Background. Previous research has confirmed the presence of increased motor overflow in schizophrenia. There are essentially two theories regarding the cortical origins of overflow. Recent research suggests that both may be correct, and that the cortical origin of overflow is highly dependent upon the population in which it presents. Motor overflow, due to an abnormally active ipsilateral corticospinal tract, may indicate a potentially severe brain abnormality arising in early development. In contrast, bilaterally active corticospinal tracts accounting for overflow probably represent a naturally occurring response during fatiguing contractions.

Method. The cortical origins of motor overflow in 20 participants with schizophrenia and 20 normal controls were investigated through the use of a number of transcranial magnetic stimulation (TMS) protocols.

Results. Each of the experimental protocols employed independently supported the contention that overflow was originating in the hemisphere contralateral to the involuntary movement.

Conclusions. Results indicated that the origins of overflow in schizophrenia are the same as those seen in the normal control group, i.e. motor overflow seems to be due to the presence of bilaterally active corticospinal tracts. Potential explanations for greater motor overflow seen in schizophrenia are discussed.

Background. The aim of this study was to estimate the extent to which anxiety disorders contribute to an increase in suicidal behaviour after controlling for both observed and non-observed sources of confounding.

Method. Data were collected from the Christchurch Health and Development Study (CHDS), a 25-year longitudinal study of over 1000 participants. Measures of anxiety disorders [phobia, generalized anxiety disorder (GAD), panic disorder], major depression (MD), substance use disorders, conduct/antisocial personality disorder, stressful life events, unemployment, and suicidal ideation/attempts for subjects aged 16–18, 18–21 and 21–25 years were used to fit random and fixed effects regression models of the associations between anxiety disorders and suicidal behaviours.

Results. Anxiety disorders were strongly associated with suicidal ideation/attempts. Any single anxiety disorder increased the odds of suicidal ideation by 7·96 times [95% confidence interval (CI) 5·69–11·13] and increased the rate of suicide attempts by 5·85 times (95% CI 3·66–9·32). Control for co-occurring mental disorders, non-observed fixed confounding factors and life stress reduced these associations [suicidal ideation odds ratio (OR) 2·80, 95% CI 1·71–4·58; suicide attempts incidence rate ratio (IRR) 1·90, 95% CI 1·07–3·39]. Rates of suicidal behaviour also increased with the number of anxiety disorders. Estimates of the population attributable risk suggested that anxiety disorders accounted for 7–10% of the suicidality in the cohort.

Conclusions. Anxiety disorders may be a risk factor for suicidality, even after controlling for confounding, with risks increasing with multiple anxiety disorders. Management of anxiety disorders may be an important component in strategies to reduce population rates of suicide.

Background. Reduction of health inequalities is a major policy goal in the UK. While there is general recognition of the disadvantaged position of people with mental health problems, the extent of inequality, particularly the association with socio-economic characteristics, has not been widely studied. We aimed to measure income-related inequality in the distribution of psychiatric disorders and to compare with inequality in other health domains.

Method. The concentration index (CI) approach was used to examine income-related inequality in mental health using data from the Psychiatric Morbidity Survey 2000 for Britain.

Results. There is marked inequality unfavourable to lower income groups with respect to mental health disorders. The extent of inequality increases with the severity of problems, with the greatest inequality observed for psychosis. Income-related inequality for psychiatric disorders is higher than for general health in the UK. Standardized CIs suggest that these inequalities are not due to the demographic composition of the income quintiles.

Conclusions. Income-related inequalities exist in mental health in Britain. As much of the observed inequality is probably due to factors associated with income and not due to the demographic composition of the income quintiles, it may be that these inequalities are potentially ‘avoidable’.

Background. There is a lack of current detailed national data on the prevalence, correlates, disability and co-morbidity of DSM-IV specific phobia (SP), the prevalence of specific objects and situations feared, and associations between impairment, treatment and co-morbidity and the number of specific situations and objects feared, among adults in the USA.

Method. The data were derived from a large (43093) representative sample of the adult population in the USA.

Results. Prevalences of 12-month and lifetime DSM-IV SP were 7·1% and 9·4% respectively. Being female, young, and low income increased risk, while being Asian or Hispanic decreased risk (p<0·05). The mean age at onset of SP was 9·7 years, the mean duration of episode was 20·1 years and only 8·0% reported treatment specifically for SP. Most specific phobias involved multiple fears, and an increasing number of fears, regardless of content, was associated with greater disability and impairment, treatment seeking and co-morbidity with other Axis I and II disorders.

