In this meta-analysis we review the findings from neuropsychological studies on set-shifting in people with eating disorders (EDs) or overweight/obesity.

Four databases (PubMed, PsycINFO, PSYNDEX and Web of Science) were searched for eligible studies. Effect sizes (ESs) were pooled using random-effects models. Moderator analyses were conducted for ED and overweight/obese subgroups, adult/adolescent samples and measures of set-shifting.

Sixty-four studies with a total of 1825 ED patients [1394 anorexia nervosa (AN), 376 bulimia nervosa (BN) and 55 binge eating disorder (BED)] and 10 studies with a total of 449 overweight/obese individuals were included. The meta-analysis revealed a small to medium ES for inefficient set-shifting across all three ED diagnoses (Hedges’ g = –0.45). Subgroup analyses yielded small to medium ESs for each ED subtype (g = –0.44 for AN, –0.53 for BED, –0.50 for BN), which did not differ significantly. There was a medium ES for restricting type AN (ANR; g = –0.51) but no significant ES for binge/purge type AN (AN/BP; g = –0.18). A medium ES was found across obesity studies (g = –0.61). The ES across overweight studies was not significant (g = –0.07). Adult samples did not differ from adolescent samples in either ED or overweight/obesity studies. The different set-shifting measures were associated with largely varying ESs.

The meta-analysis provides strong support that inefficient set-shifting is a salient neuropsychological phenomenon across ED subtypes and obesity, but is less prominent in AN/BP and overweight. Compulsivity seems to be a common underlying factor supporting a dimensional and transdiagnostic conceptualization of EDs and obesity.

True findings about schizophrenia remain elusive; many findings are not replicated and conflicting results are common. Well-conducted systematic reviews have the ability to make robust, generalizable conclusions, with good meta-analyses potentially providing the closest estimate of the true effect size. In this paper, we undertake a systematic approach to synthesising the available evidence from well-conducted systematic reviews on schizophrenia.

Reviews were identified by searching Medline, EMBASE, CINAHL, Current Contents and PsycINFO. The decision to include or exclude reviews, data extraction and quality assessments were conducted in duplicate. Evidence was graded as high quality if reviews contained large samples and robust results; and as moderate quality if reviews contained imprecision, inconsistency, smaller samples or study designs that may be prone to bias.

High- and moderate-quality evidence shows that numerous psychosocial and biomedical treatments are effective. Patients have relatively poor cognitive functioning, and subtle, but diverse, structural brain alterations, altered electrophysiological functioning and sleep patterns, minor physical anomalies, neurological soft signs, and sensory alterations. There are markers of infection, inflammation or altered immunological parameters; and there is increased mortality from a range of causes. Risk for schizophrenia is increased with cannabis use, pregnancy and birth complications, prenatal exposure to Toxoplasma gondii, childhood central nervous system viral infections, childhood adversities, urbanicity and immigration (first and second generation), particularly in certain ethnic groups. Developmental motor delays and lower intelligence quotient in childhood and adolescence are apparent.

We conclude that while our knowledge of schizophrenia is very substantial, our understanding of it remains limited.

Valuable trauma-related research may be hindered when the risks of asking participants about traumatic events are not carefully weighed against the benefits of their participation in the research.

The overall aim of our population-based survey was to improve the professional care of suicide-bereaved parents by identifying aspects of care that would be amenable to change. The study population included 666 suicide-bereaved and 377 matched (2:1) non-bereaved parents. In this article we describe the parents' perceptions of their contacts with us as well as their participation in the survey. We also present our ethical-protocol for epidemiological surveys in the aftermath of a traumatic loss.

We were able to contact 1410 of the 1423 eligible parents; eight of these parents expressed resentment towards the contact. Several participants and non-participants described their psychological suffering and received help because of the contact. A total of 666 suicide-bereaved and 377 non-bereaved parents returned the questionnaire. Just two out of the 1043 answered that they might, in the long term, be negatively affected by participation in the study; one was bereaved, the other was not. A significant minority of the parents reported being temporarily negatively affected at the end of their participation, most of them referring to feelings of sadness and painful memories. In parallel, positive experiences were widely expressed and most parents found the study valuable.

Our findings suggest, given that the study design is ethically sound, that suicide-bereaved parents should be included in research since the benefits clearly outweigh the risks.

A congenital heart defect (CHD) can increase the risk of mental health problems in affected children and their parents. The extent to which risk factors for these problems are shared in families or are specific to the individual family member is unclear.

