Previous studies of neurocognitive performance in bipolar disorder (BD) have demonstrated impairments in visuo-spatial memory. The aim of the present study was to use an object-location memory (OLM) paradigm to assess specific, dissociable processes in visuo-spatial memory and examine their relationship with broader neurocognitive performance.

Fifty participants (25 patients with BD in a current depressive episode and 25 matched healthy controls) completed the OLM paradigm which assessed three different aspects of visuo-spatial memory: positional memory, object-location binding, and a combined process. Secondary neurocognitive measures of visuo-spatial memory, verbal memory, attention and executive function were also administered.

BD patients were significantly impaired on all three OLM processes, with the largest effect in exact positional memory (d = 1.18, p < 0.0001). General deficits were also found across the secondary neurocognitive measures. Using hierarchical regression, verbal learning was found to explain significant variance on the OLM measures where object-identity was present (the object-location binding and combined processes) and accounted for the group difference. The group difference in precise positional memory remained intact.

This study demonstrates that patients with bipolar depression manifest deficits in visuo-spatial memory, with substantial impairment in fine-grain, positional memory. The differential profile of processes underpinning the visuo-spatial memory impairment suggests a form of ‘cognitive scaffolding’, whereby performance on some measures can be supported by verbal memory. These results have important implications for our understanding of the functional cognitive architecture of mood disorder.

Previous studies have shown that genetic risk for externalizing (EXT) disorders is greater in the context of adverse family environments during adolescence, but it is unclear whether these effects are long lasting. The current study evaluated developmental changes in gene–environment interplay in the concurrent and prospective associations between parent–child relationship problems and EXT at ages 18 and 25 years.

The sample included 1382 twin pairs (48% male) from the Minnesota Twin Family Study, participating in assessments at ages 18 years (mean = 17.8, s.d. = 0.69 years) and 25 years (mean = 25.0, s.d. = 0.90 years). Perceptions of parent–child relationship problems were assessed using questionnaires. Structured interviews were used to assess symptoms of adult antisocial behavior and nicotine, alcohol and illicit drug dependence.

We detected a gene–environment interaction at age 18 years, such that the genetic influence on EXT was greater in the context of more parent–child relationship problems. This moderation effect was not present at age 25 years, nor did parent-relationship problems at age 18 years moderate genetic influence on EXT at age 25 years. Rather, common genetic influences accounted for this longitudinal association.

Gene–environment interaction evident in the relationship between adolescent parent–child relationship problems and EXT is both proximal and developmentally limited. Common genetic influence, rather than a gene–environment interaction, accounts for the long-term association between parent–child relationship problems at age 18 years and EXT at age 25 years. These results are consistent with a relatively pervasive importance of gene–environmental correlation in the transition from late adolescence to young adulthood.

Military training is a chronic stressful period that often induces stress-related psychopathology. Stress vulnerability and resilience depend on personality trait anxiety, attentional threat bias and prefrontal–limbic dysfunction. However, how these neurobehavioral elements interact with regard to the development of symptoms following stress remains unclear.

Fifty-five healthy combat soldiers undergoing intensive military training completed functional magnetic resonance imaging (fMRI) testing while performing the dot-probe task (DPT) composed of angry (threat) and neutral faces. Participants were then stratified according to their bias tendency to avoidance (n = 25) or vigilance (n = 30) groups, categorized as high or low trait anxiety and assessed for post-stress symptom severity.

Avoidance compared to vigilance tendency was associated with fewer post-trauma symptoms and increased hippocampal response to threat among high anxious but not low anxious individuals. Importantly, mediation analysis revealed that only among high anxious individuals did hippocampal activity lead to lower levels of symptoms through avoidance bias tendency. However, in the whole group, avoidance bias was modulated by the interplay between the hippocampus and the dorsal anterior cingulate cortex (dACC).

Our results provide a neurobehavioral model to explain the resilience to post-trauma symptoms following chronic exposure. The model points to the importance of considering threat bias tendency in addition to personality traits when investigating the brain response and symptoms of trauma. Such a multi-parametric approach that accounts for individual behavioral sensitivities may also improve brain-driven treatments of anxiety, possibly by targeting the interplay between the hippocampus and the dACC.

Anorexia nervosa (AN) and body dysmorphic disorder (BDD) are characterized by distorted body image and are frequently co-morbid with each other, although their relationship remains little studied. While there is evidence of abnormalities in visual and visuospatial processing in both disorders, no study has directly compared the two. We used two complementary modalities – event-related potentials (ERPs) and functional magnetic resonance imaging (fMRI) – to test for abnormal activity associated with early visual signaling.

