Oppositional defiant disorder (ODD) is frequently co-occurring with attention deficit hyperactivity disorder (ADHD) in children and adolescents. Because ODD is a precursor of later conduct disorder (CD) and affective disorders, early diagnostic identification is warranted. Furthermore, the predictability of three recently confirmed ODD dimensions (ODD-irritable, ODD-headstrong and ODD-hurtful) may assist clinical decision making.

Receiver-operating characteristic (ROC) analysis was used in order to test the diagnostic accuracy of the Conners' Parent Rating Scale revised (CPRS-R) and the parent version of the Strength and Difficulties Questionnaire (PSDQ) in the prediction of ODD in a transnational sample of 1093 subjects aged 5–17 years from the International Multicentre ADHD Genetics study. In a second step, the prediction of three ODD dimensions by the same parent rating scales was assessed by backward linear regression analyses.

ROC analyses showed adequate diagnostic accuracy of the CPRS-R and the PSDQ in predicting ODD in this ADHD sample. Furthermore, the three-dimensional structure of ODD was confirmed by confirmatory factor analysis and the CPRS-R emotional lability scale significantly predicted the ODD irritable dimension.

The PSDQ and the CPRS-R are both suitable screening instruments in the identification of ODD. The emotional lability scale of the CPRS-R is an adequate predictor of irritability in youth referred for ADHD.

Elevated cortisol levels due to hypothalamic–pituitary–adrenal (HPA) axis stress response have been associated with cognitive impairment. However, the causal relationship between stress and subsequent cognitive impairment remains unclear, notably because of the small number of gender-stratified prospective studies.

Salivary cortisol secretion was evaluated in 197 non-depressed community-dwelling elderly people at three time points on the day of hospital attendance for a clinical examination and again on the following day at home, in a distinct environmental context. Cognitive performance was evaluated at baseline and at 2- and 4-year follow-up.

Cross-sectional logistic analyses adjusted for age and education indicated that men with high morning cortisol at the hospital had higher risk of low cognitive performance in verbal fluency [odds ratio (OR) 3.0, p=0.05] and visuospatial performance (OR 5.1, p=0.03). Impairment in verbal fluency was observed in women with moderate high morning cortisol (OR 3.6, p=0.05) or moderate slow diurnal rhythm (OR 3.7, p=0.04). In longitudinal analyses, slow diurnal rhythm (flatter slope) was associated with decline over 4 years in visuospatial performance (OR 7.7, p=0.03) and visual memory (OR 4.1, p=0.03) in men, and in verbal fluency (OR 6.0, p=0.01) in women. High morning cortisol was associated with decline in visual memory in women (OR 5.1, p=0.06).

HPA axis dysregulation seems to be associated with low cognitive performance in the elderly. Slower cortisol elimination rates could predict cognitive decline affecting principally non-verbal functioning in men and verbal functioning in women. The effects are independent of environmental context, apolipoprotein E (ApoE) genotype or psychopathology. Interventions blocking this pathway may provide new therapeutic options to prevent cognitive decline.

Puberty moderates genetic influences on disordered eating attitudes and behaviors, with little genetic influence before puberty but large (⩾50%) genetic effects during and after puberty. To date, however, nothing is known about the mechanisms that underlie these effects. Estradiol is a particularly promising candidate, as estrogens become elevated at puberty and regulate gene transcription within neurotransmitter systems important for eating-related phenotypes. The aim of this pilot study was to examine whether estradiol levels moderate genetic influences on disordered eating during puberty.

Participants included 198 female twins (ages 10–15 years) from the Michigan State University Twin Registry. Disordered eating attitudes and behaviors were assessed with the total score, weight preoccupation, body dissatisfaction and binge eating/compensatory behavior subscales of the Minnesota Eating Behavior Survey (MEBS). Afternoon saliva samples were assayed for estradiol levels. Moderation of genetic effects was examined by comparing twin correlations in low versus high estradiol groups.

In the low estradiol group, monozygotic (MZ) and dizygotic (DZ) twin correlations for all MEBS scales were similar, suggesting little genetic influence. In the high estradiol group, the MZ twin correlation was more than double the DZ twin correlation, indicating the presence of genetic effects. Findings could not be accounted for by age, body mass index or the physical changes of puberty.

Estradiol may be one important moderator of genetic effects on disordered eating during puberty. Larger twin studies are needed to replicate this pilot work and quantify the extent of genetic moderation.

Patients whose symptoms are ‘unexplained by disease’ often have a poor symptomatic outcome after specialist consultation, but we know little about which patient factors predict this. We therefore aimed to determine predictors of poor subjective outcome for new neurology out-patients with symptoms unexplained by disease 1 year after the initial consultation.

The Scottish Neurological Symptom Study was a 1-year prospective cohort study of patients referred to secondary care National Health Service neurology clinics in Scotland (UK). Patients were included if the neurologist rated their symptoms as ‘not at all’ or only ‘somewhat explained’ by organic disease. Patient-rated change in health was rated on a five-point Clinical Global Improvement (CGI) scale (‘much better’ to ‘much worse’) 1 year later.

