The cognitive model of depression suggests that cognitive therapy (CT) improves major depressive disorder (MDD) in part by changing depressive cognitive content (e.g. dysfunctional attitudes, hopelessness). The current analyses clarified: (1) the durability of improvements in cognitive content made by acute-phase CT responders; (2) whether continuation-phase CT (C-CT) or fluoxetine (FLX) further improves cognitive content; and (3) the extent to which cognitive content mediates continuation treatments’ effects on depressive symptoms and major depressive relapse/recurrence.

Out-patients with recurrent MDD who responded to acute-phase CT (n = 241) were randomized to 8 months of C-CT, FLX or pill placebo (PBO) and followed for an 24 additional months. Cognitive content was assessed approximately every 4 months using five standard patient-report measures.

Large improvements in cognitive content made during acute-phase CT were maintained for 32 months, with 78–90% of patients scoring in normal ranges, on average. Cognitive content varied little between C-CT, FLX and PBO arms, overall. Small, transient improvements in cognitive content in C-CT or FLX compared with PBO patients did not clearly mediate the treatments’ effects on depressive symptoms or on major depressive relapse/recurrence.

Outpatients with recurrent MDD who respond to acute-phase CT show durable improvements in cognitive content. C-CT or FLX may not continue to improve patient-reported cognitive content substantively, and thus may treat recurrent MDD by other paths.

Research evidence suggests that cognitive and neural mechanisms involved in social information processing may underlie the key aspects associated with the emergence of aggression and psychopathy. Despite extensive research in this field, it is unclear whether this deficit relates to general attentional problems or affects early stages of information processing. Therefore, the aim was to explore the link between aggression, psychopathic traits, and the early processing deficits in young antisocial violent offenders (YAVOs) and healthy controls (CTLs).

Participants were presented with rapidly changing Mondrian-like images in one eye, while a neutral or emotional (happy, angry, fearful, disgusted, surprised, sad) face was slowly introduced to the other eye. Participants indicated the location in which the face had appeared on the screen, reflecting the time when they became aware of the stimulus. The relative processing advantage was obtained by subtracting mean reaction times for emotional from neutral faces.

The results indicated that individuals with higher levels of unemotional traits tended to exhibit an extensive early processing disadvantage for fearful facial expressions; this relationship was only evident in the YAVO as opposed to the CTL sample.

These findings indicate that an emotion processing deficit in antisocial individuals is present even at the most basic levels of processing and closely related to certain psychopathic traits. Furthermore, this early processing deficit appears to be highly specific to fearful expressions, which is consistent with predictions made by influential models of psychopathy. The clinical significance and potential implications of the results are discussed.

Multiple pathway models of attention deficit hyperactivity disorder (ADHD) suggest that this disorder is the behavioural expression of dysfunction in one of several separable brain systems. One such model focuses on the brain systems underlying cognitive control, timing and reward sensitivity. It predicts separable subgroups among individuals with ADHD, with performance deficits in only one of these domains. We used latent class analysis (LCA) to identify subgroups of individuals with ADHD based on their overall pattern of neuropsychological performance, rather than grouping them based on cut-off criteria. We hypothesized that we would find separable subgroups with deficits in cognitive control, timing and reward sensitivity respectively.

Ninety-six subjects with ADHD (of any subtype) and 121 typically developing controls performed a battery assessing cognitive control, timing and reward sensitivity. LCA was used to identify subgroups of individuals with ADHD with a distinct neuropsychological profile. A similar analysis was performed for controls.

Three subgroups represented 87% of subjects with ADHD. Two of our three hypothesized subgroups were identified, with poor cognitive control and timing. Two of the ADHD subgroups had similar profiles to control subgroups, whereas one subgroup had no equivalent in controls.

Our findings support multiple pathway models of ADHD, as we were able to define separable subgroups with differing cognitive profiles. Furthermore, we found both quantitative and qualitative differences from controls, suggesting that ADHD may represent both categorical and dimensional differences. These results show that by addressing heterogeneity in ADHD, we can identify more homogeneous subsets of individuals to further investigate.

