Hypothalamic–pituitary–adrenal (HPA) axis hyperactivity, associated with increased pituitary volume, may mediate observed alterations in stress reactivity in patients with psychotic disorder. We examined the association between pituitary volume, real-life stress reactivity and genetic liability for psychotic disorder.

Pituitary volumes were derived from magnetic resonance imaging (MRI) scans of 20 patients with psychotic disorder, 37 non-psychotic siblings of these patients, and 32 controls. The Experience Sampling Method (ESM) was used to measure emotional stress reactivity [changes in negative affect (NA) associated with daily life stress] in the three groups, and biological stress reactivity (changes in cortisol associated with daily life stress) in siblings and controls. Interactions between group, stress and pituitary volume in models of NA and cortisol were examined.

Groups did not differ in pituitary volume. Patients showed significantly higher emotional stress reactivity than siblings and controls. In addition, emotional stress reactivity increased with increasing pituitary volume to a greater degree in patients than in controls and siblings. Siblings had higher cortisol levels than controls but did not show increased cortisol reactivity to stress. There was no interaction between pituitary volume, stress and group in the model of cortisol.

Higher pituitary volume was associated with increased emotional stress reactivity in patients with psychotic disorder, siblings and controls. The association was significantly stronger in the patient group, suggesting a process of progressive sensitization mediating clinical outcome.

There is evidence that patients with chronic fatigue syndrome (CFS) have mild hypocortisolism. The clinical significance of this is unclear. We aimed to determine whether hypocortisolism exerted any effect on the response of CFS to cognitive behavioural therapy (CBT).

We measured 24-h urinary free cortisol (UFC) in 84 patients with Centers for Disease Control and Prevention (CDC)-defined CFS (of whom 64 were free from psychotropic medication) who then received CBT in a specialist, tertiary out-patient clinic as part of their usual clinical care. We also measured salivary cortisol output from 0800 to 2000 h in a subsample of 56 psychotropic medication-free patients.

Overall, 39% of patients responded to CBT after 6 months of treatment. Lower 24-h UFC output was associated with a poorer response to CBT but only in psychotropic medication-free patients. A flattened diurnal profile of salivary cortisol was also associated with a poor response to CBT.

Low cortisol is of clinical relevance in CFS, as it is associated with a poorer response to CBT. Hypocortisolism could be one of several maintaining factors that interact in the persistence of CFS.

The salience of a visual stimulus is often reduced by nearby stimuli, an effect known as surround suppression of perceived contrast, which may help in locating the borders of an object. Weaker surround suppression has been observed in schizophrenia but it is unclear whether this abnormality is present in other mental disorders with similar symptomatology, or is evident in people with genetic liability for schizophrenia.

By examining surround suppression among subjects with schizophrenia or bipolar affective disorder, their unaffected biological relatives and healthy controls we sought to determine whether diminished surround suppression was specific to schizophrenia, and if subjects with a genetic risk for either disorder would show similar deficits. Measuring perceived contrast in different surround conditions also allowed us to investigate how this suppression depends on the similarity of target and surrounding stimuli.

Surround suppression was weaker among schizophrenia patients regardless of surround configuration. Subjects with bipolar affective disorder showed an intermediate deficit, with stronger suppression than in schizophrenia but weaker than control subjects. Surround suppression was normal in relatives of both patient groups. Findings support a deficit in broadly tuned (rather than sharply orientation- or direction-selective) suppression mechanisms.

Weak broadly tuned suppression during visual perception is evident in schizophrenia and bipolar affective disorder, consistent with impaired gain control related to the clinical expression of these conditions.

Rumination is an important cognitive risk factor for onset and relapse of depression. However, no studies have employed a dimensional approach in investigating the neural correlates of rumination and the relationship with depression.

Non-clinical healthy subjects (n = 306), who completed the classical rumination and depression scales, were studied using voxel-based morphometry and regional homogeneity (ReHo). Subsequently, mediation analysis was conducted to examine the influence of rumination on the relationship between brain structure and depression. Moreover, depressive patients (n = 60) and a control group (n = 63) of comparable age and education were studied with regions of interest that were identified in the healthy individuals.

For healthy individuals, regional grey-matter volume (rGMV) of dorsolateral prefrontal cortex (DLPFC) and parahippocampal gyrus (PHG) were positively correlated with rumination. In addition, rumination had a mediating effect on the relationship between the DLPFC and PHG and depression. Moreover, ReHo analysis showed that rumination had a significantly negative correlation with functional homogeneity of DLPFC. However, compared to the control group, depressed patients showed significant decrease of rGMV in the DLPFC and PHG and there was a significant negative correlation between DLPFC volume and depressive rumination.

Increased DLPFC volume (decreased ReHo) in healthy individuals while decreased in depression indicated the trend of DLPFC from inefficient inhibition (‘overload state’) to impaired regulatory mechanism (‘paralysis state’). This finding might elucidate when and why healthy individuals would develop sustained negative mood and depression eventually.

We sought to provide the first point prevalence estimates of muscle dysmorphia (MD), a form of body dysmorphic disorder characterized by a preoccupation with perceived insufficient muscularity, in adolescents.

