In general, mothers with depression experience more environmental and family risk factors, and lead riskier lifestyles, than mothers who are not depressed.

To test whether the exposure of a child to risk factors associated with mental health adds to the prediction of child psychopathology beyond exposure to maternal depression.

In 7429 mother–offspring pairs participating in the Avon Longitudinal Study of Parents and Children in the UK, maternal depression was assessed when the children were aged 1.5 years; multiple risk factor exposures were examined between birth and 2 years of age; and DSM-IV-based externalising and internalising diagnoses were evaluated when the children were 7.5 years of age.

Children of clinically depressed mothers were exposed to more risk factors associated with maternal mental health. Maternal depression increased diagnoses of externalising and internalising disorders, but a substantial portion of these associations was explained by increased risk factor exposure (41% for externalising and 37% for internalising disorders). At the same time, these risk exposures significantly increased the odds of both externalising and internalising diagnoses, over and above the influence of maternal depression.

Children of clinically depressed mothers are exposed to both maternal psychopathology and risks that are associated with maternal mental health. These results may explain why treating mothers with depression shows beneficial effects for children, but does not completely neutralise the increased risk of psychopathology and impairment.

The association between autoimmune diseases and schizophrenia has rarely been systematically investigated.

To investigate the association between schizophrenia and a variety of autoimmune diseases and to explore possible gender variation in any such association.

Taiwan's National Health Insurance Research Database was used to identify 10 811 hospital in-patients with schizophrenia and 108 110 age-matched controls. Univariate and multiple logistic regression analyses were performed, separately, to evaluate the association between autoimmune diseases and schizophrenia. We applied the false discovery rate to correct for multiple testing.

When compared with the control group, the in-patients with schizophrenia had an increased risk of Graves' disease (odds ratio (OR) = 1.32, 95% CI 1.04–1.67), psoriasis (OR = 1.48, 95% CI 1.07–2.04), pernicious anaemia (OR = 1.71, 95% CI 1.04–2.80), celiac disease (OR = 2.43, 95% CI 1.12–5.27) and hypersensitivity vasculitis (OR = 5.00, 95% CI 1.64–15.26), whereas a reverse association with rheumatoid arthritis (OR = 0.52, 95% CI 0.35–0.76) was also observed. Gender-specific variation was found for Sjögren syndrome, hereditary haemolytic anaemia, myasthenia gravis, polymyalgia rheumatica and dermatomyositis.

Schizophrenia was associated with a greater variety of autoimmune diseases than was anticipated. Further investigation is needed to gain a better understanding of the aetiology of schizophrenia and autoimmune diseases.

Young people with self-experienced cognitive thought and perception deficits (basic symptoms) may present with an early initial prodromal state (EIPS) of psychosis in which most of the disability and neurobiological deficits of schizophrenia have not yet occurred.

To investigate the effects of an integrated psychological intervention (IPI), combining individual cognitive–behavioural therapy, group skills training, cognitive remediation and multifamily psychoeducation, on the prevention of psychosis in the EIPS.

A randomised controlled, multicentre, parallel group trial of 12 months of IPI v. supportive counselling (trial registration number: NCT00204087). Primary outcome was progression to psychosis at 12- and 24-month follow-up.

A total of 128 help-seeking out-patients in an EIPS were randomised. Integrated psychological intervention was superior to supportive counselling in preventing progression to psychosis at 12-month follow-up (3.2% v. 16.9%; P = 0.008) and at 24-month follow-up (6.3% v. 20.0%; P = 0.019).

Integrated psychological intervention appears effective in delaying the onset of psychosis over a 24-month time period in people in an EIPS.

Prior research reports stronger associations between childhood maltreatment and adult psychopathology when maltreatment is assessed retrospectively compared with prospectively, casting doubt on the mental health risk conferred by maltreatment and on the validity of retrospective reports.

To investigate associations of psychopathology with prospective v. retrospective maltreatment ascertainment.

A nationally representative sample of respondents aged 16–27 years (n = 1413) in New Zealand completed a retrospective assessment of maltreatment and DSM-IV mental disorders. Survey data were linked with a national child protection database to identify respondents with maltreatment records (prospective ascertainment).

Childhood maltreatment was associated with elevated odds of mood, anxiety and drug disorders (odds ratios = 2.1–4.1), with no difference in association strength between prospective and retrospective groups. Prospectively ascertained maltreatment predicted unfavourable depression course involving early onset, chronicity and impairment.

Prospectively and retrospectively assessed maltreatment elevated the risk of psychopathology to a similar degree. Prospectively ascertained maltreatment predicted a more unfavourable depression course.