Prospective data from the Norwegian Mother and Child Cohort Study (MoBa; n = 93 009) were linked with a nationwide CHD registry, and 408 children with CHD were identified. Mothers' reports on child internalizing problems and their own distress were assessed by questionnaires at child ages 6, 18 and 36 months. A structural model was applied to distinguish between familial (shared) factors and individual-specific factors for mental health problems.

CHD was a substantial risk factor for problems in children and their mothers at all time points. CHD contributed on average 31% and 39% to the variance in children's and mothers' problems respectively. Both shared familial and individual-specific factors unique to CHD families contributed to risk for mental health problems. Whereas individual-specific risk factors contributed to the stability of problems in mothers, the effect of these factors lasted only a short time in children. Mutual influences over time were found between the mother's and the child's mental health at 18 and 36 months.

The burden of CHD in a child is shared between family members but is also specific to the individual. This study points to a need for both an individual and a family-based approach to provide psychological support to children with CHD and their parents.

A clearer understanding of the basis for the association between cannabis use and psychotic experiences (PEs) is required. Our aim was to examine the extent to which associations between cannabis and cigarette use and PEs are due to confounding.

A cohort study of 1756 adolescents with data on cannabis use, cigarette use and PEs.

Cannabis use and cigarette use at age 16 were both associated, to a similar degree, with PEs at age 18 [odds ratio (OR) 1.48, 95% confidence interval (CI) 1.18–1.86 for cannabis and OR 1.61, 95% CI 1.31–1.98 for cigarettes]. Adjustment for cigarette smoking frequency (OR 1.27, 95% CI 0.91–1.76) or other illicit drug use (OR 1.25, 95% CI 0.91–1.73) substantially attenuated the relationship between cannabis and PEs. The attenuation was to a lesser degree when cannabis use was adjusted for in the cigarette PE association (OR 1.42, 95% CI 1.05–1.92). However, almost all of the participants used cannabis with tobacco, including those who classed themselves as non-cigarette smokers.

Teasing out the effects of cannabis from tobacco is highly complex and may not have been dealt with adequately in studies to date, including this one. Complementary methods are required to robustly examine the independent effects of cannabis, tobacco and other illicit drugs on PEs.

Psychosis is characterized by a profound lack of trust and disturbed social interactions. Investigating the neural basis of these deficits is difficult because of medication effects but first-degree relatives show qualitatively similar abnormalities to patients with psychosis on various tasks. This study aimed to investigate neural activation in siblings of patients in response to an interactive task. We hypothesized that, compared to controls, siblings would show (i) less basic trust at the beginning of the task and (ii) reduced activation of the brain reward and mentalizing systems.

Functional magnetic resonance imaging (fMRI) data were acquired on 50 healthy siblings of patients with psychosis and 33 healthy controls during a multi-round trust game with a cooperative counterpart. An a priori region-of-interest (ROI) analysis of the caudate, temporoparietal junction (TPJ), superior temporal sulcus (STS), insula and medial prefrontal cortex (mPFC) was performed focusing on the investment and repayment phases. An exploratory whole-brain analysis was run to test for group-wise differences outside these ROIs.

The siblings’ behaviour during the trust game did not differ significantly from that of the controls. At the neural level, siblings showed reduced activation of the right caudate during investments, and the left insula during repayments. In addition, the whole-brain analysis revealed reduced putamen activation in siblings during investments.

The findings suggest that siblings show aberrant functioning of regions traditionally involved in reward processing in response to cooperation, which may be associated with the social reward deficits observed in psychosis.

The course of bipolar disorder progressively worsens in some patients. Although responses to pharmacotherapy appear to diminish with greater chronicity, less is known about whether patients' prior courses of illness are related to responses to psychotherapy.

Embedded in the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) was a randomized controlled trial of psychotherapy for bipolar depression comparing the efficacy of intensive psychotherapy with collaborative care (a three-session psycho-educational intervention). We assessed whether the number of previous mood episodes, age of illness onset, and illness duration predicted or moderated the likelihood of recovery and time until recovery from a depressive episode in patients in the two treatments.

Independently of treatment condition, participants with one to nine prior depressive episodes were more likely to recover and had faster time to recovery than those with 20 or more prior depressive episodes. Participants with fewer than 20 prior manic episodes had faster time to recovery than those with 20 or more episodes. Longer illness duration predicted a longer time to recovery. Participants were more likely to recover in intensive psychotherapy than collaborative care if they had 10–20 prior episodes of depression [number needed to treat (NNT) = 2.0], but equally likely to respond to psychotherapy and collaborative care if they had one to nine (NNT = 32.0) or >20 (NNT = 9.0) depressive episodes.

Number of previous mood episodes and illness duration are associated with the likelihood and speed of recovery among bipolar patients receiving psychosocial treatments for depression.

