Cognitive models have postulated that auditory hallucinations arise from the misattribution of internally generated cognitive events to external sources. Several experimental paradigms have been developed to assess this externalizing bias in clinical and non-clinical hallucination-prone samples, including source-monitoring, verbal self-monitoring and auditory signal detection tasks. This meta-analysis aims to synthesize the wealth of empirical findings from these experimental studies.

A database search was carried out for reports between January 1985 and March 2012. Additional studies were retrieved by contacting authors and screening references of eligible reports. Studies were considered eligible if they compared either (i) hallucinating and non-hallucinating patients with comparable diagnoses, or (ii) non-clinical hallucination-prone and non-prone participants using source-monitoring, verbal self-monitoring or signal detection tasks, or used correlational analyses to estimate comparable effects.

The analysis included 15 clinical (240 hallucinating patients and 249 non-hallucinating patients) and nine non-clinical studies (171 hallucination-prone and 177 non-prone participants; 57 participants in a correlation study). Moderate-to-large summary effects were observed in both the clinical and analogue samples. Robust and significant effects were observed in source-monitoring and signal detection studies, but not in self-monitoring studies, possibly due to the small numbers of eligible studies in this subgroup. The use of emotionally valenced stimuli led to effects of similar magnitude to the use of neutral stimuli.

The findings suggest that externalizing biases are important cognitive underpinnings of hallucinatory experiences. Clinical interventions targeting these biases should be explored as possible treatments for clients with distressing voices.

Anorexia nervosa is a potentially deadly psychiatric illness that develops predominantly in females around puberty but is increasingly being recognized as also affecting boys and men and women across the lifespan. The aim of this environmental scan is to provide an overview of best practices in anorexia nervosa treatment across the age spectrum.

A triangulation approach was used. First, a detailed review of randomized controlled trials (RCTs) for anorexia nervosa published between 1980 and 2011 was conducted; second, clinical practice guidelines were consulted and reviewed; third, information about RCTs currently underway was sourced. This approach facilitated a comprehensive overview, which addressed the extant evidence base, recent advances in evidence and improvements in treatment, and future directions.

The evidence base for the treatment of anorexia nervosa is advancing, albeit unevenly. Evidence points to the benefit of family-based treatment for youth. For adults no specific approach has shown superiority and, presently, a combination of renourishment and psychotherapy such as specialist supportive clinical management, cognitive behavioral therapy, or interpersonal psychotherapy is recommended. RCTs have neither sufficiently addressed the more complex treatment approaches seen in routine practice settings, such as multidisciplinary treatment or level of care, nor specifically investigated treatment in ethnically diverse populations. Methodological challenges that hinder progress in controlled research for anorexia nervosa are explained.

The review highlights evidence-based and promising treatment modalities for anorexia nervosa and presents a triangulated analysis including controlled research, practice guidelines, and emerging treatments to inform and support clinical decision making.

There are no evidence-based treatments for severe and enduring anorexia nervosa (SE-AN). This study evaluated the relative efficacy of cognitive behavioral therapy (CBT-AN) and specialist supportive clinical management (SSCM) for adults with SE-AN.

Sixty-three participants with a diagnosis of AN, who had at least a 7-year illness history, were treated in a multi-site randomized controlled trial (RCT). During 30 out-patient visits spread over 8 months, they received either CBT-AN or SSCM, both modified for SE-AN. Participants were assessed at baseline, end of treatment (EOT), and at 6- and 12-month post-treatment follow-ups. The main outcome measures were quality of life, mood disorder symptoms and social adjustment. Weight, eating disorder (ED) psychopathology, motivation for change and health-care burden were secondary outcomes.

Thirty-one participants were randomized to CBT-AN and 32 to SSCM with a retention rate of 85% achieved at the end of the study. At EOT and follow-up, both groups showed significant improvement. There were no differences between treatment groups at EOT. At the 6-month follow-up, CBT-AN participants had higher scores on the Weissman Social Adjustment Scale (WSAS; p = 0.038) and at 12 months they had lower Eating Disorder Examination (EDE) global scores (p = 0.004) and higher readiness for recovery (p = 0.013) compared to SSCM.

