically stable patients with schizophrenia and 83 controls. Using a pattern classification approach, we studied whether the features that discriminate patients from controls vary across the different stages of the illness. Using a covariance analysis, we also investigated if concurrent increases accompany decreases in cortical thickness.

Very high levels of accuracy (96.3%), specificity (98.8%) and sensitivity (88%) were noted when classifying patients with <2 years of illness from controls. Within the patient group, reduced thickness was consistently accompanied by increased thickness in distributed brain regions. A pattern of cortical amelioration or normalization (i.e. reduced deviation from controls) was noted with increasing illness duration. While temporo-limbic and fronto-parietal regions showed reduced thickness, the occipital cortex showed increased thickness, especially in those with a long-standing illness.

A compensatory remodelling process might contribute to the cortical thickness variations in different stages of schizophrenia. Subtle cerebral reorganization reflecting the inherent plasticity of brain may occur concomitantly with processes contributing to tissue reduction in adult patients with schizophrenia.

Childhood maltreatment (CM) has been associated with increased risk of attention deficit hyperactivity disorder (ADHD) in children and adults. It is, however, unclear whether this association is causal or due to familial confounding.

Data from 18 168 adult twins, aged 20–46 years, were drawn from the population-based Swedish twin registry. Retrospective self-ratings of CM (emotional and physical neglect, physical and sexual abuse and witnessing family violence), and self-ratings for DSM-IV ADHD symptoms in adulthood were analysed. Possible familial confounding was investigated using a within twin-pair design based on monozygotic (MZ) and dizygotic (DZ) twins.

CM was significantly associated with increased levels of ADHD symptom scores in adults [regression coefficient: 0.40 standard deviations, 95% confidence interval (CI) 0.37–0.43]. Within twin-pair analyses showed attenuated but significant estimates within DZ (0.29, 95% CI 0.21–0.36) and MZ (0.18, 95% CI 0.10–0.25) twin pairs. Similar results emerged for hyperactive/impulsive and inattentive ADHD symptom scores separately in association with CM. We conducted sensitivity analyses for early maltreatment, before age 7, and for abuse and neglect separately, and found similarly reduced estimates in DZ and MZ pairs. Re-traumatization after age 7 did not significantly influence results.

CM was significantly associated with increased ADHD symptoms in adults. Associations were partly due to familial confounding, but also consistent with a causal interpretation. Our findings support cognitive neuroscience studies investigating neural pathways through which exposure to CM may influence ADHD. Clinicians treating adults with ADHD should be aware of the association with maltreatment.

Our understanding of the dynamics of post-traumatic stress symptomatology and its link to functional impairment over time is limited.

Post-traumatic stress symptomatology (Post-traumatic Checklist, PCL) was assessed three times in 1-year increments (T1, T2, T3) following the Oslo bombing of 22 July, 2011, in directly (n = 257) and indirectly exposed (n = 2223) government employees, together with demographics, measures of exposure and work and social adjustment. The dynamics of post-traumatic stress disorder symptom cluster interplay were examined within a structural equation modelling framework using a cross-lagged autoregressive panel model.

Intrusions at T1 played a prominent role in predicting all symptom clusters at T2 for the directly exposed group, exhibiting especially strong cross-lagged relationships with avoidance and anxious arousal. For the indirectly exposed group, dysphoric arousal at T1 played the most prominent role in predicting all symptom clusters at T2, exhibiting a strong relationship with emotional numbing. Emotional numbing seemed to be the main driver behind prolonged stress at T3 for both groups. Functional impairment was predominately associated with dysphoric arousal and emotional numbing in both groups.

For directly exposed individuals, memories of the traumatic incident and the following intrusions seem to drive their post-traumatic stress symptomatology. However, as these memories lose their potency over time, a sequela of dysphoric arousal and emotional numbing similar to the one reported by the indirectly exposed individuals seems to be the main driver for prolonged post-traumatic stress and functional impairment. Findings are discussed using contemporary models within an exposure-dependent perspective of post-traumatic stress.

There has been considerable recent interest in possible causal linkages between exposure to bullying victimization and later psychotic symptomatology. Prior research in this area has had several limitations which make it difficult to ascertain causality, and to determine the extent to which these effects extend beyond adolescence.

