In stepped care models patients typically start with a low-intensity evidence-based treatment. Progress is monitored systematically and those patients who do not respond adequately step up to a subsequent treatment of higher intensity. Despite the fact that many guidelines have endorsed this stepped care principle it is not clear if stepped care really delivers similar or better patient outcomes against lower costs compared with other systems. We performed a systematic review and meta-analysis of all randomized trials on stepped care for depression.

We carried out a comprehensive literature search. Selection of studies, evaluation of study quality and extraction of data were performed independently by two authors.

A total of 14 studies were included and 10 were used in the meta-analyses (4580 patients). All studies used screening to identify possible patients and care as usual as a comparator. Study quality was relatively high. Stepped care had a moderate effect on depression (pooled 6-month between-group effect size Cohen's d was 0.34; 95% confidence interval 0.20–0.48). The stepped care interventions varied greatly in number and duration of treatment steps, treatments offered, professionals involved, and criteria to step up.

There is currently only limited evidence to suggest that stepped care should be the dominant model of treatment organization. Evidence on (cost-) effectiveness compared with high-intensity psychological therapy alone, as well as with matched care, is required.

Studies report the variable prevalence of attention deficit hyperactivity disorder (ADHD) in incarcerated populations. The aim of this meta-analysis was to determine the prevalence of ADHD in these populations.

Primary research studies reporting the prevalence (lifetime/current) of ADHD in incarcerated populations were identified. The meta-analysis used a mixed log-binomial model, including fixed effects for each covariate and a random study effect, to estimate the significance of various risk factors.

Forty-two studies were included in the analysis. ADHD prevalence was higher with screening diagnoses versus diagnostic interview (and with retrospective youth diagnoses versus current diagnoses). Using diagnostic interview data, the estimated prevalence was 25.5% and there were no significant differences for gender and age. Significant country differences were noted.

Compared with published general population prevalence, there is a fivefold increase in prevalence of ADHD in youth prison populations (30.1%) and a 10-fold increase in adult prison populations (26.2%).

The clinical condition of dementia is now recognized as a diagnosis that can only be applied too late in the disease process to be useful for therapeutic approaches centring on disease modification. As a result, in recent years increasing attention has been given to mild cognitive impairment (MCI) and the diagnosis of prodromal dementia. This paper reviews the evidence for the clinical presentation of prodromal dementia with Lewy bodies (DLB).

A Medline search was carried out to identify articles with original data on the prodromal presentation of DLB.

In MCI cohorts that progress to dementia, the proportion diagnosed with DLB is similar to that reported in dementia cohorts. Prodromal DLB may present as any MCI subtype, although visuospatial and executive domains may be most commonly affected. Rapid eye movement (REM) sleep behaviour disorder (RBD), autonomic symptoms, hyposmia, hallucinations and motor symptoms seem to be more common in prodromal DLB than in prodromal Alzheimer's disease (AD). Some of these symptoms can precede the diagnosis of DLB by several years. There has been little research into the use of biomarkers in prodromal DLB, although in RBD cohorts, clinical and imaging biomarkers have been associated with the development of DLB.

The evidence available suggests that prodromal DLB may be differentiated from other dementia prodromes in most cases. Further research is needed to confirm this, and to assess the utility of biomarkers such as 123I-FP-CIT and 123I-MIBG imaging.

Mothers' self-reported stroking of their infants over the first weeks of life modifies the association between prenatal depression and physiological and emotional reactivity at 7 months, consistent with animal studies of the effects of tactile stimulation. We now investigate whether the effects of maternal stroking persist to 2.5 years. Given animal and human evidence for sex differences in the effects of prenatal stress we compare associations in boys and girls.

From a general population sample of 1233 first-time mothers recruited at 20 weeks gestation we drew a random sample of 316 for assessment at 32 weeks, stratified by reported inter-partner psychological abuse, a risk indicator for child development. Of these mothers, 243 reported at 5 and 9 weeks how often they stroked their infants, and completed the Child Behavior Checklist (CBCL) at 2.5 years post-delivery.

There was a significant interaction between prenatal anxiety and maternal stroking in the prediction of CBCL internalizing (p = 0.001) and anxious/depressed scores (p < 0.001). The effects were stronger in females than males, and the three-way interaction prenatal anxiety × maternal stroking × sex of infant was significant for internalizing symptoms (p = 0.003). The interactions arose from an association between prenatal anxiety and internalizing symptoms only in the presence of low maternal stroking.

The findings are consistent with stable epigenetic effects, many sex specific, reported in animal studies. While epigenetic mechanisms may be underlying the associations, it remains to be established whether stroking affects gene expression in humans.