Patients with SE-AN can make meaningful improvements with both therapies. Both treatments were acceptable and high retention rates at follow-up were achieved. Between-group differences at follow-up were consistent with the nature of the treatments given.

Several neuroimaging studies have investigated brain grey matter in people with body dysmorphic disorder (BDD), showing possible abnormalities in the limbic system, orbitofrontal cortex, caudate nuclei and temporal lobes. This study takes these findings forward by investigating white matter properties in BDD compared with controls using diffusion tensor imaging. It was hypothesized that the BDD sample would have widespread significantly reduced white matter connectivity as characterized by fractional anisotropy (FA).

A total of 20 participants with BDD and 20 healthy controls matched on age, gender and handedness underwent diffusion tensor imaging. FA, a measure of water diffusion within a voxel, was compared between groups on a voxel-by-voxel basis across the brain using tract-based spatial statistics within the FSL package.

Results showed that, compared with healthy controls, BDD patients demonstrated significantly lower FA (p < 0.05) in most major white matter tracts throughout the brain, including in the superior longitudinal fasciculus, inferior fronto-occipital fasciculus and corpus callosum. Lower FA levels could be accounted for by increased radial diffusivity as characterized by eigenvalues 2 and 3. No area of higher FA was found in BDD.

This study provided the first evidence of compromised white matter integrity within BDD patients. This suggests that there are inefficient connections between different brain areas, which may explain the cognitive and emotion regulation deficits within BDD patients.

The boundaries of psychotic illness and the extent to which operational diagnostic categories are distinct in the long term remain poorly understood. Clarification of these issues requires prospective evaluation of diagnostic trajectory, interplay and convergence/divergence across psychotic illness, without a priori diagnostic or other restrictions.

The Cavan-Monaghan First Episode Psychosis Study (CAMFEPS), conducted using methods to attain the closest approximation to epidemiological completeness, incepts all 12 DSM-IV psychotic diagnoses. In this study we applied methodologies to achieve diagnostic reassessments on follow-up, at a mean of 6.4 years after first presentation, for 196 (97%) of the first 202 cases, with quantification of prospective and retrospective consistency.

Over 6 years, the 12 initial psychotic diagnoses were characterized by numerous transitions but only limited convergence towards a smaller number of more stable diagnostic nodes. In particular, for initial brief psychotic disorder (BrP), in 85% of cases this was the harbinger of long-term evolution to serious psychotic illness of diagnostic diversity; for initial major depressive disorder with psychotic features (MDDP), in 18% of cases this was associated with mortality of diverse causality; and for initial psychotic disorder not otherwise specified (PNOS), 31% of cases continued to defy DSM-IV criteria.

CAMFEPS methodology revealed, on an individual case basis, a diversity of stabilities in, and transitions between, all 12 DSM-IV psychotic diagnoses over 6 years; thus, psychotic illness showed longitudinal disrespect to current nosology and may be better accommodated by a dimensional model. In particular, a first episode of BrP or MDDP may benefit from more vigorous, sustained interventions.

Cognition is increasingly being recognized as an important aspect of psychotic disorders and a key contributor to functional outcome. In the past, comparative studies have been performed in schizophrenia and schizo-affective disorder with regard to cognitive performance, but the results have been mixed and the cognitive measures used have not always assessed the cognitive deficits found to be specific to psychosis. A set of optimized cognitive paradigms designed by the Cognitive Neuroscience Test Reliability and Clinical Applications for Schizophrenia (CNTRACS) Consortium to assess deficits specific to schizophrenia was used to measure cognition in a large group of individuals with schizophrenia and schizo-affective disorder.

A total of 519 participants (188 with schizophrenia, 63 with schizo-affective disorder and 268 controls) were administered three cognitive paradigms assessing the domains of goal maintenance in working memory, relational encoding and retrieval in episodic memory and visual integration.

Across the three domains, the results showed no major quantitative differences between patient groups, with both groups uniformly performing worse than healthy subjects.

The findings of this study suggests that, with regard to deficits in cognition, considered a major aspect of psychotic disorder, schizophrenia and schizo-affective disorder do not demonstrate major significant distinctions. These results have important implications for our understanding of the nosological structure of major psychopathology, providing evidence consistent with the hypothesis that there is no natural distinction between cognitive functioning in schizophrenia and schizo-affective disorder.