The 12-month outcome data were available on 716 of 1144 patients (63%). Poor outcome on the CGI (‘unchanged’, ‘worse’ or ‘much worse’) was reported by 482 (67%) out of 716 patients. The only strong independent baseline predictors were patients' beliefs [expectation of non-recovery (odds ratio [OR] 2.04, 95% confidence interval [CI] 1.40–2.96), non-attribution of symptoms to psychological factors (OR 2.22, 95% CI 1.51–3.26)] and the receipt of illness-related financial benefits (OR 2.30, 95% CI 1.37–3.86). Together, these factors predicted 13% of the variance in outcome.

Of the patients, two-thirds had a poor outcome at 1 year. Illness beliefs and financial benefits are more useful in predicting poor outcome than the number of symptoms, disability and distress.

Panic disorder (PD) is generally considered to be a chronic or intermittent disorder. This view may be biased because of a lack of general population studies investigating panic from the onset of an episode onwards. Data regarding the course of subthreshold panic disorder (sub-PD) and predictors of its course are lacking.

Using data from a large community-based survey, the Netherlands Mental Health and Incidence Study (NEMESIS), that retrospectively assessed the 2-year course of panic with a Life Chart Interview (LCI), this study investigated remission, chronicity and recurrence in subjects with new episodes of PD or sub-PD. Predictor variables of remission consisted of sociodemographics, psychobiological, environmental, psychiatric and panic-related factors.

In PD, remission of panic attacks occurred in 64.5% of subjects, mean time to remission was 5.7 months, and the remission rate was 5.8/100 person-months. In 43.3% of subjects panic was still present after 1 year. Recurrence of panic attacks occurred in 21.4% of those with PD who had achieved remission and for whom sufficient follow-up time was available. In general, the course of sub-PD was more favourable. Predictors of remission were female gender, the absence of ongoing difficulties, subthreshold panic and a low initial frequency of attacks.

These results suggest that the course of panic is diverse in the general population, thereby underlining the need for accurate predictors. This requires further research including biological data and additional psychological data. In addition, given the large proportion with a relapse, relapse prevention should be part of any treatment programme.

Several studies suggest that patients with late-onset major depression (MD) have an increased load of cerebral white-matter lesions (WMLs) compared with age-matched controls. Vascular risk factors such as hypertension and smoking may confound such findings. Our aim was to investigate the association between the localization and load of WMLs in late-onset MD with respect to vascular risk factors.

We examined 22 consecutive patients with late-onset first-episode MD and 22 age- and gender-matched controls using whole-brain magnetic resonance imaging (MRI). The localization, number and volume of WMLs were compared between patients and controls, while testing the effect of vascular risk factors.

Among subjects with one or more WMLs, patients displayed a significantly higher WML density in two white-matter tracts: the left superior longitudinal fasciculus and the right frontal projections of the corpus callosum. These tracts are part of circuitries essential for cognitive and emotional functions. Analyses revealed no significant difference in the total number and volume of WMLs between groups. Patients and controls showed no difference in vascular risk factors, except for smoking. Lesion load was highly correlated with smoking.

Our results indicate that lesion localization rather than lesion load differs between patients with late-onset MD and controls. Increased lesion density in regions associated with cognitive and emotional functions may be crucial in late-onset MD, and vascular risk factors such as smoking may play an important role in the pathophysiology of late-onset MD, consistent with the vascular depression hypothesis.

Previous findings revealed that the acquisition of new semantic concepts' labels was impaired in uncomplicated alcoholic patients. The use of errorless learning may therefore allow them to improve learning performance. However, the flexibility of the new knowledge and the memory processes involved in errorless learning remain unclear.

New concepts' labels acquisition was examined in 15 alcoholic patients and 15 control participants in an errorless learning condition compared with 19 alcoholic patients and 19 control subjects in a trial-and-error learning condition. The flexibility of the new information was evaluated using different photographs from those used in the learning sessions but representing the same concepts. All of the participants carried out an additional explicit memory task and an implicit memory task was also performed by subjects in the errorless learning condition.

The alcoholic group in the errorless condition differed significantly from the alcoholic group in the trial-and-error condition but did not differ from the two control groups. There was no significant difference between results in the learning test and the flexibility task. Finally, in the alcoholic group, the naming score in the learning test was correlated with the explicit memory score but not with the implicit memory score.

Using errorless learning, alcoholics improved their abilities to learn new concepts' labels. Moreover, new knowledge acquired with errorless learning was flexible. The errorless learning advantage may rely on explicit rather than implicit memory processes in these alcohol-dependent patients presenting only mild to moderate deficits of explicit memory capacities.

It has been hypothesized that stressful life events are associated with changes in hypothalamic–pituitary–adrenal (HPA) axis regulation, which increases susceptibility to psychiatric disorders. We investigated the association of early and late life events with HPA axis regulation in older persons.

Within the Longitudinal Aging Study Amsterdam (LASA) 1055 participants (47% male), aged 63–93 years, collected saliva within 30 min after waking and late in the evening. Early and late life events were assessed during a home interview. The associations between life events and cortisol levels were examined using linear regression and analysis of covariance with adjustments for demographics, cardiovascular risk factors and depressive symptoms.