Maternal depression and unhealthy diet are well-known risk factors for adverse child emotional–behavioural outcomes, but their developmental relationships during the prenatal and postnatal periods are largely uncharted. This study sought to examine the inter-relationships between maternal depression symptoms and unhealthy diet (assessed during pregnancy and postnatal periods) in relation to child emotional–behavioural dysregulation (assessed at the ages of 2, 4 and 7 years).

In a large prospective birth cohort of 7814 mother–child pairs, path analysis was used to examine the independent and inter-related associations of maternal depression symptoms and unhealthy diet with child dysregulation.

Higher prenatal maternal depression symptoms were prospectively associated with higher unhealthy diet, both during pregnancy and the postnatal period, which, in turn, was associated with higher child dysregulation up to the age of 7 years. In addition, during pregnancy, higher maternal depression symptoms and unhealthy diet were each independently associated with higher child dysregulation up to the age of 7 years. These results were robust to other prenatal, perinatal and postnatal confounders (such as parity and birth complications, poverty, maternal education, etc.).

Maternal depression symptoms and unhealthy diet show important developmental associations, but are also independent risk factors for abnormal child development.

Although the association between attention-deficit/hyperactivity disorder (ADHD) and drug use disorder (DUD) is well documented, it is unclear whether it is causal or results from familial confounding.

In this study we included all 551 164 individuals born in Sweden between 1991 and 1995 and used linked data from multiple nationwide registries to identify those with ADHD prior to age 15 years (1.71%). We used Cox proportional hazards models to investigate the future risk for DUD as a function of an ADHD registration and then compared the results from the entire population with the results from a co-relative design. Using the Swedish Multi-Generation Register, we identified all full-sibling, half-sibling and first-cousin pairs discordant for ADHD.

In the population sample, ADHD had a substantially increased risk for future DUD with a hazard ratio (HR) of 3.34 after accounting for gender and parental education. Examining discordant cousin pairs, discordant half-siblings and discordant siblings, those with ADHD had HRs for DUD of 3.09, 2.10 and 2.38 respectively. Controlling for the number of ADHD registrations, ADHD patients with and without stimulant treatment were similarly associated with later DUD risk.

ADHD diagnosed before 15 years of age was strongly related to future risk for DUD. The magnitude of this association was modestly reduced in relative pairs discordant for ADHD, suggesting that the ADHD–DUD association is partly causal and partly a result of familial confounding. We found no evidence to suggest that this association resulted from stimulant treatment.

Prisoners have an exceptional risk of suicide. Cognitive–behavioural therapy for suicidal behaviour has been shown to offer considerable potential, but has yet to be formally evaluated within prisons. This study investigated the feasibility of delivering and evaluating a novel, manualized cognitive–behavioural suicide prevention (CBSP) therapy for suicidal male prisoners.

A pilot randomized controlled trial of CBSP in addition to treatment as usual (CBSP; n = 31) compared with treatment as usual (TAU; n = 31) alone was conducted in a male prison in England. The primary outcome was self-injurious behaviour occurring within the past 6 months. Secondary outcomes were dimensions of suicidal ideation, psychiatric symptomatology, personality dysfunction and psychological determinants of suicide, including depression and hopelessness. The trial was prospectively registered (number ISRCTN59909209).

Relative to TAU, participants receiving CBSP therapy achieved a significantly greater reduction in suicidal behaviours with a moderate treatment effect [Cohen's d = −0.72, 95% confidence interval −1.71 to 0.09; baseline mean TAU: 1.39 (s.d. = 3.28) v. CBSP: 1.06 (s.d. = 2.10), 6 months mean TAU: 1.48 (s.d. = 3.23) v. CBSP: 0.58 (s.d. = 1.52)]. Significant improvements were achieved on measures of psychiatric symptomatology and personality dysfunction. Improvements on psychological determinants of suicide were non-significant. More than half of the participants in the CBSP group achieved a clinically significant recovery by the end of therapy, compared with a quarter of the TAU group.