The classification of anxiety and depressive disorders has long been debated and has important clinical implications. The present study combined a genetically sensitive design and multiple time points to investigate cognitive content specificity in anxiety and depressive disorder symptoms across anxiety sensitivity dimensions, a cognitive distortion implicated in both disorders.

Phenotypic and genetic correlations between anxiety sensitivity dimensions, anxiety and depressive disorder symptoms were examined at five waves of data collection within childhood, adolescence and early adulthood in two representative twin studies (n pairs = 300 and 1372).

The physical concerns dimension of anxiety sensitivity (fear of bodily symptoms) was significantly associated with anxiety but not depression at all waves. Genetic influences on physical concerns overlapped substantially more with anxiety than depression. Conversely, mental concerns (worry regarding cognitive control) were phenotypically more strongly associated with depression than anxiety. Social concerns (fear of publicly observable symptoms of anxiety) were associated with both anxiety and depression in adolescence. Genetic influences on mental and social concerns were shared to a similar extent with both anxiety and depression.

Phenotypic patterns of cognitive specificity and broader genetic associations between anxiety sensitivity dimensions, anxiety and depressive disorder symptoms were similar at all waves. Both disorder-specific and shared cognitive concerns were identified, suggesting it is appropriate to classify anxiety and depression as distinct but related disorders and confirming the clinical perspective that cognitive therapy is most likely to benefit by targeting cognitive concerns relating specifically to the individual's presenting symptoms across development.

The incidence of schizophrenia is commonly estimated by screening for psychosis among subjects presenting to psychiatric services. This approach (using a first-contact sampling frame) cannot account for cases that did not meet criteria for schizophrenia at first contact. We compared the usual approach directly with a register-based approach (using a longitudinal sampling frame) that also includes subjects initially diagnosed with other non-schizophrenic disorders.

We compared data from the Longitudinal Psychiatric Register (LPR) of The Hague over 1980–2009 with data previously collected in a first-contact study, and applied both methods to calculate the incidence of schizophrenia for subjects aged 20–54 years in the same catchment area and over the same period (October 2000 to September 2005). We reconstructed treatment pathways and diagnostic histories up to the end of 2009 and performed sensitivity analyses.

The LPR identified 843 first onsets of schizophrenia, corresponding to a treated incidence rate (IR) of 69 per 100 000 person-years [95% confidence interval (CI) 64–74]. The first-contact study identified 254 first onsets, corresponding to a treated IR of 21 per 100 000 person-years (95% CI 18–23). Two-thirds of the difference was accounted for by subjects treated for other disorders before the onset of psychosis, and by patients in older age groups.

The incidence of schizophrenia was three times higher in a longitudinal register study than in a high-quality first-contact study conducted in the same population. Risk estimates based only on first-contact studies may have been affected by selection bias.

The majority of people at ultra high risk (UHR) of psychosis also present with co-morbid affective disorders such as depression or anxiety. The neuroanatomical and clinical impact of UHR co-morbidity is unknown.

We investigated group differences in grey matter volume using baseline magnetic resonance images from 121 participants in four groups: UHR with depressive or anxiety co-morbidity; UHR alone; major depressive disorder; and healthy controls. The impact of grey matter volume on baseline and longitudinal clinical/functional data was assessed with regression analyses.

The UHR-co-morbidity group had lower grey matter volume in the anterior cingulate cortex than the UHR-alone group, with an intermediate effect between controls and patients with major depressive disorder. In the UHR-co-morbidity group, baseline anterior cingulate volume was negatively correlated with baseline suicidality/self-harm and obsessive–compulsive disorder symptoms.

Co-morbid depression and anxiety disorders contributed distinctive grey matter volume reductions of the anterior cingulate cortex in people at UHR of psychosis. These volumetric deficits were correlated with baseline measures of depression and anxiety, suggesting that co-morbid depressive and anxiety diagnoses should be carefully considered in future clinical and imaging studies of the psychosis high-risk state.

Prior research with racially/ethnically homogeneous samples has demonstrated widespread co-occurrence of psychotic experiences (PEs) and common mental health conditions, particularly multi-morbidity, suggesting that psychosis may be related to the overall severity of psychiatric disorder rather than any specific subtype. In this study we aimed to examine whether PEs are associated with the presence of specific disorders or multi-morbidity of co-occurring disorders across four large racially/ethnically diverse samples of adults in the USA.

Data were drawn from the National Comorbidity Survey Replication (NCS-R), the National Survey of American Life (NSAL) and separately from the Asian and Latino subsamples of the National Latino and Asian American Study (NLAAS). Logistic regression models were used to examine the relationship between PEs and individual subtypes of DSM-IV disorder, and to test for a linear dose–response relationship between the number of subtypes and PEs.