We acquired fMRI and ERP data in separate sessions from 15 unmedicated individuals in each of three groups (weight-restored AN, BDD, and healthy controls) while they viewed images of faces and houses of different spatial frequencies. We used joint independent component analyses to compare activity in visual systems.

AN and BDD groups demonstrated similar hypoactivity in early secondary visual processing regions and the dorsal visual stream when viewing low spatial frequency faces, linked to the N170 component, as well as in early secondary visual processing regions when viewing low spatial frequency houses, linked to the P100 component. Additionally, the BDD group exhibited hyperactivity in fusiform cortex when viewing high spatial frequency houses, linked to the N170 component. Greater activity in this component was associated with lower attractiveness ratings of faces.

Results provide preliminary evidence of similar abnormal spatiotemporal activation in AN and BDD for configural/holistic information for appearance- and non-appearance-related stimuli. This suggests a common phenotype of abnormal early visual system functioning, which may contribute to perceptual distortions.

Electroconvulsive therapy (ECT) is widely applied to treat severe depression resistant to standard treatment. Results from previous studies comparing the cost-effectiveness of this technique with treatment alternatives such as repetitive transcranial magnetic stimulation (rTMS) are conflicting.

We conducted a cost-effectiveness analysis comparing ECT alone, rTMS alone and rTMS followed by ECT when rTMS fails under the perspective of the Spanish National Health Service. The analysis is based on a Markov model which simulates the costs and health outcomes of individuals treated under these alternatives over a 12-month period. Data to populate this model were extracted and synthesized from a series of randomized controlled trials and other studies that have compared these techniques on the patient group of interest. We measure effectiveness using quality-adjusted life years (QALYs) and characterize the uncertainty using probabilistic sensitivity analyses.

ECT alone was found to be less costly and more effective than rTMS alone, while the strategy of providing rTMS followed by ECT when rTMS fails is the most expensive and effective option. The incremental cost per QALY gained of this latter strategy was found to be above the reference willingness-to-pay threshold used in these types of studies in Spain and other countries. The probability that ECT alone is the most cost-effective alternative was estimated to be around 70%.

ECT is likely to be the most cost-effective option in the treatment of resistant severe depression for a willingness to pay of €30 000 per QALY.

Psychosocial stress has been related to changes in the nervous system, with both adaptive and maladaptive consequences. The aim of this study was to examine the relationship of negative events experienced throughout the entire lifespan and hippocampal and amygdala volumes in older adults.

In 466 non-demented old adults (age range 60–96 years, 58% female), hippocampal and amygdala volumes were segmented using Freesurfer. Negative life events and the age at which these events occurred were assessed by means of a structured questionnaire. Using generalized linear models, hippocampal and amygdala volumes were estimated with life events as independent variables. The statistical analyses were adjusted for age, gender, intracranial volume, lifestyle factors, cardiovascular risk factors, depressive symptoms, and cognitive functioning.

Total number of negative life events and of late-life events, but not of early-life, early-adulthood, or middle-adulthood events, was related to larger amygdala volume. There were interactions of early-life events with age and gender. Participants who reported two or more early-life events had significantly smaller amygdala and hippocampal volumes with increasing age. Furthermore, smaller hippocampal volume was found in men who reported two or more early-life events, but not in women.

These results suggest that the effect of negative life events on the brain depends on the time when the events occurred, with the strongest effects observed during the critical time periods of early and late life.

The interactive effect of personal factors and social factors upon suicide risk is unclear. We conducted prospective cohort study to investigate whether the impact of the economic crisis in 1997–1998 upon suicide risk differed according to Neuroticism and Psychoticism personality traits.

The Miyagi Cohort Study in Japan with a follow-up for 19 years from 1990 to 2008 has 29 432 subjects aged 40–64 years at baseline who completed a questionnaire about various health habits and the Japanese version of the Eysenck Personality Questionnaire – Revised Short Form in 1990.

The suicide mortality rate increased from 4.6 per 100 000 person-years before 1998 to 27.8 after 1998. Although both Neuroticism and Psychoticism were significantly associated with an increased risk of mortality during the whole period from 1990 to 2008, the impact of the economic crisis upon suicide risk differed between the Neuroticism and Psychoticism personality traits. Compared with the lowest category, the hazard ratios (HRs) for the highest Neuroticism increased from 0.66 before 1998 to 2.45 after 1998. On the other hand, the HRs for the highest Psychoticism decreased from 7.85 before 1998 to 2.05 after 1998.

The impact of the 1997–1998 economic crisis upon suicide risk differed according to personality. Suicide risk increased among these with higher Neuroticism after the economic crisis, but this was not the case for other personality subscales.