Within our sample, the median morning and evening cortisol levels were 15.0 nmol/l [interdecile range (10–90%): 7.4–27.0 nmol/l] and 2.8 nmol/l (10–90%: 1.5–6.3 nmol/l), respectively. Persons who reported early life events showed lower levels of natural log-transformed morning cortisol [B=−0.10, 95% confidence interval (CI) −0.17 to −0.04] and flattened diurnal variability of cortisol (B=−1.06, 95% CI −2.05 to −0.08). Those reporting two or more late life events showed higher levels of natural log-transformed morning cortisol (B=0.10, 95% CI 0.02–0.18) and higher diurnal variability (B=1.19, 95% CI 0.05–2.33). No associations were found with evening cortisol.

The results of this large population-based study of older persons suggest a differential association of early and late life events with HPA axis regulation; early life events were associated with a relative hypo-secretion of morning cortisol and flattened diurnal variability, while late life events were associated with elevated secretion of morning cortisol and high diurnal variability of cortisol.

Interpersonal processes, anxiety and emotion regulation difficulties form a key part of conceptual models of eating disorders (EDs), such as anorexia nervosa (AN) and bulimia nervosa (BN), but the experimental findings to support this are limited.

The Reading the Mind in the Eyes task, the Difficulties in Emotion Regulation Scale (DERS) and a computerized pictorial (angry and neutral faces) Stroop task were administered to 190 women [50 with AN, 50 with BN and 90 healthy controls (HCs)].

Those with an ED showed attentional biases to faces in general (medium effect), but specifically to angry faces over neutral faces (large effect) compared to HCs. The ED group also reported significantly higher emotion regulation difficulties (large effect) than HCs. There was a small difference between the ED and HC groups for the emotion recognition task (small-medium effect), particularly in the restricting AN (RAN) group. Depression and attentional bias to faces significantly predicted emotion regulation difficulties in a regression model.

The data provide support for conceptualizations of EDs that emphasize the role of emotional functioning in the development and maintenance of EDs. Further research will concentrate on exploring whether these findings are state or trait features of EDs.

Recently released prisoners are at markedly higher risk of suicide than the general population. The aim of this study was to identify key risk factors for suicide by offenders released from prisons in England and Wales.

All suicides committed by offenders within 12 months of their release from prison in England and Wales, between 2000 and 2002, were identified. One control matched on gender and date of release from prison was recruited for each case. Univariate and multivariate logistic regression modelling identified key independent risk factors for suicide.

Of 256 920 released prisoners, 384 suicides occurred within a year of release. Factors significantly associated with post-release suicide were increasing age over 25 years, released from a local prison, a history of alcohol misuse or self-harm, a psychiatric diagnosis, and requiring Community Mental Health Services (CMHS) follow-up after release from prison. Non-white ethnicity and a history of previous imprisonment were protective factors.

There is a need to improve the continuity of care for people who are released from prison and for community health, offender and social care agencies to coordinate care for these vulnerable individuals.

Recent behavioral genetic studies have emphasized the importance of investigating eating disorders at the level of individual symptoms, rather than as overall diagnoses. We examined the heritability of binge eating disorder (BED) using an item-factor analytic approach, which estimates contributions of additive genetic (A), common environmental (C), and unique environmental (E) influences on liability to BED as well as individual symptoms.

Participants were 614 monozygotic and 410 dizygotic same-sex female twins from the Mid-Atlantic Twin Registry who completed a self-report measure of BED symptoms based upon DSM-IV criteria. Genetic and environmental contributions to BED liability were assessed at the diagnostic and symptom levels, using an item-factor approach.

Liability to BED was moderately heritable; 45% of the variance was due to A, with smaller proportions due to C (13%), and E (42%). Additive genetic effects accounted for 29–43% of the variance in individual items, while only 8–14% was due to C.

Results highlight the relevance of examining eating disorders at the symptom level, rather than focusing on aggregate diagnoses.

To investigate hedonic reactivity and the influence of unconscious emotional processes on the low sensitivity to positive reinforcement of food in anorexia nervosa (AN).

AN and healthy women were exposed to palatable food pictures just after a subliminal exposure to facial expressions (happy, disgust, fear and neutral faces), either while fasting or after a standardized meal (hunger versus satiety). Both implicit [facial electromyographic (EMG) activity from zygomatic and corrugator muscles, skin conductance, heart rate, and videotaped facial behavior] and explicit (self-reported pleasure and desire) measures of affective processes were recorded.

In contrast to healthy women, the AN patients did not display objective and subjective indices of pleasure to food pictures when they were in the hunger states. Pleasure to food cues (liking) was more affected than the desire to eat (wanting) in AN patients. Subliminal ‘fear faces’ increased corrugator muscle reactivity to food stimuli in fasting AN patients, as compared to controls.

The results suggest that unconscious fear cues increase the negative appraisal of alimentary stimuli in AN patients and thus contribute to decreased energy intake.