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.

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.

Recent studies among males have reported a genotype–environment interaction (G×E) in which low-activity alleles at the monoamine oxidase A (MAOA) locus conferred greater sensitivity to the effects of childhood adversity on risk for conduct disorder (CD). So far, few studies of females have controlled for gene–environment correlation or used females heterozygous for this X-linked gene.

Logistic regression analysis of a sample of 721 females ages 8–17 years from the longitudinal Virginia Twin Study of Adolescent Behavioral Development (VTSABD) assessed the additive effects of MAOA genotypes on risk for CD, together with the main effect of childhood adversity and parental antisocial personality disorder (ASP), as well as the interaction of MAOA with childhood adversity on risk for CD.

A significant main effect of genotype on risk for CD was detected, where low-activity MAOA imparted the greatest risk to CD in girls while controlling for the significant effects of maternal ASP and childhood adversity. Significant G×E with weak effect was detected when environmental exposure was untransformed, indicating a higher sensitivity to childhood adversity in the presence of the high-activity MAOA allele. The interaction was no longer statistically significant after applying a ridit transformation to reflect the sample sizes exposed at each level of childhood adversity.

The main effect of MAOA on risk for CD in females, its absence in males and directional difference of interaction is suggestive of genotype–sex interaction. As the effect of G×E on risk for CD was weak, its inclusion is not justified.

Psychological literature and clinical lore suggest that there may be systematic differences in how various demographic groups experience depressive symptoms, particularly somatic symptoms. The aim of the current study was to use methods based on item response theory (IRT) to examine whether, when equating for levels of depression symptom severity, there are demographic differences in the likelihood of reporting DSM-IV depression symptoms.

We conducted a secondary analysis of a subset (n=13 753) of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) dataset, which includes a large epidemiological sample of English-speaking Americans. We compared data from women and men, Hispanics and non-Hispanic Whites, African Americans and Whites, Asian Americans and Whites, and American Indians and Whites.

There were few differences overall, although the differences that we did find were primarily limited to somatic symptoms, and particularly appetite and weight disturbance.

For the most part, individuals responded similarly to the criteria used to diagnose major depression across gender and across English-speaking racial and ethnic groups in the USA.

Cognitive performance is often impaired in depression, and these impairments can persist even after remission from psychopathological symptoms. However, it is still unclear whether cognitive dysfunction is associated with psychopathological symptoms or represents a genuine disorder. This study examined cognitive performance in acute depression, after remission, and 6 months after remission in order to determine the nature and specificity of cognitive dysfunction as well as its relevance for the further course of depression.

Assessments of cognitive function and psychopathology were carried out on admission and prior to discharge in 53 in-patients with unipolar depression. Twenty patients were retested 6 months after discharge. To correct for practice effects, 13 healthy subjects were included and assessed twice with the same cognitive tests.

In acute depression, we found impairments of information processing/attention, memory, and executive functions. Cognitive impairments remained in a high proportion of patients, even after remission of psychopathological symptoms. After correcting for practice effects, a significant improvement was observed only for some tests of executive functioning. Severity of depression was only weakly correlated with one single cognitive measure, indicating that psychopathological and neuropsychological symptoms are dissociable. Furthermore, we found no evidence for specific cognitive dysfunction.

Our results support the hypothesis that cognitive impairments in depression are neither selective nor specific; they have trait-like features and are, therefore, not merely an epiphenomenon of depression. Whether or not cognitive dysfunction is a prognostic marker for the course of depression remains still an open issue.

Much about the long-term course of anxiety disorders is unknown. The present study utilizes a naturalistic, longitudinal, short-interval follow-up design to elucidate the course of anxiety disorders over 14 years in a largely middle-aged adult sample recruited from out-patient psychiatry and primary care facilities.

The sample consisted of 453 participants with a diagnosis of panic disorder (PD), social phobia (SP) and/or generalized anxiety disorder (GAD). Anxiety symptom ratings were tracked using weekly psychiatric status ratings (PSRs). Controlling for demographic and clinical variables, the course of PD, GAD and SP were examined using longitudinal growth models, with the most severe PSR at each follow-up point as the main outcome variable.

PSRs significantly decreased in severity over time in each of the three disorders. In the interaction effects models, age×time had a significant effect on course for PD and GAD, but not for SP, in that older age was associated with lower PSRs over time.

