It has been suggested that some psychotic symptoms reflect ‘aberrant salience’, related to dysfunctional reward learning. To test this hypothesis we investigated whether patients with schizophrenia showed impaired learning of task-relevant stimulus–reinforcement associations in the presence of distracting task-irrelevant cues.

We tested 20 medicated patients with schizophrenia and 17 controls on a reaction time game, the Salience Attribution Test. In this game, participants made a speeded response to earn money in the presence of conditioned stimuli (CSs). Each CS comprised two visual dimensions, colour and form. Probability of reinforcement varied over one of these dimensions (task-relevant), but not the other (task-irrelevant). Measures of adaptive and aberrant motivational salience were calculated on the basis of latency and subjective reinforcement probability rating differences over the task-relevant and task-irrelevant dimensions respectively.

Participants rated reinforcement significantly more likely and responded significantly faster on high-probability-reinforced relative to low-probability-reinforced trials, representing adaptive motivational salience. Patients exhibited reduced adaptive salience relative to controls, but the two groups did not differ in terms of aberrant salience. Patients with delusions exhibited significantly greater aberrant salience than those without delusions, and aberrant salience also correlated with negative symptoms. In the controls, aberrant salience correlated significantly with ‘introvertive anhedonia’ schizotypy.

These data support the hypothesis that aberrant salience is related to the presence of delusions in medicated patients with schizophrenia, but are also suggestive of a link with negative symptoms. The relationship between aberrant salience and psychotic symptoms warrants further investigation in unmedicated patients.

Anger is the main deregulated emotion in patients with antisocial personality disorder (ASPD). The aim of this study was to examine emotional, cognitive and physiological correlates of anger and compare these between ASPD patients with varying degree of psychopathy (PP) and control groups.

Assessment of the effect of anger induction on self-reported emotions and schema modes, psychophysiology and implicit reaction-time tasks measuring self-anger and aggressor–swearword associations. Participants (n=147) were patients with DSM-IV antisocial (n=21), borderline (n=45) and cluster C personality disorder (n=46) and non-patient controls (n=35).

Groups did not differ in self-reported anger. ASPD patients displayed a decrease in heart rate and systolic blood pressure (SBP) and stronger implicit self-anger associations. ASPD patients scoring low on affective PP reported less negative emotions and displayed a greater decrease in diastolic blood pressure (DBP).

ASPD patients did not display a deviant self-reported anger but physiological hyporesponsivity and cognitive hyper-responsivity. This ASPD anger response might reflect a controlled predatory-like fight preparation.

The dual task paradigm (Baddeley et al.1986; Della Sala et al.1995) has been proposed as a sensitive measure of Alzheimer's dementia, early in the disease process.

We investigated this claim by administering the modified dual task paradigm (utilising a pencil-and-paper version of a tracking task) to 33 patients with amnestic mild cognitive impairment (aMCI) and 10 with very early Alzheimer's disease, as well as 21 healthy elderly subjects and 17 controls with depressive symptoms. All groups were closely matched for age and pre-morbid intellectual ability.

There were no group differences in dual task performance, despite poor performance in episodic memory tests of the aMCI and early Alzheimer's disease groups. In contrast, the Alzheimer patients were specifically impaired in the trail-making test B, another commonly used test of divided attention.

The dual task paradigm lacks sensitivity for use in the early differential diagnosis of Alzheimer's disease.

Impairments in inhibitory function have been found in studies of cognition in schizophrenia. These have been linked to a failure to adequately maintain the task demands in working memory. As response inhibition is known to occur in both voluntary and involuntary processes, an important question is whether both aspects of response inhibition are specifically impaired in people with schizophrenia.

The subjects were 33 patients presenting with a first episode of psychosis (27 with schizophrenia and six with schizo-affective disorder) and 24 healthy controls. We administered two motor response tasks: voluntary response inhibition was indexed by the stop-signal task and involuntary response inhibition by the masked priming task. We also administered neuropsychological measures of IQ and executive function to explore their associations with response inhibition.

