The negative symptoms of psychosis and depressive symptomatology share several features, e.g. low motivation, apathy and reduced activity. Understanding the associations between these two sets of symptoms will support improved assessment and the development of interventions targeting these difficulties in people with psychosis. This is the first large systematic review and meta-analysis to quantify the relationship between these two categories of symptoms, as measured in studies to date. PsycInfo, Embase and Medline were systematically searched to identify eligible studies. Inclusion criteria ensured the studies measured both depression and negative symptoms using validated measures in a sample of over 8000 participants with non-affective psychosis diagnoses. The search led to 2020 records being screened and 56 included in the meta-analysis and review. Both meta-analyses and meta-regressions were conducted to explore the main effect and potential moderating variables. A clear pattern emerges showing that higher ratings of negative symptoms are associated with higher levels of depressive symptoms, with a small effect [standardised effect size = 0.19, p < 0.05). This did not vary greatly with the measures used (SES = 0.19–0.26) and was not moderated by demographic variables or quality ratings. Interestingly, higher depressive symptoms predict a significant relationship with co-occurring negative symptoms. However, higher negative symptoms predict that it is less likely there will be a relationship with co-occurring depressive symptoms. Heterogeneity was high across these analyses. The findings support the adoption of a symptom-specific approach to understanding the interplay between negative and depressive symptoms in psychosis, to improve assessment and intervention.

Since the 1990s, facilities for individuals at putative risk for psychosis have mushroomed and within a very short time have become part of the standard psychiatric infrastructure in many countries. The idea of preventing a severe mental disorder before its exacerbation is laudable, and early data indeed strongly suggested that the sooner the intervention, the better the outcome. In this paper, the authors provide four reasons why they think that early detection or prodromal facilities should be renamed and their treatment targets reconsidered. First, the association between the duration of untreated psychosis and outcome is empirically established but has become increasingly weak over the years. Moreover, its applicability to those who are considered at risk remains elusive. Second, instruments designed to identify future psychosis are prone to many biases that are not yet sufficiently controlled. None of these instruments allows an even remotely precise prognosis. Third, the rate of transition to psychosis in at-risk patients is likely lower than initially thought, and evidence for the success of early intervention in preventing future psychosis is promising but still equivocal. Perhaps most importantly, the treatment is not hope-oriented. Patients are more or less told that schizophrenia is looming over them, which may stigmatize individuals who will never, in fact, develop psychosis. In addition self-stigma has been associated with suicidality and depression. The authors recommend that treatment of help-seeking individuals with mental problems but no established diagnosis should be need-based, and the risk of psychosis should be de-emphasized as it is only one of many possible outcomes, including full remission. Prodromal clinics should not be abolished but should be renamed and restructured. Such clinics exist, but the transformation process needs to be facilitated.

Psychopathy is a personality type characterized by both callous emotional dysfunction and deviant behavior that affects society in the form of actions that harm others. Historically, researchers have been concerned with seeking data and arguments to support a neurobiological foundation of psychopathy. In the past few years, increasing research has begun to reveal brain alterations putatively underlying the enigmatic psychopathic personality. In this review, we describe the brain anatomical and functional features that characterize psychopathy from a synthesis of available neuroimaging research and discuss how such brain anomalies may account for psychopathic behavior. The results are consistent in showing anatomical alterations involving primarily a ventral system connecting the anterior temporal lobe to anterior and ventral frontal areas, and a dorsal system connecting the medial frontal lobe to the posterior cingulate cortex/precuneus complex and, in turn, to medial structures of the temporal lobe. Functional imaging data indicate that relevant emotional flow breakdown may occur in both these brain systems and suggest specific mechanisms via which emotion is anomalously integrated into cognition in psychopathic individuals during moral challenge. Directions for future research are delineated emphasizing, for instance, the relevance of further establishing the contribution of early life stress to a learned blockage of emotional self-exposure, and the potential role of androgenic hormones in the development of cortical anomalies.

Childhood adversities have been reported to be more common among individuals at ultra-high risk (UHR) for psychosis. This paper systematically reviewed and meta-analysed (i) the severity and prevalence of childhood adversities (childhood trauma exposure, bullying victimisation and parental separation or loss) among the UHR, and (ii) the association between adversities and transition to psychosis (TTP). PsycINFO, PubMed and Embase databases were searched for studies reporting childhood adversities among UHR individuals. Only published articles were included. Risk of bias was assessed using Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guideline (von Elm et al., 2007) and the tool developed by Hoy et al. (2012). Seventeen case–control, cross-sectional and longitudinal studies were included. UHR individuals experienced significantly more severe trauma than controls, regardless of trauma subtype. UHR were 5.5, 2.5 and 3.1 times as likely to report emotional abuse, physical abuse and bullying victimisation, respectively. There was no association with parental separation. However, childhood trauma was not significantly associated with TTP (follow-up periods: 6 months to 15 years), suggesting that trauma alone may not be a sufficient risk factor. Sexual abuse was associated with TTP but this may have been driven by a single large study. Potential confounders and low rates of TTP among UHR are limitations of this review. This is the first meta-analysis that quantitatively summarises the associations between childhood adversities and TTP among UHR, and between specific abuse subtypes and TTP. Specific recommendations have been made to increase the quality of future research. PROSPERO registration no. CRD42017054884.