The objective of this study was to examine associations between trajectories of childhood neighbourhood social cohesion and adolescent mental health and behaviour.

This study used data from the National Longitudinal Survey of Children and Youth, a nationally representative sample of Canadian children. The sample included 5577 children aged 0–3 years in 1994–1995, prospectively followed until age 12–15 years. Parental perceived neighbourhood cohesion was assessed every 2 years. Latent growth class modelling was used to identify trajectories of neighbourhood cohesion. Mental health and behavioural outcomes were self-reported at age 12–15 years. Logistic regression was used to examine associations between neighbourhood cohesion trajectories and outcomes, adjusting for potential confounders.

Five distinct trajectories were identified: ‘stable low’ (4.2%); ‘moderate increasing’ (9.1%); ‘stable moderate’ (68.5%); ‘high falling’ (8.9%); and ‘stable high’ (9.3%). Relative to those living in stable moderately cohesive neighbourhoods, those in stable low cohesive neighbourhoods were more likely to experience symptoms of anxiety/depression [odds ratio (OR) = 1.73, 95% confidence interval (CI) 1.04–2.90] and engage in indirect aggression (OR = 1.62, 95% CI 1.07–2.45). Those with improvements in neighbourhood cohesion had significantly lower odds of hyperactivity (OR = 0.67, 95% CI 0.46–0.98) and indirect aggression (OR = 0.69, 95% CI 0.49–0.96). In contrast, those with a decline in neighbourhood cohesion had increased odds of hyperactivity (OR = 1.67, 95% CI 1.21–2.29). Those in highly cohesive neighbourhoods in early childhood were more likely to engage in prosocial behaviour (‘high falling’: OR = 1.93, 95% CI 1.38–2.69; ‘stable high’: OR = 1.89, 95% CI 1.35–2.63).

These results suggest that neighbourhood cohesion in childhood may have time-sensitive effects on several domains of adolescent mental health and behaviour.

Individuals with major depressive disorder (MDD) are characterized by maladaptive responses to both positive and negative outcomes, which have been linked to localized abnormal activations in cortical and striatal brain regions. However, the exact neural circuitry implicated in such abnormalities remains largely unexplored.

In this study 26 unmedicated adults with MDD and 29 matched healthy controls (HCs) completed a monetary incentive delay task during functional magnetic resonance imaging (fMRI). Psychophysiological interaction (PPI) analyses probed group differences in connectivity separately in response to positive and negative outcomes (i.e. monetary gains and penalties).

Relative to HCs, MDD subjects displayed decreased connectivity between the caudate and dorsal anterior cingulate cortex (dACC) in response to monetary gains, yet increased connectivity between the caudate and a different, more rostral, dACC subregion in response to monetary penalties. Moreover, exploratory analyses of 14 MDD patients who completed a 12-week, double-blind, placebo-controlled clinical trial after the baseline fMRI scans indicated that a more normative pattern of cortico-striatal connectivity pre-treatment was associated with greater improvement in symptoms 12 weeks later.

These results identify the caudate as a region with dissociable incentive-dependent dACC connectivity abnormalities in MDD, and provide initial evidence that cortico-striatal circuitry may play a role in MDD treatment response. Given the role of cortico-striatal circuitry in encoding action–outcome contingencies, such dysregulated connectivity may relate to the prominent disruptions in goal-directed behavior that characterize MDD.

With psychopathology rising during adolescence and evidence suggesting that adult mental health burden is often due to disorders beginning in youth, it is important to investigate the epidemiology of adolescent mental disorders.

We analysed data gathered at ages 11 (baseline) and 19 years from the population-based Dutch TRacking Adolescents' Individual Lives Survey (TRAILS) study. At baseline we administered the Achenbach measures (Child Behavior Checklist, Youth Self-Report) and at age 19 years the World Health Organization's Composite International Diagnostic Interview version 3.0 (CIDI 3.0) to 1584 youths.

Lifetime, 12-month and 30-day prevalences of any CIDI-DSM-IV disorder were 45, 31 and 15%, respectively. Half were severe. Anxiety disorders were the most common but the least severe whereas mood and behaviour disorders were less prevalent but more severe. Disorders persisted, mostly by recurrence in mood disorders and chronicity in anxiety disorders. Median onset age varied substantially across disorders. Having one disorder increased subjects' risk of developing another disorder. We found substantial homotypic and heterotypic continuity. Baseline problems predicted the development of diagnosable disorders in adolescence. Non-intact families and low maternal education predicted externalizing disorders. Most morbidity concentrated in 5–10% of the sample, experiencing 34–55% of all severe lifetime disorders.

