There is evidence that bipolar disorder (BD) is associated with significant neurocognitive deficits and this occurs in individuals with BD type I (BD I) and with BD type II (BD II). Only a few studies have focused on cognitive impairment in BD II. The aim of this study was to describe the pattern of cognitive impairment in patients with BD II, in order to identify specific cognitive deficits that distinguish BD II from BD I patients as well as from healthy subjects.

We performed a systematic review of the literature of neuropsychological studies of BD II published between 1980 and July 2009. Fourteen articles fulfilled the inclusion criteria and were included in this review.

Main cognitive deficits found in BD II include working memory and some measures of executive functions (inhibitory control) and approximately half of the studies also detected verbal memory impairment.

There are subtle differences between the two subtypes regarding cognition. This may suggest neurobiological differences between the two subgroups which will be helpful in order to determine cognitive endophenotypes in BD subtypes.

Previous studies have shown that patients with schizophrenia are impaired on executive tasks, where positive and negative feedbacks are used to update task rules or switch attention. However, research to date using saccadic tasks has not revealed clear deficits in task switching in these patients. The present study used an oculomotor ‘rule switching’ task to investigate the use of negative feedback when switching between task rules in people with schizophrenia.

A total of 50 patients with first episode schizophrenia and 25 healthy controls performed a task in which the association between a centrally presented visual cue and the direction of a saccade could change from trial to trial. Rule changes were heralded by an unexpected negative feedback, indicating that the cue-response mapping had reversed.

Schizophrenia patients were found to make increased errors following a rule switch, but these were almost entirely the result of executing saccades away from the location at which the negative feedback had been presented on the preceding trial. This impairment in negative feedback processing was independent of IQ.

The results not only confirm the existence of a basic deficit in stimulus–response rule switching in schizophrenia, but also suggest that this arises from aberrant processing of response outcomes, resulting in a failure to appropriately update rules. The findings are discussed in the context of neurological and pharmacological abnormalities in the conditions that may disrupt prediction error signalling in schizophrenia.

The peak in age of onset of psychotic disorders such as schizophrenia during puberty and early adulthood suggests a relationship between the expression of psychopathology and the changes in the brain and body that take place during this dynamic maturational period, including a dramatic increase in circulating oestrogens and androgens. This study examined levels of salivary testosterone and oestradiol in adolescents with prepsychotic, prodromal symptoms, as this may mediate risk for psychosis by having an impact on brain development.

In 21 male adolescents with prodromal symptoms and 21 male non-clinical controls levels of testosterone and oestradiol were measured in saliva. Tanner pubertal stage and prodromal symptoms were also assessed.

Levels of testosterone were significantly lower in adolescents with prodromal symptoms as compared with non-clinical controls. No group differences in oestradiol were found. In the total sample, level of testosterone was significantly correlated with age and Tanner pubertal stage.

Our observations are in line with current hypotheses stressing the role of neuroendocrine factors during adolescence in the expression of psychotic symptoms. From a developmental perspective, susceptibility to psychotic disorders increases during adolescence. Our data suggest that testosterone might, in part, mediate this increased vulnerability. Further research is needed to assess the mediating, neural, mechanisms through which testosterone may have an impact on the development of psychotic symptoms. In the search for early risk markers for psychosis, studying neuroendocrine factors might increase our understanding of ‘at-risk’ developmental pathways.

Although antipsychotic medication still represents the treatment of choice for schizophrenia, its objective impact on symptoms is only in the medium-effect size range and at least 50% of patients discontinue medication in the course of treatment. Hence, clinical researchers are intensively looking for complementary therapeutic options. Metacognitive training for schizophrenia patients (MCT) is a group intervention that seeks to sharpen the awareness of schizophrenia patients on cognitive biases (e.g. jumping to conclusions) that seem to underlie delusion formation and maintenance. The present trial combined group MCT with an individualized cognitive-behavioural therapy-oriented approach entitled individualized metacognitive therapy for psychosis (MCT+) and compared it against an active control.

A total of 48 patients fulfilling criteria of schizophrenia were randomly allocated to either MCT+ or cognitive remediation (clinical trial NCT01029067). Blind to intervention, both groups were assessed at baseline and 4 weeks later. Psychopathology was assessed using the Positive and Negative Syndrome Scale (PANSS) and the Psychotic Symptom Rating Scales (PSYRATS). Jumping to conclusions was measured using a variant of the beads task.