Data were obtained from the Christchurch Health and Development Study, a 35-year study of a longitudinal birth cohort. This investigation used generalized estimating equation modelling to estimate the associations between bullying victimization (ages 13–16 years) and psychotic symptoms (ages 18–35 years), before and after controlling for possible confounding factors, including: gender; childhood socio-economic status; child intelligence quotient; exposure to sexual abuse in childhood; anxious/withdrawn behaviour and attention problems (ages 7–9 years); and adolescent psychotic symptoms and paranoid ideation (ages 15–16 years).

There was a significant (p < 0.0001) bivariate association between bullying victimization in adolescence and psychotic symptomatology in adulthood. Successive models controlling for covariation reduced this association to statistical non-significance. After controlling for covariates, those with the highest level of bullying victimization had rates of psychotic symptoms that were 1.21 (95% confidence interval 0.73–1.99) times higher than those who were not victimized.

The association between bullying victimization in adolescence and psychotic symptomatology in adulthood could be largely explained by childhood behavioural problems, and exposure to sexual abuse in childhood. The results suggest that bullying victimization was unlikely to have been a cause of adult psychotic symptoms, but bullying victimization remained a risk marker for these symptoms.

An increasing number of studies have investigated delay discounting (DD) in relation to obesity, but with mixed findings. This meta-analysis synthesized the literature on the relationship between monetary and food DD and obesity, with three objectives: (1) to characterize the relationship between DD and obesity in both case–control comparisons and continuous designs; (2) to examine potential moderators, including case–control v. continuous design, money v. food rewards, sample sex distribution, and sample age (<18 v. >18 years); and (3) to evaluate publication bias.

From 134 candidate articles, 39 independent investigations yielded 29 case–control and 30 continuous comparisons (total n = 10 278). Random-effects meta-analysis was conducted using Cohen's d as the effect size. Publication bias was evaluated using fail-safe N, Begg–Mazumdar and Egger tests, meta-regression of publication year and effect size, and imputation of missing studies.

The primary analysis revealed a medium effect size across studies that was highly statistically significant (d = 0.43, p < 10−14). None of the moderators examined yielded statistically significant differences, although notably larger effect sizes were found for studies with case–control designs, food rewards and child/adolescent samples. Limited evidence of publication bias was present, although the Begg–Mazumdar test and meta-regression suggested a slightly diminishing effect size over time.

Steep DD of food and money appears to be a robust feature of obesity that is relatively consistent across the DD assessment methodologies and study designs examined. These findings are discussed in the context of research on DD in drug addiction, the neural bases of DD in obesity, and potential clinical applications.

Episodes of depression and anxiety (D&A) during the transition from late adolescence to adulthood, particularly when persistent, are predictive of long-term disorders and associated public health burden. Understanding risk factors at this time is important to guide intervention. The current objective was to investigate the associations between maternal symptoms of D&A with offspring symptoms during their transition to adulthood.

Data from a large population-based birth cohort study, in South Brazil, were used. Prospective associations between maternal D&A and offspring risk of these symptoms during the transition to adulthood (18/19, 24 and 30 years) were estimated.

Maternal D&A in adolescence was associated with offspring symptoms across the transition to adulthood, associations were consistently stronger for females than for males. Daughters whose mothers reported D&A were 4.6 times (95% confidence interval 2.71–7.84) as likely to report D&A at all three time-points, than daughters of symptom-free mothers.

Maternal D&A is associated with persistent D&A during the daughter's transition to adulthood. Intervention strategies should consider the mother's mental health.

Item response theory (IRT) analyses of alcohol use disorder (AUD) and other psychological disorders are a predominant method for assessing overall and individual criterion severity for psychiatric diagnosis. However, no investigation has established the consistency of the relative criteria severities across different samples.

PubMed/Medline, PsycINFO, Web of Science and ProQuest databases were queried for entries relating to alcohol use and IRT. Study data were extracted using a standardized data entry sheet. Consistency of reported criteria severities across studies was analysed using generalizability theory to estimate generalized intraclass correlations (ICCs).