At late adolescence, 22% of youths have experienced a severe episode and 23% only mild episodes. This psychopathology is rather persistent, mostly due to recurrence, showing both monotypic and heterotypic continuity, with family context affecting particularly externalizing disorders. High problem levels at age 11 years are modest precursors of incident adolescent disorders. The burden of mental illness concentrates in 5–10% of the adolescent population.

Electroencephalography and magnetoencephalography (MEG) studies have identified alterations in gamma-band (30–80 Hz) cortical activity in schizophrenia and mood disorders, consistent with neural models of disturbed glutamate (and GABA) neuron influence over cortical pyramidal cells. Genetic evidence suggests specific deficits in GABA-A receptor function in schizoaffective bipolar disorder (SABP), a clinical syndrome with features of both bipolar disorder and schizophrenia. This study investigated gamma oscillations in this under-researched disorder.

MEG was used to measure induced gamma and evoked responses to a visual grating stimulus, known to be a potent inducer of primary visual gamma oscillations, in 15 individuals with remitted SABP, defined using Research Diagnostic Criteria, and 22 age- and sex-matched healthy controls.

Individuals with SABP demonstrated increased sustained visual cortical power in the gamma band (t35 = −2.56, p = 0.015) compared to controls. There were no group differences in baseline gamma power, transient or sustained gamma frequency, alpha band responses or pattern onset visual-evoked responses.

Gamma power is increased in remitted SABP, which reflects an abnormality in the cortical inhibitory-excitatory balance. Although an interaction between gamma power and medication can not be ruled out, there were no group differences in evoked responses or baseline measures. Further work is needed in other clinical populations and at-risk relatives. Pharmaco-magnetoencephalography studies will help to elucidate the specific GABA and glutamate pathways affected.

The National Institute of Health and Care Excellence (NICE) in England and Wales recommends the combination of pharmacotherapy and psychotherapy for the treatment of moderate to severe depression. However, the cost-effectiveness analysis on which these recommendations are based has not included psychotherapy as monotherapy as a potential option. For this reason, we aimed to update, augment and refine the existing economic evaluation.

We constructed a decision analytic model with a 27-month time horizon. We compared pharmacotherapy with cognitive–behavioural therapy (CBT) and combination treatment for moderate to severe depression in secondary care from a healthcare service perspective. We reviewed the literature to identify relevant evidence and, where possible, synthesized evidence from clinical trials in a meta-analysis to inform model parameters.

The model suggested that CBT as monotherapy was most likely to be the most cost-effective treatment option above a threshold of £22 000 per quality-adjusted life year (QALY). It dominated combination treatment and had an incremental cost-effectiveness ratio of £20 039 per QALY compared with pharmacotherapy. There was significant decision uncertainty in the probabilistic and deterministic sensitivity analyses.

Contrary to previous NICE guidance, the results indicated that even for those patients for whom pharmacotherapy is acceptable, CBT as monotherapy may be a cost-effective treatment option. However, this conclusion was based on a limited evidence base, particularly for combination treatment. In addition, this evidence cannot easily be transferred to a primary care setting.

The aetiological pathways to borderline personality disorder (BPD) remain only partly elucidated. Retrospective research indicates that prenatal adversity may be an important early risk factor in the development of BPD. This requires corroboration with prospective longitudinal studies.

A community sample of 6050 mothers and their children (born between April 1991 and December 1992) were assessed. Maternal anxiety and depression and maternal alcohol and tobacco consumption were assessed during pregnancy (18 and 32 weeks gestation). Postnatal risks, including maladaptive parenting (suboptimal parenting and parent conflict), family adversity, maternal anxiety and depression and maternal alcohol and tobacco consumption, were assessed during early childhood. Internalizing and externalizing symptoms were assessed in late childhood. Trained psychologists interviewed children in late childhood to ascertain the presence of BPD (at least five probable/definite symptoms).

In unadjusted analyses, all prenatal risk factors (i.e. maternal alcohol and tobacco consumption and maternal anxiety and depression) were significantly associated with BPD. Following adjustment for sex, birthweight and postnatal exposure to anxiety and depression respectively, maladaptive parenting, family adversity and child's internalizing and externalizing symptoms, prenatal anxiety at 18 weeks gestation [odds ratio (OR) 1.57, 95% confidence interval (CI) 1.18–2.09] and depression at 18 weeks (OR 1.59, 95% CI 1.08–2.32) and 32 weeks (OR 1.57, 95% CI 1.14–2.18) gestation remained significantly associated with BPD.

