Several prospective longitudinal studies have suggested that somatic/affective depressive symptoms, but not cognitive/affective depressive symptoms, are related to prognosis in patients with heart disease, but findings have been inconsistent. The aim of this study was to investigate the association of cognitive/affective and somatic/affective symptoms of depression with cardiovascular prognosis in patients with heart disease using a meta-analytic perspective.

A systematic search was performed in PubMed, EMBASE and PsycInfo. Thirteen prospective studies on symptom dimensions of depression and cardiovascular prognosis fulfilled the inclusion criteria, providing data on a total of 11 128 subjects. The risk estimates for each dimension of depressive symptoms, demographic and methodological variables were extracted from the included articles.

In least-adjusted analyses, both the somatic/affective [hazard ratio (HR) 1.30, 95% confidence interval (CI) 1.19–1.41, p < 0.001] and cognitive/affective (HR 1.07, 95% CI 1.00–1.15, p = 0.05) dimensions of depressive symptoms were associated with cardiovascular prognosis. In fully adjusted analyses, somatic/affective symptoms were significantly associated with adverse prognosis (HR 1.19, 95% CI 1.10–1.29, p < 0.001) but cognitive/affective symptoms were not (HR 1.04, 95% CI 0.97–1.12, p = 0.25). An increase of one standard deviation (±1 s.d.) in the scores of the somatic/affective dimension was associated with a 32% increased risk of adverse outcomes (HR 1.32, 95% CI 1.17–1.48, p < 0.001).

Somatic/affective depressive symptoms were more strongly and consistently associated with mortality and cardiovascular events in patients with heart disease compared with cognitive/affective symptoms. Future research should focus on the mechanisms by which somatic/affective depressive symptoms may affect cardiovascular prognosis.

Studies of the long-term course and outcome of psychoses tend to focus on cohorts of prevalent cases. Such studies bias samples towards those with poor outcomes, which may distort our understanding of prognosis. Long-term follow-up studies of epidemiologically robust first-episode samples are rare.

AESOP-10 is a 10-year follow-up study of 557 individuals with a first episode of psychosis initially identified in two areas in the UK (South East London and Nottingham). Detailed information was collated on course and outcome in three domains (clinical, social and service use) from case records, informants and follow-up interviews.

At follow-up, of 532 incident cases identified, at baseline 37 (7%) had died, 29 (6%) had emigrated and eight (2%) were excluded. Of the remaining 458, 412 (90%) were traced and some information on follow-up was collated for 387 (85%). Most cases (265, 77%) experienced at least one period of sustained remission; at follow-up, 141 (46%) had been symptom free for at least 2 years. A majority (208, 72%) of cases had been employed for less than 25% of the follow-up period. The median number of hospital admissions, including at first presentation, was 2 [interquartile range (IQR) 1–4]; a majority (299, 88%) were admitted a least once and a minority (21, 6%) had 10 or more admissions. Overall, outcomes were worse for those with a non-affective diagnosis, for men and for those from South East London.

Sustained periods of symptom remission are usual following first presentation to mental health services for psychosis, including for those with a non-affective disorder; almost half recover.

It has been previously demonstrated that a cognitive bias against disconfirmatory evidence (BADE) is associated with delusions. However, small samples of delusional patients, reliance on difference scores and choice of comparison groups may have hampered the reliability of these results. In the present study we aimed to improve on this methodology with a recent version of the BADE task, and compare larger groups of schizophrenia patients with/without delusions to obsessive–compulsive disorder (OCD) patients, a population with persistent and possibly bizarre beliefs without psychosis.

A component analysis was used to identify cognitive operations underlying the BADE task, and how they differ across four groups of participants: (1) high-delusional schizophrenia, (2) low-delusional schizophrenia, (3) OCD patients and (4) non-psychiatric controls.

As in past studies, two components emerged and were labelled ‘evidence integration’ (the degree to which disambiguating information has been integrated) and ‘conservatism’ (reduced willingness to provide high plausibility ratings when justified), and only evidence integration differed between severely delusional patients and the other groups, reflecting delusional subjects giving higher ratings for disconfirmed interpretations and lower ratings for confirmed interpretations.

