Mood lability is a concept widely used. However, data on its prevalence and morbid associations are scarce. We sought to establish the occurrence and importance of mood lability in a large community sample of children and adolescents by testing a priori hypotheses.

Cross-sectional data were taken from a national mental health survey including 5326 subjects aged 8–19 years in the UK. The outcomes were prevalence and characteristics of mood lability and its associations with psychopathology and overall impairment.

Mood lability occurred in more than 5% of the population of children and adolescents, both by parent and self-report. Mood lability was strongly associated with a wide range of psychopathology and was linked to significant impairment even in the absence of psychiatric disorders. Mood lability was particularly strongly associated with co-morbidity between internalizing and externalizing disorders, even when adjusting for the association with individual disorders. The pattern of results did not change after excluding youth with bipolar disorder or with episodes of elated mood.

Clinically significant mood lability is relatively common in the community. Our findings indicate that mood lability is not a mere consequence of other psychopathology in that it is associated with significant impairment even in the absence of psychiatric diagnoses. Moreover, the pattern of association of mood lability with co-morbidity suggests that it could be a risk factor shared by both internalizing and externalizing disorders. Our data point to the need for greater awareness of mood lability and its implications for treatment.

This analysis aimed to show whether symptoms of either pole change in their persistence as individuals move through two decades, whether such changes differ by age grouping, and whether age of onset plays an independent role in symptom persistence.

Participants in the National Institute of Mental Health (NIMH) Collaborative Depression Study (CDS) who completed at least 20 years of follow-up and who met study criteria for bipolar I or schizo-affective manic disorder, before intake or during follow-up, were divided by age at intake into youngest (18–29 years, n=56), middle (30–44 years, n=68) and oldest (>44 years, n=24) groups.

The persistence of depressive symptoms increased significantly in the two younger groups. Earlier ages of onset were associated with higher depressive morbidity throughout the 20 years of follow-up but did not predict changes in symptom persistence. The proportions of weeks spent in episodes of either pole correlated across follow-up periods in all age groupings, although correlations were stronger for depressive symptoms and for shorter intervals.

Regardless of age at onset, the passage of decades in bipolar illness seems to bring an increase in the predominance of depressive symptoms in individuals in their third, fourth and fifth decades and an earlier age of onset portends a persistently greater depressive symptom burden. The degree to which either depression or manic/hypomanic symptoms persist has significant stability over lengthy periods and seems to reflect traits that manifest early in an individual's illness.

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.

Previous studies have reported prefrontal cortex (PFC) pathophysiology in bipolar disorder.

We examined the hemodynamics of the PFC during resting and cognitive tasks in 29 patients with bipolar disorder and 27 healthy controls, matched for age, verbal abilities and education. The cognitive test battery consisted of letter and category fluency (LF and CF), Sets A and B of the Raven's Colored Progressive Matrices (RCPM-A and RCPM-B) and the letter cancellation test (LCT). The tissue oxygenation index (TOI), the ratio of oxygenated hemoglobin (HbO2) concentration to total hemoglobin concentration, was measured in the bilateral PFC by spatially resolved near-infrared spectroscopy. Changes in HbO2 concentration were also measured.

The bipolar group showed slight but significant impairment in performance for the non-verbal tasks (RCPM-A, RCPM-B and LCT), with no significant between-group differences for the two verbal tasks (LF and CF). A group×task×hemisphere analysis of variance (ANOVA) on the TOI revealed an abnormal pattern of prefrontal oxygenation across different types of cognitive processing in the bipolar group. Post hoc analyses following a group×task×hemisphere ANOVA on HbO2 concentration revealed that the bipolar group showed a greater increase in HbO2 concentration in the LCT and in RCPM-B, relative to controls.

Both indices of cortical activation (TOI and HbO2 concentration) indicated a discrepancy in the PFC function between verbal versus non-verbal processing, indicating task-specific abnormalities in the hemodynamic control of the PFC in bipolar disorder.

Impaired P300 auditory response has been reported in patients with psychotic bipolar disorder (BPD) and unaffected relatives of psychotic bipolar patients. Deficits in mismatch negativity (MMN), however, have not been observed in bipolar patients. To our knowledge, no family study of MMN in BPD has been reported. The current study combined the Maudsley twin and bipolar family samples using genetic model fitting analyses to: (1) assess the relationship between BPD and MMN, (2) substantiate the association between psychotic BPD and P300 variables, (3) verify the genetic overlap of BPD with P300 amplitude previously reported in the twin sample, and (4) examine the shared genetic influences between BPD and bilateral temporal scalp locations of P300 components.

