Stress is thought to exert both positive and negative effects on cognition, but the precise cognitive effects of social stress and individuals' response to stress remain unclear. We aimed to investigate the association between different measures of social stress and cognitive function in a middle- to older-aged population using data from the European Prospective Investigation into Cancer (EPIC)-Norfolk study.

Participants completed a comprehensive assessment of lifetime social adversity between 1993 and 1997 and the short form of the Mini Mental State Examination (SF-MMSE), an assessment of global cognitive function, during the third health check between 2004 and 2011 (a median of 10.5 years later). A low MMSE score was defined as a score in the bottom quartile (20–26).

Completed MMSE scores and stress measures were available for 5129 participants aged 48–90 years. Participants who reported that their lives had been more stressful over the previous 10 years were significantly more likely to have low MMSE scores [odds ratio (OR) 1.14, 95% confidence interval (CI) 1.04–1.24 per unit increase in perceived stress], independently of sociodemographic factors, physical and emotional health. The effects were restricted to the highest level of stress and the association was stronger among participants with a lower educational level. Adaptation following life event experiences also seemed to be associated with MMSE scores after adjusting for sociodemographic factors, but the association was attenuated with further adjustment.

In this generally high-functioning population, individuals' interpretations and responses to stressful events, rather than the events themselves, were associated with cognitive function.

The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) proposes aligning nicotine use disorder (NUD) criteria with those for other substances, by including the current DSM fourth edition (DSM-IV) nicotine dependence (ND) criteria, three abuse criteria (neglect roles, hazardous use, interpersonal problems) and craving. Although NUD criteria indicate one latent trait, evidence is lacking on: (1) validity of each criterion; (2) validity of the criteria as a set; (3) comparative validity between DSM-5 NUD and DSM-IV ND criterion sets; and (4) NUD prevalence.

Nicotine criteria (DSM-IV ND, abuse and craving) and external validators (e.g. smoking soon after awakening, number of cigarettes per day) were assessed with a structured interview in 734 lifetime smokers from an Israeli household sample. Regression analysis evaluated the association between validators and each criterion. Receiver operating characteristic analysis assessed the association of the validators with the DSM-5 NUD set (number of criteria endorsed) and tested whether DSM-5 or DSM-IV provided the most discriminating criterion set. Changes in prevalence were examined.

Each DSM-5 NUD criterion was significantly associated with the validators, with strength of associations similar across the criteria. As a set, DSM-5 criteria were significantly associated with the validators, were significantly more discriminating than DSM-IV ND criteria, and led to increased prevalence of binary NUD (two or more criteria) over ND.

All findings address previous concerns about the DSM-IV nicotine diagnosis and its criteria and support the proposed changes for DSM-5 NUD, which should result in improved diagnosis of nicotine disorders.

Psychological traumatic events, such as war or road traffic accidents, are widespread. A small but significant proportion of survivors develop post-traumatic stress disorder (PTSD). Distressing, sensory-based involuntary memories of trauma (henceforth ‘flashbacks’) are the hallmark symptom of PTSD. Understanding the development of flashbacks may aid their prevention. This work is the first to combine the trauma film paradigm (as an experimental analogue for flashback development) with neuroimaging to investigate the neural basis of flashback aetiology. We investigated the hypothesis that involuntary recall of trauma (flashback) is determined during the original event encoding.

A total of 22 healthy volunteers viewed a traumatic film whilst undergoing functional magnetic resonance imaging (fMRI). They kept a 1-week diary to record flashbacks to specific film scenes. Using a novel prospective fMRI design, we compared brain activation for those film scenes that subsequently induced flashbacks with both non-traumatic control scenes and scenes with traumatic content that did not elicit flashbacks (‘potentials’).

Encoding of scenes that later caused flashbacks was associated with widespread increases in activation, including in the amygdala, striatum, rostral anterior cingulate cortex, thalamus and ventral occipital cortex. The left inferior frontal gyrus and bilateral middle temporal gyrus also exhibited increased activation but only relative to ‘potentials’. Thus, these latter regions appeared to distinguish between traumatic content that subsequently flashed back and comparable content that did not.

