Despite frequent use, little is known about the metabolic and endocrine side-effects of antipsychotics in individuals with intellectual disability.

To compare indices of obesity, glucose, lipids and prolactin between antipsychotic-treated and antipsychotic-naive individuals with intellectual disability and also between participants with intellectual disability and controls from the general population.

Observational study comparing 138 antipsychotic-treated and 64 antipsychotic-naive participants with intellectual disability in one National Health Service trust with general population controls.

Antipsychotic treatment comprised: risperidone 48%, olanzapine 18%, thioxanthenes 10%, other 24%; monotherapy 95% of participants; mean treatment duration 8 years; median daily chlorpromazine equivalent dose 108mg (range 16–667). Metabolic indices were the same or more favourable in the intellectual disability group than the general population control group but overweight/obesity and type 2 diabetes were more prevalent in the women in the intellectual disability group than the control group. Metabolic indices were similar, statistically or clinically, between the antipsychotic-treated and the antipsychotic-naive groups but there was a non-significant trend towards a higher rate of type 2 diabetes in the antipsychotic group. A total of 100% and 70% of participants on amisulpride/sulpiride and risperidone respectively had hyperprolactinaemia, with secondary hypogonadism in 77% and 4% of affected women and men.

Antipsychotics, on average, did not increase metabolic risk, although the existence of a susceptible subgroup at risk of diabetes cannot be excluded. Some antipsychotics induced hyperprolactinaemic hypogonadism, requiring active management. However, our findings suggest that antipsychotics at the low doses routinely prescribed for people with intellectual disability are generally safe in relation to metabolic adverse effects, even if efficacy remains poorly defined.

Biological or genetic models of mental illness are commonly expected to increase tolerance towards people with mental illness, by reducing notions of responsibility and blame.

To investigate whether biogenetic causal attributions of mental illness among the general public are associated with more tolerant attitudes, whether such attributions are related to lower perceptions of guilt and responsibility, to what extent notions of responsibility are associated with rejection of people who are mentally ill, and how prevalent notions of responsibility are among the general public with regard to different mental disorders.

A systematic review was conducted of representative population studies examining attitudes towards people with mental illness and beliefs about such disorders.

We identified 33 studies relevant to this review. Generally, biogenetic causal attributions were not associated with more tolerant attitudes; they were related to stronger rejection in most studies examining schizophrenia. No published study reported on associations of biogenetic causal attributions and perceived responsibility. The stereotype of self-responsibility was unrelated to rejection in most studies. Public images of mental disorder are generally dominated by the stereotypes of unpredictability and dangerousness, whereas responsibility is less relevant.

Biogenetic causal models are an inappropriate means of reducing rejection of people with mental illness.

Munchausen's syndrome by proxy (recently renamed fabricated or induced illness) is a rare form of child abuse, but relatively little is known about the psychopathology of the perpetrators.

To examine the medical, psychiatric, social work and forensic records of mothers referred for detailed psychiatric assessment from 1996 to 2009.

Twenty-eight consecutive individuals with a putative diagnosis of fabricated or induced illness were referred to the authors for detailed psychiatric assessment and recommendations about management (25 from family courts). We scrutinised all medical and psychiatric records and interviewed them, as well as informants.

In total, 16 (57%) had evidence of a current somatoform disorder, and factitious disorders (either past or current) were identified in 18 (64%): 11 participants had both somatoform and factitious disorders. Nine participants (32%) had non-epileptic attacks. We found evidence of pathological lying (pseudologia fantastica) in 17 (61%) of the participants; in some there were key links between early abusive experiences, the development of pathological lying and the eventual fabrication of illness in the child victim.

A chronic somatoform disorder or factitious disorder (or both) was detected in almost two-thirds of the participants. Over half of the mothers exhibited pathological lying, in some dating from adolescence, and this often continued into adult life eventually involving the child in a web of deceit and abuse. Psychiatrists whose work brings them into contact with women with chronic somatoform or factitious disorders, especially if there is evidence of lying from an early age, should always be alert to the impact of these illnesses on any dependent children.

Most people with schizophrenia in low- and middle-income (LAMI) countries receive minimal formal care, and there are high rates of non-adherence to medication.

To evaluate the effectiveness of an intervention that involves a family member in supervising medication administration – supervised treatment in out-patients for schizophrenia (STOPS) – in improving treatment adherence and clinical outcomes.

Individuals (n = 110) with schizophrenia or schizoaffective disorders were allocated to STOPS or to treatment as usual (TAU) and followed up for 1 year. The primary outcome was adherence to the treatment regimen. Positive and Negative Syndrome Scale for Schizophrenia and Global Assessment of Functioning scores were also assessed.