These data support the finding that a reduced willingness to adjust beliefs when confronted with disconfirming evidence may be a cognitive underpinning of delusions specifically, rather than obsessive beliefs or other aspects of psychosis such as hallucinations, and illustrates a cognitive process that may underlie maintenance of delusions in the face of counter-evidence. This supports the possibility of the BADE operation being a useful target in cognitive-based therapies for delusions.

Both language and music are thought to have evolved from a musical protolanguage that communicated social information, including emotion. Individuals with perceptual music disorders (amusia) show deficits in auditory emotion recognition (AER). Although auditory perceptual deficits have been studied in schizophrenia, their relationship with musical/protolinguistic competence has not previously been assessed.

Musical ability was assessed in 31 schizophrenia/schizo-affective patients and 44 healthy controls using the Montreal Battery for Evaluation of Amusia (MBEA). AER was assessed using a novel battery in which actors provided portrayals of five separate emotions. The Disorganization factor of the Positive and Negative Syndrome Scale (PANSS) was used as a proxy for language/thought disorder and the MATRICS Consensus Cognitive Battery (MCCB) was used to assess cognition.

Highly significant deficits were seen between patients and controls across auditory tasks (p < 0.001). Moreover, significant differences were seen in AER between the amusia and intact music-perceiving groups, which remained significant after controlling for group status and education. Correlations with AER were specific to the melody domain, and correlations between protolanguage (melody domain) and language were independent of overall cognition.

This is the first study to document a specific relationship between amusia, AER and thought disorder, suggesting a shared linguistic/protolinguistic impairment. Once amusia was considered, other cognitive factors were no longer significant predictors of AER, suggesting that musical ability in general and melodic discrimination ability in particular may be crucial targets for treatment development and cognitive remediation in schizophrenia.

Cannabis use is high amongst young people who have recently had their first episode of psychosis, and is associated with worse outcomes. To date, interventions to reduce cannabis consumption have been largely ineffective, and it has been suggested that longer treatment periods are required.

In a pragmatic single-blind randomized controlled trial 110 participants were randomly allocated to one of three conditions: a brief motivational interviewing and cognitive behavioural therapy (MI-CBT) intervention (up to 12 sessions over 4.5 months) with standard care from an early intervention service; a long MI-CBT intervention (up to 24 sessions over 9 months) with standard care; or standard care alone. The primary outcome was change in cannabis use as measured by Timeline Followback.

Neither the extended nor the brief interventions conferred benefit over standard care in terms of reductions in frequency or amount of cannabis use. Also the interventions did not result in improvements in the assessed clinical outcomes, including symptoms, functioning, hospital admissions or relapse.

Integrated MI and CBT for people with cannabis use and recent-onset psychosis does not reduce cannabis use or improve clinical outcomes. These findings are consistent with those in the published literature, and additionally demonstrate that offering a more extended intervention does not confer any advantage. Many participants were not at an action stage for change and for those not ready to reduce or quit cannabis, targeting associated problems rather than the cannabis use per se may be the best current strategy for mental health services to adopt.

We investigated whether source-monitoring deficits (here a discrimination between imagined and performed actions) underlie hallucinations among patients with a history of hallucinations in the course of their alcohol dependence.

We assessed 29 patients with alcohol dependence who had no history of hallucinations during their course of alcoholism and 29 patients with a history of at least one episode of hallucinations of any modality during their course of alcohol dependency. The control group consisted of 24 healthy participants. Participants were assessed with an action memory task. Simple actions were presented to the participants verbally or non-verbally. Some actions were performed physically and others were imagined. In the recognition phase, participants were asked whether the action was presented verbally or non-verbally (action presentation type discrimination) and whether the action was performed or imagined (self-monitoring). A confidence score related to self-monitoring responses was also obtained.

Alcoholics with a history of hallucinations misremembered imagined actions as perceived ones more frequently than patients without hallucinations, but not the reverse. Only patients with a history of hallucinations committed more errors of this type than healthy subjects. There were no group differences regarding discrimination between an action presentation type. Both clinical groups committed errors with a higher degree of confidence than healthy subjects.

Our results tentatively suggest that a specific type of source-monitoring deficit (i.e. confusing imagery with reality) may be involved in the hallucinations in patients with alcohol dependence. The findings are discussed in the light of a transdiagnostic approach to hallucinations.

