The aims of this meta-analysis are (i) to estimate the pooled relative risk (RR) of developing non-affective psychotic disorder (NAPD) and affective psychotic disorder (APD) among migrants and their children; (ii) to adjust these results for socioeconomic status (SES); (iii) to examine the sources of heterogeneity that underlie the risk of NAPD.

We included population-based incidence studies that reported an age-adjusted RR with 95% confidence interval (CI) published 1 January 1977–12 October 2017 and used a random-effects model.

We retrieved studies performed in Europe (n = 43), Israel (n = 3), Canada (n = 2) and Australia (n = 1). The meta-analysis yielded a RR, adjusted for age and sex, of 2.13 (95% CI 1.99–2.27) for NAPD and 2.94 (95% CI 2.28–3.79) for APD. The RRs diminished, but persisted after adjustment for SES. With reference to NAPD: a personal or parental history of migration to Europe from countries outside Europe was associated with a higher RR (RR = 2.94, 95% CI 2.63–3.29) than migration within Europe (RR = 1.88, 95% 1.62–2.18). The corresponding RR was lower in Israel (RR = 1.22; 0.99–1.50) and Canada (RR = 1.21; 0.85–1.74). The RR was highest among individuals with a black skin colour (RR = 4.19, 95% CI 3.42–5.14). The evidence of a difference in risk between first and second generation was insufficient.

Positive selection may explain the low risk in Canada, while the change from exclusion to inclusion may do the same in Israel. Given the high risks among migrants from developing countries in Europe, social exclusion may have a pathogenic role.

Social attention ability is crucial for human adaptive social behaviors and interpersonal communications, and the malfunction of which has been implicated in autism spectrum disorder (ASD), a highly genetic neurodevelopmental disorder marked by striking social deficits.

Using a classical twin design, the current study investigated the genetic contribution to individual variation in social and non-social attention abilities, and further probed their potential genetic linkage. Moreover, individual autistic traits were further measured in an independent group of non-twin participants to examine the hypothetical link between the core social attention ability and ASD.

We found reliable genetic influences on the social attentional effects induced by two distinct cues (eye gaze and walking direction), with 91% of their covariance accounted for by common genetic effects. However, no evidence of heritability or shared genetic effects was observed for the attentional effect directed by a non-social cue (i.e. arrow direction) and its correlation with the social attention ability. Remarkably, one's autistic traits could well predict his/her heritable core social attention ability extracted from the conventional social attentional effect.

These findings together suggest that human social attention ability is supported by unique genetic mechanisms that can be shared across different social, but not non-social, processing. Moreover, they also encourage the identification of ‘social attention genes’ and highlight the critical role of the core human social attention ability in seeking the endophenotypes of social cognitive disorders including ASD.

Limbic-cortical imbalance is an established model for the neurobiology of major depressive disorder (MDD), but imaging genetics studies have been contradicting regarding potential risk and resilience mechanisms. Here, we re-assessed previously reported limbic-cortical alterations between MDD relatives and controls in combination with a newly acquired sample of MDD patients and controls, to disentangle pathology, risk, and resilience.

We analyzed functional magnetic resonance imaging data and negative affectivity (NA) of MDD patients (n = 48), unaffected first-degree relatives of MDD patients (n = 49) and controls (n = 109) who performed a faces matching task. Brain response and task-dependent amygdala functional connectivity (FC) were compared between groups and assessed for associations with NA.

Groups did not differ in task-related brain activation but activation in the superior frontal gyrus (SFG) was inversely correlated with NA in patients and controls. Pathology was associated with task-independent decreases of amygdala FC with regions of the default mode network (DMN) and decreased amygdala FC with the medial frontal gyrus during faces matching, potentially reflecting a task-independent DMN predominance and a limbic-cortical disintegration during faces processing in MDD. Risk was associated with task-independent decreases of amygdala-FC with fronto-parietal regions and reduced faces-associated amygdala-fusiform gyrus FC. Resilience corresponded to task-independent increases in amygdala FC with the perigenual anterior cingulate cortex (pgACC) and increased FC between amygdala, pgACC, and SFG during faces matching.

Our results encourage a refinement of the limbic-cortical imbalance model of depression. The validity of proposed risk and resilience markers needs to be tested in prospective studies. Further limitations are discussed.