A total of 301 subjects were included in this study, including 94 twin pairs, 31 bipolar families, and 39 unrelated healthy controls. Statistical analyses were based on structural equation modelling.

Both P300 and MMN are heritable, with heritability estimates of 0.58 for MMN, 0.68–0.80 for P300 amplitude, and 0.21–0.56 for P300 latency. The bipolar patients and their relatives showed normal MMN. No significant association, either genetic or environmental, was found with BPD. BPD was significantly associated with reduced P300 amplitude and prolonged latency on midline and bilateral temporal-posterior scalp areas. Shared genetic factors were the main source of these associations.

The results confirm that MMN is not an endophenotype for psychotic BPD whereas P300 amplitude and latency components are valid endophenotypes for psychotic BPD.

Bipolar disorder and schizophrenia have both been associated with deficits in extra-dimensional set shifting (EDS). Deficits in reversal learning (RL) have also been shown in schizophrenia but not in bipolar disorder. This study sought to assess the specificity of these findings in a direct comparison of clinically stable patients with each disorder.

The intra-dimensional/extra-dimensional (IDED) set-shifting task, part of the Cambridge Neuropsychological Test Automated Battery (CANTAB), was administered to 30 patients with schizophrenia, 47 with bipolar disorder and a group of 44 unaffected controls. EDS and RL errors were compared between the groups and related to measures of current and past psychiatric symptoms and medication.

Both groups of patients with schizophrenia or bipolar disorder made more EDS and RL errors than controls. Neither measure separated the two disorders, even when the analysis was restricted to euthymic patients. No relationship was found with prescribed medication.

Patients with bipolar disorder or schizophrenia show common deficits in EDS and RL. These deficits do not seem to be attributable to current symptoms and are consistent with disrupted networks involving the ventral prefrontal cortex.

Suicide tends to concentrate in disadvantaged neighborhoods, and neighborhood disadvantage is associated with many important risk factors for youth suicide. However, no study has directly investigated the link between neighborhood poverty and youth suicidal behaviors, while controlling for pre-existing vulnerabilities. The objective of this study was to determine whether living in a poor neighborhood is associated with suicidal thoughts and attempts in late adolescence over and above background vulnerabilities, and whether this association can be explained by late-adolescence psychosocial risks: depression, social support, negative life events (NLEs), delinquent activities, substance abuse and exposure to suicide. The potential moderating role of neighborhood poverty was also examined.

A subset of 2776 participants was selected from the Canadian National Longitudinal Survey of Children and Youth (NLSCY). Late-adolescence suicidal behaviors and risk factors were self-reported. The 2001 Canadian Census was used to characterize neighborhoods during early and middle adolescence. Late-childhood family and individual controls were assessed through parent-report.

At the bivariate level, the odds of reporting suicidal thoughts were about twice as high in poor than non-poor neighborhoods, and the odds of attempting suicide were about four times higher. After controlling for background vulnerabilities, neighborhood poverty remained significantly associated with both suicidal thoughts and attempts. However, these associations were not explained by late-adolescence psychosocial risks. Rather, youth living in poor neighborhoods may be at greater risk through the amplification of other risk factors in disadvantaged neighborhoods.

Potential explanations for the increased vulnerability of youth living in poor neighborhoods are discussed.

The impact of antidepressant drug treatment (ADT) on the risk of suicide is uncertain. The aim of this study was to determine in a real-life setting whether ADT is associated with an increased or a reduced risk of suicide compared to absence of ADT (no-ADT) in patients with depression.

A decision analysis method was used to estimate the number of suicides prevented or induced by ADT in children and adolescents (10–19 years old), adults (20–64 years old) and the elderly (⩾65 years) diagnosed with major depression. The impact of gender and parasuicide history on the findings was explored within each age group. Sensitivity analyses were used to assess the robustness of the models.

Prescribing ADT to all patients diagnosed with depression would prevent more than one out of three suicide deaths compared to the no-ADT strategy, irrespective of age, gender or parasuicide history. Sensitivity analyses showed that persistence in taking ADT would be the main characteristic influencing the effectiveness of ADT on suicide risk.

Public health decisions that contribute directly or indirectly to reducing the number of patients with depression who are effectively administered ADT may paradoxically induce a rise in the number of suicides.

The relationship between the Bali (Indonesia) bombings of October 2002 and suicide has not previously been investigated, despite anecdotal evidence of the economic and psychological consequences of these attacks.

Suicide rates were calculated over the period 1994–2006 in three Bali regencies to determine whether suicide increased in the period following the first Bali bombings. Poisson regression and time-series models were used to assess the change in suicide rates by sex, age and area in the periods before and after October 2002.