Results provide the first prospective evidence that the brain behaves differently whilst experiencing emotional events that will subsequently become involuntary memories – flashbacks. Understanding the neural basis of analogue flashback memory formation may aid the development of treatment interventions for this PTSD feature.

Studying the distribution of anatomical abnormalities over the entire cortical surface can help to identify key neural circuits implicated in generating symptoms of neuropsychiatric disorders. There is a significant inconsistency among studies investigating the neuroanatomy of obsessive–compulsive disorder (OCD) because of the confounding influence of co-morbid depression and medication use and the lack of unbiased estimation of whole-brain morphometric changes. It is also unknown whether the distinct surface anatomical properties of thickness, surface area and gyrification, which collectively contribute to grey matter volume (GMV), are independently affected in OCD.

The cortical maps of thickness, gyrification and surface areal change were acquired from 23 unmedicated OCD patients and 20 healthy controls using an unbiased whole-brain surface-based morphometric (SBM) method to detect regional changes in OCD. Subcortical structures were not assessed in this study.

Patients showed a significant increase in the right inferior parietal cortical thickness. Significant increases in gyrification were also noted in the left insula, left middle frontal and left lateral occipital regions extending to the precuneus and right supramarginal gyrus in OCD. Areal contraction/expansion maps revealed no significant regional differences between the patients and controls. In patients, gyrification of the insula significantly predicted the symptom severity measured using Yale–Brown Obsessive–Compulsive Scale (YBOCS).

An alteration in the cortical surface anatomy is an important feature of OCD seen in unmedicated samples that relates to the severity of the illness. The results underscore the presence of a neurodevelopmental aberration underlying the pathophysiology of OCD.

Parent and teacher ratings of attention deficit hyperactivity disorder (ADHD) symptoms yield high estimates of heritability whereas self-ratings typically yield lower estimates. To understand why, the present study examined the etiological overlap between parent, teacher and self-ratings of ADHD symptoms in a population-based sample of 11–12-year-old twins.

Participants were from the Twins Early Development Study (TEDS). ADHD symptoms were assessed using the Strengths and Difficulties Questionnaire (SDQ) hyperactivity scale completed by parents, teachers and children. Structural equation modeling was used to examine genetic and environmental contributions to phenotypic variance/covariance.

The broad-sense heritability of ADHD symptoms was 82% for parent ratings, 60% for teacher ratings and 48% for self-ratings. Post-hoc analyses revealed significantly higher heritability for same-teacher than different-teacher ratings of ADHD (76% v. 49%). A common pathway model best explained the relationship between different informant ratings, with common genetic influences accounting for 84% of the covariance between parent, teacher and self-rated ADHD symptoms. The remaining variance was explained by rater-specific genetic and non-shared environmental influences.

Despite different heritabilities, there were shared genetic influences for parent, teacher and self-ratings of ADHD symptoms, indicating that different informants rated some of the same aspects of behavior. The low heritability estimated for self-ratings and different-teacher ratings may reflect increased measurement error when different informants rate each twin from a pair, and/or greater non-shared environmental influences. Future studies into the genetic influences on ADHD should incorporate informant data in addition to self-ratings to capture a pervasive, heritable component of ADHD symptomatology.

We examined the cross-sectional relationship between environmental tobacco smoke exposure, continuous performance test (CPT) measures, and attention deficit hyperactivity disorder (ADHD) or learning disability symptoms in school-aged children.

In total, 989 children (526 boys, mean age 9.1 ± 0.7 years), recruited from five South Korean cities participated in this study. We used urine cotinine as a biomarker for environmental tobacco smoke exposure, and obtained the children's scores on a CPT. Parents completed the Korean versions of the ADHD Rating Scale – IV (ADHD-RS) and Learning Disability Evaluation Scale (LDES). Using generalized linear mixed model (GLMM), we assessed the associations between urine cotinine concentrations, neuropsychological variables, and symptoms of ADHD and learning disabilities. Additionally, we conducted structural equation models to explore the effects' pathways.