Improving Access to Psychological Therapies (IAPT) services treat most patients in England who present to primary care with major depression. Psychodynamic psychotherapy is one of the psychotherapies offered. Dynamic Interpersonal Therapy (DIT) is a psychodynamic and mentalization-based treatment for depression. 16 sessions are delivered over approximately 5 months. Neither DIT's effectiveness relative to low-intensity treatment (LIT), nor the feasibility of randomizing patients to psychodynamic or cognitive-behavioural treatments (CBT) in an IAPT setting has been demonstrated.

147 patients were randomized in a 3:2:1 ratio to DIT (n = 73), LIT (control intervention; n = 54) or CBT (n = 20) in four IAPT treatment services in a combined superiority and feasibility design. Patients meeting criteria for major depressive disorder were assessed at baseline, mid-treatment (3 months) and post-treatment (6 months) using the Hamilton Rating Scale for Depression (HRSD-17), Beck Depression Inventory-II (BDI-II) and other self-rated questionnaire measures. Patients receiving DIT were also followed up 6 months post-completion.

The DIT arm showed significantly lower HRSD-17 scores at the 6-month primary end-point compared with LIT (d = 0.70). Significantly more DIT patients (51%) showed clinically significant change on the HRSD-17 compared with LIT (9%). The DIT and CBT arms showed equivalence on most outcomes. Results were similar with the BDI-II. DIT showed benefit across a range of secondary outcomes.

DIT delivered in a primary care setting is superior to LIT and can be appropriately compared with CBT in future RCTs.

Previous research has implicated demographic, psychological, behavioral, and cognitive variables in the onset and maintenance of pediatric overweight/obesity. No adequately-powered study has simultaneously modeled these variables to assess their relative associations with body mass index (BMI; kg/m2) in a nationally representative sample of youth.

Multiple machine learning regression approaches were employed to estimate the relative importance of 43 demographic, psychological, behavioral, and cognitive variables previously associated with BMI in youth to elucidate the associations of both fixed (e.g. demographics) and potentially modifiable (e.g. psychological/behavioral) variables with BMI in a diverse representative sample of youth. The primary analyses consisted of 9–10 year olds divided into a training (n = 2724) and test (n = 1123) sets. Secondary analyses were conducted by sex, ethnicity, and race.

The full sample model captured 12% of the variance in both the training and test sets, suggesting good generalizability. Stimulant medications and demographic factors were most strongly associated with BMI. Lower attention problems and matrix reasoning (i.e. nonverbal abstract problem solving and inductive reasoning) and higher social problems and screen time were robust positive correlates in the primary analyses and in analyses separated by sex.

Beyond demographics and stimulant use, this study highlights abstract reasoning as an important cognitive variable and reaffirms social problems and screen time as significant correlates of BMI and as modifiable therapeutic targets. Prospective data are needed to understand the predictive power of these variables for BMI gain.

The association between incarceration and psychiatric disorders has been noted. Yet, existing studies are cross-sectional or examine the risk of recidivism, which has limited the predictive validity of psychiatric disorders as a risk factor for incarceration. To overcome this limitation, this study used a prospective cohort to examine whether psychiatric diagnoses in early adulthood predicted incarceration throughout a 30-year follow-up. It tested the association between psychiatric diagnoses with future incarcerations, their number and durations, controlling for education and ethnic status.

This study merged data from three sources in Israel: a prospective 10-year birth cohort study of young adults aged 25–34, conducted in the 1980s (N = 4914) that included a psychiatric interview; data from the Prison Service, including the cause, number and duration of incarcerations; and from the Vital Statistics Registry on death records.

Multivariate analysis showed that substance-use disorders, antisocial personality and lower levels of education predicted future incarceration, their number and maximum duration. The remainder diagnoses were not significantly associated with future incarceration.

Results limited the prediction of future incarcerations to persons diagnosed with substance use and antisocial personality, and do not support an independent predictive association between additional psychiatric diagnoses and future incarceration.

Causes of the comorbidity of substance misuse with anxiety-related and depressive disorders (anxiety/depression) remain poorly known. We estimated associations of substance misuse and anxiety/depression in the general population and tested them while accounting for genetic and shared environmental factors.

