Most research on interventions to counter stigma and discrimination has focused on short-term outcomes and has been conducted in high-income settings.

To synthesise what is known globally about effective interventions to reduce mental illness-based stigma and discrimination, in relation first to effectiveness in the medium and long term (minimum 4 weeks), and second to interventions in low- and middle-income countries (LMICs).

We searched six databases from 1980 to 2013 and conducted a multi-language Google search for quantitative studies addressing the research questions. Effect sizes were calculated from eligible studies where possible, and narrative syntheses conducted. Subgroup analysis compared interventions with and without social contact.

Eighty studies (n = 422 653) were included in the review. For studies with medium or long-term follow-up (72, of which 21 had calculable effect sizes) median standardised mean differences were 0.54 for knowledge and −0.26 for stigmatising attitudes. Those containing social contact (direct or indirect) were not more effective than those without. The 11 LMIC studies were all from middle-income countries. Effect sizes were rarely calculable for behavioural outcomes or in LMIC studies.

There is modest evidence for the effectiveness of anti-stigma interventions beyond 4 weeks follow-up in terms of increasing knowledge and reducing stigmatising attitudes. Evidence does not support the view that social contact is the more effective type of intervention for improving attitudes in the medium to long term. Methodologically strong research is needed on which to base decisions on investment in stigma-reducing interventions.

Low income is a widely studied risk factor for child and adolescent behavioural difficulties. Previous research on this relationship has produced mixed findings.

To investigate the level, shape and homogeneity of income gradients in different types of antisocial behaviour.

A representative sample of 7977 British children and adolescents, aged 5–16 years, was analysed. Hypotheses concerning the shapes and homogeneity of the relationships between family socioeconomic status and multiple antisocial behaviour outcomes, including clinical diagnoses of oppositional-defiant disorder, conduct disorder and symptom subscales, such as irritability and hurtfulness, were tested by structural equation models.

Consistent income gradients were demonstrated across all antisocial behaviours studied. Disorder prevalence and mean symptom counts decreased across income quintiles in a non-linear fashion.

Our findings emphasise that income gradients are similar across different forms of antisocial behaviour and indicate that income may lead to greater behavioural differences in the mid-income range and less variation at low- and high-income extremes.

People with callous–unemotional traits and also those with autism spectrum disorder (ASD) display sociocognitive difficulties. However, the frequency and neurocognitive correlates of callous–unemotional traits within individuals with ASD are unknown.

To determine the prevalence of callous–unemotional traits in individuals with ASD and test their association with behavioural and cognitive measures.

Parents of 92 adolescents with ASD completed the Antisocial Processes Screening Device (APSD) for callous–unemotional traits. Adolescents participated in tasks of emotion recognition, theory of mind and cognitive flexibility.

In total 51% (n = 47) scored above a cut-off expected to identify the top 6% on the APSD. Of these 17% (n = 8) had concurrent conduct problems. Regression analyses found callous–unemotional traits were associated with specific impairment in fear recognition but not with theory of mind or cognitive flexibility.

Adolescents with ASD show high rates of callous–unemotional traits but, unlike in the general population, these are not strongly associated with conduct problems. The relationship of callous–unemotional traits to impairments in fear recognition suggests similar affective difficulties as in individuals with callous–unemotional traits without ASD.

Autism research has previously focused on either identifying a latent dimension or searching for subgroups. Research assessing the concurrently categorical and dimensional nature of autism is needed.

To investigate the latent structure of autism and identify meaningful subgroups in a sample spanning the full spectrum of genetic vulnerability.

Factor mixture models were applied to data on empathy, systemising and autistic traits from individuals on the autism spectrum, parents and general population controls.

A two-factor three-class model was identified, with two factors measuring empathy and systemising. Class one had high systemising and low empathy scores and primarily consisted of individuals with autism. Mainly comprising controls and parents, class three displayed high empathy scores and lower systemising scores, and class two showed balanced scores on both measures of systemising and empathy.

Autism is best understood as a dimensional construct, but meaningful subgroups can be identified based on empathy, systemising and autistic traits.

Empathy is a basic human ability, and patients with schizophrenia show dysfunctional empathic abilities on the behavioural and neural level.

These dysfunctions may precede the onset of illness; thus, it seems mandatory to examine the empathic abilities in individuals at clinical high risk for psychosis.

Using functional magnetic resonance imaging, we measured 15 individuals at clinical high risk of psychosis (CHR group) and compared their empathy performance with 15 healthy volunteers and 15 patients with schizophrenia.

Behavioural data analysis indicated no significant deficit in the CHR group. Functional data analysis revealed hyperactivation in a frontotemporoparietal network including the amygdala in the CHR group compared with the other two groups.

Despite normal behavioural performance, the CHR group activated the neural empathy network differently and specifically showed hyperactivation in regions critical for emotion processing. This could suggest a compensatory mechanism reflecting emotional hypersensitivity or dysfunctional emotion regulation. Further investigations should clarify the role of these neural alterations for development and exacerbation of psychosis.

Evidence suggests that auditory hallucinations may result from abnormally enhanced auditory sensitivity.

To investigate whether there is an auditory processing bias in healthy individuals who are prone to experiencing auditory hallucinations.