The delivery and evaluation of CBSP therapy within a prison is feasible. CBSP therapy offers significant promise in the prevention of prison suicide and an adequately powered randomized controlled trial is warranted.

Previous studies have provided inconsistent evidence that chronic exposure to opioid drugs, including heroin and methadone, may be associated with impairments in executive neuropsychological functioning, specifically cognitive impulsivity. Further, it remains unclear how such impairments may relate of the nature, level and extent of opioid exposure, the presence and severity of opioid dependence, and hazardous behaviours such as injecting.

Participants with histories of illicit heroin use (n = 24), former heroin users stabilized on prescribed methadone (methadone maintenance treatment; MMT) (n = 29), licit opioid prescriptions for chronic pain without history of abuse or dependence (n = 28) and healthy controls (n = 28) were recruited and tested on a task battery that included measures of cognitive impulsivity (Cambridge Gambling Task, CGT), motor impulsivity (Affective Go/NoGo, AGN) and non-planning impulsivity (Stockings of Cambridge, SOC).

Illicit heroin users showed increased motor impulsivity and impaired strategic planning. Additionally, they placed higher bets earlier and risked more on the CGT. Stable MMT participants deliberated longer and placed higher bets earlier on the CGT, but did not risk more. Chronic opioid exposed pain participants did not differ from healthy controls on any measures on any tasks. The identified impairments did not appear to be associated specifically with histories of intravenous drug use, nor with estimates of total opioid exposure.

These data support the hypothesis that different aspects of neuropsychological measures of impulsivity appear to be associated with exposure to different opioids. This could reflect either a neurobehavioural consequence of opioid exposure, or may represent an underlying trait vulnerability to opioid dependence.

Prenatal stress is hypothesized to have a disruptive impact on neurodevelopmental trajectories, but few human studies have been conducted on the long-term neural correlates of prenatal exposure to stress. The aim of this study was to explore the relationship between prenatal stress exposure and gray-matter volume and resting-state functional connectivity in a sample of 35 healthy women aged 14–40 years.

Voxel-based morphometry and functional connectivity analyses were performed on the whole brain and in specific regions of interest (hippocampus and amygdala). Data about prenatal/postnatal stress and obstetric complications were obtained by interviewing participants and their mothers, and reviewing obstetric records.

Higher prenatal stress was associated with decreased gray-matter volume in the left medial temporal lobe (MTL) and both amygdalae, but not the hippocampus. Variance in gray-matter volume of these brain areas significantly correlated with depressive symptoms, after statistically adjusting for the effects of age, postnatal stress and obstetric complications. Prenatal stress showed a positive linear relationship with functional connectivity between the left MTL and the pregenual cortex. Moreover, connectivity between the left MTL and the left medial-orbitofrontal cortex partially explained variance in the depressive symptoms of offspring.

In young women, exposure to prenatal stress showed a relationship with the morphometry and functional connectivity of brain areas involved in the pathophysiology of depressive disorders. These data provide evidence in favor of the hypothesis that early exposure to stress affects brain development and identified the MTL and amygdalae as possible targets of such exposure.

Telomere attrition might be one of the mechanisms through which psychosocial stress leads to somatic disease. To date it is unknown if exposure to adverse life events in adulthood is associated with telomere shortening prospectively. In the current study we investigated whether life events are associated with shortening of telomere length (TL).

Participants were 1094 adults (mean age 53.1, range 33–79 years) from the PREVEND cohort. Data were collected at baseline (T1) and at two follow-up visits after 4 years (T2) and 6 years (T3). Life events were assessed with an adjusted version of the List of Threatening Events (LTE). TL was measured by monochrome multiplex quantitative PCR at T1, T2, and T3. A linear mixed model was used to assess the effect of recent life events on TL prospectively. Multivariable regression analyses were performed to assess whether the lifetime life events score or the score of life events experienced before the age of 12 predicted TL cross-sectionally. All final models were adjusted for age, sex, body mass index, presence of chronic diseases, frequency of sports, smoking status, and level of education.