We studied individuals born in Sweden 1968–1997 (n = 2 996 398) with follow-up in nationwide register data for 1997–2013. To account for familial effects, stratified analyses were conducted within siblings and twin pairs. Substance misuse was defined as ICD-10 alcohol or drug use disorder or an alcohol/drug-related criminal conviction. Three dimensions of ICD-10 anxiety and depressive disorders and a substance misuse dimension were identified through exploratory factor analysis.

Substance misuse was associated with a 4.5-fold (95% CI 4.50–4.58) elevated risk of lifetime generalized anxiety/depression, 4.7-fold (95% CI 4.63–4.82) elevated risk of panic disorder and agora/social phobia, and 2.9-fold elevated risk of phobias/OCD (95% CI 2.82–3.02) as compared to those without substance misuse. The associations were attenuated in within-family analyses but we found elevated risks in monozygotic twin pairs discordant for substance misuse as well as significant non-shared environmental correlations. The association between anxiety/depression and substance misuse was mainly driven by generalized anxiety/depression, whereas other anxiety/depression dimensions had minor or no independent associations with substance misuse.

Substance misuse and anxiety/depression are associated at the population level, and these associations are partially explained by familial liabilities. Our findings indicate a common genetic etiology but are also compatible with a potential partially causal relationship between substance misuse and anxiety/depression.

Childhood trauma, psychosis risk, cognition, and depression have been identified as important risk markers for suicidal behaviors. However, little is known about the interplay between these distal and proximal markers in influencing the risk of suicide. We aim to investigate the interplay between childhood trauma, cognitive biases, psychotic-like experiences (PLEs) and depression in predicting suicidal behaviors in a non-clinical sample of young adults.

In total, 3495 young adults were recruited to an online computer-assisted web interview. We used the Prodromal Questionnaire to assess PLEs. Childhood trauma was assessed with the Traumatic Experience Checklist (three items) and Childhood Experience of Care and Abuse Questionnaire (CECA.Q, three items). Cognitive biases were assessed with a short version of the Davos Assessment of Cognitive Biases Scale. Suicidality, psychiatric diagnoses, and substance use were screened with a self-report questionnaire.

Childhood trauma, as well as PLEs, was associated with an approximately five-fold increased risk of suicidal thoughts and plans as well as suicide attempts. Participants with depression were six times more likely to endorse suicidal behaviors. Path analysis revealed that PLEs, depression and cognitive biases are significant mediators of the relationship between trauma and suicidal behaviors. The model explained 44.6% of the variance in lifetime suicidality.

Cognitive biases, PLEs, and depression partially mediate the relationship between childhood trauma and suicidal behaviors. The interplay between distal and proximal markers should be recognized and become part of clinical screening and therapeutic strategies for preventing risk of suicidality.

Childhood maltreatment (CM) plays an important role in the development of major depressive disorder (MDD). The aim of this study was to examine whether CM severity and type are associated with MDD-related brain alterations, and how they interact with sex and age.

Within the ENIGMA-MDD network, severity and subtypes of CM using the Childhood Trauma Questionnaire were assessed and structural magnetic resonance imaging data from patients with MDD and healthy controls were analyzed in a mega-analysis comprising a total of 3872 participants aged between 13 and 89 years. Cortical thickness and surface area were extracted at each site using FreeSurfer.

CM severity was associated with reduced cortical thickness in the banks of the superior temporal sulcus and supramarginal gyrus as well as with reduced surface area of the middle temporal lobe. Participants reporting both childhood neglect and abuse had a lower cortical thickness in the inferior parietal lobe, middle temporal lobe, and precuneus compared to participants not exposed to CM. In males only, regardless of diagnosis, CM severity was associated with higher cortical thickness of the rostral anterior cingulate cortex. Finally, a significant interaction between CM and age in predicting thickness was seen across several prefrontal, temporal, and temporo-parietal regions.

Severity and type of CM may impact cortical thickness and surface area. Importantly, CM may influence age-dependent brain maturation, particularly in regions related to the default mode network, perception, and theory of mind.

This study investigated whether higher maternal choline levels mitigate effects of marijuana on fetal brain development. Choline transported into the amniotic fluid from the mother activates α7-nicotinic acetylcholine receptors on fetal cerebro-cortical inhibitory neurons, whose development is impeded by cannabis blockade of their cannabinoid-1(CB1) receptors.

Marijuana use was assessed during pregnancy from women who later brought their newborns for study. Mothers were informed about choline and other nutrients, but not specifically for marijuana use. Maternal serum choline was measured at 16 weeks gestation.