A total of 451 citations were screened and 34 papers (30 unique samples) included in the research synthesis. The AUD criteria set exhibited low consistency in the ordering of criteria using both traditional [ICC = 0.16, 95% confidence interval (CI) 0.06–0.56] and generalized (ICC = 0.18, 95% CI 0.15–0.21) approaches. These results were partially accounted for by previously studied factors such as age and type of sample (e.g. clinical v. community), but the largest source of unreliability was the diagnostic instrument employed.

Despite the robust finding of unidimensional structure of AUDs, inconsistency in the relative severities across studies suggests low replicability, challenging the generalizability of findings from any given study. Explicit modeling of well-studied factors like age and sample type is essential and increases the generalizability of findings. Moreover, while the development of structured diagnostic interviews is considered a landmark contribution toward improving psychiatric research, variability across instruments has not been fully appreciated and is substantial.

The genetic influences in human brain structure and function and impaired functional connectivities are the hallmarks of the schizophrenic brain. To explore how common genetic variants affect the connectivities in schizophrenia, we applied genome-wide association studies assaying the abnormal neural connectivities in schizophrenia as quantitative traits.

We recruited 161 first-onset and treatment-naive patients with schizophrenia and 150 healthy controls. All the participants underwent scanning with a 3 T-magnetic resonance imaging scanner to acquire structural and functional imaging data and genotyping using the HumanOmniZhongHua-8 BeadChip. The brain-wide association study approach was employed to account for the inherent modular nature of brain connectivities.

We found differences in four abnormal functional connectivities [left rectus to left thalamus (REC.L–THA.L), left rectus to right thalamus (REC.L–THA.R), left superior orbital cortex to left thalamus (ORBsup.L–THA.L) and left superior orbital cortex to right thalamus (ORBsup.L–THA.R)] between the two groups. Univariate single nucleotide polymorphism (SNP)-based association revealed that the SNP rs6800381, located nearest to the CHRM3 (cholinergic receptor, muscarinic 3) gene, reached genomic significance (p = 1.768 × 10−8) using REC.L–THA.R as the phenotype. Multivariate gene-based association revealed that the FAM12A (family with sequence similarity 12, member A) gene nearly reached genomic significance (nominal p = 2.22 × 10–6, corrected p = 0.05).

Overall, we identified the first evidence that the CHRM3 gene plays a role in abnormal thalamo-orbital frontal cortex functional connectivity in first-episode treatment-naive patients with schizophrenia. Identification of these genetic variants using neuroimaging genetics provides insights into the causes of variability in human brain development, and may help us determine the mechanisms of dysfunction in schizophrenia.

According to diathesis–stress models, personality traits, such as negative emotionality (NE) and positive emotionality (PE), may moderate the effects of stressors on the development of depression. However, relatively little empirical research has directly examined whether NE and PE act as diatheses in the presence of stressful life events, and no research has examined whether they moderate the effect of disaster exposure on depressive symptoms. Hurricane Sandy, the second costliest hurricane in US history, offers a unique opportunity to address these gaps.

A total of 318 women completed measures of NE and PE 5 years prior to Hurricane Sandy. They were also assessed for lifetime depressive disorders on two occasions, the latter occurring an average of 1 year before the hurricane. Approximately 8 weeks after the disaster (mean = 8.40, s.d. = 1.48 weeks), participants completed a hurricane stress exposure questionnaire and a measure of current depressive symptoms.

Adjusting for lifetime history of depressive disorders, higher levels of stress from Hurricane Sandy predicted elevated levels of depressive symptoms, but only in participants with high levels of NE or low levels of PE.

These findings support the role of personality in the development of depression and suggest that personality traits can be useful in identifying those most vulnerable to major stressors, including natural disasters.

Complicated grief is a distinct psychological response of individuals facing the loss of a loved one and can lead to many types of adverse health outcomes. Although social support may be beneficial, few studies have examined the beneficial effects of helpful support on complicated grief following bereavement.

A randomized controlled trial was conducted. Bereaved participants and supporters were randomized to psychoeducation on complicated grief and helpful social support or psychoeducation on complicated grief. The primary outcome was the Inventory of Complicated Grief.