Data were taken from a survey of 3618 Australian adolescents (11.172–19.76 years; 49.3% girls). Measures captured demographic characteristics, symptoms of MD and eating disorders, psychological distress and functional impairment. Diagnostic criteria for MD developed by Pope et al. (1997, Psychosomatics, 38(6), 548–557) were applied, entailing preoccupation with insufficient muscularity causing significant levels of distress or disability that cannot be better accounted for by an eating disorder.

The point prevalence of MD was 2.2% [95% confidence interval (CI) 1.6–3.0%] among boys and 1.4% (95% CI 0.9–2.0%) among girls. Prevalence was not associated with gender (V = 0.031) or socioeconomic status (SES) (partial η2< 0.001), but was marginally associated with older age (partial η2 = 0.001). Boys with MD were more likely than girls with MD to report severe preoccupation with muscularity (V = 0.259) and a weight-lifting regime that interfered with their life (V = 0.286), whereas girls with MD were more likely to report discomfort with body exposure (V = 0.380).

While future epidemiological research using diagnostic interviews is needed to verify these estimates, the findings suggest that MD is relatively common from early to late adolescence. Gender differences in MD prevalence may be minimal; however, the symptom profile appears to diverge between boys and girls. These findings provide a platform for future, analytical research designed to inform clinical and public health interventions.

Establishing an evidence-based diagnostic system informed by the biological (dys)function of the nervous system is a major priority in psychiatry. This objective, however, is often challenged by difficulties in identifying homogeneous clinical populations. Melancholia, a biological and endogenous subtype for major depressive disorder, presents a canonical test case in the search of biological nosology.

We employed a unique combination of naturalistic functional magnetic resonance imaging (fMRI) paradigms – resting state and free viewing of emotionally salient films – to search for neurobiological signatures of depression subtypes. fMRI data were acquired from 57 participants; 17 patients with melancholia, 17 patients with (non-melancholic) major depression and 23 matched healthy controls.

Patients with melancholia showed a prominent loss of functional connectivity in hub regions [including ventral medial prefrontal cortex, anterior cingulate cortex (ACC) and superior temporal gyrus] during natural viewing, and in the posterior cingulate cortex while at rest. Of note, the default mode network showed diminished reactivity to external stimuli in melancholia, which correlated with the severity of anhedonia. Intriguingly, the subgenual ACC, a potential target for treating depression with deep brain stimulation (DBS), showed divergent changes between the two depression subtypes, with increased connectivity in the non-melancholic and decreased connectivity in the melancholic subsets.

These findings reveal neurobiological changes specific to depression subtypes during ecologically valid behavioural conditions, underscoring the critical need to respect differing neurobiological processes underpinning depressive subtypes.

We evaluated the effectiveness and cost-effectiveness of the Incredible Years® Teacher Classroom Management (TCM) programme as a universal intervention, given schools’ important influence on child mental health.

A two-arm, pragmatic, parallel group, superiority, cluster randomised controlled trial recruited three cohorts of schools (clusters) between 2012 and 2014, randomising them to TCM (intervention) or Teaching As Usual (TAU-control). TCM was delivered to teachers in six whole-day sessions, spread over 6 months. Schools and teachers were not masked to allocation. The primary outcome was teacher-reported Strengths and Difficulties Questionnaire (SDQ) Total Difficulties score. Random effects linear regression and marginal logistic regression models using Generalised Estimating Equations were used to analyse the outcomes. Trial registration: ISRCTN84130388.

Eighty schools (2075 children) were enrolled; 40 (1037 children) to TCM and 40 (1038 children) to TAU. Outcome data were collected at 9, 18, and 30-months for 96, 89, and 85% of children, respectively. The intervention reduced the SDQ-Total Difficulties score at 9 months (mean (s.d.):5.5 (5.4) in TCM v. 6.2 (6.2) in TAU; adjusted mean difference = −1.0; 95% CI−1.9 to −0.1; p = 0.03) but this did not persist at 18 or 30 months. Cost-effectiveness analysis suggested that TCM may be cost-effective compared with TAU at 30-months, but this result was associated with uncertainty so no firm conclusions can be drawn. A priori subgroup analyses suggested TCM is more effective for children with poor mental health.

TCM provided a small, short-term improvement to children's mental health particularly for children who are already struggling.

The National Psychiatric Morbidity Survey (NPMS) programme was partly designed to monitor trends in mental disorders, including depression, with comparable data spanning 1993 to 2007. Findings already published from this programme suggest that concerns about increasing prevalence of common mental disorders (CMDs) may be unfounded. This article focuses on depression and tests the hypothesis that successive birth cohorts experience the same prevalence of depression as they age.

We carried out a pseudo-cohort analysis of a sequence of three cross-sectional surveys of the English household population using identical diagnostic instruments. The main outcome was ICD-10 depressive episode or disorder. Secondary outcomes were the depression subscales of the Clinical Interview Schedule – Revised (CIS-R).

