Ethnic minority status and childhood trauma are established risk factors for psychotic disorders. Both are found to be associated with increased level of positive symptoms, in particular auditory hallucinations. Our main aim was to investigate the experience and effect of childhood trauma in patients with psychosis from ethnic minorities, hypothesizing that they would report more childhood trauma than the majority and that this would be associated with more current and lifetime hallucinations.

In this cross-sectional study we included 454 patients with a SCID-I DSM-IV diagnosis of non-affective or affective psychotic disorder. Current hallucinations were measured with the Positive and Negative Syndrome Scale (P3; Hallucinatory Behaviour). Lifetime hallucinations were assessed with the SCID-I items: auditory hallucinations, voices commenting and two or more voices conversing. Childhood trauma was assessed with the Childhood Trauma Questionnaire, self-report version.

Patients from ethnic minority groups (n = 69) reported significantly more childhood trauma, specifically physical abuse/neglect, and sexual abuse. They had significantly more current hallucinatory behaviour and lifetime symptoms of hearing two or more voices conversing. Regression analyses revealed that the presence of childhood trauma mediated the association between ethnic minorities and hallucinations.

More childhood trauma in ethnic minorities with psychosis may partially explain findings of more positive symptoms, especially hallucinations, in this group. The association between childhood trauma and these first-rank symptoms may in part explain this group's higher risk of being diagnosed with a schizophrenia-spectrum diagnosis. The findings show the importance of childhood trauma in symptom development in psychosis.

Patients with major depressive disorder (MDD) present with highly heterogeneous symptom profiles. We aimed to examine whether individual differences in amygdala activity to emotionally salient stimuli were related to heterogeneity in lifetime levels of depressive and subthreshold manic symptoms among adults with MDD.

We compared age- and gender-matched adults with MDD (n = 26) with healthy controls (HC, n = 28). While undergoing functional magnetic resonance imaging, participants performed an implicit emotional faces task: they labeled a color flash superimposed upon initially neutral faces that dynamically morphed into one of four emotions (angry, fearful, sad, happy). Region of interest analyses examined group differences in amygdala activity. For conditions in which adults with MDD displayed abnormal amygdala activity versus HC, within-group analyses examined amygdala activity as a function of scores on a continuous measure of lifetime depression-related and mania-related pathology.

Adults with MDD showed significantly greater right-sided amygdala activity to angry and happy conditions than HC (p < 0.05, corrected). Multiple regression analyses revealed that greater right-amygdala activity to the happy condition in adults with MDD was associated with higher levels of subthreshold manic symptoms experienced across the lifespan (p = 0.002).

Among depressed adults with MDD, lifetime features of subthreshold mania were associated with abnormally elevated amygdala activity to emerging happy faces. These findings are a first step toward identifying biomarkers that reflect individual differences in neural mechanisms in MDD, and challenge conventional mood disorder diagnostic boundaries by suggesting that some adults with MDD are characterized by pathophysiological processes that overlap with bipolar disorder.

Limbic-cortical imbalance is an established model for the neurobiology of major depressive disorder (MDD), but imaging genetics studies have been contradicting regarding potential risk and resilience mechanisms. Here, we re-assessed previously reported limbic-cortical alterations between MDD relatives and controls in combination with a newly acquired sample of MDD patients and controls, to disentangle pathology, risk, and resilience.

We analyzed functional magnetic resonance imaging data and negative affectivity (NA) of MDD patients (n = 48), unaffected first-degree relatives of MDD patients (n = 49) and controls (n = 109) who performed a faces matching task. Brain response and task-dependent amygdala functional connectivity (FC) were compared between groups and assessed for associations with NA.

Groups did not differ in task-related brain activation but activation in the superior frontal gyrus (SFG) was inversely correlated with NA in patients and controls. Pathology was associated with task-independent decreases of amygdala FC with regions of the default mode network (DMN) and decreased amygdala FC with the medial frontal gyrus during faces matching, potentially reflecting a task-independent DMN predominance and a limbic-cortical disintegration during faces processing in MDD. Risk was associated with task-independent decreases of amygdala-FC with fronto-parietal regions and reduced faces-associated amygdala-fusiform gyrus FC. Resilience corresponded to task-independent increases in amygdala FC with the perigenual anterior cingulate cortex (pgACC) and increased FC between amygdala, pgACC, and SFG during faces matching.

Our results encourage a refinement of the limbic-cortical imbalance model of depression. The validity of proposed risk and resilience markers needs to be tested in prospective studies. Further limitations are discussed.

There is limited research that explores the association between exclusion from school and mental health, but it seems intuitively plausible that the recognition of mental difficulties by key teachers and parents would influence the likelihood of exclusion from school.

A secondary analysis of the British Child and Adolescent Mental Health survey 2004, (n = 7997) and the 2007 follow-up (n = 5326) was conducted. Recognition of difficulty was assessed via a derived variable that combined the first item of the Impact supplement of the Strengths and Difficulties Questionnaire which asked parents and teachers if they thought that the child has difficulties with emotions, behaviour and concentration, and the presence/absence of psychiatric disorder measured by the Development and Well-being Assessment.