Suicide rates (age-adjusted) increased in males from an average of 2.84 (per 100 000) in the period pre-2002 to 8.10 in the period post-2002, and for females from 1.51 to 3.68. The greatest increases in suicide in the post-2002 period were in the age groups 20–29 and ⩾60 years, for both males and females. Tourist arrivals fell significantly after the bombings, and addition of tourism to models reduced relative risk estimates of suicide, suggesting that some of the increase may be attributable to the socio-economic effects of declines in tourism.

There was an almost fourfold increase in male suicide risk and a threefold increase in female suicide risk in the period following the 2002 bombings in Bali. Trends in tourism did not account for most of the observed increases. Other factors such as indirect socio-economic effects and Balinese notions of collective guilt and anxieties relating to ritual neglect are important in understanding the rise in suicide in the post-2002 period.

Because the diagnosis of attention deficit hyperactivity disorder (ADHD) in higher education settings is rapidly becoming a contentious issue, particularly among patients with high IQs, we sought to assess the validity of diagnosing ADHD in high-IQ adults and to further characterize the clinical features associated with their ADHD.

We operationalized high IQ as having a full-scale IQ⩾120. We identified 53 adults with a high IQ who did not have ADHD and 64 adults with a high IQ who met diagnostic criteria for ADHD. Groups did not differ on IQ, socio-economic status or gender.

High-IQ adults with ADHD reported a lower quality of life, had poorer familial and occupational functioning, and had more functional impairments, including more speeding tickets, accidents and arrests. Major depressive disorder, obsessive-compulsive disorder and generalized anxiety disorder diagnoses were higher in high-IQ adults with ADHD. All other psychiatric co-morbidities, including antisocial personality disorder and substance abuse, did not differ between the two high-IQ groups. ADHD was more prevalent in first-degree relatives of adults with ADHD relative to controls.

Our data suggest that adults with ADHD and a high IQ display patterns of functional impairments, familiality and psychiatric co-morbidities that parallel those found in the average-IQ adult ADHD population.

Despite the growing recognition that the clinical symptom characteristics associated with attention deficit hyperactivity disorder (ADHD) persist into adulthood in a high proportion of subjects, little is known about the persistence of neurocognitive deficits in ADHD. The objective was twofold: (1) to conduct a meta-analysis of neuropsychological studies to characterize attentional performance in subjects with adult ADHD by examining differences in ADHD versus normal control subjects; and (2) to investigate whether these differences vary as a function of age and gender.

Twenty-five neuropsychological studies comparing subjects with adult ADHD and healthy controls were evaluated. Statistical effect size was determined to characterize the difference between ADHD and control subjects. Meta-regression analysis was applied to investigate whether the difference between ADHD and control subjects varied as a function of age and gender across studies.

Tests measuring focused and sustained attention yielded an effect size with medium to large magnitude whereas tests of simple attention resulted in a small to medium effect size in terms of poorer attention functioning of ADHD subjects versus controls. On some of the measures (e.g. Stroop interference), a lower level of attention functioning in the ADHD group versus the controls was associated with male gender.

Adult ADHD subjects display significantly poorer functioning versus healthy controls on complex but not on simple tasks of attention, and the degree of impairment varies with gender, with males displaying a higher level of impairment.

Although several studies have examined brainstem volume in autism, results have been mixed and no investigation has specifically measured gray- and white-matter structures. The aim of this investigation was to assess gray- and white-matter volumes in children with autism.

Subjects included 22 right-handed, non-mentally retarded boys with autism and 22 gender- and age-matched controls. Magnetic resonance imaging (MRI) scans were obtained using a 1.5-T scanner and volumetric measurements were performed using the BRAINS2 software package. Gray- and white-matter volumes were measured using a semi-automated segmentation process.

There were no significant differences in age and total brain volume (TBV) between the two groups but full-scale IQ was higher in controls. A decrease in brainstem gray-matter volume was observed in the autism group before and after controlling for TBV. No significant differences were observed in white-matter volume. A significant relationship was observed between brainstem gray-matter volume and oral sensory sensitivity as measured by the Sensory Profile Questionnaire (SPQ).

Findings from this study are suggestive of brainstem abnormalities in autism involving gray-matter structures with evidence supporting the existence of a relationship between these alterations and sensory deficits. These results are consistent with previous investigations and support the existence of disturbances in brainstem circuitry thought to be implicated in the sensory dysfunction observed in autism.

Calendar calculation is the ability to quickly name the day that a given date falls on. Previous research has suggested that savant calendar calculation is based on rote memory and the use of rule-based arithmetic skills. The objective of this study was to identify the cognitive processes that distinguish calendar calculation in savant individuals from healthy calendar calculators.