There were 8670, 6977 and 6815 participants in 1993, 2000 and 2007 respectively. In men, the prevalence of depression increased between cohorts born in 1943–1949 and 1950–1956 [odds ratio (OR) 2.5, 95% confidence interval (CI) 1.4–4.2], then remained relatively stable across subsequent cohorts. In women, there was limited evidence of change in prevalence of depression. Women born in 1957–1963, surveyed aged 44–50 years in 2007, had exceptionally high prevalence. It is not clear whether this represents a trend or a quirk of sampling.

There is no evidence of an increase in the prevalence of depression in male cohorts born since 1950. In women, there is limited evidence of increased prevalence. Demand for mental health services may stabilize or even fall for men.

In an effort to group mental disorders on the basis of aetiology, five clusters have been proposed. In this paper, we consider the validity of the first cluster, neurocognitive disorders, within this proposal. These disorders are categorized as ‘Dementia, Delirium, and Amnestic and Other Cognitive Disorders’ in DSM-IV and ‘Organic, including Symptomatic Mental Disorders’ in ICD-10.

We reviewed the literature in relation to 11 validating criteria proposed by a Study Group of the DSM-V Task Force as applied to the cluster of neurocognitive disorders.

‘Neurocognitive’ replaces the previous terms ‘cognitive’ and ‘organic’ used in DSM-IV and ICD-10 respectively as the descriptor for disorders in this cluster. Although cognitive/organic problems are present in other disorders, this cluster distinguishes itself by the demonstrable neural substrate abnormalities and the salience of cognitive symptoms and deficits. Shared biomarkers, co-morbidity and course offer less persuasive evidence for a valid cluster of neurocognitive disorders. The occurrence of these disorders subsequent to normal brain development sets this cluster apart from neurodevelopmental disorders. The aetiology of the disorders is varied, but the neurobiological underpinnings are better understood than for mental disorders in any other cluster.

Neurocognitive disorders meet some of the salient criteria proposed by the Study Group of the DSM-V Task Force to suggest a classification cluster. Further developments in the aetiopathogenesis of these disorders will enhance the clinical utility of this cluster.

In women, anxiety symptoms are common and increase during midlife, but little is known about whether these symptoms predict onsets of major depressive disorder (MDD) episodes. We examined whether anxiety symptoms are associated with subsequent episodes of MDD in midlife African-American and Caucasian women, and whether they confer a different risk for first versus recurrent MDD episodes.

A longitudinal analysis was conducted using 12 years of data from the Study of Women's Health Across the Nation (SWAN) Mental Health Study (MHS). The baseline sample comprised 425 Caucasian (n = 278) and African American (n = 147) community-dwelling women, aged 46.1 ± 2.5 years. Anxiety symptoms measured annually using a self-report questionnaire were examined in relation to MDD episodes in the subsequent year, assessed with the SCID. Multivariable models were estimated with random effects logistic regression.

Higher anxiety symptoms scores were associated with a significantly higher adjusted odds of developing an episode of MDD at the subsequent annual visit [odds ratio (OR) 1.47, p = 0.01], specifically for a recurrent episode (OR 1.49, p = 0.03) but non-significant for a first episode (OR 1.32, p = 0.27). There were no significant racial effects in the association between anxiety symptoms and subsequent MDD episodes.

Anxiety symptoms often precede MDD and may increase the vulnerability of midlife women to depressive episodes, particularly recurrences. Women with anxiety symptoms should be monitored clinically during the ensuing year for the development of an MDD episode.

Accumulating evidence suggests that fetal growth restriction may increase risk of later schizophrenia but this issue has not been addressed directly in previous studies. We examined whether the degree of fetal growth restriction was linearly related to risk of schizophrenia, and also whether maternal pre-eclampsia, associated with both placental dysfunction and poor fetal growth, was related to risk of schizophrenia.

A population-based cohort of single live births in the Medical Birth Registry of Norway (MBRN) between 1967 and 1982 was followed to adulthood (n = 873 612). The outcome was schizophrenia (n=2207) registered in the National Insurance Scheme (NIS). The degree of growth restriction was assessed by computing sex-specific z scores (standard deviation units) of ‘birth weight for gestational age’ and ‘birth length for gestational age’. Analyses were adjusted for potential confounders. Maternal pre-eclampsia was recorded in the Medical Birth Registry by midwives or obstetricians using strictly defined criteria.

The odds ratio (OR) for schizophrenia increased linearly with decreasing birth weight for gestational age z scores (p value for trend = 0.005). Compared with the reference group (z scores 0.01–1.00), the adjusted OR [95% confidence interval (CI)] for the lowest z-score category (< − 3.00) was 2.0 (95% CI 1.2–3.5). A similar pattern was observed for birth length for gestational age z scores. Forty-nine individuals with schizophrenia were identified among 15 622 births with pre-eclampsia. The adjusted OR for schizophrenia following maternal pre-eclampsia was 1.3 (95% CI 1.0–1.8).

Associations of schizophrenia risk with degree of fetal growth restriction and pre-eclampsia suggest future research into schizophrenia etiology focusing on mechanisms that influence fetal growth, including placental function.