PANSS delusion severity declined significantly in the combined MCT treatment compared with the control condition. PSYRATS delusion conviction as well as jumping to conclusions showed significantly greater improvement in the MCT group. In line with prior studies, treatment adherence and subjective efficacy was excellent for the MCT.

The results suggest that the combination of a cognition-oriented and a symptom-oriented approach ameliorate psychotic symptoms and cognitive biases and represents a promising complementary treatment for schizophrenia.

There is a general consensus in the literature that schizophrenia causes difficulties with facial emotion perception and discrimination. Functional brain imaging studies have observed reduced limbic activity during facial emotion perception but few studies have examined the relation to flat affect severity.

A total of 26 people with schizophrenia and 26 healthy controls took part in this event-related functional magnetic resonance imaging study. Sad, happy and neutral faces were presented in a pseudo-random order and participants indicated the gender of the face presented. Manual segmentation of the amygdala was performed on a structural T1 image.

Both the schizophrenia group and the healthy control group rated the emotional valence of facial expressions similarly. Both groups exhibited increased brain activity during the perception of emotional faces relative to neutral ones in multiple brain regions, including multiple prefrontal regions bilaterally, the right amygdala, right cingulate cortex and cuneus. Group comparisons, however, revealed increased activity in the healthy group in the anterior cingulate, right parahippocampal gyrus and multiple visual areas. In schizophrenia, the severity of flat affect correlated significantly with neural activity in several brain areas including the amygdala and parahippocampal region bilaterally.

These results suggest that many of the brain regions involved in emotional face perception, including the amygdala, are equally recruited in both schizophrenia and controls, but flat affect can also moderate activity in some other brain regions, notably in the left amygdala and parahippocampal gyrus bilaterally. There were no significant group differences in the volume of the amygdala.

Both past depressive episodes and the personality trait of depressive rumination are strong risk factors for future depression. Depression is associated with abnormal emotional processing, which may be a neurobiological marker for vulnerability to depression. A consistent picture has yet to emerge as to how a history of depression and the tendency to ruminate influence emotional processing. The aim of this study was to investigate the relationship between rumination, past depression and neural responses when processing face emotions.

The Ruminative Responses Scale (RRS) was completed by 30 remitted depressives and 37 controls who underwent functional magnetic resonance imaging (fMRI) scanning while viewing happy, sad, fearful and neutral faces.

The remitted depressives showed overall reductions in neural responses to negative emotions relative to the controls. However, in the remitted depressives, but not the controls, RRS scores were correlated with increased neural responses to negative emotions and decreased responses to happiness in limbic regions.

Automatic emotion processing biases and rumination seem to be correlated to aspects of vulnerability to depression. However, remission from depression may be maintained by a general suppression of limbic responsiveness to negative emotion.

The determinants of depression following acute coronary syndrome (ACS) are poorly understood. Triggering of ACS by emotional stress and low socio-economic status (SES) are predictors of adverse outcomes. We therefore investigated whether emotional triggering and low SES predict depression and anxiety following ACS.

This prospective observational clinical cohort study involved 298 patients with clinically verified ACS. Emotional stress was assessed for the 2 h before symptom onset and compared with the equivalent period 24 h earlier using case-crossover methods. SES was defined by household income and education. Depression was measured with the Beck Depression Inventory and the Hamilton Rating Scale for Depression and anxiety with the Hospital Anxiety and Depression Scale 3 weeks after ACS and again at 6 and 12 months. Age, gender, ethnicity, marital status, the Global Registry of Acute Coronary Events risk score, duration of hospital stay and history of depression were included as covariates.

Emotional stress during the 2-h hazard period was associated with increased risk of ACS (odds ratio 1.88, 95% confidence interval 1.01–3.61). Both low income and emotional triggering predicted depression and anxiety at 3 weeks and 6/12 months independently of covariates. The two factors interacted, with the greatest depression and anxiety in lower income patients who experienced acute emotional stress. Education was not related to depression.