Patients with schizophrenia compared to healthy controls showed significantly increased duration of the voluntary response inhibition process, as indexed by the stop-signal reaction time (SSRT). By contrast, there were no group differences on the pattern of priming on the masked priming task, indicative of intact involuntary response inhibition. Neuropsychological measures revealed that voluntary response inhibition is not necessarily dependent on working memory.

These data provide evidence for a specific impairment of voluntary response inhibition in schizophrenia.

Previous work suggests that daily life stress-sensitivity may be an intermediary phenotype associated with both genetic risk for depression and developmental stress exposures. In the current analysis we hypothesized that genetic risk for depression and three environmental exposures over the course of development [prenatal stress, childhood adversity and adult negative life events (NLEs)] combine synergistically to produce the phenotype of stress-sensitivity.

Twin pairs (n=279) participated in a momentary assessment study using the Experience Sampling Method (ESM), collecting appraisals of stress and negative affect (NA) in the flow of daily life. Prospective data on birthweight and gestational age, questionnaire data on childhood adversity and recent NLEs, and interview data on depression were used in the analyses. Daily life stress-sensitivity was modelled as the effect of ESM daily life stress appraisals on ESM NA.

All three developmental stress exposures were moderated by genetic vulnerability, modelled as dizygotic (DZ) or monozygotic (MZ) co-twin depression status, in their effect on daily life stress-sensitivity. Effects were much stronger in participants with MZ co-twin depression and a little stronger in participants with DZ co-twin depression status, compared to those without co-twin depression. NLE main effects and NLE genetic moderation were reducible to birthweight and childhood adversity.

The findings are consistent with the hypothesis that adult daily life stress-sensitivity is the result of sensitization processes initiated by developmental stress exposures. Genes associated with depression may act by accelerating the process of stress-induced sensitization.

Neurocognitive impairment is a well-recognized feature of depression that has been reported in younger and older adults. Similar deficits occur with ageing and it is unclear whether the greater deficits in late-life depression are an ageing-related phenomenon or due to a difference in the nature of late-life depression itself. We hypothesized that ageing alone would not fully explain the increased neurocognitive impairment in late-life depression but that differences in the illness explain the greater decrements in memory and executive function.

Comparison of the neuropsychological performance of younger (<60 years) and older (⩾60 years) adults with major depressive disorder (MDD) and healthy comparison subjects. Scores for each depression group were normalized against their respective age-matched control group and the primary comparisons were on four neurocognitive domains: (i) attention and executive function; (ii) verbal learning and memory; (iii) visuospatial learning and memory; and (iv) motor speed.

We recruited 75 subjects with MDD [<60 years (n=44), ⩾60 years (n=31)] and 82 psychiatrically healthy comparison subjects [<60 years (n=42), ⩾60 years (n=40)]. The late-life depression group had greater impairment in verbal learning and memory and motor speed but not in executive function. The two depressed groups did not differ in depression severity, global cognitive function, intelligence or education.

Late-life depression is associated with more severe impairment in verbal learning and memory and motor speed than depression in earlier adult life and this is not due to ageing alone.

Previous research has demonstrated that various types of verbal source memory error are associated with positive symptoms in patients with schizophrenia. Notably, intrusions in free recall have been associated with hallucinations and delusions. We tested the hypothesis that extra-list intrusions, assumed to arise from poor monitoring of internally generated words, are associated with verbal hallucinations and that intra-list intrusions are associated with global hallucination scores.

A sample of 41 patients with schizophrenia was administered four lists of words, followed by free recall. The number of correctly recalled words and the number of extra- and intra-list intrusions were tallied.

The verbal hallucination score was significantly correlated with the number of extra-list intrusions, whereas it was unrelated to the number of correctly recalled words. The number of intra-list intrusions was significantly correlated with the global, but not with the verbal, hallucination score in the subsample of hallucinating patients. It was marginally significantly correlated with the delusion score in delusional patients.

The data corroborate the view that verbal hallucinations are linked to defective monitoring of internal speech, and that errors in context processing are involved in hallucinations and delusions.

The correlates of insight in early-onset psychosis have received little previous attention.