Marijuana use for the first 10 weeks gestation or more by 15% of mothers decreased newborns' inhibition of evoked potentials to repeated sounds (d’ = 0.55, p < 0.05). This effect was ameliorated if women had higher gestational choline (rs = −0.50, p = 0.011). At 3 months of age, children whose mothers continued marijuana use through their 10th gestational week or more had poorer self-regulation (d’ = −0.79, p < 0.05). This effect was also ameliorated if mothers had higher gestational choline (rs = 0.54, p = 0.013). Maternal choline levels correlated with the children's improved duration of attention, cuddliness, and bonding with parents.

Prenatal marijuana use adversely affects fetal brain development and subsequent behavioral self-regulation, a precursor to later, more serious problems in childhood. Stopping marijuana use before 10 weeks gestational age prevented these effects. Many mothers refuse to cease use because of familiarity with marijuana and belief in its safety. Higher maternal choline mitigates some of marijuana's adverse effects on the fetus.

Reward processing deficits have been implicated in the etiology of depression. A blunted reward positivity (RewP), an event-related potential elicited by feedback to monetary gain relative to loss, predicts new onsets and increases in depression symptoms. Etiological models of depression also highlight stressful life events. However, no studies have examined whether stressful life events moderate the effect of the RewP on subsequent depression symptoms. We examined this question during the key developmental transition from childhood to adolescence.

A community sample of 369 children (mean age of 9) completed a self-report measure of depression symptoms. The RewP to winning v. losing was elicited using a monetary reward task. Three years later, we assessed stressful life events occurring in the year prior to the follow-up. Youth depressive symptoms were rated by the children and their parents at baseline and follow-up.

Stressful life events moderated the effect of the RewP on depression symptoms at follow-up such that a blunted RewP predicted higher depression symptoms in individuals with higher levels of stressful life events. This effect was also evident when events that were independent of the youth's behavior were examined separately.

These results suggest that the RewP reflects a vulnerability for depression that is activated by stress.

The diet of most adults is low in fish and, therefore, provides limited quantities of the long-chain, omega-3 fatty acids (LCn-3FAs), eicosapentaenoic and docosahexaenoic acids (EPA, DHA). Since these compounds serve important roles in the brain, we sought to determine if healthy adults with low-LCn-3FA consumption would exhibit improvements in neuropsychological performance and parallel changes in brain morphology following repletion through fish oil supplementation.

In a randomized, controlled trial, 271 mid-life adults (30–54 years of age, 118 men, 153 women) consuming ⩽300 mg/day of LCn-3FAs received 18 weeks of supplementation with fish oil capsules (1400 mg/day of EPA and DHA) or matching placebo. All participants completed a neuropsychological test battery examining four cognitive domains: psychomotor speed, executive function, learning/episodic memory, and fluid intelligence. A subset of 122 underwent neuroimaging before and after supplementation to measure whole-brain and subcortical tissue volumes.

Capsule adherence was over 95%, participant blinding was verified, and red blood cell EPA and DHA levels increased as expected. Supplementation did not affect performance in any of the four cognitive domains. Exploratory analyses revealed that, compared to placebo, fish oil supplementation improved executive function in participants with low-baseline DHA levels. No changes were observed in any indicator of brain morphology.

In healthy mid-life adults reporting low-dietary intake, supplementation with LCn-3FAs in moderate dose for moderate duration did not affect neuropsychological performance or brain morphology. Whether salutary effects occur in individuals with particularly low-DHA exposure requires further study.

The present paper presents a fundamentally novel approach to model individual differences of persons with the same biologically heterogeneous mental disorder. Unlike prevalent case-control analyses, that assume a clear distinction between patient and control groups and thereby introducing the concept of an ‘average patient’, we describe each patient's biology individually, gaining insights into the different facets that characterize persistent attention-deficit/hyperactivity disorder (ADHD).

Using a normative modeling approach, we mapped inter-individual differences in reference to normative structural brain changes across the lifespan to examine the degree to which case-control analyses disguise differences between individuals.

At the level of the individual, deviations from the normative model were frequent in persistent ADHD. However, the overlap of more than 2% between participants with ADHD was only observed in few brain loci. On average, participants with ADHD showed significantly reduced gray matter in the cerebellum and hippocampus compared to healthy individuals. While the case-control differences were in line with the literature on ADHD, individuals with ADHD only marginally reflected these group differences.