Participants in the STOPS group had better adherence (complete adherence: 37 (67.3%) in STOPS v. 25 (45.5%) in TAU; P<0.02) and significant improvement in symptoms and functioning.

STOPS may be useful in enhancing adherence to treatment for schizophrenia in LAMI countries.

Cognitive impairment is an established feature of schizophrenia. However, little is known about its relationship to the structural and functional brain abnormalities that characterise the disorder.

To identify structural and/or functional brain abnormalities associated with schizophrenic cognitive impairment.

We carried out structural magnetic resonance imaging (MRI) and voxel-based morphometry in 26 participants who were cognitively impaired and 23 who were cognitively preserved, all with schizophrenia, plus 39 matched controls. Nineteen of those who were cognitively impaired and 18 of those who were cognitively preserved plus 34 controls also underwent functional MRI during performance of a working memory task.

No differences were found between the participants who were cognitively intact and those who were cognitively impaired in lateral ventricular volume or whole brain volume. Voxel-based morphometry also failed to reveal clusters of significant difference in grey and white matter volume between these two groups. However, during performance of the n-back task, the participants who were cognitively impaired showed hypoactivation compared with those who were cognitively intact in the dorsolateral prefrontal cortex among other brain regions.

Cognitive impairment in schizophrenia is not a function of the structural brain abnormality that accompanies the disorder but has correlates in altered brain function.

A number of studies in a range of samples attest a link between childhood sexual abuse and psychosis.

To use data from a large representative general population sample (Adult Psychiatric Morbidity Survey 2007) to test hypotheses that childhood sexual abuse is linked to psychosis, and that the relationship is consistent with mediation by revictimisation experiences, heavy cannabis use, anxiety and depression.

The prevalence of psychosis was established operationally in a representative cross-sectional survey of the adult household population of England (n = 7353). Using computer-assisted self-interview, a history of various forms of sexual abuse was established, along with the date of first abuse.

Sexual abuse before the age of 16 was strongly associated with psychosis, particularly if it involved non-consensual sexual intercourse (odds ratio (OR) = 10.14, 95% CI 4.8–21.3, population attributable risk fraction 14%). There was evidence of partial mediation by anxiety and depression, but not by heavy cannabis use nor revictimisation in adulthood.

The association between childhood sexual abuse and psychosis was large, and may be causal. These results have important implications for the nature and aetiology of psychosis, for its treatment and for primary prevention.

There is a long-standing belief that creativity is coupled with psychopathology.

To test this alleged association and to investigate whether any such association is the result of environmental or genetic factors.

We performed a nested case–control study based on Swedish registries. The likelihood of holding a creative occupation in individuals who had received in-patient treatment for schizophrenia, bipolar disorder or unipolar depression between 1973 and 2003 and their relatives without such a diagnosis was compared with that of controls.

Individuals with bipolar disorder and healthy siblings of people with schizophrenia or bipolar disorder were overrepresented in creative professions. People with schizophrenia had no increased rate of overall creative professions compared with controls, but an increased rate in the subgroup of artistic occupations. Neither individuals with unipolar depression nor their siblings differed from controls regarding creative professions.

A familial cosegregation of both schizophrenia and bipolar disorder with creativity is suggested.

Generalised anxiety disorder (GAD) in older adults is associated with neuropsychological impairment.

We examined neuropsychological functioning in older adults with GAD in comparison with psychiatrically healthy older adults at baseline, and we examined changes following a 12-week placebo-controlled trial of escitalopram.

A total of 160 participants without dementia aged ⩾60 with current GAD and 37 individuals in a comparison group without psychiatric history underwent neuropsychological assessment. Of these, 129 participants with GAD were reassessed post-treatment (trial registration: NCT00105586).

The participants with GAD performed worse than the comparison group in information processing speed, working memory, inhibition, problem-solving (including concept formation and mental flexibility) and immediate and delayed memory. Neuropsychological functioning was correlated with everyday functioning. After treatment, those with low cognitive scores experienced working memory, delayed memory and visuospatial ability improvement and those who reported clinical improvement in anxiety exhibited improvement in the ability to engage inhibition and episodic recall. These improvements were modest and of similar magnitude in both treatment conditions.

Generalised anxiety disorder in older adults is associated with neuropsychological impairments, which are associated with functional impairment. Those with GAD who either have a low cognitive performance or report clinical improvement in anxiety post-treatment, show improvement in multiple cognitive domains. These findings underscore the importance of treatments that aid cognition as well as anxiety symptoms.

Short-term structured risk assessment is presumed to reduce incidents of aggression and seclusion on acute psychiatric wards. Controlled studies of this approach are scarce.