The results showed that psychoeducation of supporters of bereaved individuals has significant beneficial effects. Particularly, symptoms of complicated grief were decreased in bereaved individuals with supporters that received psychoeducation.

The results highlight the potential of psychoeducation to facilitate helpful social support and reduce complicated grief.

Sodium nitroprusside (SNP) has been reported to rapidly reduce psychotic symptoms in patients with schizophrenia. This has the potential to revolutionize treatment for schizophrenia. In this study, we tested the hypothesis that SNP leads to a reduction in psychotic symptoms and an improvement in spatial working memory (SWM) performance in patients with schizophrenia.

This was a single-centre, randomized, double-blind, placebo-controlled trial performed from 27 August 2014 to 10 February 2016 (clinicaltrials.gov identifier: NCT02176044). Twenty patients with schizophrenia aged 18–60 years with a diagnosis of schizophrenia or schizoaffective disorder were recruited from psychiatric outpatient clinics in the South London and Maudsley NHS Trust, London, UK. Baseline symptoms were measured using the Positive and Negative Syndrome Scale (PANSS) and the 18-item Brief Psychiatric Rating Scale (BPRS-18), and SWM was assessed using the CANTAB computerized test. Participants received either an infusion of SNP (0.5 μg/kg per min for 4 h) or placebo and were re-assessed for symptoms and SWM performance immediately after the infusion, and 4 weeks later.

SNP did not lead to any reduction in psychotic symptoms or improvement in SWM performance compared to placebo.

Although this study was negative, it is possible that the beneficial effects of SNP may occur in patients with a shorter history of illness, or with more acute exacerbation of symptoms.

While oral antidepressants reach efficacy after weeks, single-dose intravenous (i.v.) ketamine has rapid, yet time-limited antidepressant effects. We aimed to determine the efficacy and safety of single-dose i.v. ketamine augmentation of escitalopram in major depressive disorder (MDD).

Thirty outpatients with severe MDD (17-item Hamilton Rating Scale for Depression total score ⩾24) were randomized to 4 weeks double-blind treatment with escitalopram 10 mg/day+single-dose i.v. ketamine (0.5 mg/kg over 40 min) or escitalopram 10 mg/day + placebo (0.9% i.v. saline). Depressive symptoms were measured using the Montgomery–Asberg Depression Rating Scale (MADRS) and the Quick Inventory of Depressive Symptomatology – Self-Report (QIDS-SR). Suicidal ideation was evaluated with the QIDS-SR item 12. Adverse psychopathological effects were measured with the Brief Psychiatric Rating Scale (BPRS)-positive symptoms, Young Mania Rating Scale (YMRS) and Clinician Administered Dissociative States Scale (CADSS). Patients were assessed at baseline, 1, 2, 4, 24 and 72 h and 7, 14, 21 and 28 days. Time to response (⩾50% MADRS score reduction) was the primary outcome.

By 4 weeks, more escitalopram + ketamine-treated than escitalopram + placebo-treated patients responded (92.3% v. 57.1%, p = 0.04) and remitted (76.9% v. 14.3%, p = 0.001), with significantly shorter time to response [hazard ratio (HR) 0.04, 95% confidence interval (CI) 0.01–0.22, p < 0.001] and remission (HR 0.11, 95% CI 0.02–0.63, p = 0.01). Compared to escitalopram + placebo, escitalopram + ketamine was associated with significantly lower MADRS scores from 2 h to 2 weeks [(peak = 3 days–2 weeks; effect size (ES) = 1.08–1.18)], QIDS-SR scores from 2 h to 2 weeks (maximum ES = 1.27), and QIDS-SR suicidality from 2 to 72 h (maximum ES = 2.24). Only YMRS scores increased significantly with ketamine augmentation (1 and 2 h), without significant BPRS or CADSS elevation.

Single-dose i.v. ketamine augmentation of escitalopram was safe and effective in severe MDD, holding promise for speeding up early oral antidepressant efficacy.

The effects of cognitive behavioural therapy of anxiety disorders on depression has been examined in previous meta-analyses, suggesting that these treatments have considerable effects on depression. In the current meta-analysis we examined whether the effects of treatments of anxiety disorders on depression differ across generalized anxiety disorder (GAD), social anxiety disorder (SAD) and panic disorder (PD). We also compared the effects of these treatments with the effects of cognitive and behavioural therapies of major depression (MDD).