After adjusting for a range of relevant covariates, GLMM showed urinary cotinine levels were significantly and positively associated with CPT scores on omission errors, commission errors, response time, and response time variability, and with parent- and teacher-rated ADHD-RS scores. In addition, urine cotinine levels were negatively associated with LDES scores on spelling and mathematical calculations. The structural equation model revealed that CPT variables mediated the association between urine cotinine levels and parental reports of symptoms of ADHD and learning disabilities.

Our data indicate that environmental exposure to tobacco smoke is associated with ADHD and learning disabilities in children, and that impairments in attention and inhibitory control probably mediate the effect.

An understanding of the exact nature of executive function (EF) deficits in conduct disorder (CD) remains elusive because of issues of co-morbidity with attention deficit hyperactivity disorder (ADHD).

Seventy-two adolescents with CD, 35 with CD + ADHD and 20 healthy controls (HCs) were assessed on a computerized battery of putative ‘cool’ and ‘hot’ EFs. Participants also completed the Child Behaviour Checklist (CBCL).

In the cool EF tasks such as planning, the CD + ADHD group in particular showed most notable impairments compared to HCs. This pattern was less evident for set shifting and behavioural inhibition but there were significant correlations between errors scores on these tasks and indices of externalizing behaviours on the CBCL across the sample. For hot EF tasks, all clinical groups performed worse than HCs on delay of gratification and poor performance was correlated with externalizing scores. Although there were no notable group differences on the punishment-based card-playing task, there were significant correlations between ultimate payout and externalizing behaviour across groups.

Overall, our findings highlight the fact that there may be more common than distinguishing neuropsychological underpinnings to these co-morbid disorders and that a dimensional symptom-based approach may be the way forward.

The goal of the current study was to investigate asthma and mental health among youth in the community, and to consider the role of asthma severity and persistence in this link.

Data were drawn from the Raine Study, a population-based birth cohort study in Western Australia. Logistic regression models and generalized estimating equations were used to examine the relationship between asthma at age 5 years and the range of internalizing and externalizing mental health problems at ages 5–17 years. Analyses were stratified by asthma severity and persistence, and adjusted for a range of potential confounders.

More severe and persistent asthma at age 5 was associated with significantly increased odds of affective, anxiety, somatic, oppositional defiant and conduct problems at ages 5–17. Mild asthma and remitted asthma were not associated with heightened vulnerability to mental disorders.

Our results suggest that youth with symptomatic asthma are more likely to suffer from a wide range of mental health problems, and that the likelihood of mental health problems appears to increase as a function of asthma severity. Youth with poorly controlled and/or more severe and persistent asthma may be considered a vulnerable group who might benefit from mental health screening in clinical, school and community settings.

Employment is associated with health benefits over unemployment, but the psychosocial characteristics of work also influence health. There has, however, been little research contrasting the prevalence of psychiatric disorders among people who are unemployed with those in jobs of differing psychosocial quality.

Analysis of data from the English Adult Psychiatric Morbidity Survey (APMS) considered the prevalence of common mental disorders (CMDs) among 2603 respondents aged between 21 and 54 years who were either (i) employed or (ii) unemployed and looking for work at the time of interview in 2007. Quality of work was assessed by the number of adverse psychosocial job conditions reported (low control, high demands, insecurity and low job esteem).

The prevalence of CMDs was similar for those respondents who were unemployed and those in the poorest quality jobs. This pattern remained after controlling for relevant demographic and socio-economic covariates.

Although employment is thought to promote mental health and well-being, work of poor psychosocial quality is not associated with any better mental health than unemployment. Policy efforts to improve community mental health should consider psychosocial job quality in conjunction with efforts to increase employment rates.

In this global study we sought to estimate the degree to which a family member might feel embarrassed when a close relative is suffering from an alcohol, drug, or mental health condition (ADMC) versus a general medical condition (GMC). To date, most studies have considered embarrassment and stigma in society and internalized by the afflicted individual but have not assessed family embarrassment in a large-scale study.