To evaluate the effect of risk assessment on the number of aggression incidents and time in seclusion for patients admitted to acute psychiatric wards.

A cluster randomised controlled trial was conducted in four wards over a 40-week period (n = 597 patients). Structured risk assessment scales were used on two experimental wards, and the numbers of incidents of aggression and seclusion were compared with two control wards where assessment was based purely on clinical judgement.

The numbers of aggressive incidents (relative risk reduction −68%, P<0.001) and of patients engaging in aggression (relative risk reduction RRR =–50%, P<0.05) and the time spent in seclusion (RRR =–45%, P<0.05) were significantly lower in the experimental wards than in the control wards. Neither the number of seclusions nor the number of patients exposed to seclusion decreased.

Routine application of structured risk assessment measures might help reduce incidents of aggression and use of restraint and seclusion in psychiatric wards.

In a baseline study among 7- and 8-year-old children with auditory vocal hallucinations, only limited functional impact was observed.

To assess 5-year course and predictors of auditory vocal hallucinations, as well as 5-year incidence and its risk factors.

A sample of 337 children, 12 and 13 years of age, were reassessed on auditory vocal hallucinations and associated symptoms after a mean follow-up period of 5.1 years.

The 5-year persistence and incidence rates were 24% and 9% respectively, with more new cases arising in urban areas. Both persistent and incident auditory vocal hallucinations were associated with problem behaviour in the clinical range of psychopathology as measured with the Child Behavior Checklist, particularly at follow-up, as well as with other psychotic symptoms, particularly at baseline. Persistence was predicted by baseline auditory vocal hallucinations severity, particularly in terms of external attribution of voices and hearing multiple voices, and was associated with worse primary school test scores and lower secondary school level.

First onset of auditory vocal hallucinations in middle childhood is not uncommon and is associated with psychopathological and behavioural comorbidity. Similarly, persistence of auditory vocal hallucinations in childhood is not uncommon and is associated with psychopathological, behavioural and cognitive alterations.

Although genetic epidemiological studies have confirmed increased rates of major depressive disorder among the relatives of people with bipolar affective disorder, no report has compared the clinical characteristics of depression between these two groups.

To compare clinical features of depressive episodes across participants with major depressive disorder and bipolar disorder from within bipolar disorder pedigrees, and assess the utility of a recently proposed probabilistic approach to distinguishing bipolar from unipolar depression. A secondary aim was to identify subgroups within the relatives with major depression potentially indicative of ‘genetic’ and ‘sporadic’ subgroups.

Patients with bipolar disorder types 1 and 2 (n = 246) and patients with major depressive disorder from bipolar pedigrees (n = 120) were assessed using the Diagnostic Interview for Genetic Studies. Logistic regression was used to identify distinguishing clinical features and assess the utility of the probabilistic approach. Hierarchical cluster analysis was used to identify subgroups within the major depressive disorder sample.

Bipolar depression was characterised by significantly higher rates of psychomotor retardation, difficulty thinking, early morning awakening, morning worsening and psychotic features. Depending on the threshold employed, the probabilistic approach yielded a positive predictive value ranging from 74% to 82%. Two clusters within the major depressive disorder sample were found, one of which demonstrated features characteristic of bipolar depression, suggesting a possible ‘genetic’ subgroup.

A number of previously identified clinical differences between unipolar and bipolar depression were confirmed among participants from within bipolar disorder pedigrees. Preliminary validation of the probabilistic approach in differentiating between unipolar and bipolar depression is consistent with dimensional distinctions between the two disorders and offers clinical utility in identifying patients who may warrant further assessment for bipolarity. The major depressive disorder clusters potentially reflect genetic and sporadic subgroups which, if replicated independently, might enable an improved phenotypic definition of underlying bipolarity in genetic analyses.

A putative interaction between cannabis and variation at rs4680 within the catechol-methyl-transferase (COMT) gene on psychosis has been reported, but not adequately replicated.

To examine whether the relative risk of developing psychosis following use of cannabis is dependent upon variation within COMT.

A longitudinal study of 2630 individuals from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort who completed questionnaire-based assessments for cannabis use at age 14 and incident psychotic experiences at age 16. Six SNPs within COMT were genotyped.

There was no evidence of an interaction under multiplicative models between cannabis use and COMT on the risk of developing psychotic experiences in our primary analyses. In sensitivity analyses we observed highly variable evidence of interaction, whereby psychotomimetic effects of cannabis were greater in methionine homozygotes under some scenarios, but in valine homozygotes under others.

Cannabis increases risk of psychosis irrespective of underlying COMT genotypes. These findings argue against the widely held belief that the relative risk of developing psychosis following use of cannabis is dependent upon variation within COMT. The public health message about the potential increase in risk of psychotic disorders following cannabis use should not be tempered by reports that this harm is subgroup specific in the absence of robust evidence of replication.