Research evidence suggests that cognitive and neural mechanisms involved in social information processing may underlie the key aspects associated with the emergence of aggression and psychopathy. Despite extensive research in this field, it is unclear whether this deficit relates to general attentional problems or affects early stages of information processing. Therefore, the aim was to explore the link between aggression, psychopathic traits, and the early processing deficits in young antisocial violent offenders (YAVOs) and healthy controls (CTLs).

Participants were presented with rapidly changing Mondrian-like images in one eye, while a neutral or emotional (happy, angry, fearful, disgusted, surprised, sad) face was slowly introduced to the other eye. Participants indicated the location in which the face had appeared on the screen, reflecting the time when they became aware of the stimulus. The relative processing advantage was obtained by subtracting mean reaction times for emotional from neutral faces.

The results indicated that individuals with higher levels of unemotional traits tended to exhibit an extensive early processing disadvantage for fearful facial expressions; this relationship was only evident in the YAVO as opposed to the CTL sample.

These findings indicate that an emotion processing deficit in antisocial individuals is present even at the most basic levels of processing and closely related to certain psychopathic traits. Furthermore, this early processing deficit appears to be highly specific to fearful expressions, which is consistent with predictions made by influential models of psychopathy. The clinical significance and potential implications of the results are discussed.

Evidence synthesis methods enabling direct and indirect comparisons over the entire set of relevant clinical data produce quantitative point estimates for the treatments contrasts between competing interventions, and provide a hierarchical rank ordering between them. We aimed to provide evidence-based guidance on the efficacy and all-cause discontinuation of antimanic treatments.

We conducted a network meta-analysis within a Bayesian framework. We searched all standard literature databases without language restrictions up to 15 January 2014 to identify reports of short-term, randomized, blinded trials of putative antimanic drugs as monotherapy for adults with bipolar-I mania.

Altogether, 14256 manic patients randomized to one of 18 active treatments or placebo provided 95 direct comparisons on 128 data points. For the primary outcome, standardized mean difference as Hedges’ g (standardized mean difference; SMD), the hierarchies indicated by surface under the cumulative ranking (SUCRA) probabilities were in agreement with the point estimates for all antimanic drugs identified as effective. For the 12 effective antimanic drugs on clinical use, SMDs against placebo ranged from 0.32 to 0.66 without superiority of one over another, except for risperidone v. aripiprazole and valproate. Aripiprazole, olanzapine, quetiapine, risperidone, and valproate had less all-cause discontinuation rates than placebo. Sensitivity analysis by drug class indicated similar efficacy profiles for haloperidol, second-generation antipsychotics, and mood stabilizers.

Hierarchical rank ordering by comparative efficacy and risk of all-cause discontinuations should help to guide antimanic treatment choices by clinicians, healthcare policy makers, and guideline developers.

Although there is a clear phenotypic relationship between the quality of the interparental or marital relationship and child conduct problems (CP), the etiology of this association is as yet unclear. One possibility is that this association takes the form of a genotype–environment interaction (G × E), whereby the quality of the interparental relationship acts to moderate the etiology of child CP. The current study sought to evaluate this possibility.

We examined multiple measures and informant reports of the quality of the interparental relationship in a sample of more than 700 child twin families from the Michigan State University Twin Registry (MSUTR). Analyses consisted of a series of latent G × E models.

The ‘no moderation’ model provided the best fit to the data in nearly all cases, findings that collectively provide strong evidence against the possibility that the etiology of CP is moderated by the quality of the interparental relationship.

Our findings suggest that, contrary to implicit (and sometimes explicit) assumptions in the field, it is not the case that every environmental risk (or protective) factor exacerbates (or suppresses) genetic influences on CP. Future research should seek to delineate the specific environmental experiences that do serve as etiologic moderators of CP, and to clarify how this G × E interplay might change over the course of development.

Previous studies have shown that genetic risk for externalizing (EXT) disorders is greater in the context of adverse family environments during adolescence, but it is unclear whether these effects are long lasting. The current study evaluated developmental changes in gene–environment interplay in the concurrent and prospective associations between parent–child relationship problems and EXT at ages 18 and 25 years.

The sample included 1382 twin pairs (48% male) from the Minnesota Twin Family Study, participating in assessments at ages 18 years (mean = 17.8, s.d. = 0.69 years) and 25 years (mean = 25.0, s.d. = 0.90 years). Perceptions of parent–child relationship problems were assessed using questionnaires. Structured interviews were used to assess symptoms of adult antisocial behavior and nicotine, alcohol and illicit drug dependence.