The interaction of physical and mental vulnerability and environmental constraints is thought to foster the development of psychiatric disorders such as major depressive disorder (MDD). A central factor in the development of psychopathology is mental stress. Despite some evidence for parasympathetic withdrawal and sympathetic overactivity in MDD, the psychophysiological response to stress in depression is not clear-cut. Given the growing interest in heart rate and heart rate variability as indicators for remote monitoring of patients, it is important to understand how patients with MDD react to stress in a laboratory-controlled environment. We conducted a systematic review of studies using electrocardiography to derive heart rate and heart rate variability during stress in patients with clinical depression. We focused on well-validated stress tasks- the mental arithmetic stress task, the Trier social stress task and public speaking task- to minimize confounding effects due to the nature of the stressor. The majority of studies found hypo-reactivity during stress as a hallmark of depression as evidenced by lower fluctuation in heart rate and heart rate variability in the high-frequency band. We address the potential underlying biological mechanisms, the influence of covariates on these measures and briefly discuss the specificity and potential for remote monitoring by using these variables.

Despite the clinical impact of motor symptoms such as agitation or retardation on the course of depression, these symptoms are poorly understood. Novel developments in the field of instrumentation and mobile devices allow for dimensional and continuous recording of motor behavior in various settings, particularly outside the laboratory. Likewise, the use of novel assessments enables to combine multimodal neuroimaging with behavioral measures in order to investigate the neural correlates of motor dysfunction in depression. The research domain criteria (RDoC) framework will soon include a motor domain that will provide a framework for studying motor dysfunction in mood disorders. In addition, new studies within this framework will allow investigators to study motor symptoms across different stages of depression as well as other psychiatric diagnoses. Finally, the introduction of the RDoC motor domain will help test how motor symptoms integrate with the original five RDoC domains (negative valence, positive valence, cognitive, social processes, and arousal/regulation).

Adults with autism spectrum disorder (ASD) are thought to be at disproportionate risk of developing mental health comorbidities, with anxiety and depression being considered most prominent amongst these. Yet, no systematic review has been carried out to date to examine rates of both anxiety and depression focusing specifically on adults with ASD. This systematic review and meta-analysis examined the rates of anxiety and depression in adults with ASD and the impact of factors such as assessment methods and presence of comorbid intellectual disability (ID) diagnosis on estimated prevalence rates. Electronic database searches for studies published between January 2000 and September 2017 identified a total of 35 studies, including 30 studies measuring anxiety (n = 26 070; mean age = 30.9, s.d. = 6.2 years) and 29 studies measuring depression (n = 26 117; mean age = 31.1, s.d. = 6.8 years). The pooled estimation of current and lifetime prevalence for adults with ASD were 27% and 42% for any anxiety disorder, and 23% and 37% for depressive disorder. Further analyses revealed that the use of questionnaire measures and the presence of ID may significantly influence estimates of prevalence. The current literature suffers from a high degree of heterogeneity in study method and an overreliance on clinical samples. These results highlight the importance of community-based studies and the identification and inclusion of well-characterized samples to reduce heterogeneity and bias in estimates of prevalence for comorbidity in adults with ASD and other populations with complex psychiatric presentations.

Unnatural causes of death due to traffic accidents (TA) and suicide attempts (SA) constitute a major burden on global health, which remained stable in the last decade despite widespread efforts of prevention. Recently, latent infection with Toxoplasma gondii (T. gondii) has been suggested to be a biological risk factor for both TA and SA. Therefore, a systematic search concerning the relationship of T. gondii infection with TA and/or SA according to PRISMA guidelines in Medline, Pubmed and PsychInfo was conducted collecting papers up to 11 February 2019 (PROSPERO #CRD42018090206). The random-effect model was applied and sensitivity analyses were subsequently performed. Lastly, the population attributable fraction (PAF) was calculated. We found a significant association for antibodies against T. gondii with TA [odds ratio (OR) = 1.69; 95% confidence interval (CI) 1.20–2.38, p = 0.003] and SA (OR = 1.39; 95% CI 1.10–1.76, p = 0006). Indication of publication bias was found for TA, but statistical adjustment for this bias did not change the OR. Heterogeneity between studies on SA was partly explained by type of control population used (ORhealthy controls = 1.9, p < 0.001 v. ORpsychiatric controls = 1.06, p = 0.87) and whether subjects with schizophrenia only were analysed (ORschizophrenia = 0.87, p = 0.62 v. ORvarious = 1.8, p < 0.001). The association was significantly stronger with higher antibody titres in TA and in studies that did not focus on schizophrenia subjects concerning SA. PAF of a T. gondii infection was 17% for TA and 10% for SA. This indicates that preventing T. gondii infection may play a role in the prevention of TA or SA, although uncertainty remains whether infection and outcome are truly causally related.