Case-control comparisons, disguise inter-individual differences in brain biology in individuals with persistent ADHD. The present results show that the ‘average ADHD patient’ has limited informative value, providing the first evidence for the necessity to explore different biological facets of ADHD at the level of the individual and practical means to achieve this end.

Whether severe obstetric complications (OCs), which harm neural function in offspring, contribute to impaired cognition found in psychiatric disorders is currently unknown. Here, we sought to evaluate how a history of severe OCs is associated with cognitive functioning, indicated by Intelligence Quotient (IQ).

We evaluated the associations of a history of OCs and IQ in 622 healthy controls (HC) and 870 patients on the schizophrenia (SCZ) – bipolar disorder (BIP) spectrum from the ongoing Thematically Organized Psychosis study cohort, Oslo, Norway. Participants underwent assessments using the NART (premorbid IQ) and the WASI (current IQ). Information about OCs was obtained from the Medical Birth Registry of Norway. Multiple linear regression models were used for analysis.

Severe OCs were equally common across groups. SCZ patients with OCs had lower performances on both premorbid and current IQ measures, compared to those without OCs. However, having experienced more than one co-occurring severe OC was associated with lower current IQ in all groups.

Severe OCs were associated with lower IQ in the SCZ group and in the BIP and HC groups, but only if they had experienced more than one severe OC. Low IQ might be a neurodevelopmental marker for SCZ; wherein, severe OCs influence cognitive abilities and increase the risk of developing SCZ. Considering OCs as a variable of neurodevelopmental risk for severe mental illness may promote the development of neuroprotective interventions, improve outcome in vulnerable newborns and advance our ability to make clinical prognoses.

Recently, the MONARCA I randomized controlled trial (RCT) was the first to investigate the effect of smartphone-based monitoring in bipolar disorder (BD). Findings suggested that smartphone-based monitoring sustained depressive but reduced manic symptoms. The present RCT investigated the effect of a new smartphone-based system on the severity of depressive and manic symptoms in BD.

Randomized controlled single-blind parallel-group trial. Patients with BD, previously treated at The Copenhagen Clinic for Affective Disorder, Denmark and currently treated at community psychiatric centres, private psychiatrists or GPs were randomized to the use of a smartphone-based system or to standard treatment for 9 months. Primary outcomes: differences in depressive and manic symptoms between the groups.

A total of 129 patients with BD (ICD-10) were included. Intention-to-treat analyses showed no statistically significant effect of smartphone-based monitoring on depressive (B = 0.61, 95% CI −0.77 to 2.00, p = 0.38) and manic (B = −0.25, 95% CI −1.1 to 0.59, p = 0.56) symptoms. The intervention group reported higher quality of life and lower perceived stress compared with the control group. In sub-analyses, the intervention group had higher risk of depressive episodes, but lower risk of manic episodes compared with the control group.

There was no effect of smartphone-based monitoring. In patient-reported outcomes, patients in the intervention group reported improved quality of life and reduced perceived stress. Patients in the intervention group had higher risk of depressive episodes and reduced risk of manic episodes. Despite the widespread use and excitement of electronic monitoring, few studies have investigated possible effects. Further studies are needed.

Across psychopathologies, trauma-exposed individuals suffer from difficulties in inhibiting emotions and regulating attention. In trauma-exposed individuals without psychopathology, only subtle alterations of neural activity involved in regulating emotions have been reported. It remains unclear how these neural systems react to demanding environments, when acute (non-traumatic but ordinary) stress serves to perturbate the system. Moreover, associations with subthreshold clinical symptoms are poorly understood.

The present fMRI study investigated response inhibition of emotional faces before and after psychosocial stress situations. Specifically, it compared 25 women (mean age 31.5 ± 9.7 years) who had suffered severe early life trauma but who did not have a history of or current psychiatric disorder, with 25 age- and education-matched trauma-naïve women.

Under stress, response inhibition related to fearful faces was reduced in both groups. Compared to controls, trauma-exposed women showed decreased left inferior frontal gyrus (IFG) activation under stress when inhibiting responses to fearful faces, while activation of the right anterior insula was slightly increased. Also, groups differed in brain–behaviour correlations. Whereas stress-induced false alarm rates on fearful stimuli negatively correlated with stress-induced IFG signal in controls, in trauma-exposed participants, they positively correlated with stress-induced insula activation.