We detected a gene–environment interaction at age 18 years, such that the genetic influence on EXT was greater in the context of more parent–child relationship problems. This moderation effect was not present at age 25 years, nor did parent-relationship problems at age 18 years moderate genetic influence on EXT at age 25 years. Rather, common genetic influences accounted for this longitudinal association.

Gene–environment interaction evident in the relationship between adolescent parent–child relationship problems and EXT is both proximal and developmentally limited. Common genetic influence, rather than a gene–environment interaction, accounts for the long-term association between parent–child relationship problems at age 18 years and EXT at age 25 years. These results are consistent with a relatively pervasive importance of gene–environmental correlation in the transition from late adolescence to young adulthood.

With psychopathology rising during adolescence and evidence suggesting that adult mental health burden is often due to disorders beginning in youth, it is important to investigate the epidemiology of adolescent mental disorders.

We analysed data gathered at ages 11 (baseline) and 19 years from the population-based Dutch TRacking Adolescents' Individual Lives Survey (TRAILS) study. At baseline we administered the Achenbach measures (Child Behavior Checklist, Youth Self-Report) and at age 19 years the World Health Organization's Composite International Diagnostic Interview version 3.0 (CIDI 3.0) to 1584 youths.

Lifetime, 12-month and 30-day prevalences of any CIDI-DSM-IV disorder were 45, 31 and 15%, respectively. Half were severe. Anxiety disorders were the most common but the least severe whereas mood and behaviour disorders were less prevalent but more severe. Disorders persisted, mostly by recurrence in mood disorders and chronicity in anxiety disorders. Median onset age varied substantially across disorders. Having one disorder increased subjects' risk of developing another disorder. We found substantial homotypic and heterotypic continuity. Baseline problems predicted the development of diagnosable disorders in adolescence. Non-intact families and low maternal education predicted externalizing disorders. Most morbidity concentrated in 5–10% of the sample, experiencing 34–55% of all severe lifetime disorders.

At late adolescence, 22% of youths have experienced a severe episode and 23% only mild episodes. This psychopathology is rather persistent, mostly due to recurrence, showing both monotypic and heterotypic continuity, with family context affecting particularly externalizing disorders. High problem levels at age 11 years are modest precursors of incident adolescent disorders. The burden of mental illness concentrates in 5–10% of the adolescent population.

The DSM criteria for adult attention-deficit/hyperactivity disorder (ADHD) have not been tested in American Psychiatric Association (APA) field trials for either DSM-IV or DSM-5. This study aimed to assess: (a) the prevalence of ADHD according to DSM-5 criteria; (b) the factor solution that provides the best fit for ADHD symptoms; (c) the symptoms with the highest predictive value for clinical impairment; and (d) the best symptomatic threshold for each ADHD dimension (inattention and hyperactivity/impulsivity).

Trained psychologists evaluated 4000 young adults from the 1993 Pelotas Birth Cohort Study with an instrument covering all DSM-5 ADHD criteria. A series of confirmatory factor analyses (CFAs) tested the best factor structure. Complex logistic regressions assessed differential contributions of each symptom to clinical impairment. Receiver-operating characteristic (ROC) analyses tested which would be the best symptomatic cut-off in the number of symptoms for predicting impairment.

The prevalence of DSM-5 ADHD was 3.55% [95% confidence interval (CI) 2.98–4.12]. The estimated prevalence of DSM-IV ADHD was 2.8%. CFA revealed that a bifactor model with a single general factor and two specific factors provided the best fit for DSM-5 symptoms. Inattentive symptoms continued to be the most important predictors of impairment in adults. The best cut-offs were five symptoms of inattention and four symptoms of hyperactivity/impulsivity.

Our results, combined with previous findings, suggest a 27% increase in the expected prevalence of ADHD among young adults, comparing DSM-IV to DSM-5 criteria. The DSM-5 symptomatic organization derived a similar factor structure for adults as DSM-IV symptoms. Data using DSM-5 criteria support lowering the symptomatic threshold for diagnosing ADHD in adults.

Major depression is associated with abnormalities in reward processing at neural and behavioural levels. Neural abnormalities in reward have been described in young people at familial risk of depression but behavioural changes in reward-based decision making have been less studied in this group.

We studied 63 young people (mean age 18.9 years) with a parent with a diagnosis of major depression but who had never been depressed themselves, that is with a positive family history of depression (the FH+ group). Participants performed the Cambridge Gambling Task (CGT), which provides several measures of decision making including deliberation time, quality of decision making, risk taking, risk adjustment and delay aversion. A control group of 49 age- and gender-matched young people with no history of mood disorder in a first-degree relative undertook the same task.