Understanding pre-existing neural vulnerabilities found in youth who are family history positive (FHP) for alcohol use disorders could help inform preventative interventions created to delay initiation age and escalation of heavy drinking. The goal of this study was to compare indices of white matter integrity using diffusion tensor imaging (DTI) between FHP and family history negative (FHN) youth using a sample of 94 alcohol-naive adolescents and to examine if differences were associated with global and domain-specific cognitive functioning.

Participants were 48 FHP and 46 FHN demographically matched, healthy, substance-naive 12- to 14-year-olds (54% female) recruited from local middle schools. Participants completed a neuropsychological test battery and magnetic resonance imaging session, including DTI.

FHP youth had higher fractional anisotropy and axial diffusivity, and lower radial and mean diffusivity, than FHN youth in 19 clusters spanning projection, association and interhemispheric white matter tracts. Findings were replicated after controlling for age, gender, socio-economic status, grade and pubertal development. Groups did not differ significantly on global or domain-specific neuropsychological test scores.

FHP teens showed higher white matter integrity, but similar cognitive functioning, to FHN youth. More mature neural features could be related to more precocious behaviors, such as substance use initiation, in FHP youth. Future research exploring white matter maturation before and after substance use initiation will help elucidate the neurodevelopmental trajectories in youth at risk for substance use disorders, to inform preventive efforts and better understand the sequelae of adolescent alcohol and drug use.

Impulsive decision making is a hallmark of frequently occurring addiction disorders including alcohol dependence (AD). Therefore, ameliorating impulsive decision making is a promising target for the treatment of AD. Previous studies have shown that modafinil enhances cognitive control functions in various psychiatric disorders. However, the effects of modafinil on delay discounting and its underlying neural correlates have not been investigated as yet. The aim of the current study was to investigate the effects of modafinil on neural correlates of impulsive decision making in abstinent AD patients and healthy control (HC) subjects.

A randomized, double-blind, placebo-controlled, within-subjects cross-over study using functional magnetic resonance imaging (fMRI) was conducted in 14 AD patients and 16 HC subjects. All subjects participated in two fMRI sessions in which they either received a single dose of placebo or 200 mg of modafinil 2 h before the session. During fMRI, subjects completed a delay-discounting task to measure impulsive decision making.

Modafinil improved impulsive decision making in AD pateints, which was accompanied by enhanced recruitment of frontoparietal regions and reduced activation of the ventromedial prefrontal cortex. Moreover, modafinil-induced enhancement of functional connectivity between the superior frontal gyrus and ventral striatum was specifically associated with improvement in impulsive decision making.

These findings indicate that modafinil can improve impulsive decision making in AD patients through an enhanced coupling of prefrontal control regions and brain regions coding the subjective value of rewards. Therefore, the current study supports the implementation of modafinil in future clinical trials for AD.

The effect of prenatal distress on the risk of a small for gestational age (SGA) infant is uncertain. We have addressed the influences of prenatal stress, anxiety and depression on the risk of SGA. We also examined the effects of infant sex and timing of distress during pregnancy on any observed associations.

The study population comprised 5606 healthy nulliparous pregnant women who participated in the international prospective Screening for Obstetric and Pregnancy Endpoints (SCOPE) study. Women completed the Perceived Stress Scale (PSS), the short form of the Spielberger State–Trait Anxiety Inventory (STAI) and the Edinburgh Postnatal Depression Scale (EPDS) at 15 ± 1 and 20 ± 1 weeks' gestation. SGA was defined as birthweight below the 10th customized percentile. Logistic regression was used for data analysis, adjusting for several potential confounders such as maternal age, body mass index (BMI), smoking, socio-economic status and physical exercise.

The risk of SGA was increased in relation to mild [adjusted odds ratio (aOR) 1.35, 95% confidence interval (CI) 1.07–1.71], moderate (aOR 1.26, 95% CI 1.06–1.49), high (aOR 1.45, 95% CI 1.08–1.95) and very high stress scores (aOR 1.56, 95% CI 1.03–2.37); very high anxiety score (aOR 1.45, 95% CI 1.13–1.86); and very high depression score (aOR 1.14, 95% CI 1.05–1.24) at 20 ± 1 weeks' gestation. Sensitivity analyses showed that very high anxiety and very high depression increases the risk of SGA in males but not in females whereas stress increases the risk of SGA in both males and females.