In 16 sites of the World Mental Health Surveys (WMHS), standardized assessments were completed including items on family embarrassment. Site matching was used to constrain local socially shared determinants of stigma-related feelings, enabling a conditional logistic regression model that estimates the embarrassment close relatives may hold in relation to family members affected by an ADMC, a GMC, or both conditions.

There was a statistically robust association such that subgroups with an ADMC-affected relative were more likely to feel embarrassed compared to subgroups with a relative affected by a GMC (p < 0.001), even with covariate adjustments for age and sex.

The pattern of evidence from this research is consistent with conceptual models for interventions that target individual- and family-level stigma-related feelings of embarrassment as possible obstacles to effective early intervention and treatment for an ADMC. Macro-level interventions are under way but micro-level interventions may also be required among family members, along with care for each person with an ADMC.

The psychobiological model of personality by Cloninger and colleagues originally hypothesized that interindividual variability in the temperament dimension ‘harm avoidance’ (HA) is explained by differences in the activity of the brain serotonin system. We assessed brain serotonin transporter (5-HTT) density in vivo with positron emission tomography (PET) in healthy individuals with high or low HA scores using an ‘oversampling’ study design.

Subjects consistently in either upper or lower quartiles for the HA trait were selected from a population-based cohort in Finland (n = 2075) with pre-existing Temperament and Character Inventory (TCI) scores. A total of 22 subjects free of psychiatric and somatic disorders were included in the matched high- and low-HA groups. The main outcome measure was regional 5-HTT binding potential (BPND) in high- and low-HA groups estimated with PET and [11C]N,N-dimethyl-2-(2-amino-4-methylphenylthio)benzylamine ([11C]MADAM). In secondary analyses, 5-HTT BPND was correlated with other TCI dimensions.

5-HTT BPND did not differ between high- and low-HA groups in the midbrain or any other brain region. This result remained the same even after adjusting for other relevant TCI dimensions. Higher 5-HTT BPND in the raphe nucleus predicted higher scores in ‘self-directedness’.

This study does not support an association between the temperament dimension HA and serotonin transporter density in healthy subjects. However, we found a link between high serotonin transporter density and high ‘self-directedness’ (ability to adapt and control one's behaviour to fit situations in accord with chosen goals and values). We suggest that biological factors are more important in explaining variability in character than previously thought.

The extent to which specific factors influence diagnostic delays in dementia is unclear. Therefore, the aim of the present study was to compare duration from symptom onset to diagnosis for young-onset dementia (YOD) and late-onset dementia (LOD) and to assess the effect of age at onset, type of dementia, gender, living situation, education and family history of dementia on this duration.

Data on 235 YOD and 167 LOD patients collected from caregivers from two prospective cohort studies were used. Multiple linear regression analysis was performed.

The duration between symptom onset and the diagnosis of YOD exceeded that of LOD by an average of 1.6 years (2.8 v. 4.4 years). Young age and being diagnosed with frontotemporal dementia were related to increases in the time to diagnosis. Subjects with vascular dementia experienced shorter time to diagnosis.

There is a need to raise special awareness of YOD to facilitate a timely diagnosis.

Survivors of critical illnesses often have clinically significant post-traumatic stress disorder (PTSD) symptoms. This study describes the 2-year prevalence and duration of PTSD symptoms after acute lung injury (ALI), and examines patient baseline and critical illness/intensive care-related risk factors.

This prospective, longitudinal cohort study recruited patients from 13 intensive care units (ICUs) in four hospitals, with follow-up 3, 6, 12 and 24 months after ALI onset. The outcome of interest was an Impact of Events Scale – Revised (IES-R) mean score ⩾1.6 (‘PTSD symptoms’).