We studied clinical correlates of insight in a sample of 110 adolescent recent-onset psychosis patients (mean age 15.53 years; psychotic symptoms present for <6 months). Insight was measured with the Scale to Assess Unawareness of Mental Disorder (SUMD) at baseline, 6 months and 12 months follow-up.

Insight improved over the early phases of the illness, in parallel with psychopathological improvement. Poor insight at baseline and 6 months correlated with poor functioning at 6 and 12 months respectively. Schizophrenia patients had poorer insight than patients with bipolar disorder at 6 and 12 months but not at baseline. Logistic and linear regressions were used to predict 12-month diagnoses and functioning based on insight measurements. Baseline awareness of illness was a significant predictor for diagnosis [odds ratio (OR) 1.4, 95% confidence interval (CI) 1.05–1.97]. Treatment compliance at 6 months did not correlate with baseline SUMD subscores, but correlated with insight into having a disorder (Spearman's ρ=0.21, p=0.039), its consequences (Spearman's ρ=0.28, p=0.006) and the need for treatment (Spearman's ρ=0.26, p=0.012) at 6 months. The ‘attribution of symptoms’ dimension of insight is poorly correlated with other insight dimensions and with other clinical variables.

Poor insight correlates with symptom severity and global functioning but also has some trait value for schizophrenia, which is apparent once acute psychotic symptomatology is not prominent. A multi-dimensional approach to the assessment of insight is necessary, as different dimensions are influenced by different factors.

Taxometric research on depression has yielded mixed results, with some studies supporting dimensional solutions and others supporting taxonic solutions. Although supplementary tests of construct validity might clarify these mixed findings, to date such analyses have not been reported. The present study represents a follow-up to our previous taxometric study of depression designed to evaluate the relative predictive validities of dimensional and categorical models of depression.

Two sets of dimensional and categorical models of depression were constructed from the depression items of the Composite International Diagnostic Interview: (1) empirically derived models obtained using latent structure analyses and (2) rationally selected models, including an additive depressive symptoms scale (dimensional) and DSM major depressive episodes (categorical). Both sets of dimensional and categorical models were compared in terms of their abilities to predict various clinically relevant outcomes (psychiatric diagnoses and impairment).

Factor analyses suggested a two-factor model (‘cognitive–affective’ and ‘somatic’ symptoms) and latent class analyses suggested a three-class model (‘severe depression’, ‘moderate depression’ and ‘cognitive–affective distress’). In predictive analyses that simultaneously included dimensional and categorical models as predictors, the dimensional models remained significant unique predictors of outcomes while the categorical models did not.

Both dimensional models provided superior predictive validity relative to their categorical counterparts. These results provide construct validity evidence for the dimensional findings from our previous taxometric study and thus inspire confidence in dimensional conceptualizations of depression. It remains for future research to evaluate the construct validity of the taxonic solutions reported in the literature.

Previous surveys on depression in China focused on prevalence estimates without providing a detailed epidemiological profile.

Face-to-face household interviews were conducted with a multi-stage household probability sample of 2633 adults (age ⩾18 years) in Beijing and 2568 in Shanghai between November 2001 and February 2002. The World Health Organization Composite International Diagnostic Interview (CIDI) was used to assess major depressive episode (MDE) according to Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV criteria.

The lifetime prevalence and 1-year prevalence estimates of DSM-IV/CIDI MDE were 3.6% [95% confidence interval (CI) 2.8–4.4%] and 1.8% (95% CI 1.2–2.4%) respectively. No significant gender difference was found in these estimates. Respondents born in 1967 or later were at elevated lifetime risk compared with respondents born in earlier cohorts. The mean age of onset was 30.3 years. Among those reporting 1-year MDE, 15.7, 51.8, 25.3 and 6.4% reported mild, moderate, severe and very severe symptoms respectively; 4.8, 2.6 and 3.2% reported suicidal ideation, plans, and recent attempts in the same year respectively. Respondents with 1-year MDE reported a mean of 27.5 days out of role owing to their depression in the year before interview. Significant co-morbidity was found between MDE and other mental disorders [odds ratio (OR) 22.0] and chronic physical disorders (OR 3.2). Only 22.7% of respondents with 1-year MDE sought treatment.