Neural facilitation of emotion inhibition during stress appears to be altered in trauma-exposed women, even without a history of or current psychopathology. Decreased activation of the IFG in concert with heightened bottom-up salience of fear related cues may increase vulnerability to stress-related diseases.

Early life maltreatment (ELM), borderline personality disorder (BPD), and major depressive disorder (MDD) have been associated with empathy deficits in different domains. Lack of maternal empathy has also been related to child behavioral problems. As ELM, BPD, and MDD often co-occur, we aimed to identify dissociable effects on empathy due to these three factors. In addition, we aimed to investigate their indirect effects via empathy on child psychopathology.

We included 251 mothers with and without MDD (in remission), BPD and ELM and their children, aged 5–12. We used the Interpersonal Reactivity Index as a measure of empathy on four different dimensions (personal distress, empathic concern, perspective taking, and fantasy) and the Child Behavior Checklist as a measure of child psychopathology.

Having included all three factors (ELM, MDD, BPD) in one analysis, we found elevated personal distress in MDD and BPD, and lower levels of perspective-taking in BPD, but no effects from ELM on any empathy subscales. Furthermore, we found indirect effects from maternal BPD and MDD on child psychopathology, via maternal personal distress.

The present study demonstrated the dissociable effects of maternal ELM, MDD, and BPD on empathy. Elevated personal distress in mothers with BPD and MDD may lead to higher levels of child psychopathology.

Preliminary evidence suggests that hoarding disorder (HD) and obsessive-compulsive disorder (OCD) may show distinct patterns of brain activation during executive performance, although results have been inconclusive regarding the specific neural correlates of their differential executive dysfunction. In the current study, we aim to evaluate differences in brain activation between patients with HD, OCD and healthy controls (HCs) during response inhibition, response switching and error processing.

We assessed 17 patients with HD, 18 patients with OCD and 19 HCs. Executive processing was assessed inside a magnetic resonance scanner by means of two variants of a cognitive control protocol (i.e. stop- and switch-signal tasks), which allowed for the assessment of the aforementioned executive domains.

OCD patients performed similar to the HCs, differing only in the number of successful go trials in the switch-signal task. However, they showed an anomalous hyperactivation of the right rostral anterior cingulate cortex during error processing in the switch-signal task. Conversely, HD patients performed worse than OCD and HC participants in both tasks, showing an impulsive-like pattern of response (i.e. shorter reaction time and more commission errors). They also exhibited hyperactivation of the right lateral orbitofrontal cortex during successful response switching and abnormal deactivation of frontal regions during error processing in both tasks.

Our results support that patients with HD and OCD present dissimilar cognitive profiles, supported by distinct neural mechanisms. Specifically, while alterations in HD resemble an impulsive pattern of response, patients with OCD present increased error processing during response conflict protocols.

Bipolar disorder (BD) is associated with attentional and processing abnormalities. Such abnormalities are also seen in healthy subjects with sleep disruption. We hypothesised cognitive abnormalities in BD patients would be worse in those with objectively verified sleep abnormalities.

Forty-six BD patients and 42 controls had comprehensive sleep/circadian rhythm assessment over 21 days alongside mood questionnaires. Cognitive function was assessed with a range of tasks including Psychomotor Vigilance Test (PVT), Attention Network Task (ANT) and Digit Symbol Substitution Test (DSST). BD participants with normal and abnormal sleep were compared with age- and sex-matched controls.

BD patients had longer response times and made more lapses (responses >500 ms) than controls on the PVT (both p < 0.001). However, patients with normal sleep patterns did not differ from controls while those with sleep abnormalities did (p < 0.001). An identical pattern of effects were seen with the ANT response times, with the abnormality in bipolar abnormal sleepers related to the executive attentional network. Similarly, patients made fewer correct responses on the DSST compared with the controls (p < 0.001). Bipolar normal sleepers did not differ while those with abnormal sleep did (p < 0.001). All these differences were seen in bipolar abnormal sleepers who were euthymic (p < 0.01) and across the main abnormal sleep phenotypes.

We confirm impairment in attention and processing speed in BD. Rather than sleep abnormalities exacerbating such dysfunction, the impairments were confined to bipolar abnormal sleepers, consistent with sleep disturbance being the main driver of cognitive dysfunction.