The well-established relationship between childhood adversity and psychosis is likely to involve other factors such as genetic variants that can help us to understand why not everyone exposed to adverse events develops psychotic symptoms later in life.

We investigated the influence of childhood abuse and neglect on positive and negative psychotic-like experiences in adulthood and the potential moderating effect of the BDNF-Val66Met polymorphism.

Psychotic-like experiences and childhood adversity were assessed in 533 individuals from the general population.

Childhood abuse showed a strong independent effect on the positive dimension of psychotic-like experiences (β = 0.16, s.e. = 0.05, P = 0.002). Furthermore, this association was moderated by the BDNF-Val66Met polymorphism (β = 0.27, s.e. = 0.10, P = 0.004).

Individuals exposed to childhood abuse are more likely to report positive psychotic-like experiences. Met carriers reported more positive psychotic-like experiences when exposed to childhood abuse than did individuals carrying the Val/Val genotype. Therefore, the observed gene–environment interaction effect may be partially responsible for individual variation in response to childhood abuse.

Preliminary studies in the UK, all using screening instruments of unknown cultural validity, indicate that there may be an increased prevalence of dementia in African–Caribbean people, possibly related to vascular risk factors and potentially amenable to preventative measures.

To determine the prevalence of dementia in older people of African–Caribbean country of birth compared with their White UK-born counterparts.

A total of 218 people of African–Caribbean country of birth and 218 White UK-born people aged ⩾60 years were recruited from five general practices in North London. Those who screened positive for cognitive impairment using a culturally valid instrument were offered a standardised diagnostic interview. Two independent assessors diagnosed dementia according to standard operationalised criteria.

African–Caribbean participants were 2 years younger, and those with dementia nearly 8 years younger than their White counterparts. The prevalence of dementia was significantly higher in the African–Caribbean (9.6%) than the White group (6.9%) after adjustment for the confounders age and socioeconomic status (odds ratio (OR) = 3.1, 95%CI 1.3–7.3, P = 0.012).

There is an increased prevalence of dementia in older people of African–Caribbean country of birth in the UK and at younger ages than in the indigenous White population. These findings have implications for service provision and preventive interventions. Further research is needed to explore the role of vascular risk factors and social adversity in the excess of dementia in this population.

It is unclear whether common affective disorders and anxiety disorders increase the risk of alcohol dependence and alcohol misuse.

To investigate whether affective disorders and anxiety disorders increase the risk of alcohol dependence and alcohol misuse.

This study is a retrospective cohort study based on data collected from the 2007 Australia Mental Health and Well-Being survey. Both Poisson and logistic regression models were used for multivariate analysis.

Participants with affective disorders (relative risk (RR) = 5.46, 95% CI 4.08–7.31 for alcohol dependence within 5 years of onset; RR = 2.77, 95% CI 1.93–3.99 after first 5 years) and anxiety disorders (RR = 3.33, 95% CI 2.37–4.68 for alcohol dependence within first 5 years of onset; RR = 3.56, 95% CI 2.72–4.64 after first 5 years) were at higher risk of alcohol misuse and alcohol dependence.

Common affective disorders and anxiety disorders may increase the risk of alcohol dependence and alcohol misuse among the Australian population.

Presentations to hospital with self-harm are common, associated with suicide and have an increased mortality, yet there is no accepted effective intervention.

To investigate whether problem-solving therapy would improve outcomes in adults presenting to hospital with self-harm, compared with usual care.

A Zelen randomised controlled trial was conducted in four district health boards in New Zealand. A second hospital presentation with self-harm at 1 year for all episodes, plus separate comparisons of first-time and repeat presentations at the index episode, were the a priori primary outcomes. The trial registration number was ACTRN12605000337673.

In an intention-to-treat analysis of all randomised patients (n = 1094) there was no significant difference at 12 months in the proportion of people who had presented again with self-harm when comparing all episodes (intervention 13.4%, usual care 14.1%; relative risk reduction RR = 0.05, 95% CI −0.28 to 0.30, P = 0.79) or where the index episode was the first episode (intervention 13.4%, usual care 9.4%, RR =–0.42, 95% CI −1.17 to 0.08, P = 0.37). Where the index episode was repeated self-harm, those who received therapy were less likely to present again with self-harm (intervention 13.5%, usual care 22.1%, RR = 0.39, 95% CI 0.07 to 0.60, number needed to treat 12, P = 0.03).

Problem-solving therapy is not recommended for everyone who presents to hospital with self-harm. Among adults with a history of self-harm it may be an effective intervention.