The present findings suggest that the severity of anxiety disorders declines over time, although this decline is modest and depends on the specific disorder being assessed. Older individuals with PD and GAD have a better prognosis than their younger counterparts, as their course is characterized by a steeper decline in severity. The present findings provide important information about the course of anxiety disorders in mid-life.

Birth cohort studies have shown that individuals who develop non-affective psychoses display subtle deviations in behaviour during childhood and adolescence. We had the opportunity to examine the widely used Child Behavior Checklist (CBCL) and the Youth Self-Report (YSR) to explore the antecedents of non-affective psychosis.

Based on a birth cohort of 3801 young adults, psychopathology was assessed at years 5 and 14 using the CBCL and/or the YSR. Screen-positive non-affective psychosis (SP-NAP) was assessed at year 21 by using the Composite International Diagnostic Interview (CIDI) or a self-report checklist. The association between childhood symptoms and SP-NAP was examined using logistic regression.

Of the cohort, 60 subjects were classified as SP-NAP. In males, SP-NAP was associated with higher scores: (a) on year 5 CBCL ‘Total’, ‘Aggression’ and ‘Social, Attention and Thought’ scores; (b) on year 14 CBCL ‘Social’, ‘Attention’ and ‘Delinquency’ scores, and (c) YSR ‘Total’ and many YSR subscores. These associations were less clear for females. Hallucinations at year 14 were associated with SP-NAP for both sexes. Boys with high ‘Total’ scores at both years 5 and 14 were at greatest risk of SP-NAP (a 5-fold risk), followed by boys and girls whose ‘Social, Attention and Thought’ scores either increased or remained high from years 5 to 14 (3- to 13-fold risk).

Individuals who screen positive for non-affective psychosis show increased psychopathology during childhood and adolescence. The psychopathological trajectory of children who go on to develop schizophrenia anticipates the heterogeneity associated with the full clinical syndrome.

Schizophrenia patients show disturbances on a range of tasks that assess mentalizing or ‘Theory of Mind’ (ToM). However, these tasks are often developmentally inappropriate, make large demands on verbal abilities and explicit problem-solving skills, and involve after-the-fact reflection as opposed to spontaneous mentalizing.

To address these limitations, 55 clinically stable schizophrenia out-patients and 44 healthy controls completed a validated Animations Task designed to assess spontaneous attributions of social meaning to ambiguous abstract visual stimuli. In this paradigm, 12 animations depict two geometric shapes ‘interacting’ with each other in three conditions: (1) ToM interactions that elicit attributions of mental states to the agents, (2) Goal-Directed (GD) interactions that elicit attributions of simple actions, and (3) Random scenes in which no interaction occurs. Verbal descriptions of each animation are rated for the degree of Intentionality attributed to the agents and for accuracy.

Patients had lower Intentionality ratings than controls for ToM and GD scenes but the groups did not significantly differ for Random scenes. The descriptions of the patients less closely matched the situations intended by the developers of the task. Within the schizophrenia group, performance on the Animations Task showed minimal associations with clinical symptoms.

Patients demonstrated disturbances in the spontaneous attribution of mental states to abstract visual stimuli that normally evoke such attributions. Hence, in addition to previously established impairment on mentalizing tasks that require logical inferences about others' mental states, individuals with schizophrenia show disturbances in implicit aspects of mentalizing.

Interpersonal communication problems are common among persons with schizophrenia and may be linked, in part, to deficits in theory of mind (ToM), the ability to accurately perceive the attitudes, beliefs and intentions of others. Particular difficulties might be expected in the processing of counterfactual information such as sarcasm or lies.

The present study included 50 schizophrenia or schizo-affective out-patients and 44 demographically comparable healthy adults who were administered Part III of The Awareness of Social Inference Test (TASIT; a measure assessing comprehension of sarcasm versus lies) as well as measures of positive and negative symptoms and community functioning.

TASIT data were analyzed using a 2 (group: patients versus healthy adults)×2 (condition: sarcasm versus lie) repeated-measures ANOVA. The results show significant effects for group, condition, and the group×condition interaction. Compared to controls, patients performed significantly worse on sarcasm but not lie scenes. Within-group contrasts showed that patients performed significantly worse on sarcasm versus lie scenes; controls performed comparably on both. In patients, performance on TASIT showed a significant correlation with positive, but not negative, symptoms. The group and interaction effects remained significant when rerun with a subset of patients with low-level positive symptoms. The findings for a relationship between TASIT performance and community functioning were essentially negative.