Conclusions. SP is a highly prevalent, disabling and co-morbid disorder in the US adult population. The early onset of SP and the disorders most strongly associated with it highlights the need for longitudinal studies beginning in early childhood. Results suggest the existence of a generalized subtype of SP much like social phobia, which, once revealed, may lead to a classification of SP that is more etiologically and therapeutically meaningful.

Background. We identified the need to develop a scientifically rigorous measure of health-related quality of life (HRQL) in dementia that would be appropriate for use at all stages of dementia severity and would be available in both self- and proxy-report versions.

Method. We used standard psychometric methods to eliminate items with poor psychometric properties (item-reduction field test) and to assess the acceptability, reliability and validity of the item-reduced instruments (psychometric evaluation field test). We developed and validated two versions of DEMQOL: a 28-item interviewer-administered questionnaire that is self-reported by the person with dementia (DEMQOL) and a 31-item interviewer-administered questionnaire that is proxy-reported by a caregiver (DEMQOL-Proxy).

Results. DEMQOL shows high reliability (internal consistency and test–retest) and moderate validity in people with mild/moderate dementia. DEMQOL-Proxy shows good acceptability and internal consistency and moderate evidence of validity in people with mild/moderate and severe dementia. Test–retest reliability and performance in people with severe dementia need further testing.

Conclusions. DEMQOL and DEMQOL-Proxy show psychometric properties that are comparable with the best available dementia-specific measures of HRQL. We recommend that DEMQOL and DEMQOL-Proxy are used together. Reliability and validity need to be confirmed in independent samples and responsiveness needs to be evaluated.

Background. Deficits in a patient's ‘theory of mind’ (TOM) have been proposed to lead to psychosis. However, it remains unclear whether TOM deficits constitute a trait- or a state-related deficit and whether they respond to antipsychotic treatment, and also whether the change in TOM and change in psychosis are associated.

Method. In the cross-sectional component of this study, 71 patients with psychotic disorders were included and TOM ability was measured using a hinting task in which subjects had to infer real intentions behind indirect speech. In the longitudinal study, a different cohort of 17 drug-free patients were included wherein they received antipsychotic treatment for 6 weeks and the effect on psychotic symptoms and TOM was measured every 2 weeks. Associations between TOM and psychopathology were assessed and a mixed effects model was used to investigate the rate of change over time.

Results. Positive and Negative Syndrome Scale (PANSS) total scores were significantly associated with TOM scores. The hinting task was not associated with positive symptoms but was significantly associated with negative and general symptoms. The longitudinal arm of the study showed that both PANSS positive scores and TOM improved after medication was started, particularly during the first 2 weeks of antipsychotic treatment, but these changes were not associated. The TOM response at 2 weeks of antipsychotic treatment reached similar values to those obtained in the cross-sectional sample.

Conclusions. Although TOM and psychotic symptoms are related to each other, antipsychotic treatment impacts each independently, suggesting a dissimilar cognitive or neurobiological substrate for the two.

Background. The close association between generalized anxiety disorder (GAD) and major depressive disorder (MDD) prompts questions about how to characterize them in future diagnostic systems. We tested whether risk factors for MDD and GAD are similar or different.

Method. The representative 1972–73 Dunedin birth cohort of 1037 males and females was followed to age 32 with 96% retention. Adult GAD and MDD were diagnosed at ages 18, 21, 26, and 32 years, and juvenile anxiety/depression were also taken into account. Thirteen prospective risk measures indexed domains of family history, adverse family environment, childhood behavior, and adolescent self-esteem and personality traits.

Results. Co-morbid MDD+GAD was antedated by highly elevated risk factors broadly across all domains. MDD+GAD was further characterized by the earliest onset, most recurrence, and greatest use of mental health services and medication. Pure GAD had levels of risk factors similar to the elevated levels for co-morbid MDD+GAD; generally, pure MDD did not. Pure GAD had risks during childhood not shared by pure MDD, in domains of adverse family environment (low SES, somewhat more maltreatment) and childhood behavior (internalizing problems, conduct problems, somewhat more inhibited temperament). Pure MDD had risks not shared by pure GAD, in domains of family history (of depression) and personality (low positive emotionality).

Conclusions. Specific antecedent risk factors for pure adult MDD versus GAD may suggest partly different etiological pathways. That GAD and co-morbid MDD+GAD share many risk markers suggests that the presence of GAD may signal a pathway toward relatively more severe internalizing disorder.