Prevalence of PEs was moderately greater among individuals with each subtype of disorder in each data set [odds ratios (ORs) 1.8–3.8], although associations were only variably significant when controlling for clinical and demographic variables. However, the sum of disorder subtypes was related to odds for PEs in a linear dose–response fashion across all four samples.

PEs are related primarily to the extent or severity of psychiatric illness, as indicated by the presence of multiple psychiatric disorders, rather than to any particular subtype of disorder in these data. This relationship applies to the general population and across diverse racial/ethnic groups.

Deep brain stimulation (DBS) is a promising new treatment for patients with treatment-refractory obsessive–compulsive disorder (OCD). However, since most DBS patients only show a partial response, the treatment still needs to be improved. In this study we hypothesized that cognitive–behavioural therapy (CBT) could optimize the post-operative management in DBS and we evaluated the efficacy of CBT as augmentation to DBS targeted at the nucleus accumbens.

A total of 16 patients with treatment-refractory OCD were treated with DBS targeted at the nucleus accumbens. After stabilization of decline in OCD symptoms, a standardized 24-week CBT treatment programme was added to DBS in an open-phase trial of 8 months. Changes in obsessive–compulsive, anxiety and depressive symptoms were evaluated using the Yale–Brown Obsessive Compulsive Scale, Hamilton Anxiety Scale and Hamilton Rating Scale for Depression.

Following the addition of CBT to DBS, a significant decrease in obsessive–compulsive symptoms was observed, but not in anxiety and depressive symptoms. In a subsequent double-blind phase, in which stimulation was discontinued, OCD symptoms returned to baseline (relapse) and anxiety and depressive symptoms worsened (rebound) compared with baseline.

The results of this explorative study suggest that a combined treatment of accumbens DBS and CBT may be optimal for improving obsessive–compulsive symptoms in treatment-refractory OCD. However, a subsequent randomized controlled trial is necessary to draw firm conclusions. It seems that DBS results in affective changes that may be required to enable response prevention in CBT. This may indicate that DBS and CBT act as two complementary treatments.

Oxytocin (OT) is associated with our ability to empathize and has been shown to play a major role in mediating social behaviors within the context of intergroup dynamics. Schizophrenia is associated with impaired empathy, and with a dysfunctional oxytocinergic system. The effect of OT on the empathic responses of patients with schizophrenia within the context of intergroup relationships has not been studied. The present study examined the effect of OT on the patients' empathic responses to pain experienced by in-group, conflictual out-group and neutral out-group members.

In a double-blind, placebo-controlled, within-subject cross-over design, the responses on the Pain Evaluation Task of 28 male patients with schizophrenia were compared to 27 healthy male controls. All participants received a single intranasal dose of 24 IU OT or placebo, 1 week apart.

OT induced an empathy bias in the healthy controls towards the conflictual out-group members. Although this effect was absent in the patient group, OT seems to heighten an empathic bias in the patient group towards the in-group members when rating non-painful stimuli.

The study demonstrates that the administration of OT can result in empathic bias towards adversary out-group members in healthy controls but not in patients with schizophrenia. However, the OT-induced bias in both the patients (in the no-pain condition towards the in-group members) and the healthy controls (in the no-pain and pain conditions towards the adversary out-group) suggests that OT enhances the distinction between conflictual in-group and out-group members.

Deep brain stimulation (DBS) is increasingly being applied to psychiatric conditions such as obsessive–compulsive disorder (OCD), major depression and anorexia nervosa. Double-blind, randomized controlled trials (RCTs) of active versus sham treatment have been limited to small numbers. We therefore undertook a systematic review and meta-analysis of the effectiveness of DBS in psychiatric conditions to maximize study power.

We conducted a systematic literature search for double-blind, RCTs of active versus sham treatment using Pubmed/Medline and EMBASE up to April 2013. Where possible, we combined results from studies in a meta-analysis. We assessed differences in final values between the active and sham treatments for parallel-group studies and compared changes from baseline score for cross-over designs.

Inclusion criteria were met by five studies, all of which were of OCD. Forty-four subjects provided data for the meta-analysis. The main outcome was a reduction in obsessive symptoms as measured by the Yale–Brown Obsessive Compulsive Scale (YBOCS). Patients on active, as opposed to sham, treatment had a significantly lower mean score [mean difference (MD) −8.93, 95% confidence interval (CI) −13.35 to −5.76, p < 0.001], representing partial remission. However, one-third of patients experienced significant adverse effects (n = 16). There were no differences between the two groups in terms of other outcomes.