There is a debate over whether disruptive behaviour should be regarded as a central component of, or rather as an epiphenomenon with little diagnostic value for, psychopathy.

To test whether callous–unemotional traits and conduct disorder can be dissociated in the English and Romanian Adoptee Study, a prospective longitudinal study of adopted individuals with a history of severe early institutional deprivation.

The Child and Adolescent Psychiatric Assessment was used to establish DSM-IV diagnoses for conduct disorder (and also oppositional defiant disorder) at the 15-year follow-up stage. The Inventory of Callous–Unemotional Traits questionnaire was administered to assess psychopathy traits.

There was no significant association between callous–unemotional traits and conduct disorder, both according to parent and youth self-report assessed categorically and dimensionally after controlling for confounds.

The majority of individuals with high callous–unemotional traits did not show conduct disorder in this special sample of children. This supports the view that, while common, an overlap between these aspects of psychopathology is not inevitable and so provides evidence for the dissociation of these two concepts. In terms of classification, we argue for a diagnostic scheme where psychopathy can be diagnosed independently of conduct disorder.

Maternal smoking during pregnancy may increase the risk of nicotine dependence, especially in girls, but data are conflicting and confounding by other familial factors cannot be ruled out.

To clarify the relationship between prenatal tobacco exposure and adolescent tobacco uptake and dependence in boys and girls respectively, while taking confounding factors into close consideration.

We conducted a prospective longitudinal study, comprising 3020 Swedish youths followed from 11 to 18 years of age. Exposure and outcome information was elicited via self-administered parental and repeated youth questionnaires. Hazard ratios (HRs), odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were calculated as measures of associations.

Girls prenatally exposed to maternal tobacco use had a two-to threefold increased odds of experiencing a high number of withdrawal symptoms (OR = 2.83, 95% CI 1.68–4.87), craving for tobacco (OR = 2.04, 95% CI 1.28–3.32) and heavy tobacco use (five or more cigarettes or snus dips per day) (OR = 1.93, 95% CI 1.30–2.86). These associations were weaker among boys, and did not reach formal statistical significance. Associations between prenatal tobacco exposure and onset of regular tobacco use in both genders appeared to be mostly explained by parents' social position and postnatal smoking behaviour.

Prenatal exposure to tobacco is linked to an increased risk of nicotine dependence among adolescent girls.

Thalamic volume deficits are associated with psychosis but it is unclear whether the volume reduction is uniformly distributed or whether it is more severe in particular thalamic regions.

To quantify whole and regional thalamic volume in males with early-onset psychosis and healthy male controls.

Brain scans were obtained for 80 adolescents: 46 individuals with early-onset psychosis with a duration of positive symptoms less than 6 months and 34 healthy controls. All participants were younger than 19 years. Total thalamic volumes were assessed using FreeSurfer and FSL-FIRST, group comparisons of regional thalamic volumes were studied with a surface-based approach.

Total thalamic volume was smaller in participants with early-onset psychosis relative to controls. Regional thalamic volume reduction was most significant in the right anterior mediodorsal area and pulvinar.

In males with minimally treated early-onset psychosis, thalamic volume deficits may be most pronounced in the anterior mediodorsal and posterior pulvinar regions, adding strength to findings from post-mortem studies in adults with psychosis.

Previous studies in schizophrenia have shown a strong relationship between memory deficits and a poor clinical outcome. However, no previous study has identified the functional neural correlates of memory encoding in relation to remission.

To determine whether functional magnetic resonance imaging (fMRI) activation patterns differed between individuals that later achieved remission v. those who did not.

Forty-two participants with first-episode schizophrenia were divided into two groups after 1 year of treatment as per the 2005 remission in schizophrenia consensus definition. We then examined fMRI activation using three contrasts (associative v. item-oriented strategy, semantically unrelated v. related image pairs, and successful v. unsuccessful memory encoding) among 15 participants who had achieved remission (remitted group), 27 who had not (non-remitted group) and 31 healthy controls (control group).

Participants in the non-remitted group displayed a positive activation in the posterior cingulate compared with those in the remitted group when encoding related images; no significant differences between the two groups were identified for the other contrasts. From the behavioural data, compared with the remitted and control groups, the non-remitted group demonstrated an inability to encode related images and displayed worse recognition memory overall.

This is the first study to identify differential neural activation between individuals with first-episode schizophrenia that later achieved remission v. those who did not. The behavioural and functional results together add to the growing evidence relating a poor clinical outcome in schizophrenia to memory-related deficits.

Inconsistent findings have been reported on the role of comorbid alcohol use disorders as risk factors for a persistent course of depressive and anxiety disorders.