Both FH+ participants and controls had low and equivalent scores on anxiety and depression self-rating scales. Compared to controls, the FH+ participants showed overall lower risk taking, although like controls they made more risky choices as the odds of a favourable outcome increased. No other measures of decision making differed between the two groups.

Young people at increased familial risk of depression have altered risk taking that is not accounted for by current affective symptomatology. Lowered risk taking might represent an impairment in reward seeking, which is one of several changes in reward-based behaviours seen in acutely depressed patients; however, our findings suggest that decreased reward seeking could be part of a risk endophenotype for depression.

Schizophrenia (SZ) is characterized by a broad global cognitive impairment that precedes the onset of the disease. By contrast, some studies suggest that premorbid deficits are absent, or even reversed, in bipolar disorder (BD). However, studies have shown impairments in cognitive functioning after the illness onset in both disorders. The aim of this study was to systematically review and meta-analyze those studies that compared premorbid and/or post-onset global cognitive function between SZ and BD.

We searched Medline (PubMed), EMBASE and PsycINFO for studies where information on cognitive functioning was collected in both SZ and BD within the same study or using the same methods.

Compared to healthy comparison groups, SZ patients showed a significant premorbid cognitive impairment [standardized mean difference (SMD) −0.597, 95% confidence interval (CI) −0.707 to −0.487, p < 0.0001] and a large post-onset impairment (SMD −1.369, 95% CI −1.578 to −1.160, p < 0.0001). We found small significant deficits in premorbid intellectual function in the BD group when this was assessed retrospectively (−0.147, 95% CI −0.238 to −0.056, p = 0.001) but not prospectively (−0.029, 95% CI −0.199 to + 0.142, p = 0.744), and moderate cognitive impairment after onset (SMD −0.623, 95% CI −0.717 to −0.529, p < 0.0001).

SZ is characterized by significant deficits in premorbid intellectual function but the evidence regarding premorbid function in BD is equivocal. After illness onset, patients with both disorders seem to suffer a further decline in cognitive function but the magnitude of the impairment remains greater in SZ than in BD.

Cognitive deficits are well documented in ecstasy (3,4-methylenedioxymethamphetamine; MDMA) users, with such deficits being taken as evidence of dysregulation of the serotonin (5-hydroxytryptamine; 5-HT) system. More recently neuroimaging has been used to corroborate these deficits. The present study aimed to assess multitasking performance in ecstasy polydrug users, polydrug users and drug-naive individuals. It was predicted that ecstasy polydrug users would perform worse than non-users on the behavioural measure and this would be supported by differences in cortical blood oxygenation.

In the study, 20 ecstasy-polydrug users, 17 polydrug users and 19 drug-naive individuals took part. On day 1, drug use history was taken and questionnaire measures were completed. On day 2, participants completed a 20-min multitasking stressor while brain blood oxygenation was measured using functional near infrared spectroscopy (fNIRS).

There were no significant differences between the three groups on the subscales of the multitasking stressor. In addition, there were no significant differences on self-report measures of perceived workload (NASA Task Load Index). In terms of mood, ecstasy users were significantly less calm and less relaxed compared with drug-naive controls. There were also significant differences at three voxels on the fNIRS, indicating decreased blood oxygenation in ecstasy users compared with drug-naive controls at voxel 2 (left dorsolateral prefrontal cortex), voxel 14 and voxel 16 (right dorsolateral prefrontal cortex), and compared with polydrug controls at V14.

The results of the present study provide support for changes in brain activation during performance of demanding tasks in ecstasy polydrug users, which could be related to cerebral vasoconstriction.

Although cannabis abuse (CA) is known to be associated with schizophrenia, the causal nature of this association is unclear, with prodromal effects complicating its interpretation.

From Swedish national registry databases, we used a co-relative case–control design with full-sibling, half-sibling and first-cousin comparisons, alongside a general Swedish population sample. Using ICD codes, 5456 individuals with an initial diagnosis of schizophrenia (2000–2010) were matched with five schizophrenia-free controls. We further identified first-cousin, half-sibling and full-sibling pairs discordant for CA and statistically extrapolated results for discordant monozygotic (MZ) twins.

Within the general Swedish population, CA was strongly associated with later schizophrenia [odds ratio (OR) 10.44, 95% confidence interval (CI) 8.99–12.11]. This association was substantially attenuated both by increasing temporal delays between CA exposure and schizophrenia diagnosis and by controlling for increasing degrees of familial confounding. Extrapolated discordant MZ pairs suggested that fully controlling for confounding familial factors reduced the association between CA and later schizophrenia to more modest levels (ORs of approximately 3.3 and 1.6 with 3- and 7-year temporal delays respectively). Opiate, sedative, cocaine/stimulant and hallucinogen abuse were also strongly associated with subsequent schizophrenia in the general population. After controlling for familial confounding, only cocaine/stimulant exposure remained associated.