During the 2-year follow-up, 66/186 patients (35%) had PTSD symptoms, with the greatest prevalence by the 3-month follow-up. Fifty-six patients with post-ALI PTSD symptoms survived to the 24-month follow-up, and 35 (62%) of these had PTSD symptoms at the 24-month follow-up; 50% had taken psychiatric medications and 40% had seen a psychiatrist since hospital discharge. Risk/protective factors for PTSD symptoms were pre-ALI depression [hazard odds ratio (OR) 1.96, 95% confidence interval (CI) 1.06–3.64], ICU length of stay (for a doubling of days, OR 1.39, 95% CI 1.06–1.83), proportion of ICU days with sepsis (per decile, OR 1.08, 95% CI 1.00–1.16), high ICU opiate doses (mean morphine equivalent ⩾100 mg/day, OR 2.13, 95% CI 1.02–4.42) and proportion of ICU days on opiates (per decile, OR 0.83, 95% CI 0.74–0.94) or corticosteroids (per decile, OR 0.91, 95% CI 0.84–0.99).

PTSD symptoms are common, long-lasting and associated with psychiatric treatment during the first 2 years after ALI. Risk factors include pre-ALI depression, durations of stay and sepsis in the ICU, and administration of high-dose opiates in the ICU. Protective factors include durations of opiate and corticosteroid administration in the ICU.

Prior studies of adult post-traumatic stress disorder (PTSD) suggest abnormal functioning of prefrontal and limbic regions. Cumulative childhood and adult trauma exposures are major risk factors for developing adult PTSD, yet their contribution to neural dysfunction in PTSD remains poorly understood. This study aimed to examine the neural correlates of childhood and adult trauma exposure and post-traumatic stress symptoms (PTSS) within a single model.

Medication-free male combat veterans (n = 28, average age 26.6 years) with a wide range of PTSS were recruited from the community between 2010 and 2011. Subjects completed an emotional face-morphing task while undergoing functional magnetic resonance imaging (fMRI). Clinical ratings included the Clinician-Administered PTSD Scale (CAPS), Childhood Trauma Questionnaire (CTQ) and Combat Exposure Scale (CES). A priori regions were examined through multivariate voxelwise regression in SPM8, using depressive symptoms and IQ as covariates.

In the angry condition, CAPS scores correlated positively with activation in the medial prefrontal cortex [mPFC; Brodmann area (BA) 10, z = 3.51], hippocampus (z = 3.47), insula (z = 3.62) and, in earlier blocks, the amygdala. CES and CTQ correlated positively with activation in adjacent areas of the dorsal anterior cingulate cortex (dACC; BA 32, z = 3.70 and BA 24, z = 3.88 respectively). In the happy condition, CAPS, CTQ and CES were not correlated significantly with activation patterns.

dACC activation observed in prior studies of PTSD may be attributable to the cumulative effects of childhood and adult trauma exposure. By contrast, insula, hippocampus and amygdala activation may be specific to PTSS. The specificity of these results to threat stimuli, but not to positive stimuli, is consistent with abnormalities in threat processing associated with PTSS.

Attention deficit hyperactivity disorder (ADHD) is recognized as an early-onset neuropsychiatric disorder with executive dysfunctions and neurobiological deficits. The authors compared executive functions and microstructural integrity of the frontostriatal circuit in children with ADHD and typically developing children.

We assessed 25 children with ADHD and 25 age-, sex-, handedness- and intelligence-matched typically developing children by using psychiatric interviews, the Wechsler Intelligence Scale for Children – third edition, and the tasks involving executive functions in the Cambridge Neuropsychological Test Automated Battery. The frontostriatal tracts were reconstructed by diffusion spectrum imaging tractography and were subdivided into four functionally distinct segments, including dorsolateral, medial prefrontal, orbitofrontal and ventrolateral tracts. Tract-specific and matched case-control analyses were used and generalized fractional anisotropy values were computed.

Children with ADHD had lower generalized fractional anisotropy of all the bilateral frontostriatal fiber tracts and poorer performance in verbal and spatial working memory, set-shifting, sustained attention, cognitive inhibition and visuospatial planning. The symptom severity of ADHD and the executive functioning performance significantly correlated with integrity of the frontostriatal tracts, particularly the left orbitofrontal and ventrolateral tracts. Children with ADHD also demonstrated loss of the leftward asymmetry in the dorsolateral and medial prefrontal tracts that was present in typically developing children.