To determine whether the course of depressive and/or anxiety disorders is conditional on the type (abuse or dependence) or severity of comorbid alcohol use disorders.

In a large sample of participants with current depression and/or anxiety (n = 1369) we examined whether the presence and severity of DSM-IV alcohol abuse or alcohol dependence predicted the 2-year course of depressive and/or anxiety disorders.

The persistence of depressive and/or anxiety disorders at the 2-year follow-up was significantly higher in those with remitted or current alcohol dependence (persistence 62% and 67% respectively), but not in those with remitted or current alcohol abuse (persistence 51% and 46% respectively), compared with no lifetime alcohol use disorder (persistence 53%). Severe (meeting six or seven diagnostic criteria) but not moderate (meeting three to five criteria) current dependence was a significant predictor as 95% of those in the former group still had a depressive and/or anxiety disorder at follow-up. This association remained significant after adjustment for severity of depression and anxiety, psychosocial factors and treatment factors.

Alcohol dependence, especially severe current dependence, is a risk factor for an unfavourable course of depressive and/or anxiety disorders, whereas alcohol abuse is not.

Symptoms of obsessive–compulsive disorder (OCD) have been described in neuropsychiatric syndromes associated with streptococcal infections. It is proposed that antibodies raised against streptococcal proteins cross-react with neuronal proteins (antigens) in the brain, particularly in the basal ganglia, which is a brain region implicated in OCD pathogenesis.

To test the hypothesis that post-streptococcal autoimmunity, directed against neuronal antigens, may contribute to the pathogenesis of OCD in adults.

Ninety-six participants with OCD were tested for the presence of anti-streptolysin-O titres (ASOT) and the presence of anti-basal ganglia antibodies (ABGA) in a cross-sectional study. The ABGA were tested for with western blots using three recombinant antigens; aldolase C, enolase and pyruvate kinase. The findings were compared with those in a control group of individuals with depression (n = 33) and schizophrenia (n = 17).

Positivity for ABGA was observed in 19/96 (19.8%) participants with OCD compared with 2/50 (4%) of controls (Fisher's exact test P = 0.012). The majority of positive OCD sera (13/19) had antibodies against the enolase antigen. No clinical variables were associated with ABGA positivity. Positivity for ASOT was not associated with ABGA positivity nor found at an increased incidence in participants with OCD compared with controls.

These findings support the hypothesis that central nervous system autoimmunity may have an aetiological role in some adults with OCD. Further study is required to examine whether the antibodies concerned are pathogenic and whether exposure to streptococcal infection in vulnerable individuals is a risk factor for the development of OCD.

Antidepressant prescribing is widespread. Nonetheless, response to antidepressants is variable. If it was possible to predict response to medication and thus tailor treatment accordingly, this would not only improve patient outcomes but may also have economic benefits.

To test the hypothesis that individuals with more severe depression would benefit more from noradrenaline reuptake inhibitors (NARIs) than selective serotonin reuptake inhibitors (SSRIs) compared with individuals with less severe depression.

Individuals recruited from UK primary care who met ICD-10 criteria for a depressive episode and scored 15 or more on the Beck Depression Inventory (BDI) were randomised to either an SSRI (citalopram 20mg daily) or a NARI (reboxetine 4mg twice daily). Randomisation was by means of a remote automated telephone system. The main outcome was depressive symptoms measured by the BDI total score 6 weeks after randomisation. (Trial registration: ISRCTN31345163.)

In total, 601 participants were randomised (citalopram: n = 298, reboxetine: n = 303). Ninety-one per cent were followed up at 6 weeks (citalopram: n = 274, reboxetine: n = 272). There was little evidence to support an interaction between treatment and severity of depression (interaction term: 0.02, 95% CI −0.59 to 0.62, P = 0.96). Adjustment for potential confounders (age, gender, employment status, history of depression, number of life events and social support) did not affect the findings (interaction term: 0.06, 95% CI −0.54 to 0.66, P = 0.85).

Treatment with NARIs does not confer any advantage over SSRI treatment for outcome in those with more severe depressive illness presenting in primary care.

Sleep disturbances comparable with insomnia occur in up to 80% of people with schizophrenia, but very little is known about the contribution of circadian coordination to these prevalent disruptions.

A systematic exploration of circadian time patterns in individuals with schizophrenia with recurrent sleep disruption.

We examined the relationship between sleep–wake activity, recorded actigraphically over 6 weeks, along with ambient light exposure and simultaneous circadian clock timing, by collecting weekly 48 h profiles of a urinary metabolite of melatonin in 20 out-patients with schizophrenia and 21 healthy control individuals matched for age, gender and being unemployed.