The findings replicate a prior demonstration of difficulty in the comprehension of sarcasm using a different test, but are not consistent with previous studies showing global ToM deficits in schizophrenia.

Despite the popularity of inner-speech theories of auditory verbal hallucinations (AVHs), little is known about the phenomenological qualities of inner speech in patients with schizophrenia who experience AVHs (Sz-AVHs), or how this compares to inner speech in the non-voice-hearing general population.

We asked Sz-AVHs (n=29) and a non-voice-hearing general population sample (n=42) a series of questions about their experiences of hearing voices, if present, and their inner speech.

The inner speech reported by patients and controls was found to be almost identical in all respects. Furthermore, phenomenological qualities of AVHs (e.g. second- or third-person voices) did not relate to corresponding qualities in inner speech.

No discernable differences were found between the inner speech reported by Sz-AVHs and healthy controls. Implications for inner-speech theories of AVHs are discussed.

There may be important public health implications of increasing our knowledge of factors associated with age of dementia onset. The pre-morbid personality domain of Neuroticism constituted an interesting and theoretically plausible, yet uninvestigated, candidate for such an association. We aimed to examine whether midlife Neuroticism was associated with earlier age of onset of Alzheimer's disease (AD).

This was a case–comparison study of 213 patients with probable AD. Detailed clinical information was collected for all patients including age of onset of dementia symptoms. One or two knowledgeable informants rated each patient's midlife personality retrospectively using the Neuroticism, Extraversion, Openness Five-Factor Inventory (NEO-FFI) questionnaire. The relationship between midlife Neuroticism and age of dementia onset was evaluated using both correlational analysis and backward linear regression analysis.

Midlife Neuroticism predicted younger age of dementia onset in females but not in males. The association found in females was independent of pre-morbid history of affective disorder.

This finding and its potential mechanism warrant further investigation.

Individuals with Down's syndrome (DS) are at high risk of developing Alzheimer's disease (AD). However, few studies have investigated brain anatomy in DS individuals with AD.

We compared whole brain anatomy, as measured by volumetric magnetic resonance imaging (MRI), in DS individuals with and without AD. We also investigated whether volumetric differences could reliably classify DS individuals according to AD status. We used volumetric MRI and manual tracing to examine regional brain anatomy in 19 DS adults with AD and 39 DS adults without AD.

DS individuals with AD had significantly smaller corrected volumes bilaterally of the hippocampus and caudate, and right amygdala and putamen, and a significantly larger corrected volume of left peripheral cerebrospinal fluid (CSF), compared to DS individuals without AD. The volume of the hippocampus and caudate nucleus correctly categorized 92% and 92% respectively of DS individuals without AD, and 75% and 80% respectively of DS individuals with AD.

DS individuals with AD have significant medial temporal and striatal volume reductions, and these may provide markers of clinical AD.

Diagnosing attention deficit hyperactivity disorder (ADHD) in adults is difficult when diagnosticians cannot establish onset prior to the DSM-IV criterion of age 7 or if the number of symptoms does not achieve the DSM threshold for diagnosis. Previous work has assessed the validity of such diagnoses based on psychiatric co-morbidity, family history and neuropsychological functions but none of these studies have used personality as a validation criterion.

We compared four groups of adults: (1) full ADHD subjects who met all DSM-IV criteria for childhood-onset ADHD; (2) late-onset subjects who met all criteria except the age at onset criterion, (3) subthreshold subjects who did not meet full symptom criteria and (4) non-ADHD subjects who did not meet any of the above criteria. Diagnoses were made by using the Structured Clinical Interview for DSM-IV (SCID) and the Temperament and Character Inventory (TCI) was used to assess personality traits.

We found that full ADHD and late-onset ADHD showed similar personality profiles with significant deviations on all TCI scales except reward dependence and self-transcendence. By contrast, subthreshold cases only showed deviations on novelty seeking and self-directiveness.

These data call into question the stringent age of onset of ADHD symptom criteria for adults when making retrospective diagnoses of ADHD. Subthreshold ADHD seems to be a milder form of the disorder that is consistent with dimensional views of the disorder.