CA has an appreciable causal impact on future risk for schizophrenia. However, population-based estimates of cannabis–schizophrenia co-morbidity substantially overestimate their causal association. Predictions of the cases of schizophrenia that might be prevented by reduced cannabis consumption based on population associations are therefore likely to be considerably overestimated.

Anorexia nervosa (AN) is a serious disorder incurring high costs due to hospitalization. International treatments vary, with prolonged hospitalizations in Europe and shorter hospitalizations in the USA. Uncontrolled studies suggest that longer initial hospitalizations that normalize weight produce better outcomes and fewer admissions than shorter hospitalizations with lower discharge weights. This study aimed to compare the effectiveness of hospitalization for weight restoration (WR) to medical stabilization (MS) in adolescent AN.

We performed a randomized controlled trial (RCT) with 82 adolescents, aged 12–18 years, with a DSM-IV diagnosis of AN and medical instability, admitted to two pediatric units in Australia. Participants were randomized to shorter hospitalization for MS or longer hospitalization for WR to 90% expected body weight (EBW) for gender, age and height, both followed by 20 sessions of out-patient, manualized family-based treatment (FBT).

The primary outcome was the number of hospital days, following initial admission, at the 12-month follow-up. Secondary outcomes were the total number of hospital days used up to 12 months and full remission, defined as healthy weight (>95% EBW) and a global Eating Disorder Examination (EDE) score within 1 standard deviation (s.d.) of published means. There was no significant difference between groups in hospital days following initial admission. There were significantly more total hospital days used and post-protocol FBT sessions in the WR group. There were no moderators of primary outcome but participants with higher eating psychopathology and compulsive features reported better clinical outcomes in the MS group.

Outcomes are similar with hospitalizations for MS or WR when combined with FBT. Cost savings would result from combining shorter hospitalization with FBT.

Recent cross-sectional studies have shown psychotic experiences (PEs) are associated with suicidal ideation and behaviours. We aimed to examine associations between psychotic experiences (including persistent PE), and contemporaneous and incident non-suicidal self-injury (NSSI) and suicide attempts.

Participants were from an Australian longitudinal cohort of 1896 adolescents (12–17 years). NSSI and suicide attempts were measured using the Self-Harm Behaviour Questionnaire. Items from the Diagnostic Interview Schedule for Children were used to assess psychotic experiences, and the General Health Questionnaire-12 measured psychological distress.

Adolescents both psychologically distressed and endorsing psychotic experiences had increased odds of contemporaneous and incident NSSI and attempted suicide. Psychotic experiences alone did not predict future risk. Persistent psychotic experiences were associated with increased risk of NSSI and suicide attempts.

Psychological distress with accompanying psychotic experiences and persistent psychotic experiences are important predictors of NSSI and suicide attempts. Screening these phenotypes in adolescents will assist in discerning those adolescents most at risk, providing opportunities for targeted suicide prevention strategies.

Many studies have examined the efficacy of psychotherapy for major depressive disorder (MDD) but publication bias against null results may exist in this literature. However, to date, the presence of an excess of significant findings in this literature has not been explicitly tested.

We used a database of 1344 articles on the psychological treatment of depression, identified through systematic search in PubMed, PsycINFO, EMBASE and the Cochrane database of randomized trials. From these we identified 149 studies eligible for inclusion that provided 212 comparisons. We tested for an excess of significant findings using the method developed by Ioannidis and Trikalinos (2007), and compared the distribution of p values in this literature with the distribution in the antidepressant literature, where publication bias is known to be operating.

The average statistical power to detect the effect size indicated by the meta-analysis was 49%. A total of 123 comparisons (58%) reported a statistically significant difference between treatment and control groups, but on the basis of the average power observed, we would only have expected 104 (i.e. 49%) to do so. There was therefore evidence of an excess of significance in this literature (p = 0.010). Similar results were obtained when these analyses were restricted to studies including a cognitive behavioural therapy (CBT) arm. Finally, the distribution of p values for psychotherapy studies resembled that for published antidepressant studies, where publication bias against null results has already been established.

The small average size of individual psychotherapy studies is only sufficient to detect large effects. Our results indicate an excess of significant findings relative to what would be expected, given the average statistical power of studies of psychotherapy for major depression.