DBS may show promise for treatment-resistant OCD but there are insufficient randomized controlled data for other psychiatric conditions. DBS remains an experimental treatment in adults for severe, medically refractory conditions until further data are available.

Neurocognitive deficits are important aspects of the schizophrenic disorders because they have a strong impact on social and vocational outcomes. We expanded on previous research by focusing on the neurocognitive profiles of persons at high risk (HR) or ultra-high risk (UHR) for schizophrenic and affective psychoses. Our main aim was to determine whether neurocognitive measures are sufficiently sensitive to predict a group affiliation based on deficits in functional domains.

This study included 207 help-seeking individuals identified as HR (n = 75), UHR (n = 102) or at high risk for bipolar disorder (HRBip; n = 30), who were compared with persons comprising a matched, healthy control group (CG; n = 50). Neuropsychological variables were sorted according to their load in a factor analysis and were compared among groups. In addition, the likelihood of group membership was estimated using logistic regression analyses.

The performance of HR and HRBip participants was comparable, and intermediate between the controls and UHR. The domain of processing speed was most sensitive in discriminating HR and UHR [odds ratio (OR) 0.48, 95% confidence interval (CI) 0.28–0.78, p = 0.004] whereas learning and memory deficits predicted a conversion to schizophrenic psychosis (OR 0.47, 95% CI 0.25–0.87, p = 0.01).

Performances on neurocognitive tests differed among our three at-risk groups and may therefore be useful in predicting psychosis. Overall, cognition had a profound effect on the extent of general functioning and satisfaction with life for subjects at risk of psychosis. Thus, this factor should become a treatment target in itself.

Elucidating the cognitive architecture of schizophrenia promises to advance understanding of the clinical and biological substrates of the illness. Traditional cross-sectional neuropsychological approaches differentiate impaired from normal cognitive abilities but are limited in their ability to determine latent substructure. The current study examined the latent architecture of abnormal cognition in schizophrenia via a systematic approach.

Exploratory factor analysis (EFA) and confirmatory factor analysis (CFA) were carried out on a large neuropsychological dataset including the Brief Assessment of Cognition in Schizophrenia, Continuous Performance Test, Wisconsin Card Sorting Test, Benton Judgment of Line Orientation Test, and Wechsler Abbreviated Scale of Intelligence matrix reasoning derived from 1012 English-speaking ethnic Chinese healthy controls and 707 schizophrenia cases recruited from in- and out-patient clinics.

An initial six-factor model fit cognitive data in healthy and schizophrenia subjects. Further modeling, which accounted for methodological variance between tests, resulted in a three-factor model of executive functioning, vigilance/speed of processing and memory that appeared to best discriminate schizophrenia cases from controls. Factor analytic-derived g estimands and conventionally calculated g showed similar case–control discrimination. However, agreement analysis suggested systematic differences between both g indices.

Factor structures derived in the current study were broadly similar to those reported previously. However, factor structures between schizophrenia subjects and healthy controls were different. Roles of factor analytic-derived g estimands and conventional composite score g were further discussed. Cognitive structures underlying cognitive deficits in schizophrenia may prove useful for interrogating biological substrates and enriching effect sizes for subsequent work.

Emotional lability (EL), characterized by negative emotional traits and emotional instability, is frequently reported in children and adults with attention deficit hyperactivity disorder (ADHD). However, EL is primarily assessed using retrospective self-report, which is subject to reporting bias and does not consider the potential influence of positive and negative everyday experiences.

Ambulatory assessment was carried out in 41 men with ADHD without co-morbidity, current medication or substance abuse, and 47 healthy control participants. Reports of negative and positive emotions (irritability, frustration, anger, happiness, excitement) and the occurrence of bad and good events were completed eight times daily during a working week. Group differences in emotional intensity and instability were investigated using multilevel models, and explored in relation to bad and good events and the Affective Lability Scale – Short Form (ALS-SF), an EL questionnaire.

The ADHD group reported significantly more frequent bad events, heightened intensity and instability of irritability and frustration, and greater intensity of anger. The results for positive emotions were equivocal or negative. Bad events significantly contributed to the intensity and instability of negative emotions, and showed a stronger influence in the ADHD group. However, covariation for their effect did not eliminate group differences. Small-to-moderate correlations were seen between intensity and instability of negative emotions and the ALS-SF.

Adults with ADHD report heightened intensity and instability of negative emotions in daily life. The results suggest two components of EL in ADHD: a reactive component responsive to bad events and an endogenous component, independent of negative everyday events.