Patients who experience acute emotional stress during their ACS and are lower SES as defined by current affluence and access to resources are particularly vulnerable to subsequent depression and anxiety.

Teenage motherhood is relatively common in the UK, but little is known about related health inequalities in this population. We estimated cause-specific mortality risks over three decades in a nationally representative cohort.

We examined premature mortality in a 1.1% sample of all women who were teenagers in England and Wales during the 1970s, 1980s and 1990s using data from the Office for National Statistics Longitudinal Study (ONS LS). Our primary outcome was suicide. Long-term follow-up to 31 December 2006, to a potential maximum age of 49 years, was achieved through near-complete routine linkage to national mortality records. We created a time-dependent exposure variable, with relative risks estimated according to age when women first experienced motherhood versus a reference group of those currently without children.

Women who were teenage mothers were around 30% more likely to die prematurely by any cause and almost 60% more likely to die unnaturally, whereas first-time motherhood at mature age conferred lower risk compared to women without children. Teenage motherhood was associated with a more than doubled risk of suicide [mortality rate ratio (MRR) 2.23, 95% confidence interval (CI) 1.30–3.83], and elevated risks of fatal cancer of the cervix and lung were also found. Changing the reference category to first-time mothers at 20 years and above also revealed a significant elevation in risk of accidental death.

The complex psychosocial needs of these women require greater attention from clinicians, public health professionals, social services and policymakers. Their elevated risk of poor health outcomes may persist well beyond the actual teenage motherhood years.

It is unclear whether risk for major depression during the menopausal transition or immediately thereafter is increased relative to pre-menopause. We aimed to examine whether the odds of experiencing major depression were greater when women were peri- or post-menopausal compared to when they were pre-menopausal, independent of a history of major depression at study entry and annual measures of vasomotor symptoms (VMS), serum levels of, or changes in, estradiol (E2), follicular stimulating hormone (FSH) or testosterone (T) and relevant confounders.

Participants included the 221 African American and Caucasian women, aged 42–52 years, who were pre-menopausal at entry into the Pittsburgh site of a community-based study of menopause, the Study of Women's Health Across the Nation (SWAN). We conducted the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID) to assess diagnoses of lifetime, annual and current major depression at baseline and at annual follow-ups. Psychosocial and health factors, and blood samples for assay of reproductive hormones, were obtained annually.

Women were two to four times more likely to experience a major depressive episode (MDE) when they were peri-menopausal or early post-menopausal. Repeated-measures logistic regression analyses showed that the effect of menopausal status was independent of history of major depression and annually measured upsetting life events, psychotropic medication use, VMS and serum levels of or changes in reproductive hormones. History of major depression was a strong predictor of major depression throughout the study.

The risk of major depression is greater for women during and immediately after the menopausal transition than when they are pre-menopausal.

The cross-sectional association between impaired glucose/diabetes and depression is inconsistent. We examined the longitudinal associations between diabetes, indicators of glucose metabolism and depressive symptoms over 2 years of follow-up.

Participants were 4338 men and women from the English Longitudinal Study of Ageing, a prospective study of community-dwelling older adults [aged 62.9 (s.d.=9.0) years, 45.2% men]. Depressive symptoms were assessed at baseline and after 2 years of follow-up using the eight-item Centre of Epidemiological Studies – Depression (CES-D) scale. Glycated haemoglobin (HbA1c) levels, fasting glucose and other biological and behavioural risk factors were also assessed at baseline.

Approximately 11.5% of the sample were categorized with elevated depressive symptoms at follow-up (a score ⩾4 on the CES-D). There was an association between HbA1c and depressive symptoms at follow-up [per unit increase, odds ratio (OR) 1.17, 95% confidence interval (CI) 1.03–1.33] after adjustment for age and baseline CES-D. Cross-sectionally, the probability of depressive symptoms increased with increasing HbA1c levels until the value of 8.0% after which there was a plateau [p(curve)=0.03]. Compared with those with normal fasting glucose, participants with diabetes (confirmed through self-report or elevated fasting blood glucose) at baseline had an elevated risk of depressive symptoms at follow-up (OR 1.52, 95% CI 1.01–2.30) after adjusting for depressive symptoms at baseline, behavioural and sociodemographic variables, adiposity and inflammation.