Recent life events significantly predicted telomere attrition prospectively (B = −0.031, p = 0.007). We were not able to demonstrate a significant cross-sectional relationship between the lifetime LTE score and TL. Nor did we find exposure to adverse life events before the age of 12 to be associated with TL in adulthood.

Exposure to recent adverse life events in adulthood is associated with telomere attrition prospectively.

This study prospectively assesses the mental health outcomes among women seeking abortions, by comparing women having later abortions with women denied abortions, up to 2 years post-abortion seeking.

We present the first 2 years of a 5-year telephone interview study that is following 956 women who sought an abortion from 30 facilities throughout the USA. We use adjusted linear mixed-effects regression analyses to assess whether symptoms of depression and anxiety, as measured by the Brief Symptom Inventory-short form and the Primary Care Evaluation of Mental Disorders Patient Health Questionnaire, differ over time among women denied an abortion due to advanced gestational age, compared with women who received abortions.

Baseline predicted mean depressive symptom scores for women denied abortion (3.07) were similar to women receiving an abortion just below the gestational limit (2.86). Depressive symptoms declined over time, with no difference between groups. Initial predicted mean anxiety symptoms were higher among women denied care (2.59) than among women who had an abortion just below the gestational limit (1.91). Anxiety levels in the two groups declined and converged after 1 year.

Women who received an abortion had similar or lower levels of depression and anxiety than women denied an abortion. Our findings do not support the notion that abortion is a cause of mental health problems.

Clinical and ethical implications of personality and mood changes in Parkinson's disease (PD) patients treated with subthalamic deep brain stimulation (STN-DBS) are under debate. Although subjectively perceived personality changes are often mentioned by patients and caregivers, few empirical studies concerning these changes exist. Therefore, we analysed subjectively perceived personality and mood changes in STN-DBS PD patients.

In this prospective study of the ELSA-DBS group, 27 PD patients were assessed preoperatively and 1 year after STN-DBS surgery. Two categories, personality and mood changes, were analysed with semi-structured interviews. Patients were grouped into personality change yes/no, as well as positive/negative mood change groups. Caregivers were additionally interviewed about patients’ personality changes. Characteristics of each group were assessed with standard neurological and psychiatric measurements. Predictors for changes were analysed.

Personality changes were perceived by six of 27 (22%) patients and by 10 of 23 caregivers (44%). The preoperative hypomania trait was a significant predictor for personality change perceived by patients. Of 21 patients, 12 (57%) perceived mood as positively changed. Higher apathy and anxiety ratings were found in the negative change group.

Our results show that a high proportion of PD patients and caregivers perceived personality changes under STN-DBS, emphasizing the relevance of this topic. Mood changed in positive and negative directions. Standard measurement scales failed to adequately reflect personality or mood changes subjectively perceived by patients. A more individualized preoperative screening and preparation for patients and caregivers, as well as postoperative support, could therefore be useful.

Major depressive disorder (MDD) that onsets by adolescence is associated with various deficits in psychosocial functioning. However, adolescent-onset MDD often follows a recurrent course that may drive its associated impairment.

To tease apart these two clinical features, we examined the relative associations of age of onset (adolescent versus adult) and course (recurrent versus single episodes) of MDD with a broad range of psychosocial functioning outcomes assessed in early adulthood. Participants comprised a large, population-based sample of male and female twins from the Minnesota Twin Family Study (MTFS; n = 1252) assessed prospectively from ages 17 to 29 years.

A recurrent course of MDD predicted impairment in several psychosocial domains in adulthood, regardless of whether the onset was in adolescence or adulthood. By contrast, adolescent-onset MDD showed less evidence of impairment in adulthood after accounting for recurrence. Individuals with both an adolescent onset and recurrent episodes of MDD represented a particularly severe group with pervasive psychosocial impairment in adulthood.

