A number of enhancement strategies have been proposed to improve the quality and outcome of care for depression in primary care settings. Decision-makers are likely to need to know whether these interventions are cost-effective in routine primary care settings.

We conducted a systematic review of all full economicevaluations (cost-effectiveness and cost-utility analyses) accompanying randomised controlled trials of enhanced primary care for depression. Costs were standardised to UK pounds/US dollars and incremental cost-effectiveness ratios (ICERs) were visually summarised using a permutation matrix.

We identified 11 full economic evaluations (4757 patients). A near-uniform finding was that the interventions based upon collaborative care/case management resulted in improved outcomes but were also associated with greater costs. When considering primary care depression treatment costs alone, ICER estimates ranged from £7 ($13, no confidence interval given) to £13 ($24, 95% CI—105 to 148) per additional depression-free day. Educational interventions alone were associated with increased cost and no clinical benefit.

Improved outcomes through depression management programmes using a collaborative care/case management approach can be expected, but are associated with increased cost and will require investment.

Although selective serotonin reuptake inhibitors (SSRIs) are frequently used for major depressive disorder, only 50–60% of patients respond to a standard dose. For non-responders, dose escalation is often applied.

To systematically review the evidence for dose escalation of SSRIs.

A systematic literature search in MEDLINE, EMBASE, CINAHL and PsycInfo was performed. Randomised controlled trials and meta-analyses investigating dose escalation of SSRIs were identified. Relevant articles were retrieved and critically appraised. Results were summarised in an evidence table. Pooling was not justified because of heterogeneity of the identified studies.

Eight true dose-escalation studies and three meta-analyses were identified. The available data provided no unequivocal base for dose escalation. Dose escalation before 4 weeks of treatment at a standard dose appeared to be ineffective.

Dose escalation of SSRIs is equivocally supported by evidence of randomised controlled trials; methodological difficulties in the studies may account for this lack of evidence.

We have previously reported the Val66Met and GT(n) repeat polymorphisms of the brain-derived neurotrophic factor (BDNF) gene to be associated with bipolar disorder. However, these findings have not been replicated consistently.

To dissect the association of the BDNF gene with bipolar disorder by examining additional markers at the DNA level and by testing the illness categories of bipolar disorder I and II and rapid cycling.

We performed a family-based association study and haplotype analyses with 312 nuclear families using four single nucleotide polymorphisms (SNPs) and the Val66Met and GT(n) repeat polymorphisms.

The SNPs hCVI1592756 and rs2049045, the Val66Met and GT(n) were significantly associated with bipolar disorder using transmission disequilibrium analyses (P=0.02, 0.009, 0.001 and 0.008 respectively). The effect at these markers was mainly driven by the rapid-cycling patients.

Within bipolar disorder, variation in the BDNF gene appears to predict risk for developing rapid cycling according to DSM–IV. Incorporating this clinical sub-phenotyping into other studies of the BDNF gene may help to resolve some of the inconsistencies reported thus far concerning BDNF and bipolar disorder.

Children of mothers with eating disorders are at increased risk of developmental disturbance, but there has been little research in middle childhood, when disturbed eating habits tend to emerge.

To examine whether maternal eating disorders identified in the postnatal year are associated with the development of disturbed eating habits and attitudes in children at 10 years of age.

Follow-up comparative study of 56 families (33 mothers with eating disorders and 23 controls). Psychopathology of children, mothers and fathers was assessed by interview, and mother-child interaction observed.

The index group of children scored higher than controls on three of four domains of eating disorder psychopathology and on a global score. Children's eating disturbance was associated with length of exposure to mothers' eating disorder and mother-child mealtime conflict at 5 years. There was some evidence of increased emotional problems in index children.

The children of mothers with eating disorders manifested disturbed eating habits and attitudes compared with controls, and may be at heightened risk of developing frank eating disorder psychopathology.

Routine use of standardised outcome measures is not universal.

To evaluate the effectiveness of standardised outcome assessment.

A randomised controlled trial, involving 160 representative adult mental health patients and paired staff (ISRCTN16971059). The intervention group (n=101) (a) completed monthly postal questionnaires assessing needs, quality of life, mental health problem severity and therapeutic alliance, and (b) received 3-monthly feedback. The control group (n=59) received treatment as usual.

The intervention did not improve primary outcomes of patient-rated unmet need and of quality of life. Other subjective secondary outcome measures were also not improved. The intervention reduced psychiatric inpatient days (3.5 v. 16.4 mean days, bootstrapped 95% CI 1.6-25.7), and hence service use costs were £2586 (95% CI 102-5391) less for intervention-group patients. Net benefit analysis indicated that the intervention was cost-effective.

Routine use of outcome measures as implemented in this study did not improve subjective outcomes, but was associated with reduced psychiatric inpatient admissions.

Evaluation of individuals at high genetic risk of schizophrenia is a powerful method for identifying precursors of the illness.