Savant calendar calculators with autism (ACC, n=3), healthy calendar calculators (HCC, n=3), non-savant subjects with autism (n=6) and healthy calendar calculator laymen (n=18) were included in the study. All participants calculated dates of the present (current month). In addition, ACC and HCC also calculated dates of the past and future 50 years.

ACC showed shorter reaction times and fewer errors than HCC and non-savant subjects with autism, and significantly fewer errors than healthy calendar calculator laymen when calculating dates of the present. Moreover, ACC performed faster and more accurate than HCC regarding past dates. However, no differences between ACC and HCC were detected for future date calculation.

The findings may imply distinct calendar calculation strategies in ACC and HCC, with HCC relying on calendar regularities for all types of dates and an involvement of (rote) memory in ACC when processing dates of the past and the present.

Although mental disorders have been shown to predict subsequent substance disorders, it is not known whether substance disorders could be cost-effectively prevented by large-scale interventions aimed at prior mental disorders. Although experimental intervention is the only way to resolve this uncertainty, a logically prior question is whether the associations of mental disorders with subsequent substance disorders are strong enough to justify mounting such an intervention. We investigated this question in this study using simulations to estimate the number of substance disorders that might be prevented under several hypothetical intervention scenarios focused on mental disorders.

Data came from the National Comorbidity Survey Replication (NCS-R), a nationally representative US household survey that retrospectively assessed lifetime history and age of onset of DSM-IV mental and substance disorders. Survival analysis using retrospective age-of-onset reports was used to estimate associations of mental disorders with subsequent substance dependence. Simulations based on the models estimated effect sizes in several hypothetical intervention scenarios.

Although successful intervention aimed at mental disorders might prevent some proportion of substance dependence, the number of cases of mental disorder that would have to be treated to prevent a single case of substance dependence is estimated to be so high that this would not be a cost-effective way to prevent substance dependence (in the range 76–177 for anxiety-mood disorders and 40–47 for externalizing disorders).

Treatment of prior mental disorders would not be a cost-effective way to prevent substance dependence. However, prevention of substance dependence might be considered an important secondary outcome of interventions for early-onset mental disorders.

Mild traumatic brain injury (mTBI) is being claimed as the ‘signature’ injury of the Iraq war, and is believed to be the cause of long-term symptomatic ill health (post-concussional syndrome; PCS) in an unknown proportion of military personnel.

We analysed cross-sectional data from a large, randomly selected cohort of UK military personnel deployed to Iraq (n=5869). Two markers of PCS were generated: ‘PCS symptoms’ (indicating the presence of mTBI-related symptoms: none, 1–2, 3+) and ‘PCS symptom severity’ (indicating the presence of mTBI-related symptoms at either a moderate or severe level of severity: none, 1–2, 3+).

PCS symptoms and PCS symptom severity were associated with self-reported exposure to blast whilst in a combat zone. However, the same symptoms were also associated with other in-theatre exposures such as potential exposure to depleted uranium and aiding the wounded. Strong associations were apparent between having PCS symptoms and other health outcomes, in particular being a post-traumatic stress disorder or General Health Questionnaire case.

PCS symptoms are common and some are related to exposures such as blast injury. However, this association is not specific, and the same symptom complex is also related to numerous other risk factors and exposures. Post-deployment screening for PCS and/or mTBI in the absence of contemporaneous recording of exposure is likely to be fraught with hazards.

Mental capacity is now a core part of UK mental health law and clinicians will increasingly be expected to assess it. Because it is a legal concept there is a need to clarify associations with variables that clinicians are more familiar with, especially insight.

In this cross-sectional study we recruited consecutive psychiatric admissions to the Maudsley Hospital, London. We carried out structured assessments of decision making using the MacArthur Competence Assessment Tool for Treatment (MacCAT-T), resulting in a clinical judgement about capacity status. We analysed associations with a range of sociodemographic and clinical variables, including insight score on the Expanded Schedule for the Assessment of Insight (SAI-E). The same variables were compared in an analysis stratified according to diagnostic group: psychotic disorders/bipolar affective disorder (BPAD)/non-psychotic disorders.

Psychotic disorders and manic episodes of BPAD are most strongly associated with incapacity. In such patients, insight is the best discriminator of capacity status. In patients with non-psychotic disorders, insight is less strongly associated with capacity; in this group depressed mood discriminates capacity status whereas it does not in psychotic disorders. Cognitive performance does not discriminate capacity status in patients with psychotic disorders.

Mental capacity has complex relationships with psychopathological variables, and these relationships are different according to diagnostic group. Insight is the best discriminator of capacity status in psychotic disorders and BPAD but not in non-psychotic disorders.