The low prevalence and insignificant gender difference, but not patterns of onset, course, co-morbidity, and impairment, distinguish the epidemiological profile of MDE in metropolitan China from those in other countries.

There is growing evidence for the familiality of pediatric bipolar disorder (BPD) and its association with impairments on measures of processing speed, verbal learning and ‘executive’ functions. The current study investigated whether these neurocognitive impairments index the familial risk underlying the diagnosis.

Subjects were 170 youth with BPD (mean age 12.3 years), their 118 non-mood-disordered siblings and 79 non-mood-disordered controls. Groups were compared on a battery of neuropsychological tests from the Wechsler Intelligence Scales, the Stroop Color Word Test, the Wisconsin Card Sorting Test (WCST), the Rey–Osterrieth Complex Figure (ROCF), an auditory working memory Continuous Performance Test (CPT) and the California Verbal Learning Test – Children's Version (CVLT-C). Measures were factor analyzed for data reduction purposes. All analyses controlled for age, sex and attention-deficit/hyperactivity disorder (ADHD).

Principal components analyses with a promax rotation yielded three factors reflecting: (1) processing speed/verbal learning, (2) working memory/interference control and (3) abstract problem solving. The CPT working memory measure with interference filtering demands (WM INT) was only administered to subjects aged ⩾12 years and was therefore analyzed separately. BPD youth showed impairments versus controls and unaffected relatives on all three factors and on the WM INT. Unaffected relatives exhibited impairments versus controls on the abstract problem-solving factor and the WM INT. They also showed a statistical trend (p=0.07) towards worse performance on the working memory/interference control factor.

Neurocognitive impairments in executive functions may reflect the familial neurobiological risk mechanisms underlying pediatric BPD and may have utility as endophenotypes in molecular genetic studies of the condition.

A key neuropsychological proposal in schizophrenia is that negative and disorganization symptoms are associated with different patterns of impairment on executive tasks.

Studies reporting correlations between positive, negative or disorganization symptoms and any type of executive test were meta-analysed. The influence of moderating factors was also examined, including age, treatment and stage of illness and whether symptoms were relapsing or persistent. The magnitudes of the correlations were compared with those for general intellectual impairment.

Pooled correlations between executive impairment and both negative symptoms and disorganization were significant in the small-to-moderate range. That for positive symptoms (‘reality distortion’), however, was close to zero. The pattern of correlations among different executive tests differed significantly for negative symptoms and disorganization. Patients with stable clinical pictures showed significantly higher correlations with executive impairment than those with relapsing and remitting illnesses. Both negative symptoms and disorganization also correlated significantly with general intellectual function as indexed by current IQ.

Meta-analysis supports the view that negative symptoms and disorganization are associated with partially dissociable patterns of executive impairment. However, co-existent general intellectual impairment has been an important confounding factor in the studies to date.

The relationship between mental and physical disorders is well established, but there is less consensus as to the nature of their joint association with disability, in part because additive and interactive models of co-morbidity have not always been clearly differentiated in prior research.

Eighteen general population surveys were carried out among adults as part of the World Mental Health (WMH) Survey Initiative (n=42 697). DSM-IV disorders were assessed using face-to-face interviews with the Composite International Diagnostic Interview (CIDI 3.0). Chronic physical conditions (arthritis, heart disease, respiratory disease, chronic back/neck pain, chronic headache, and diabetes) were ascertained using a standard checklist. Severe disability was defined as on or above the 90th percentile of the WMH version of the World Health Organization Disability Assessment Schedule (WHODAS-II).

The odds of severe disability among those with both mental disorder and each of the physical conditions (with the exception of heart disease) were significantly greater than the sum of the odds of the single conditions. The evidence for synergy was model dependent: it was observed in the additive interaction models but not in models assessing multiplicative interactions. Mental disorders were more likely to be associated with severe disability than were the chronic physical conditions.

This first cross-national study of the joint effect of mental and physical conditions on the probability of severe disability finds that co-morbidity exerts modest synergistic effects. Clinicians need to accord both mental and physical conditions equal priority, in order for co-morbidity to be adequately managed and disability reduced.