The negative implications of adolescent-onset MDD for psychosocial functioning in adulthood seem to be due primarily to its frequently recurrent course, rather than its early onset, per se. The results highlight the importance of considering both age of onset and course for understanding MDD and its implications for functioning, and also in guiding targeted intervention efforts.

Although risk for psychosis in velocardiofacial (22q11.2 deletion) syndrome (VCFS) is well established, the cognitive and familial factors that moderate that risk are poorly understood.

A total of 75 youth with VCFS were assessed at three time points, at 3-year intervals. Time 1 (T1) psychiatric risk was assessed with the Behavior Assessment System for Children (BASC). Data reduction of BASC scores yielded avoidance–anxiety and dysregulation factors. Time 2 (T2) neuropsychological and family function and time 3 (T3) prodromal/overt psychosis were assessed. Poisson regression models tested associations between T3 positive prodromal symptoms/overt psychosis and T1 psychiatric risk, T2 cognitive and familial factors, and their interactions.

T1 avoidance–anxiety ratings predicted T3 prodromal/overt psychosis. T2 verbal learning scores moderated this association, such that individuals with low avoidance–anxiety scores and stronger verbal learning skills were the least likely to demonstrate prodromal/overt psychosis at T3. Low scores on a T2 visual vigilance task also predicted T3 prodromal/overt psychosis, independently of the effect of T1 avoidance–anxiety scores. T1 dysregulation scores did not predict T3 prodromal/overt psychosis in a linear manner. Instead, the association between dysregulation and prodromal/overt psychosis was amplified by T2 levels of family organization, such that individuals with low dysregulation scores and low family organization scores were the most likely to exhibit T3 prodromal/overt psychosis.

Significant moderators of psychiatric risk in VCFS include verbal learning skills as well as levels of family organization, carrying implications for early identification and preventative treatment of youth with VCFS at highest risk for psychosis.

Fluoxetine is generally regarded as the first-line pharmacological treatment for young people, as it is believed to show a more favourable benefit:risk ratio than other antidepressants. However, the mechanisms through which fluoxetine influences symptoms in youth have been little investigated. This study examined whether acute administration of fluoxetine in a sample of young healthy adults altered the processing of affective information, including positive, sad and anger cues.

A total of 35 male and female volunteers aged between 18 and 21 years old were randomized to receive a single 20 mg dose of fluoxetine or placebo. At 6 h after administration, participants completed a facial expression recognition task, an emotion-potentiated startle task, an attentional dot-probe task and the Rapid Serial Visual Presentation. Subjective ratings of mood, anxiety and side effects were also taken pre- and post-fluoxetine/placebo administration.

Relative to placebo-treated participants, participants receiving fluoxetine were less accurate at identifying anger and sadness and did not show the emotion-potentiated startle effect. There were no overall significant effects of fluoxetine on subjective ratings of mood.

Fluoxetine can modulate emotional processing after a single dose in young adults. This pattern of effects suggests a potential cognitive mechanism for the greater benefit:risk ratio of fluoxetine in adolescent patients.

Smaller hippocampal volume has often been observed in patients with post-traumatic stress disorder (PTSD). However, there is no consensus whether this is a result of stress/trauma exposure, or constitutes a vulnerability factor for the development of PTSD. Second, it is unclear whether hippocampal volume normalizes with successful treatment of PTSD, or whether a smaller hippocampus is a risk factor for the persistence of PTSD.

Magnetic resonance imaging (MRI) scans and clinical interviews were collected from 47 war veterans with PTSD, 25 healthy war veterans (combat controls) and 25 healthy non-military controls. All veterans were scanned a second time with a 6- to 8-month interval, during which PTSD patients received trauma-focused therapy. Based on post-treatment PTSD symptoms, patients were divided into a PTSD group who was in remission (n = 22) and a group in whom PTSD symptoms persisted (n = 22). MRI data were analysed with Freesurfer.