Group-level results suggest that relative to healthy controls (HCs), ultra-high-risk (UHR) and first-episode psychosis (FEP) subjects show alterations in neuroanatomy, neurofunction and cognition that may be mediated genetically. It is unclear, however, whether these groups can be differentiated at single-subject level, for instance using the machine learning analysis support vector machine (SVM). Here, we used a multimodal approach to examine the ability of structural magnetic resonance imaging (sMRI), functional MRI (fMRI), diffusion tensor neuroimaging (DTI), genetic and cognitive data to differentiate between UHR, FEP and HC subjects at the single-subject level using SVM.

Three age- and gender-matched SVM paired comparison groups were created comprising 19, 19 and 15 subject pairs for FEP versus HC, UHR versus HC and FEP versus UHR, respectively. Genetic, sMRI, DTI, fMRI and cognitive data were obtained for each participant and the ability of each to discriminate subjects at the individual level in conjunction with SVM was tested.

Successful classification accuracies (p < 0.05) comprised FEP versus HC (genotype, 67.86%; DTI, 65.79%; fMRI, 65.79% and 68.42%; cognitive data, 73.69%), UHR versus HC (sMRI, 68.42%; DTI, 65.79%), and FEP versus UHR (sMRI, 76.67%; fMRI, 73.33%; cognitive data, 66.67%).

The results suggest that FEP subjects are identifiable at the individual level using a range of biological and cognitive measures. Comparatively, only sMRI and DTI allowed discrimination of UHR from HC subjects. For the first time FEP and UHR subjects have been shown to be directly differentiable at the single-subject level using cognitive, sMRI and fMRI data. Preliminarily, the results support clinical development of SVM to help inform identification of FEP and UHR subjects, though future work is needed to provide enhanced levels of accuracy.

Schizophrenia is associated with lower pre-morbid intelligence (IQ) in addition to (pre-morbid) cognitive decline. Both schizophrenia and IQ are highly heritable traits. Therefore, we hypothesized that genetic variants associated with schizophrenia, including copy number variants (CNVs) and a polygenic schizophrenia (risk) score (PSS), may influence intelligence.

IQ was estimated with the Wechsler Adult Intelligence Scale (WAIS). CNVs were determined from single nucleotide polymorphism (SNP) data using the QuantiSNP and PennCNV algorithms. For the PSS, odds ratios for genome-wide SNP data were calculated in a sample collected by the Psychiatric Genome-Wide Association Study (GWAS) Consortium (8690 schizophrenia patients and 11 831 controls). These were used to calculate individual PSSs in our independent sample of 350 schizophrenia patients and 322 healthy controls.

Although significantly more genes were disrupted by deletions in schizophrenia patients compared to controls (p = 0.009), there was no effect of CNV measures on IQ. The PSS was associated with disease status (R2 = 0.055, p = 2.1 × 10−7) and with IQ in the entire sample (R2 = 0.018, p = 0.0008) but the effect on IQ disappeared after correction for disease status.

Our data suggest that rare and common schizophrenia-associated variants do not explain the variation in IQ in healthy subjects or in schizophrenia patients. Thus, reductions in IQ in schizophrenia patients may be secondary to other processes related to schizophrenia risk.

Hyperprolactinemia is frequent in patients with schizophrenic psychoses. It is usually regarded as an adverse effect of antipsychotics but has recently also been shown in patients without antipsychotic medication. Our objective was to test whether hyperprolactinemia occurs in antipsychotic-naive first-episode patients (FEPs).

In the framework of the European First Episode Schizophrenia Trial (EUFEST), 249 out of 498 FEPs were eligible for this study, of whom 74 were antipsychotic naive. All patients were investigated regarding their serum prolactin levels with immunoassays standardized against the 3rd International Reference Standard 84/500.

Twenty-nine (39%) of the 74 antipsychotic-naive patients showed hyperprolactinemia not explained by any other reason, 11 (50%) of 22 women and 18 (35%) of 52 men.

Hyperprolactinemia may be present in patients with schizophrenic psychoses independent of antipsychotic medication. It might be stress induced. As enhanced prolactin can increase dopamine release through a feedback mechanism, this could contribute to explaining how stress can trigger the outbreak of psychosis.