To identify factors which may help or hinder decision-making ability in people with psychosis, we did a systematic review and meta-analysis of their performance on the Iowa and Cambridge Gambling Tasks. Analysis of 47 samples found they had moderately poorer performance than healthy individuals (N = 4264, g = −0.57, 95% confidence interval (CI) −0.66 to −0.48). Few studies (k = 8) used non-psychotic clinical comparator groups, although very low-quality evidence (k = 3) found people with bipolar disorder may perform better. Negative symptoms (k = 13, N = 648, r = −0.17, 95% CI −0.26 to −0.07) and lower IQ (k = 11, N = 525, r = 0.20, 95% CI 0.29–0.10), but not positive symptoms (k = 10, N = 512, r = −0.01, 95% CI −0.11 to 0.08), each had small-moderate associations with poorer decision-making. Lower quality evidence suggested general symptoms, working memory, social functioning, awareness of emotional responses to information, and attentional bias towards gain are associated with decision-making, but not education, executive functioning or overall symptoms. Meta-regression suggested an inverse association between decision-making and depression severity (k = 6, Q = 6.41, R2 100%, p = 0.01). Those taking first-generation (k = 6, N = 305, g = −0.17, 95% CI −0.40 to 0.06, p = 0.147) or low-dose antipsychotics (k = 5, N = 442, g = −0.19, 95% CI −0.44 to 0.06, p = 0.139) had unimpaired decision-making. Although meta-regression found no linear association between dose and performance, non-reporting of the dose was common and associated with larger impairments (k = 46, Q = 4.71, R2 14%, p = 0.03). Those supporting people with psychosis to make decisions, including treatment decisions, should consider the potential effect of these factors. Interventionist-causal trials are required to test whether reducing antipsychotic dose and treating anxiety and depression can improve decision-making in this group.

New studies of long-term outcomes claim to show that taking antipsychotics on a continuous and indefinite basis is the best approach for people diagnosed with a first episode of psychosis or schizophrenia. A 10-year follow-up of a trial of quetiapine maintenance, for example, found a higher proportion of people with a poor composite outcome in the group initially randomised to placebo. However, most people classified as showing poor outcome were rated as having a mild score on a single psychotic symptom; there were no differences in overall symptoms, positive or negative symptoms or level of functioning. Moreover, 16% of participants did not have a follow-up interview and data from the end of the original trial were used instead. A study using a Finnish database suggested that mortality and readmission were higher in people who did not start long-term antipsychotic treatment or who discontinued it as compared with long-term continuous users. However, the analysis did not control for important confounders and is likely to reflect the fact that people who do not comply with treatment are at higher risk of death due to underlying health risks and behaviours. The analysis showed a slightly higher risk of readmission among non-users of antipsychotics compared with long-term users and a more substantial increased risk among people who discontinued treatment. However, follow-up ceased at the first readmission and therefore eventual, long-term outcome was not assessed. Speed of reduction and whether it was done with or without clinical support were also not distinguished.

Depression is common in primary care, and most patients prefer psychological treatment over pharmacotherapy. Cognitive behaviour therapy (CBT) is an effective treatment, but there are gaps in current knowledge about CBT in the primary care context, especially with regard to long-term effects and the efficacy of specific delivery formats. This is an obstacle to the integration of primary care and specialist psychiatry. We conducted a systematic review and meta-analysis of randomised controlled trials of CBT for primary care patients with depression to investigate the effect of CBT for patients with depression in primary care. A total of 34 studies, with 2543 patients in CBT and 2815 patients in control conditions, were included. CBT was more effective than the control conditions [g = 0.22 (95% confidence interval (CI) 0.15–0.30)], and the effect was sustained at follow-up [g = 0.17 (95% CI 0.10–0.24)]. CBT also led to a higher response rate [odds ratio (OR) = 2.47 (95% CI 1.60–3.80)] and remission rate [OR = 1.56 (95% CI 1.15–2.14)] than the control conditions. Heterogeneity was moderate. The controlled effect of CBT was significant regardless of whether patients met diagnostic criteria for depression, scored above a validated cut-off for depression, or merely had depressive symptoms. CBT also had a controlled effect regardless of whether the treatment was delivered as individual therapy, group therapy or therapist-guided self-help. We conclude that CBT appears to be effective for patients with depression in primary care, and recommend that patients with mild to moderate depression be offered CBT in primary care.