We searched PubMed, PsycINFO, EMBASE and the Cochrane database, and included 47 trials on anxiety disorders and 34 trials on MDD.

Baseline depression severity was somewhat lower in anxiety disorders than in MDD, but still mild to moderate in most studies. Baseline severity differed across the three anxiety disorders. The effect sizes found for treatment of the anxiety disorders ranged from g = 0.47 for PD, g = 0.68 for GAD and g = 0.69 for SAD. Differences between these effect sizes and those found in the treatment of MDD (g = 0.81) were not significant in most analyses and we found few indications that the effects differed across anxiety disorders. We did find that within-group effect sizes resulted in significantly (p < 0.001) larger effect sizes for depression (g = 1.50) than anxiety disorders (g = 0.73–0.91). Risk of bias was considerable in the majority of studies.

Patients participating in trials of cognitive behavioural therapy for anxiety disorders have high levels of depression. These treatments have considerable effects on depression, and these effects are comparable to those of treatment of primary MDD.

Depression and diabetes commonly co-occur; however, the strength of the physiological effects of diabetes as mediating factors towards depression is uncertain.

We analyzed extensive clinical, epidemiological and laboratory data from n = 2081 Mexican Americans aged 35–64 years, recruited from the community as part of the Cameron County Hispanic Cohort (CCHC) divided into three groups: Diagnosed (self-reported) diabetes (DD, n = 335), Undiagnosed diabetes (UD, n = 227) and No diabetes (ND, n = 1519). UD participants denied being diagnosed with diabetes, but on testing met the 2010 American Diabetes Association and World Health Organization definitions of diabetes. Depression was measured using the Center for Epidemiological Studies – Depression (CES-D) scale. Weighted data were analyzed using dimensional and categorical outcomes using univariate and multivariate models.

The DD group had significantly higher CES-D scores than both the ND and UD (p ⩽ 0.001) groups, whereas the ND and UD groups did not significantly differ from each other. The DD subjects were more likely to meet the CES-D cut-off score for depression compared to both the ND and UD groups (p = 0.001), respectively. The UD group was also less likely to meet the cut-off score for depression than the ND group (p = 0.003). Our main findings remained significant in models that controlled for socio-demographic and clinical confounders.

Meeting clinical criteria for diabetes was not sufficient for increased depressive symptoms. Our findings suggest that the ‘knowing that one is ill’ is associated with depressive symptoms in diabetic subjects.

The aim of this study was to analyse a possible synergistic effect between back pain and common mental disorders (CMDs) in relation to future disability pension (DP).

All 4 823 069 individuals aged 16–64 years, living in Sweden in December 2004, not pensioned in 2005 and without ongoing sickness absence at the turn of 2004/2005 formed the cohort of this register-based study. Hazard ratios (HRs) and 95% confidence intervals (CIs) for DP (2006–2010) were estimated. Exposure variables were back pain (M54) (sickness absence or inpatient or specialized outpatient care in 2005) and CMD (F40-F48) [sickness absence or inpatient or specialized outpatient care or antidepressants (N06a) in 2005].

HRs for DP were 4.03 (95% CI 3.87–4.21) and 3.86 (95% CI 3.68–4.04) in women and men with back pain. HRs for DP in women and men with CMD were 4.98 (95% CI 4.88–5.08) and 6.05 (95% CI 5.90–6.21). In women and men with both conditions, HRs for DP were 15.62 (95% CI 14.40–16.94) and 19.84 (95% CI 17.94–21.94). In women, synergy index, relative excess risk due to interaction, and attributable proportion were 1.24 (95% CI 1.13–1.36), 0.18 (95% CI 0.11–0.25), and 2.08 (95% CI 1.09–3.06). The corresponding figures for men were 1.45 (95% CI 1.29–1.62), 0.29 (95% CI 0.22–0.36), and 4.21 (95% CI 2.71–5.70).

Co-morbidity of back pain and CMD is associated with a higher risk of DP than either individual condition, when added up, which has possible clinical implications to prevent further disability and exclusion from the labour market.