Adjusted logistic regression models demonstrated that children with recognised difficulties were more likely to be excluded [adjusted odds ratio (OR) 5.78, confidence interval 3.45–9.64, p < 0.001], but children with unrecognised difficulties [adjusted OR 3.58 (1.46–8.81) p < 0.005] or recognised subclinical difficulties [adjusted OR 3.42 (2.04–5.73) p < 0.001] were also more likely to be excluded than children with no difficulties. Children with conduct disorder and attention deficit hyperactivity disorder were most likely to be excluded compared with other types of disorder.

Exclusion from school may result from a failure to provide timely and effective support rather than a failure to recognise psychopathology.

Maladaptive cognitive biases such as negative attributional style and hopelessness have been implicated in the development and maintenance of depression. According to the hopelessness theory of depression, hopelessness mediates the association between attributional style and depression. The aetiological processes underpinning this influential theory remain unknown. The current study investigated genetic and environmental influences on hopelessness and its concurrent and longitudinal associations with attributional style and depression across adolescence and emerging adulthood. Furthermore, given high co-morbidity between depression and anxiety, the study investigated whether these maladaptive cognitions constitute transdiagnostic cognitive content common to both internalizing symptoms.

A total of 2619 twins/siblings reported attributional style (mean age 15 and 17 years), hopelessness (mean age 17 years), and depression and anxiety symptoms (mean age 17 and 20 years).

Partial correlations revealed that attributional style and hopelessness were uniquely associated with depression but not anxiety symptoms. Hopelessness partially mediated the relationship between attributional style and depression. Hopelessness was moderately heritable (A = 0.37, 95% confidence interval 0.28–0.47), with remaining variance accounted for by non-shared environmental influences. Independent pathway models indicated that a set of common genetic influences largely accounted for the association between attributional style, hopelessness and depression symptoms, both concurrently and across development.

The results provide novel evidence that associations between attributional style, hopelessness and depression symptoms are largely due to shared genetic liability, suggesting developmentally stable biological pathways underpinning the hopelessness theory of depression. Both attributional style and hopelessness constituted unique cognitive content in depression. The results inform molecular genetics research and cognitive treatment approaches.

Classic conceptual frameworks explaining the relationship of personality traits to depression include the precursor and predisposition models. The former hypothesizes that depression is predicted by traits alone whereas the latter hypothesizes that stress, together with personality, predicts depression. Dynamic vulnerability models (DVM) expand on these perspectives by incorporating fluctuations in personality over time. The stress generation model provides an alternative view, positing that depression generates stress, creating a self-perpetuating cycle. However, these conceptual models are rarely directly compared.

We tested these models, focusing on neuroticism and stressful life events that the participant may have contributed to, using path analysis in a sample of 550 never-depressed, adolescent females assessed five times over 3 years.

A dynamic precursor model with stress generation was best supported. For the precursor component, neuroticism predicted subsequent depression across four assessment intervals. For the dynamic trait component, stressful life events predicted subsequent neuroticism at three of four intervals. Finally, in line with stress generation, depression consistently predicted subsequent stressful life events, and life events then predicted depression.

Finding support for the DVM is noteworthy, as this is the first comprehensive test of this model. Moreover, results supported integrating stress generation with trait vulnerability. Continued use of integrated approaches and refining the statistical implementation of these theories is necessary to advance understanding of the development of depression.

Neurocognitive deficits are important aspects of schizophrenic disorder because they have a strong impact on social and vocational outcomes. Previously it was assumed that cognitive abilities progressively deteriorate with illness onset. However, recent research results have contradicted this with observations of continuous or even improved performance in individuals at risk for psychosis or manifest schizophrenia. The objective of our longitudinal study was to examine neurocognitive functioning in help-seeking individuals meeting basic symptoms or ultra-high-risk criteria for schizophrenic psychosis (HRSchiz) or risk criteria for affective psychosis (HRBip). The progression of cognitive functioning in individuals converting to psychosis was compared with that of at-risk individuals who did not convert during the follow-up period.

Data were available from 86 study participants who completed neurocognitive and clinical assessments at baseline and, on average, 12.8 (s.d. = 1.5) months later. Neurocognitive measures were grouped according to their load in factor analysis to five cognitive domains: speed, attention, fluency, learning and memory, and working memory.

Neurocognitive functioning in HRSchiz and HRBip individuals generally improved over time. Subjects converting to manifest psychosis displayed a stable neurocognitive profile from baseline to follow-up. Compared with non-converters, they had already demonstrated a significantly lower level of performance during their baseline examinations.

Our data provide no evidence for a progressive cognitive decline in individuals at risk of psychosis. In line with the neurodevelopmental model, our findings suggest that cognitive deficits are already present very early, before or during the prodromal stage of the illness.