Our findings demonstrate disturbed structural connectivity of the frontostriatal circuitry in children with ADHD and add new evidence of associations between integrity of the frontostriatal tracts and measures of core symptoms of ADHD and a wide range of executive dysfunctions in both groups.

Although numerous studies have examined the latent structure of major depression, less attention has focused on mania. This paper presents the first investigation outside the USA to evaluate the psychometric properties of the DSM-IV criterion B mania symptoms using item response theory (IRT).

Data were drawn from the Australian 2007 National Survey of Mental Health and Well-Being (NSMHWB, n = 8841). The psychometric performance of the mania symptoms was evaluated using a two-parameter logistic model. Because substance use disorders (SUDs) frequently co-occur with mania and can influence manic symptom expression, differential item functioning (DIF) between mania respondents with/without a SUD diagnosis was also assessed.

Factor analysis supported a unidimensional trait underlying mania. The grandiosity symptom displayed the highest discrimination whereas discrimination was lowest for decreased need for sleep. Relatively speaking, grandiosity tapped the severe end and increased goal-oriented activities tapped the mild end of the mania severity continuum. The symptoms generally performed equivalently between those with/without a SUD diagnosis, with one exception; the activities with painful consequences symptom was endorsed at lower levels of severity, and hence more frequently, by those with a SUD diagnosis versus those without a SUD diagnosis.

Accurate conceptualization of latent structure has crucial theoretical, statistical and clinical implications. The symptoms generally performed well in distinguishing between respondents with differing levels of liability, but others did not, suggesting modification is warranted to ensure optimal use in epidemiological samples. Given the dearth of psychometric evaluation studies of mania, further research replicating these results is necessary.

There is a large body of evidence indicating that eating disorders (EDs) are characterized by particular neuropsychological profiles. We aimed to further explore whether impairments in neuropsychological functioning previously found in ED groups are present prior to onset, or are secondary to the disorder.

This is the first study to explore neuropsychological functioning in children born to a mother with a lifetime ED, who are therefore at high risk of developing an ED, in a large cohort sample. We investigated intelligence and attention at age 8 years (n = 6201) and working memory (WM) and inhibition at age 10 years (6192) in children who are at high risk of developing an ED, compared to children who are not.

The children of women with lifetime anorexia nervosa (AN) showed high full-scale and performance IQ, increased WM capacity, better visuo-spatial functioning, and decreased attentional control. The children of women with lifetime bulimia nervosa (BN) showed comparatively poor visuo-spatial functioning.

Our findings suggest that high intelligence, increased WM capacity and impaired attentional control might be intermediate phenotypes on the pathway between genetic vulnerability and the development of an ED.

This report prospectively examines the 4-year course, and predictors of course, of body dysmorphic disorder (BDD), a common and often severe disorder. No prior studies have prospectively examined the course of BDD in individuals ascertained for BDD.

The Longitudinal Interval Follow-Up Evaluation (LIFE) assessed weekly BDD symptoms and treatment received over 4 years for 166 broadly ascertained adults and adolescents with current BDD at intake. Kaplan–Meier life tables were constructed for time to remission and relapse. Full remission was defined as minimal or no BDD symptoms, and partial remission as less than full DSM-IV criteria, for at least 8 consecutive weeks. Full relapse and partial relapse were defined as meeting full BDD criteria for at least 2 consecutive weeks after attaining full or partial remission respectively. Cox proportional hazards regression examined predictors of remission and relapse.

Over 4 years, the cumulative probability was 0.20 for full remission and 0.55 for full or partial remission from BDD. A lower likelihood of full or partial remission was predicted by more severe BDD symptoms at intake, longer lifetime duration of BDD, and being an adult. Among partially or fully remitted subjects, the cumulative probability was 0.42 for subsequent full relapse and 0.63 for subsequent full or partial relapse. More severe BDD at intake and earlier age at BDD onset predicted full or partial relapse. Eighty-eight percent of subjects received mental health treatment during the follow-up period.

In this observational study, BDD tended to be chronic. Several intake variables predicted greater chronicity of BDD.