Exposure to life stress is known to adversely impact the course of bipolar disorder. Few studies have disentangled the effects of multiple types of stressors on the longitudinal course of bipolar I disorder. This study examines whether severity of chronic stressors and exposure to trauma are prospectively associated with course of illness among bipolar patients.

One hundred and thirty-one participants diagnosed with bipolar I disorder were recruited through treatment centers, support groups and community advertisements. Severity of chronic stressors and exposure to trauma were assessed at study entry with in-person interviews using the Bedford College Life Event and Difficulty Schedule (LEDS). Course of illness was assessed by monthly interviews conducted over the course of 24 months (over 3000 assessments).

Trauma exposure was related to more severe interpersonal chronic stressors. Multiple regression models provided evidence that severity of overall chronic stressors predicted depressive but not manic symptoms, accounting for 7.5% of explained variance.

Overall chronic stressors seem to be an important determinant of depressive symptoms within bipolar disorder, highlighting the importance of studying multiple forms of life stress.

Bipolar disorder (BD) has been reported to be associated with high risk of suicide. We aimed to investigate the frequency and characteristics of suicide in people with BD in a national sample.

Suicide in BD in England from 1996 to 2009 was explored using descriptive statistics on data collected by the National Confidential Inquiry into Suicide and Homicide by People with Mental Illness (NCI). Suicide cases with a primary diagnosis of BD were compared to suicide cases with any other primary diagnosis.

During the study period 1489 individuals with BD died by suicide, an average of 116 cases/year. Compared to other primary diagnosis suicides, those with BD were more likely to be female, more than 5 years post-diagnosis, current/recent in-patients, to have more than five in-patient admissions, and to have depressive symptoms. In BD suicides the most common co-morbid diagnoses were personality disorder and alcohol dependence. Approximately 40% were not prescribed mood stabilizers at the time of death. More than 60% of BD suicides were in contact with services the week prior to suicide but were assessed as low risk.

Given the high rate of suicide in BD and the low estimates of risk, it is important that health professionals can accurately identify patients most likely to experience poor outcomes. Factors such as alcohol dependence/misuse, personality disorder, depressive illness and current/recent in-patient admission could characterize a high-risk group. Future studies need to operationalize clinically useful indicators of suicide risk in BD.

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of elevated alanine aminotransferase (ALT). NAFLD is associated with insulin resistance and hepatic inflammation. Similarly, patients with depression exhibit insulin resistance and increased inflammatory markers. However, no study has shown a clear association between elevated ALT and the development of depression. The aim of the study was to test whether elevated ALT, a surrogate marker for NAFLD, predicts the development of depression.

The present prospective cohort study investigated 12 180 employed adults referred for health examinations that included fasting blood tests and anthropometric measurements between 2003 and 2010. Exclusion criteria were: baseline minor/major depression, excessive alcohol consumption and other causes for ALT elevation. Depression was evaluated by the eight-item Patient Health Questionnaire (PHQ-8) score.

The final cohort included 5984 subjects [69.4% men, aged 45.0 (s.d. = 10.24) years]. The incidence rate of minor and major depression was 3.8% and 1.4%, respectively. Elevated ALT was a significant independent predictor for the occurrence of minor [odds ratio (OR) 2.02, 95% confidence interval (CI) 1.40–2.92] and major (OR 3.132, 95% CI 1.81–5.40) depression after adjusting for age, gender, body mass index, education level, serum levels of lipids, glucose, smoking and physical activity. Adding subjective health and affective state parameters (sleep disturbances, self-rated health, anxiety and burnout) as potential mediators only slightly ameliorated the association. Persistently elevated ALT was associated with the greatest risk for minor or major depression as compared with elevation only at baseline or follow-up (p for trend < 0.001).

Elevated ALT was associated with developing depressive symptoms, thus suggesting that NAFLD may represent an independent modifiable risk factor for depression.

Previous studies suggest a link between parental separation or divorce and risk of depression in adolescence. There are, however, few studies that have prospectively examined the effects of timing of biological father absence on risk for depressive symptoms in adolescence while controlling for a range of confounding factors.