In reattribution, general practitioners (GPs) request psychosocial information directly and explain medically unexplained symptoms (MUS) using psychosocial information in the consultation. We explored whether reattribution training (RT) increased the communication of psychosocial information and decreased communication about somatic intervention between GPs and their MUS patients.

A cluster randomized controlled trial (RCT) of RT versus usual treatment in GPs from 16 practices and 141 patients with MUS on audio-recorded and transcribed doctor–patient communication in an index consultation. In a secondary data analysis, the Liverpool Clinical Interaction Analysis Scheme (LCIAS) was applied by an experienced rater to each turn of speech in the transcript from the index consultation blind to treatment allocation.

After RT, patients were more likely to disclose and discuss psychosocial problems, and propose psychosocial explanations for symptoms; around 25% of patients discussed psychosocial information extensively. In the RT group, GPs did not seek new psychosocial disclosure but they reduced advocacy for somatic intervention. After RT, GPs suggested, on average, two utterances of psychosocial explanation and six utterances of somatic intervention.

After RT, some patients discussed psychosocial issues extensively but GPs did not probe underlying psychosocial issues. They gave mixed psychosocial and somatic messages about MUS, which may have increased patients' concerns about their health. GPs should actively seek the disclosure of underlying psychosocial problems and give clear, unambiguous messages to MUS patients when they are willing to discuss psychosocial issues.

The aim of this study was to extend an earlier retrospective cohort study of schizophrenia via a prospective study to a follow-up of 34 years, with an emphasis on describing the life-course of the illness.

Subjects were 128 first-ever admissions for schizophrenia in 1963 to either of two mental hospital in Alberta, Canada. Follow-up continued until death or 1997. A symptom severity scale, with scores ranging from 0 (no symptoms) to 3 (hospitalized), was used to collect time-series data on each subject and create life-course curves. Indices were constructed to summarize the information in each curve. Information on social functioning was also collected.

Results were similar for men and women. The life-course curves showed marked variability of symptom severity across subjects and over time. The average score over the entire period of follow-up for the cohort indicated ‘moderate’ symptoms, and the change in average score from beginning to end of follow-up demonstrated a slight worsening of symptoms. The measures of social functioning indicated that only about one quarter of the patients had a good to excellent outcome.

The long-term course in schizophrenia is one of varying symptom severity, and for many patients, there is a poor overall outcome.

Strategies are needed to identify youth developing schizophrenia. The present study aimed to determine whether adolescents treated for substance misuse were at elevated risk to develop schizophrenia, whether this risk has changed since the late 1960s, and whether substance misuse in adolescence predicted poorer outcomes through adulthood.

In a Swedish city, since the mid-1960s there has been only one clinic for adolescent substance misuse. Three samples from this clinic were studied: 1992 individuals treated from 1968 to 1971 followed to age 50 years; 1576 treated from 1980 to 1984 followed to age 35 years; and 180 treated in 2004 followed to age 22 years. Each clinical sample was matched on age, sex and place of birth to an equal, or larger, number of randomly selected individuals from the general population. Schizophrenia, substance use disorders, physical disorders related to substance misuse, criminal convictions, poverty and death were identified using national registers.

Individuals treated for substance misuse in adolescence were at increased risk to subsequently develop schizophrenia: in males the increase was approximately four-fold and in females between five- and seven-fold. There was no difference in risk for those treated in 1968–1971 and from 1980 to 1984 when cannabis use increased from 37.6% to 49.8% of the clinical samples. Among males who developed schizophrenia, treatment for substance misuse was associated with increased risk of substance use disorders and criminal convictions through adulthood.

Treatment programmes for adolescents misusing substances include a disproportionate number developing schizophrenia. Early detection and treatment have the potential to improve long-term outcomes.

Previous efforts to derive empirically based eating disorder (ED) typologies through latent structure modeling have been limited by the ethnic and cultural homogeneity of their study populations and their reliance on DSM-IV ED signs and symptoms as indicator variables.

Ethnic Fijian schoolgirls (n=523) responded to a self-report battery assessing ED symptoms, herbal purgative use, co-morbid psychopathology, clinical impairment, cultural orientation, and peer influences. Participants who endorsed self-induced vomiting or herbal purgative use in the past 28 days (n=222) were included in a latent profile analysis (LPA) to identify unique subgroups of bulimic symptomatology.

LPA identified a bulimia nervosa (BN)-like class (n=86) characterized by high rates of binge eating and self-induced vomiting, and a herbal purgative class (n=136) characterized primarily by the use of indigenous Fijian herbal purgatives. Both ED classes endorsed greater eating pathology and general psychopathology than non-purging participants, and the herbal purgative class endorsed greater clinical impairment than either the BN-like or non-purging participants. Cultural orientation did not differ between the two ED classes.

Including study populations typically under-represented in mental health research and broadening the scope of relevant signs and symptoms in latent structure models may increase the generalizability of ED nosological schemes to encompass greater cultural diversity.