These data suggest that poor glucose metabolism and diabetes are risk factors for future depression in older adults. There was no evidence of a U-shaped association.

We present the incidence and risk factors for major depressive disorder (MDD) among community-dwelling elderly Nigerians.

A cohort study of persons aged ⩾65 years residing in eight contiguous Yoruba-speaking states in south-west and north-central Nigeria was conducted between November 2003 and December 2007. Of the 2149 baseline sample, 1408 (66%) were successfully followed up after approximately 39 months. Face-to-face in-home assessments were conducted with the World Health Organization (WHO) Composite International Diagnostic Interview, version 3 (CIDI.3) and diagnosis was based on the DSM-IV. Incident MDD was determined in the group with no prior lifetime history of MDD at baseline and who were free of dementia at follow-up (n=892).

During the follow-up period, 308 persons had developed incident MDD, representing a rate of 104.3 [95% confidence interval (CI) 93.3–116.6] per 1000 person-years. Compared to males, the age-adjusted hazard for females was 1.63 (95% CI 1.30–2.06). Lifetime or current subsyndromal symptoms of depression at baseline did not increase the risk of incident MDD. Among females, but not males, rural residence and poor social network were risk factors for incident MDD. Physical health status at baseline did not predict new onset of MDD.

The finding of a high incidence of MDD among elderly Nigerians complements earlier reports of a high prevalence of the disorder in this understudied population. Social factors, in particular those relating to social isolation, constitute a risk for incident MDD.

Genetic and environmental factors are important in the etiology of substance use. However, little is known about the stability of these factors across development. We aimed to answer three crucial questions about this etiology that have never been addressed in a single study: (1) Is there a general vulnerability to substance consumption from early adolescence to young adulthood? (2) If so, do the genetic and environmental influences on this vulnerability change across development? (3) Do these developmental processes differ in males and females?

Subjects included 1480 twin pairs from the Swedish Twin Study of Child and Adolescent Development who have been followed since 1994. Prospective, self-reported regular smoking, alcohol intoxication and illicit drug use were assessed at ages 13–14, 16–17 and 19–20 years. Structural modeling was performed with the program Mx.

An underlying common factor accounted for the association between smoking, alcohol and illicit drug consumption for the three age groups. Common genetic and shared environmental effects showed substantial continuity. In general, as participants aged, the influence of the shared environment decreased, and genetic effects became more substance specific in their effect.

The current report answers three important questions in the etiology of substance use. The genetic and environmental risk for substance consumption is partly mediated through a common factor and is partly substance specific. Developmentally, evidence was strongest for stability of common genetic effects, with less evidence for genetic innovation. These processes seem to be the same in males and females.

Increased impulsivity is considered to be a core characteristic of borderline personality disorder (BPD) and has been shown to play a significant role in decision making and planning. Neuropsychological studies in BPD revealed impairments of executive functions, and it is assumed that these deficits are related to altered feedback processing. However, research on executive functions in BPD is still limited and the underlying deficits remain an open question. The present study, therefore, explored whether decision-making deficits are related to altered feedback evaluation in BPD.

A total of 18 BPD patients and 18 matched healthy controls underwent a modified version of the Iowa Gambling Task while an electroencephalogram was recorded. Feedback processing was examined by measuring the feedback-related negativity (FRN) and the P300 as electrophysiological correlates of feedback evaluation.

Behavioural results revealed that BPD patients, relative to controls, made more risky choices and did not improve their performance. With regard to the FRN, amplitudes in BPD patients did not discriminate between positive and negative feedback information. Further, BPD patients showed reduced FRN amplitudes, which were associated with enhanced impulsivity and enhanced risk taking. In contrast, the P300 amplitudes following negative feedback were increased in BPD patients, relative to controls.

This study indicates that BPD patients are impaired in decision making, which might be related to a dysfunctional use of feedback information. Specifically, BPD patients did not learn to avoid disadvantageous selections, even though they attended to negative consequences.

Disturbances in social interaction are a defining feature of patients with borderline personality disorder (BPD). In this study, facial emotional expressions, which are crucial for adaptive interactions in social contexts, were assessed in patients with BPD in response to social exclusion.