These findings suggest that prenatal stress, anxiety and depression measured at 20 weeks' gestation increase the risk of SGA. The effects of maternal anxiety and depression on SGA were strongest in male infants.

The high rate of depression among children of depressed mothers is well known. Suggestions that improvement in maternal acute depression has a positive effect on the child have emerged. However, data on the mechanisms of change have been sparse. The aim was to understand how remission and relapse in the mother might explain the changes in the child's outcome.

Participants were 76 depressed mothers who entered into a medication clinical trial for depression and 135 of their eligible offspring ages 7–17 years. The mothers and children were assessed at baseline and periodically over 9 months by independent teams to understand the relationship between changes in children's symptoms and functioning and maternal remission or relapse. The main outcome measures were, for mothers, the Hamilton Depression Rating Scale (HAMD), the Social Adjustment Scale (SAS) and the Parental Bonding Instrument (PBI) and, for children, the Children's Depression Inventory (CDI), the Columbia Impairment Scale (CIS), the Multidimensional Anxiety Scale for Children (MASC) and the Children's Global Assessment Scale (CGAS).

Maternal remission was associated with a decrease in the child's depressive symptoms. The mother's subsequent relapse was associated with an increase in the child's symptoms over 9 months. The effect of maternal remission on the child's improvement was partially explained by an improvement in the mother's parenting, particularly the change in the mother's ability to listen and talk to her child, but also reflected in her improvement in parental bonding. These findings could not be explained by the child's treatment.

A depressed mother's remission is associated with her improvement in parenting and a decrease in her child's symptoms. Her relapse is associated with an increase in her child's symptoms.

This study surveyed the characteristics of white matter (WM) micro-integrity in patients who were diagnosed with major depressive disorder (MDD) without co-morbidities.

A total of 44 patients with MDD and 27 normal controls were enrolled in our study. Diffusion tensor imaging images of patients and controls were pre-processed and analysed to estimate differences in WM micro-integrity between patients and controls by performing comparisons of the values obtained from fractional anisotropy (FA). FA outputs of patients and controls were compared by a non-parametric permutation-based method with global brain volume, age and gender as covariates. In addition, the between-group differences of radial diffusivity (RD) and axial diffusivity (AD) were assessed to explain the alterations in FA values. Correlations between clinical variables (such as depression severity, anxiety severity, illness duration) and FA values were also estimated in each group and across both groups.

The patients with MDD had significantly lower FA values than the controls, for the left superior longitudinal fasciculus (SLF) and the right anterior thalamic radiation (ATR). The reductions in FA values occurred in combination with elevated RD values in the bilateral SLF and decreased AD values in the bilateral ATR. FA values were negatively correlated with depression severity in the SLF and with illness duration in the right SLF and ATR.

MDD patients had significant alterations in the WM micro-integrity of the left SLF and the right ATR.

Studies investigating structural brain abnormalities in depression have typically employed a categorical rather than dimensional approach to depression [i.e. comparing subjects with Diagnostic and Statistical Manual of Mental Disorders (DSM)-defined major depressive disorder (MDD) v. healthy controls]. The National Institute of Mental Health, through their Research Domain Criteria initiative, has encouraged a dimensional approach to the study of psychopathology as opposed to an over-reliance on categorical (e.g. DSM-based) diagnostic approaches. Moreover, subthreshold levels of depressive symptoms (i.e. severity levels below DSM criteria) have been found to be associated with a range of negative outcomes, yet have been relatively neglected in neuroimaging research.

To examine the extent to which depressive symptoms – even at subclinical levels – are linearly related to gray matter volume reductions in theoretically important brain regions, we employed whole-brain voxel-based morphometry in a sample of 54 participants.

The severity of mild depressive symptoms, even in a subclinical population, was associated with reduced gray matter volume in the orbitofrontal cortex, anterior cingulate, thalamus, superior temporal gyrus/temporal pole and superior frontal gyrus. A conjunction analysis revealed concordance across two separate measures of depression.

Reduced gray matter volume in theoretically important brain regions can be observed even in a sample that does not meet DSM criteria for MDD, but who nevertheless report relatively elevated levels of depressive symptoms. Overall, these findings highlight the need for additional research using dimensional conceptual and analytic approaches, as well as further investigation of subclinical populations.