Significant sleep/circadian disruption occurred in all the participants with schizophrenia. Half these individuals showed severe circadian misalignment ranging from phase-advance/delay to non-24 h periods in sleep–wake and melatonin cycles, and the other half showed patterns from excessive sleep to highly irregular and fragmented sleep epochs but with normally timed melatonin production.

Severe circadian sleep/wake disruptions exist despite stability in mood, mental state and newer antipsychotic treatment. They cannot be explained by the individuals' level of everyday function.

Longitudinal studies of delirium phenomenology are lacking.

We studied features that characterise subsyndromal delirium and persistent delirium over time.

Twice-weekly evaluations of 100 adults with DSM-IV delirium using the Delirium Rating Scale – Revised-98 (DRS-R98) and Cognitive Test for Delirium (CTD). The generalised estimating equation method identified symptom patterns distinguishing full syndromal from subsyndromal delirium and resolving from persistent delirium.

Participants (mean age 70.2 years (s.d. = 10.5)) underwent 323 assessments (range 2–9). Full syndromal delirium was significantly more severe than subsyndromal delirium for DRS-R98 thought process abnormalities, delusions, hallucinations, agitation, retardation, orientation, attention, and short- and long-term memory items, and CTD attention, vigilance, orientation and memory. Persistent full syndromal delirium had greater disturbance of DRS-R98 thought process abnormalities, delusions, agitation, orientation, attention, and short- and long-term memory items, and CTD attention, vigilance and orientation.

Full syndromal delirium differs from subsyndromal delirium over time by greater severity of many cognitive and non-cognitive symptoms. Persistent delirium involves increasing prominence of recognised core diagnostic features and cognitive impairment.

People with major depressive disorder who fail to respond to adequate trials of antidepressant treatment may harbour hidden bipolar disorder.

We aimed to compare the rates of a change in diagnosis to bipolar disorder among people with major depressive disorder with stratified responses to antidepressants during an 8-year follow-up period.

Information on individuals with major depressive disorder identified during 2000 (cohort 2000, n = 1485) and 2003 (cohort 2003, n = 2459) were collected from a nationally representative cohort of 1 000 000 health service users in Taiwan. Participants responding well to antidepressants were compared with those showing poor responses to adequate trials of antidepressants.

In 7.6–12.1% of those with a diagnosis of unipolar major depressive disorder this diagnosis was subsequently changed to bipolar disorder, with a mean time to change of 1.89–2.98 years. Difficult-to-treat participants presented higher rates of change to a bipolar diagnosis (25.6% in cohort 2000; 26.6% in cohort 2003) than easy-to-treat participants (8.8–8.9% in cohort 2000; 6.8–8.6% in cohort 2003; P<0.0001). Regression analysis showed that the variable most strongly associated with the change in diagnosis was antidepressant use history. The difficult-to-treat participants were associated most with diagnostic changing (cohort 2000: odds ratio (OR) = 1.88 (95% CI 1.12–3.16); cohort 2003: OR = 4.94 (95% CI 2.81–8.68)).

This is the first large-scale study to report an association between antidepressant response history and subsequent change in diagnosis from major depressive disorder to bipolar disorder. Our findings support the view that a history of poor response to antidepressants in unipolar depression could be a useful predictor for bipolar diathesis.

Most previous attempts to determine the psychological cost of military deployment have been limited by reliance on convenience samples, lack of pre-deployment data or confidentiality and cross-sectional designs.

This study addressed these limitations using a population-based, prospective cohort of US military personnel deployed in support of the operations in Iraq and Afghanistan.

The sample consisted of US military service members in all branches including active duty, reserve and national guard who deployed once (n = 3393) or multiple times (n = 4394). Self-reported symptoms of post-traumatic stress were obtained prior to deployment and at two follow-ups spaced 3 years apart. Data were examined for longitudinal trajectories using latent growth mixture modelling.

Each analysis revealed remarkably similar post-traumatic stress trajectories across time. The most common pattern was low–stable post-traumatic stress or resilience (83.1% single deployers, 84.9% multiple deployers), moderate–improving (8.0%, 8.5%), then worsening–chronic posttraumatic stress (6.7%, 4.5%), high–stable (2.2% single deployers only) and high–improving (2.2% multiple deployers only). Covariates associated with each trajectory were identified.

The final models exhibited similar types of trajectories for single and multiple deployers; most notably, the stable trajectory of low post-traumatic stress pre- to post-deployment, or resilience, was exceptionally high. Several factors predicting trajectories were identified, which we hope will assist in future research aimed at decreasing the risk of post-traumatic stress disorder among deployers.