We examined facial emotional reactions of 35 patients with BPD and 33 healthy controls when playing Cyberball, a virtual ball-tossing game that reliably induces social exclusion. Besides self-reported emotional responses, facial emotional expressions were analyzed by applying the Emotional Facial Action Coding System (EMFACS).

Patients with BPD showed a biased perception of participation. They more readily reported feeling excluded compared to controls even when they were included. In BPD, social exclusion led to an increase in self-reported other-focused negative emotions. Overall, EMFACS analyses revealed that BPD patients reacted with fewer positive expressions and with significantly more mixed emotional expressions (two emotional facial expressions at the same time) compared to the healthy control group when excluded.

Besides a negative bias for perceived social participation, ambiguous facial emotional expressions may play an important role in the disturbed relatedness in patients with BPD.

Numerous longitudinal studies have identified risk factors for the onset of most eating disorders (EDs). Identifying women at highest risk within a high-risk sample would allow for focusing of preventive resources and also suggests different etiologies.

A longitudinal cohort study over 3 years in a high-risk sample of 236 college-age women randomized to the control group of a prevention trial for EDs. Potential risk factors and interactions between risk factors were assessed using the methods developed previously. Main outcome measures were time to onset of a subthreshold or full ED.

At the 3-year follow-up, 11.2% of participants had developed a full or partial ED. Seven of 88 potential risk factors could be classified as independent risk factors, seven as proxies, and two as overlapping factors. Critical comments about eating from teacher/coach/siblings and a history of depression were the most potent risk factors. The incidence for participants with either or both of these risk factors was 34.8% (16/46) compared to 4.2% (6/144) for participants without these risk factors, with a sensitivity of 0.75 and a specificity of 0.82.

Targeting preventive interventions at women with high weight and shape concerns, a history of critical comments about eating weight and shape, and a history of depression may reduce the risk for EDs.

The aim of this study was to explore the extent of lack of insight and its components in eating disorders (EDs) and to investigate the relationship between insight and clinical and cognitive characteristics in this group.

Seventy-five participants were enrolled in the study: 25 with anorexia nervosa (AN), 15 with bulimia nervosa (BN) and 35 healthy controls (HC). Insight was assessed with a modified version of the Schedule for the Assessment of Insight for EDs (SAI-ED) and multi-dimensional scaling (MDS) analysis was used to clarify the internal structure of the scale. Neuropsychological tests included the Trail Making Test (TMT), the Brixton Test and a Verbal Fluency Task.

Only a subgroup of AN patients (24%) had severe impairment of insight. Patients with the restricting type of AN (AN-R) had poorer overall insight than patients with the binge-purge type of the disorder (AN-B/P). More of the ED patients displayed a deliberate denial of illness rather than a lack of awareness of the illness. A regression model revealed that only performance in part B of the TMT (TMT-B) was a moderate predictor of insight level. No association was found between insight and other cognitive or clinical variables.

Impaired insight is a significant feature of some ED patients. Insight in EDs seems to be partially dependent on intact mental flexibility.

The stress response involves the activation of the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system (SNS). As a role for stress in determining of the onset and the natural course of eating disorders (EDs) has been proposed, the study of the psychobiology of the stress response in patients with anorexia nervosa (AN) and bulimia nervosa (BN) should be helpful in understanding the pathophysiology of these disorders. The two neurobiological components of the stress response can be easily explored in humans by the measurement of salivary cortisol and α-amylase response to a stressor. Therefore, we assessed salivary cortisol and α-amylase responses to the Trier Social Stress Test (TSST) in symptomatic patients with AN and BN compared to healthy controls.

Seven AN women, eight BN women and eight age-matched healthy females underwent the TSST between 1530 and 1700 h. Salivary cortisol and α-amylase levels were measured by an enzyme-linked immunosorbent assay (ELISA).

Compared to healthy women, AN patients showed a normal cortisol response to the TSST, although this occurred at significantly increased hormone levels, and an almost complete absence of response of α-amylase. BN women, however, exhibited enhanced pre-stress levels of salivary α-amylase but a normal response of the enzyme and cortisol to the TSST.

These findings demonstrate, for the first time, the occurrence of an asymmetry between the HPA axis and SNS components of the stress response in the acute phase of AN but not in BN. The pathophysiological significance of this asymmetry remains to be determined.