To identify aspects of personality, psychopathology and social development that differentiate high-risk and control individuals.

Adolescent and young-adult first-degree relatives (n=35) of people with schizophrenia or schizoaffective disorder and a control group (n=55) were compared on 36 measures at baseline of a longitudinal study Measures differentiating high-risk and control participants were related to four genetic loading indices.

High-risk participants older than 17 years showed more physical anhedonia, less positive involvement with peers and more problems with peers, siblings and the opposite gender. Older high-risk individuals also were less cooperative, less self-directed and less reward-dependent. Problems with peers and the opposite gender, as well as reward dependence, were related linearly to genetic loading.

Alterations in personality traits and social development are present in high-risk individuals, and may be markers for genetic liability toward the illness.

Dimensional structures are established for many psychiatric diagnoses, but dimensions have not been compared between diagnostic groups.

To examine the structure of dimensions in psychosis, to analyse their correlations with disease characteristics and to assess the relative contribution of dimensions v. diagnosis in explaining these characteristics.

Factor analysis of the OPCRIT items of 191 Maudsley Family Study patients with schizophrenia, mood disorders with psychosis, schizoaffective disorder, and other psychotic illnesses, followed by regression of disease characteristics from factor scores and diagnosis.

Five factors were identified (mania, reality distortion, depression, disorganisation, negative); all were more variable in schizophrenia than in affective psychosis. Mania was the best discriminator between schizophrenia and affective psychosis; the negative factor was strongly correlated with poor premorbid functioning, insidious onset and worse course. Dimensions explained more of the disease characteristics than did diagnosis, but the explanatory power of the latter was also high.

Kraepelinian diagnostic categories suffice for understanding illness characteristics, but the use of dimensions adds substantial information.

Research has uncovered many characteristics related to violence committed by people with mental illness. However, relatively few studies have focused on understanding the connection between violence and dynamic, malleable variables such as a patient's level of treatment engagement.

To explore the link between community violence and patients' beliefs about psychiatric treatment benefit.

A sample of 1011 adults receiving out-patient treatment for a psychiatric disorder in the public mental health systems of five US states were interviewed.

Bivariate analyses revealed community violence was inversely related to treatment adherence, perceived treatment need and perceived treatment effectiveness. Multivariate analyses showed these three variables were associated with reduced odds of violent and other aggressive acts.

The results suggest clinical consideration of patients' perceptions of treatment benefit can help enhance violence risk assessment in psychiatric practice settings.

Mental health problems in people with learning disabilities and autism are poorly understood.

To investigate the prevalence of episodic psychiatric disorders in a sample of teenagers with learning disabilities with and without autism.

Teenagers with learning disabilities living in one geographical area were identified. Those with autism were matched to those without. A semi– structured investigator-based interview linked to Research Diagnostic Criteria was used to assess prevalence and type of episodic disorders.

Significantly more individuals with autism had a lifetime episodic disorder, most commonly major depression. Two individuals with autism had bipolar affective disorder. Other episodic disorders with mood components and behaviour change were also evident, as were un classifiable disorders characterised by complex psychiatric symptoms, chronicity and general deterioration. Antipsychotics and stimulants were most frequently prescribed; the former associated with episodic disorder, the latter with autism.

Teenagers with learning disabilities and autism have higher rates of episodic psychiatric disorders than those with learning disabilities alone.

The extent to which depression impairs health-related quality of life (HRQoL) in the physically ill has not been clearly established.

To quantify the adverse influence of depression and anxiety assessed at the time of first myocardial infarction and 6 months later, on the physical aspect of HRQoL 12 months after the infarction.

In all, 260 in-patients, admitted following first myocardial infarction, completed the Hospital Anxiety and Depression Scale and the Medical Outcomes Study SF–36 assessment before discharge and at 6- and 12-month follow-up.

Depression and anxiety 6 months after myocardial infarction predicted subsequent impairment in the physical aspects of HRQoL (attributable adjusted R2=9%, P<0.0005). These negative effects of depression and anxiety on outcome were mediated by feelings of fatigue. Depression and anxiety present before myocardial infarction did not predict HRQoL 12 months after myocardial infarction.

Detection and treatment of depression and anxiety following myocardial infarction improve the patient's health-related quality of life.

Social cognition has been implicated in the relationship between cognition and social functioning.

To test the hypothesis that social cognition mediates the relationship between cognitive and social functioning.

This was a 1-year longitudinal cohort study comparing three groups: 50 people with first-episode psychosis, 53 people with multi-episode schizophrenia and 55 people without psychiatric disorder as controls. Participants were assessed on social perception, social knowledge, interpersonal problem-solving, cognition and social functioning.

There were significant associations between social cognition, cognition and social functioning in all three groups. Deficits in social cognition were stable over time. In the first two groups, controlling for social cognition reduced the relationship between cognitive and social functioning.

This study provides some evidence that social cognition mediates the relationship between cognitive and social functioning.