Despite its importance as a paradigmatic personality disorder, little is known about the measurement invariance of the DSM-IV borderline personality disorder (BPD) criteria; that is, whether the criteria assess the disorder equivalently across different groups.

BPD criteria were evaluated at interview in 2794 young adult Norwegian twins. Analyses, based on item-response modeling, were conducted to test for differential age and sex moderation of the individual BPD criteria characteristics given factor-level covariate effects.

Confirmatory factor analytic results supported a unidimensional structure for the nine BPD criteria. Compared to males, females had a higher BPD factor mean, larger factor variance and there was a significant age by sex interaction on the factor mean. Strong differential sex and age by sex interaction effects were found for the ‘impulsivity’ criterion factor loading and threshold. Impulsivity related to the BPD factor poorly in young females but improved significantly in older females. Males reported more impulsivity compared to females and this difference increased with age. The ‘affective instability’ threshold was also moderated, with males reporting less than expected.

The results suggest the DSM-IV BPD ‘impulsivity’ and ‘affective instability’ criteria function differentially with respect to age and sex, with impulsivity being especially problematic. If verified, these findings have important implications for the interpretation of prior research with these criteria. These non-invariant age and sex effects may be identifying criteria-level expression features relevant to BPD nosology and etiology. Criterion functioning assessed using modern psychometric methods should be considered in the development of DSM-V.

Anhedonia and stress sensitivity have been identified as promising depressive phenotypes. Research suggests that stress-induced anhedonia is a possible mechanism underlying the association between stress and depression. The present proof-of-concept study assessed whether hedonic capacity and stress perception are heritable and whether their genetic and environmental contributions are shared.

Twenty monozygotic (MZ) and 15 dizygotic (DZ) twin pairs completed a probabilistic reward task that provides an objective behavioral measure of hedonic capacity (reward responsiveness) and completed several questionnaires including the Perceived Stress Scale (PSS). Bivariate Cholesky models were used to investigate whether covariation between (1) depressive symptoms and hedonic capacity, (2) depressive symptoms and perceived stress, and (3) perceived stress and hedonic capacity resulted from shared or residual genetic and environmental factors.

Additive genetic (A) and individual-specific environment (E) factors contributed to 46% and 54% of the variance in hedonic capacity, respectively. For perceived stress, 44% and 56% of the variance was accounted for by A and E factors, respectively. The genetic correlation between depression and hedonic capacity was moderate (ra=0.29), whereas the correlation between depression and stress perception was large (ra=0.67). Genetic and environmental correlations between hedonic capacity and stress perception were large (ra=0.72 and re=−0.43).

The present study provides initial feasibility for using a twin approach to investigate genetic contributions of a laboratory-based anhedonic phenotype. Although these preliminary findings indicate that hedonic capacity and perceived stress are heritable, with substantial shared additive genetic contributions, replications in larger samples will be needed.

Little information exists on treatment effectiveness in antisocial personality disorder (ASPD). We investigated the feasibility and effectiveness of carrying out a randomized controlled trial of cognitive behaviour therapy (CBT) in men with ASPD who were aggressive.

This was an exploratory two-centre, randomized controlled trial in a community setting. Fifty-two adult men with a diagnosis of ASPD, with acts of aggression in the 6 months prior to the study, were randomized to either treatment as usual (TAU) plus CBT, or usual treatment alone. Change over 12 months of follow-up was assessed in the occurrence of any act of aggression and also in terms of alcohol misuse, mental state, beliefs and social functioning.

The follow-up rate was 79%. At 12 months, both groups reported a decrease in the occurrence of any acts of verbal or physical aggression. Trends in the data, in favour of CBT, were noted for problematic drinking, social functioning and beliefs about others.

CBT did not improve outcomes more than usual treatment for men with ASPD who are aggressive and living in the community in this exploratory study. However, the data suggest that a larger study is required to fully assess the effectiveness of CBT in reducing aggression, alcohol misuse and improving social functioning and view of others. It is feasible to carry out a rigorous randomized controlled trial in this group.