This study sought to determine the social and emotional impact of maternal loss on Aboriginal children and young people using data from the Western Australian Aboriginal Child Health Survey (WAACHS).

Data were from a population-based random sample of 5289 Aboriginal children aged under 18 years. Interview data about the children were gathered from primary carers and from their school teachers. Probabilistic record linkage to death registrations was used to ascertain deaths. Association between maternal death and subsequent psychosocial outcomes was assessed using univariate analyses and logistic regression.

Of the 5289 Aboriginal children, 57 had experienced the death of their birth mother prior to the survey. Multi-variable adjustment accounting for age and gender found that, relative to children who were living with their birth mother, children whose birth mother had died were at higher risk for sniffing glue or other substances [odds ratio (OR) 3.4, 95% confidence interval (CI) 1.3–8.7], using other drugs (OR 2.8, 95% CI 1.2–6.8), talking about suicide (OR 2.6, 95% CI 1.2–5.7) and attempting suicide (OR 7.0, 95% CI 1.6–31.1).

Although the death of a birth mother is relatively rare and the vast majority of Aboriginal children with adverse developmental outcomes live in families and are cared for by their birth mother, the findings here suggest that the loss of a birth mother and the circumstances arising from this impart a level of onward developmental risk for mental health morbidity in Australian Aboriginal children.

Non-suicidal self-injury (NSSI) has received increased attention in the mental health literature and has been proposed as a diagnostic entity for DSM-5. However, data on NSSI in the United States adult population are lacking.

The prevalence and nature of NSSI were examined in a random-digit dialing sample of 439 adults in the United States. Participants were recruited during July and August of 2008.

Lifetime prevalence of NSSI was 5.9%, including 2.7% who had self-injured five or more times. The 12-month prevalence was 0.9%. Methods of NSSI reported included cutting/carving, burning, biting, scraping/scratching skin, hitting, interfering with wound healing and skin picking. Half of self-injurers reported multiple methods. The average age of onset was 16 years (median 14 years). Instances of NSSI infrequently co-occurred with suicidal thoughts and with use of alcohol or drugs and rarely required medical treatment. Most injurers reported that NSSI functioned to alleviate negative emotions. Fewer reported that they self-injured to punish themselves, to communicate with others/get attention or to escape a situation or responsibility. NSSI was associated with younger age, being unmarried and a history of mental health treatment, but not with gender, ethnicity, educational history or household income.

Results are largely consistent with previous research in adolescent and young adult samples. Study limitations notwithstanding, this study provides the most definitive and detailed information to date regarding the prevalence and characteristics of NSSI in US adults. In the future, it will be important for large-scale epidemiological studies of psychopathology to include questions about NSSI.

To explore the genetic and environmental factors underlying the co-occurrence of lifetime diagnoses of DSM-IV phobia.

Female twins (n=1430) from the population-based Norwegian Institute of Public Health Twin Panel were assessed at personal interview for DSM-IV lifetime specific phobia, social phobia and agoraphobia. Comorbidity between the phobias were assessed by odds ratios (ORs) and polychoric correlations and multivariate twin models were fitted in Mx.

Phenotypic correlations of lifetime phobia diagnoses ranged from 0.55 (agoraphobia and social phobia, OR 10.95) to 0.06 (animal phobia and social phobia, OR 1.21). In the best fitting twin model, which did not include shared environmental factors, heritability estimates for the phobias ranged from 0.43 to 0.63. Comorbidity between the phobias was accounted for by two common liability factors. The first loaded principally on animal phobia and did not influence the complex phobias (agoraphobia and social phobia). The second liability factor strongly influenced the complex phobias, but also loaded weak to moderate on all the other phobias. Blood phobia was mainly influenced by a specific genetic factor, which accounted for 51% of the total and 81% of the genetic variance.

Phobias are highly co-morbid and heritable. Our results suggest that the co-morbidity between phobias is best explained by two distinct liability factors rather than a single factor, as has been assumed in most previous multivariate twin analyses. One of these factors was specific to the simple phobias, while the other was more general. Blood phobia was mainly influenced by disorder specific genetic factors.