We examine the association between father absence occurring in early (the first 5 years) and middle childhood (5–10 years) and adolescent depressive symptoms in a sample comprising 5631 children from the UK-based Avon Longitudinal Study of Parents and Children (ALSPAC). Self-reported depressive symptoms at 14 years were assessed using the Short Mood and Feelings Questionnaire (SMFQ). Father absence was assessed from maternal questionnaires completed at regular intervals from the birth of the study child up to 10 years.

There was evidence for an association between father absence in early childhood and increased odds of depressive symptoms at 14 years. This association was stronger in girls than in boys and remained after adjusting for a range of socio-economic, maternal and familial confounders assessed prior to the father's departure. Conversely, there was no evidence for an association between father absence in middle childhood and depressive symptoms at 14 years.

Father absence in early childhood increases risk for adolescent depressive symptoms, particularly in girls. Future research should be aimed at identifying possible biological and psychosocial mechanisms linking father absence to depressive symptomatology to enable the development of family-based early prevention and intervention programmes targeting young children at risk.

It is not clear whether the prevalence of dementia and depression among the elderly has changed during the past 30 years.

Population-based samples from Gothenburg, Sweden were examined with identical psychiatric and neuropsychiatric examinations at age 70 years in 1976–1977 (n = 404, response rate 78.8%) and 2000–2001 (n = 579, response rate 66.4%), and at age 75 in 1976–1977 (n = 303, response rate 78%) and 2005–2006 (n = 753, response rate 63.4%). Depression was diagnosed according to DSM-IV and dementia according to Kay's criteria. General linear models (GLMs) were used to test for differences between groups.

Dementia was related to age but not to birth cohort or sex. Major depression was related to sex (higher in women) but not to birth cohort or age. Minor depression was related to birth cohort, sex (higher in women), age (higher at age 75) and the interaction effect of birth cohort × age; that is, the prevalence of minor depression increased with age in the 2000s but not in the 1970s. Thus, the prevalence of minor depression was higher in 2005–2006 than in 1976–1977 among 75-year-olds for both men (12.4% v. 3.7%) and women (19.1% v. 5.6%) whereas there were no birth cohort differences at age 70.

Secular changes were observed only for minor depression, which is considered to be related more to psychosocial factors than major depression. The high prevalence of minor depression in later-born birth cohorts emphasizes the importance of detecting minor depression in the elderly.

Major depressive disorder (MDD) and generalized anxiety disorder (GAD) have the highest co-morbidity rates within the internalizing disorders cluster, yet no Internet-based cognitive behavioural therapy (iCBT) programme exists for their combined treatment.

We designed a six-lesson therapist-assisted iCBT programme for mixed anxiety and depression. Study 1 was a randomized controlled trial (RCT) comparing the iCBT programme (n = 46) versus wait-list control (WLC; n = 53) for patients diagnosed by structured clinical interview with MDD, GAD or co-morbid GAD/MDD. Primary outcome measures were the Patient Health Questionnaire nine-item scale (depression), Generalized Anxiety Disorder seven-item scale (generalized anxiety), Kessler 10-item Psychological Distress scale (distress) and 12-item World Health Organization Disability Assessment Schedule II (disability). The iCBT group was followed up at 3 months post-treatment. In study 2, we investigated the adherence to, and efficacy of the same programme in a primary care setting, where patients (n = 136) completed the programme under the supervision of primary care clinicians.

The RCT showed that the iCBT programme was more effective than WLC, with large within- and between-groups effect sizes found (>0.8). Adherence was also high (89%), and gains were maintained at 3-month follow-up. In study 2 in primary care, adherence to the iCBT programme was low (41%), yet effect sizes were large (>0.8). Of the non-completers, 30% experienced benefit.

Together, the results show that iCBT is effective and adherence is high in research settings, but there is a problem of adherence when translated into the ‘real world’. Future efforts need to be placed on developing improved adherence to iCBT in primary care settings.

Diagnosis of depressive disorder using interviewer-administered instruments is expensive and frequently impractical in large epidemiological surveys. The aim of this study was to assess the validity of three self-completion measures of depressive disorder and other psychiatric disorders in older people against an interviewer-administered instrument.