The aetiology of depression is multifactorial, with biological, cognitive and environmental factors across the life course influencing risk of a depressive episode. There is inconsistent evidence linking early life development and later depression. The aim of this study was to investigate relationships between low birthweight (LBW), infant neurodevelopment, and acute and chronic stress as components in pathways to depression in adulthood.

The sample included 4627 members of the National Survey of Health and Development (NSHD; the 1946 British birth cohort). Weight at birth, age of developmental milestones, economic deprivation in early childhood, acute stressors in childhood and adulthood, and socio-economic status (SES) in adulthood were assessed for their direct and indirect effects on adolescent (ages 13 and 15 years) and adult (ages 36, 43 and 53 years) measures of depressive symptoms in a structural equation modelling (SEM) framework. A structural equation model developed to incorporate all variables exhibited excellent model fit according to several indices.

The path of prediction from birthweight to age of developmental milestones to adolescent depression/anxiety to adult depression/anxiety was significant (p < 0.001). Notably, direct paths from birthweight (p = 0.25) and age of developmental milestones (p = 0.23) to adult depression were not significant. Childhood deprivation and stressors had important direct and indirect effects on depression. Stressors in adulthood were strongly associated with adult depression.

Depression in adulthood is influenced by an accumulation of stressors across the life course, including many that originate in the first years of life. Effects of early-life development on mental health appear by adolescence.

Meta-analyses suggest that reboxetine may be less effective than other antidepressants. Such comparisons may be biased by lower adherence to reboxetine and subsequent handling of missing outcome data. This study illustrates how to adjust for differential non-adherence and hence derive an unbiased estimate of the efficacy of reboxetine compared with citalopram in primary care patients with depression.

A structural mean modelling (SMM) approach was used to generate adherence-adjusted estimates of the efficacy of reboxetine compared with citalopram using GENetic and clinical Predictors Of treatment response in Depression (GENPOD) trial data. Intention-to-treat (ITT) analyses were performed to compare estimates of effectiveness with results from previous meta-analyses.

At 6 weeks, 92% of those randomized to citalopram were still taking their medication, compared with 72% of those randomized to reboxetine. In ITT analysis, there was only weak evidence that those on reboxetine had a slightly worse outcome than those on citalopram [adjusted difference in mean Beck Depression Inventory (BDI) scores: 1.19, 95% confidence interval (CI) –0.52 to 2.90, p = 0.17]. There was no evidence of a difference in efficacy when differential non-adherence was accounted for using the SMM approach for mean BDI (–0.29, 95% CI –3.04 to 2.46, p = 0.84) or the other mental health outcomes.

There was no evidence of a difference in the efficacy of reboxetine and citalopram when these drugs are taken and tolerated by depressed patients. The SMM approach can be implemented in standard statistical software to adjust for differential non-adherence and generate unbiased estimates of treatment efficacy for comparisons of two (or more) active interventions.

Until recently, hoarding was considered an obsessive–compulsive symptom (OCS). However, current evidence suggests that these two phenotypes may be clinically, and perhaps etiologically, distinct. Both hoarding and OCS have a genetic etiology, but the degree of unique and shared genetic contributions to these phenotypes has not been well studied.

Prevalence rates were assessed for hoarding and OCS in a sample of adult twin pairs (n = 7906 twins) and their family members from the Netherlands Twin Register (total sample = 15 914). Using Mplus, genetic analyses using liability threshold models were conducted for both phenotypes, for their co-morbidity, and for specific hoarding symptoms (cluttering, discarding and acquiring).

Of the total sample, 6.7% met criteria for clinically significant hoarding; endorsement of all three hoarding symptoms was ⩾79%. Men had slightly higher rates than women. Also, 5.7% met criteria for clinically significant OCS; rates were similar in males and females. Genetic factors accounted for 36% of the variance for hoarding and 40% of the variance for OCS. The genetic correlation between hoarding and OCS was 0.10. There was no evidence of sex-specific genetic contributions for hoarding or OCS. There was evidence for a genetic contribution to all hoarding symptom subtypes. Only cluttering showed evidence of a contribution from the shared environment.