Smaller left hippocampal volume was observed in PTSD patients compared with both control groups. Hippocampal volume of the combat controls did not differ from healthy controls. Second, pre- and post-treatment analyses of the PTSD patients and combat controls revealed reduced (left) hippocampal volume only in the persistent patients at both time points. Importantly, hippocampal volume did not change with treatment.

Our findings suggest that a smaller (left) hippocampus is not the result of stress/trauma exposure. Furthermore, hippocampal volume does not increase with successful treatment. Instead, we demonstrate for the first time that a smaller (left) hippocampus constitutes a risk factor for the persistence of PTSD.

Altered corticostriatothalamic encoding of reinforcement is a core feature of depression. Here we examine reinforcement learning in late-life depression in the theoretical framework of the vascular depression hypothesis. This hypothesis attributes the co-occurrence of late-life depression and poor executive control to prefrontal/cingulate disconnection by vascular lesions.

Our fMRI study compared 31 patients aged ⩾60 years with major depression to 16 controls. Using a computational model, we estimated neural and behavioral responses to reinforcement in an uncertain, changing environment (probabilistic reversal learning).

Poor executive control and depression each explained distinct variance in corticostriatothalamic response to unexpected rewards. Depression, but not poor executive control, predicted disrupted functional connectivity between the striatum and prefrontal cortex. White-matter hyperintensities predicted diminished corticostriatothalamic responses to reinforcement, but did not mediate effects of depression or executive control. In two independent samples, poor executive control predicted a failure to persist with rewarded actions, an effect distinct from depressive oversensitivity to punishment. The findings were unchanged in a subsample of participants with vascular disease. Results were robust to effects of confounders including psychiatric comorbidities, physical illness, depressive severity, and psychotropic exposure.

Contrary to the predictions of the vascular depression hypothesis, altered encoding of rewards in late-life depression is dissociable from impaired contingency learning associated with poor executive control. Functional connectivity and behavioral analyses point to a disruption of ascending mesostriatocortical reward signals in late-life depression and a failure of cortical contingency encoding in elderly with poor executive control.

Despite elevated risk profiles for depression among South Asian and Black Caribbean people in the UK, prevalences of late-life depressive symptoms across the UK's three major ethnic groups have not been well characterized.

Data were collected at baseline and 20-year follow-up from 632 European, 476 South Asian and 181 Black Caribbean men and women (aged 58–88 years), of a community-based cohort study from north-west London. The 10-item Geriatric Depression Scale was interviewer-administered during a clinic visit (depressive symptoms defined as a score of ⩾4 out of 10), with clinical data (adiposity, diabetes, cardiovascular disease, cognitive function) also collected. Sociodemographic, psychosocial, behavioural, disability, and medical history information was obtained by questionnaire.

Prevalence of depressive symptoms varied by ethnic group, affecting 9.7% of White European, 15.5% of South Asian, and 17.7% of Black Caribbean participants. Compared with White Europeans, South Asian and Black Caribbean participants were significantly more likely to have depressive symptoms (odds ratio 1.79, 95% confidence interval 1.24–2.58 and 1.80, 1.11–2.92, respectively). Adjustment for co-morbidities had most effect on the excess South Asian odds, and adjustment for socioeconomic position had most effect on the elevated Black Caribbean odds.

Higher prevalence of depressive symptoms observed among South Asian people were attenuated after adjustment for physical health, whereas the Black Caribbean increased prevalence was most explained by socioeconomic disadvantage. It is important to understand the reasons for these ethnic differences to identify opportunities for interventions to address inequalities.

While drug abuse (DA) is strongly familial, we still have limited knowledge about the causes of its cross-generational transmission.

We examined DA ascertained from national registers in offspring of three family types from the Swedish population [intact (n = 2 111 074), ‘not-lived-with’ (n = 165 315, where biological parents never lived with their offspring) and ‘step’ (n = 124 800 offspring)], which reflected, respectively, the effects of genes + rearing, genes only and rearing only. We replicated these results in three high-risk co-relative designs.