Two hundred healthy volunteers performed a temporal order judgement task in which they determined whether an auditory or a visual stimulus came first under conditions of directed attention (‘attend-auditory’ and ‘attend-visual’ conditions). The Launay–Slade Hallucination Scale was used to divide the sample into high and low hallucination-proneness groups.

The high hallucination-proneness group exhibited a reduced sensitivity to auditory stimuli under the attend-auditory condition. By contrast, attention-directed visual sensitivity did not differ significantly between groups.

Healthy individuals prone to hallucinatory experiences may possess a bias in attention towards internal auditory stimuli at the expense of external sounds. Interventions involving the redistribution of attentional resources would have therapeutic benefit in patients experiencing auditory hallucinations.

Studies have produced conflicting evidence regarding whether cognitive control deficits in patients with schizophrenia result from dysfunction within the cognitive control network (CCN; top-down) and/or unisensory cortex (bottom-up).

To investigate CCN and sensory cortex involvement during multisensory cognitive control in patients with schizophrenia.

Patients with schizophrenia and healthy controls underwent functional magnetic resonance imaging while performing a multisensory Stroop task involving auditory and visual distracters.

Patients with schizophrenia exhibited an overall pattern of response slowing, and these behavioural deficits were associated with a pattern of patient hyperactivation within auditory, sensorimotor and posterior parietal cortex. In contrast, there were no group differences in functional activation within prefrontal nodes of the CCN, with small effect sizes observed (incongruent–congruent trials). Patients with schizophrenia also failed to upregulate auditory cortex with concomitant increased attentional demands.

Results suggest a prominent role for dysfunction within auditory, sensorimotor and parietal areas relative to prefrontal CCN nodes during multisensory cognitive control.

It is unclear to what extent the traditional distinction between neurological and psychiatric disorders reflects biological differences.

To examine neuroimaging evidence for the distinction between neurological and psychiatric disorders.

We performed an activation likelihood estimation meta-analysis on voxel-based morphometry studies reporting decreased grey matter in 14 neurological and 10 psychiatric disorders, and compared the regional and network-level alterations for these two classes of disease. In addition, we estimated neuroanatomical heterogeneity within and between the two classes.

Basal ganglia, insula, sensorimotor and temporal cortex showed greater impairment in neurological disorders; whereas cingulate, medial frontal, superior frontal and occipital cortex showed greater impairment in psychiatric disorders. The two classes of disorders affected distinct functional networks. Similarity within classes was higher than between classes; furthermore, similarity within class was higher for neurological than psychiatric disorders.

From a neuroimaging perspective, neurological and psychiatric disorders represent two distinct classes of disorders.

The contribution of education and intelligence to resilience against age-related cognitive decline is not clear, particularly in the presence of ‘normal for age’ minor brain abnormalities.

Participants (n = 208, mean age 69.2 years, s.d. = 5.4) in the Whitehall II imaging substudy attended for neuropsychological testing and multisequence 3T brain magnetic resonance imaging. Images were independently rated by three trained clinicians for global and hippocampal atrophy, periventricular and deep white matter changes.

Although none of the participants qualified for a clinical diagnosis of dementia, a screen for cognitive impairment (Montreal Cognitive Assessment (MoCA) <26) was abnormal in 22%. Hippocampal atrophy, in contrast to other brain measures, was associated with a reduced MoCA score even after controlling for age, gender, socioeconomic status, years of education and premorbid IQ. Premorbid IQ and socioeconomic status were associated with resilience in the presence of hippocampal atrophy.

Independent contributions from a priori risk (age, hippocampal atrophy) and resilience (premorbid function, socioeconomic status) combine to predict measured cognitive impairment.

There is little research evidence as to whether general adult psychiatry or old age psychiatry should look after old people with enduring mental illness.

To compare the extent to which general adult and old age psychiatric services meet the needs of older people with enduring mental illness.

A total of 74 elderly patients with functional psychiatric disorders were identified by reviewing the notes of patients over the age of 60 living in a defined inner urban catchment area. Data were collected on the morbidity and needs of the sample. Needs were assessed using the Elderly Psychiatric Needs Schedule (EPNS).

The participants in contact with old age psychiatry had significantly fewer unmet needs compared with those in contact with general adult psychiatry (2.8 v. 5.6, t = 2.2, P<0.03). Total needs were not significantly different between those managed by old age and general adult services (8.0 v. 6.5 respectively, t = 1.2, P = 0.2).

This study found that old age psychiatry services were better placed to meet the needs of elderly people with mental illness. This finding supports the need for a separate old age psychiatry service.

Behavioural and psychological symptoms of dementia are frequently treated with antipsychotics.

To determine the incidence of antipsychotic use in relation to diagnosis of Alzheimer's disease.

Cohort of all community-dwellers in Finland diagnosed with Alzheimer's disease in 2005 and matched controls. All antipsychotics dispensed between 1995 and 2009 were extracted from the Finnish National Prescription Register.

Altogether 1996/6087 (32.8%) persons with Alzheimer's disease initiated antipsychotic use. The incidence of antipsychotic use was fivefold among persons with Alzheimer's disease compared with controls, started to increase 2–3 years before diagnosis and was highest during the first 6 months after diagnosis.

A distinct increase in antipsychotic initiations occurs in the same time window as Alzheimer's disease diagnosis.