A random sample stratified by sex, age and social position was selected from the Whitehall II study participants. This sample was supplemented by inclusion of depressed Whitehall II participants. Depressive disorder and other mental disorders were assessed by the interviewer-administered structured revised Clinical Interview Schedule (CIS-R) in 277 participants aged 58–80 years. Participants also completed a computerized self-completion version of the CIS-R in addition to the General Health Questionnaire (GHQ) and the Center for Epidemiologic Studies Depression Scale (CES-D).

The mean total score was similar for the interviewer-administered (4.43) and self-completion (4.35) versions of the CIS-R [95% confidence interval (CI) for difference −0.31 to 0.16]. Differences were not related to sex, age, social position or presence of chronic physical illness. Sensitivity/specificity of self-completion CIS-R was 74%/98% for any mental disorder and 75%/98% for depressive episode. The corresponding figures were 86%/87% and 78%/83% for GHQ and 77%/89% and 89%/86% for CES-D.

The self-completion computerized version of the CIS-R is feasible and has good validity as a measure of any mental disorder and depression in people aged ⩾ 60 years. GHQ and CES-D also have good criterion validity as measures of any mental disorder and depressive disorder respectively.

Survivors of critical illnesses often have clinically significant post-traumatic stress disorder (PTSD) symptoms. This study describes the 2-year prevalence and duration of PTSD symptoms after acute lung injury (ALI), and examines patient baseline and critical illness/intensive care-related risk factors.

This prospective, longitudinal cohort study recruited patients from 13 intensive care units (ICUs) in four hospitals, with follow-up 3, 6, 12 and 24 months after ALI onset. The outcome of interest was an Impact of Events Scale – Revised (IES-R) mean score ⩾1.6 (‘PTSD symptoms’).

During the 2-year follow-up, 66/186 patients (35%) had PTSD symptoms, with the greatest prevalence by the 3-month follow-up. Fifty-six patients with post-ALI PTSD symptoms survived to the 24-month follow-up, and 35 (62%) of these had PTSD symptoms at the 24-month follow-up; 50% had taken psychiatric medications and 40% had seen a psychiatrist since hospital discharge. Risk/protective factors for PTSD symptoms were pre-ALI depression [hazard odds ratio (OR) 1.96, 95% confidence interval (CI) 1.06–3.64], ICU length of stay (for a doubling of days, OR 1.39, 95% CI 1.06–1.83), proportion of ICU days with sepsis (per decile, OR 1.08, 95% CI 1.00–1.16), high ICU opiate doses (mean morphine equivalent ⩾100 mg/day, OR 2.13, 95% CI 1.02–4.42) and proportion of ICU days on opiates (per decile, OR 0.83, 95% CI 0.74–0.94) or corticosteroids (per decile, OR 0.91, 95% CI 0.84–0.99).

PTSD symptoms are common, long-lasting and associated with psychiatric treatment during the first 2 years after ALI. Risk factors include pre-ALI depression, durations of stay and sepsis in the ICU, and administration of high-dose opiates in the ICU. Protective factors include durations of opiate and corticosteroid administration in the ICU.

Being physically assaulted is known to increase the risk of the occurrence of post-traumatic stress disorder (PTSD) symptoms but it may also skew judgements about the intentions of other people. The objectives of the study were to assess paranoia and PTSD after an assault and to test whether theory-derived cognitive factors predicted the persistence of these problems.

At 4 weeks after hospital attendance due to an assault, 106 people were assessed on multiple symptom measures (including virtual reality) and cognitive factors from models of paranoia and PTSD. The symptom measures were repeated 3 and 6 months later.

Factor analysis indicated that paranoia and PTSD were distinct experiences, though positively correlated. At 4 weeks, 33% of participants met diagnostic criteria for PTSD, falling to 16% at follow-up. Of the group at the first assessment, 80% reported that since the assault they were excessively fearful of other people, which over time fell to 66%. Almost all the cognitive factors (including information-processing style during the trauma, mental defeat, qualities of unwanted memories, self-blame, negative thoughts about self, worry, safety behaviours, anomalous internal experiences and cognitive inflexibility) predicted later paranoia and PTSD, but there was little evidence of differential prediction.

Paranoia after an assault may be common and distinguishable from PTSD but predicted by a strikingly similar range of factors.