Combined across mothers and fathers, the hazard ratio (HR) for DA in offspring given DA in parents was 3.52 in intact, 2.73 in ‘not-lived-with’ and 1.79 in stepfamilies. In 968 biological full or half-sibling pairs one of whom was reared by and the other never lived with their parent with DA, the HR for DA was greater in the reared than ‘not-lived-with’ child (HR 1.57). In 64 offspring pairs of a parent with DA, the HR for DA was greater in a reared biological v. step-parented non-biological child (HR 3.33). In 321 pairs of offspring of a parent with DA one of whom was a not-lived-with biological child and the second a step-parented non-biological child, the HR for DA was greater in the biological v. stepchild (HR 1.80).

Both genetic and environmental factors contribute substantially to parent–offspring resemblance for DA. The general population contains informative family constellations that can complement more traditional adoption designs in clarifying the sources of parent–offspring resemblance.

Impulsivity is a hallmark characteristic of substance use disorders. Recently, studies have begun to explore whether increased impulsivity in substance-dependent individuals (SDIs) is associated with a greater propensity to relapse following treatment. Despite growing recognition of its multidimensional nature, however, most studies have treated impulsivity unilaterally. Accordingly, it remains unclear whether certain facets of impulsivity are more relevant to relapse than others. The aim of the current study was to examine the relationship between multiple facets of impulsivity and short-term relapse in SDIs. As a secondary aim, we explored the role of treatment retention in this relationship.

A personality-based impulsivity questionnaire (UPPS) and three neurocognitive tasks of impulsivity [stop-signal task (SST), delay discounting task (DDT) and Iowa gambling task (IGT)] were administered in a heterogeneous sample of 70 SDIs shortly following their entry in an in-patient detoxification programme. Mediation analyses were performed to explore whether the effects of impulsivity on relapse were mediated by treatment retention.

Performance on two neurocognitive indices of impulsive choice (i.e. delay discounting and impulsive decision-making) significantly predicted short-term relapse. The effects of delay discounting and impulsive decision-making on relapse propensity were mediated by treatment retention.

Neurocognitive indices of impulsivity may be more sensitive to the prediction of relapse than trait-based self-report questionnaires. Post-treatment relapse in SDIs may be reduced by targeting the processes involved in impulsive choice and by improving treatment retention in SDIs with inflated impulsivity.

Attentional impairment is a core cognitive feature of major depressive disorder (MDD) and bipolar disorder (BD). However, little is known of the characteristics of response time (RT) distributions from attentional tasks. This is crucial to furthering our understanding of the profile and extent of cognitive intra-individual variability (IIV) in mood disorders.

A computerized sustained attention task was administered to 138 healthy controls and 158 patients with a mood disorder: 86 euthymic BD, 33 depressed BD and 39 medication-free MDD patients. Measures of IIV, including individual standard deviation (iSD) and coefficient of variation (CoV), were derived for each participant. Ex-Gaussian (and Vincentile) analyses were used to characterize the RT distributions into three components: mu and sigma (mean and standard deviation of the Gaussian portion of the distribution) and tau (the ‘slow tail’ of the distribution).

Compared with healthy controls, iSD was increased significantly in all patient samples. Due to minimal changes in average RT, CoV was only increased significantly in BD depressed patients. Ex-Gaussian modelling indicated a significant increase in tau in euthymic BD [Cohen's d = 0.39, 95% confidence interval (CI) 0.09–0.69, p = 0.011], and both sigma (d = 0.57, 95% CI 0.07–1.05, p = 0.025) and tau (d = 1.14, 95% CI 0.60–1.64, p < 0.0001) in depressed BD. The mu parameter did not differ from controls.

Increased cognitive variability may be a core feature of mood disorders. This is the first demonstration of differences in attentional RT distribution parameters between MDD and BD, and BD depression and euthymia. These data highlight the utility of applying measures of IIV to characterize neurocognitive variability and the great potential for future application.