OCS and hoarding are common in this population-based sample, have prevalence rates similar to those previously reported, and show significant heritability. Genetic factors contributed to the co-morbidity of both traits, although the genetic correlation between them was low.

As relapse after completed cognitive behavior therapy (CBT) for obsessive–compulsive disorder (OCD) is common, many treatment protocols include booster programs to improve the long-term effects. However, the effects of booster programs are not well studied. In this study, we investigated the long-term efficacy of Internet-based CBT (ICBT) with therapist support for OCD with or without an Internet-based booster program.

A total of 101 participants were included in the long-term follow-up analysis of ICBT. Of these, 93 were randomized to a booster program or no booster program. Outcome assessments were collected at 4, 7, 12 and 24 months after receiving ICBT.

The entire sample had sustained long-term effects from pre-treatment to all follow-up assessments, with large within-group effect sizes (Cohen's d = 1.58–2.09). The booster group had a significant mean reduction in OCD symptoms compared to the control condition from booster baseline (4 months) to 7 months, but not at 12 or 24 months. Participants in the booster group improved significantly in terms of general functioning at 7, 12 and 24 months, and had fewer relapses. Kaplan–Meier analysis also indicated a significantly slower relapse rate in the booster group.

The results suggest that ICBT has sustained long-term effects and that adding an Internet-based booster program can further improve long-term outcome and prevent relapse for some OCD patients.

Studies in borderline personality disorder (BPD) have consistently revealed abnormalities in fronto-limbic brain regions during emotional, somatosensory and cognitive challenges. Here we investigated changes in resting-state functional connectivity (RSFC) of three fronto-limbic core regions of specific importance to BPD.

Functional magnetic resonance imaging data were acquired in 20 unmedicated female BPD patients and 17 healthy controls (HC, matched for age, sex and education) during rest. The amygdala, and the dorsal and ventral anterior cingulate cortex (ACC) were defined as seeds to investigate RSFC patterns of a medial temporal lobe network, the salience network and default mode network. The Dissociation Experience Scale (DES), a measure of trait dissociation, was additionally used as a predictor of RSFC with these seed regions.

Compared with HC, BPD patients showed a trend towards increased RSFC between the amygdala and the insula, orbitofrontal cortex and putamen. Compared with controls, patients furthermore exhibited diminished negative RSFC between the dorsal ACC and posterior cingulate cortex, a core region of the default mode network, and regions of the dorsomedial prefrontal cortex. Last, increased negative RSFC between the ventral ACC and medial occipital regions was observed in BPD patients. DES scores were correlated with amygdala connectivity with the dorsolateral prefrontal cortex and fusiform gyrus.

Our findings suggest alterations in resting-state networks associated with processing of negative emotions, encoding of salient events, and self-referential processing in individuals with BPD compared with HC. These results shed more light on the role of abnormal brain connectivity in BPD.

Somatoform disorders are costly for society in terms of increased healthcare expenditure. Patients' illness perceptions have been found to play a role in somatoform disorders. However, it is unclear whether illness perceptions predict higher health costs in these patients.

A total of 1785 primary care patients presenting a new health complaint completed a questionnaire on their illness perceptions and emotional distress before the consultation. The physicians completed a questionnaire for each patient on diagnostics after the consultation. In a stratified subsample, physician interviewers established diagnoses of DSM-IV somatization and undifferentiated somatoform disorders (n = 144) using the Schedules for Clinical Assessment in Neuropsychiatry. Healthcare expenditure was obtained from Danish health registers for a 2-year follow-up period.

Patients had more negative perceptions of their well-defined physical health problems when they had a co-morbid somatoform disorder. A strong illness identity [β = 0.120, 95% confidence interval (CI) 0.029–0.212, p = 0.012], perceived negative consequences (β = 0.010, 95% CI 0.001–0.019, p = 0.024), a long timeline perspective (β = 0.013, 95% CI 0.005–0.021, p = 0.001), low personal control (β = − 0.009, 95% CI –0.015 to −0.002, p = 0.011) and negative emotional representations (β = 0.009, 95% CI 0.002–0.017, p = 0.020) predicted healthcare expenditure in somatoform disorders.

The results suggest that illness perceptions play a role in the perpetuation of symptoms in somatoform disorders and predict higher future healthcare expenditure among a subgroup of these patients.