This study provides prospective evidence of associations between prenatal adversities and BPD at 11–12 years. Prenatal anxiety and depression were independently associated with BPD, suggesting that they may exert direct effects on BPD during the prenatal period. This highlights the importance of programmes to reduce maternal stress during pregnancy.

Parental depressive symptoms are associated with emotional and behavioural problems in offspring. However, genetically informative studies are needed to distinguish potential causal effects from genetic confounds, and longitudinal studies are required to distinguish parent-to-child effects from child-to-parent effects.

We conducted cross-sectional analyses on a sample of Swedish twins and their adolescent offspring (n = 876 twin families), and longitudinal analyses on a US sample of children adopted at birth, their adoptive parents, and their birth mothers (n = 361 adoptive families). Depressive symptoms were measured in parents, and externalizing and internalizing problems measured in offspring. Structural equation models were fitted to the data.

Results of model fitting suggest that associations between parental depressive symptoms and offspring internalizing and externalizing problems remain after accounting for genes shared between parent and child. Genetic transmission was not evident in the twin study but was evident in the adoption study. In the longitudinal adoption study child-to-parent effects were evident.

We interpret the results as demonstrating that associations between parental depressive symptoms and offspring emotional and behavioural problems are not solely attributable to shared genes, and that bidirectional effects may be present in intergenerational associations.

Meta-analyses support the efficacy of cognitive–behavioural therapy (CBT) for schizophrenia in western cultures. This study aimed to compare the efficacy of CBT and supportive therapy (ST) for patients with schizophrenia in China.

A multicentre randomized controlled, single-blinded, parallel-group trial enrolled a sample of 192 patients with schizophrenia. All patients were offered 15 sessions of either CBT or ST over 24 weeks and followed up for an additional 60 weeks. All measures used were standardized instruments with good reliability and validity. The Positive and Negative Syndrome Scale (PANSS) was used to assess symptoms of schizophrenia. The Schedule for Assessing Insight (SAI) was used to assess patients’ insight and the Personal and Social Performance Scale (PSP) was used to assess their social functioning.

Effect-size analysis showed that patients made rapid improvements in all symptoms, insight and social functioning as measured by the PANSS, SAI and PSP at 12 and 24 weeks and maintained these improvements over the course of the study to 84 weeks. Patients in the CBT group showed significantly greater and more durable improvement in PANSS total score (p = 0.045, between-group d = 0.48), positive symptoms (p = 0.018, between-group d = 0.42) and social functioning (p = 0.037, between-group d = 0.64), with significant differences emerging after completion of therapy.

Both CBT and ST combined with medication had benefits on psychopathology, insight and social functioning of patients with schizophrenia. CBT was significantly more effective than ST on overall, positive symptoms and social functioning of patients with schizophrenia in the long term.

Body dysmorphic disorder (BDD) and anorexia nervosa (AN) are both characterized by distorted perception of appearance. Previous studies in BDD suggest abnormalities in visual processing of own and others’ faces, but no study has examined visual processing of faces in AN, nor directly compared the two disorders in this respect.

We collected functional magnetic resonance imaging data on 60 individuals of equivalent age and gender in each of three groups – 20 BDD, 20 weight-restored AN, and 20 healthy controls (HC) – while they viewed images of others’ faces that contained only high or low spatial frequency information (HSF or LSF). We tested hypotheses about functional connectivity within specialized sub-networks for HSF and LSF visual processing, using psychophysiological interaction analyses.

The BDD group demonstrated increased functional connectivity compared to HC between left anterior occipital face area and right fusiform face area (FFA) for LSF faces, which was associated with symptom severity. Both BDD and AN groups had increased connectivity compared to HC between FFA and precuneous/posterior cingulate gyrus for LSF faces, and decreased connectivity between FFA and insula. In addition, we found that LSF connectivity between FFA and posterior cingulate gyrus was significantly associated with thoughts about own appearance in AN.

Results suggest similar abnormal functional connectivity within higher-order systems for face processing in BDD and AN, but distinct abnormal connectivity patterns within occipito-temporal visual networks. Findings may have implications for understanding relationships between these disorders, and the pathophysiology underlying perceptual distortions.

Previous studies of the dimensional structure of panic attack symptoms have mostly identified a respiratory and a vestibular/mixed somatic dimension. Evidence for additional dimensions such as a cardiac dimension and the allocation of several of the panic attack symptom criteria is less consistent. Clarifying the dimensional structure of the panic attack symptoms should help to specify the relationship of potential risk factors like anxiety sensitivity and fear of suffocation to the experience of panic attacks and the development of panic disorder.

In an outpatient multicentre study 350 panic patients with agoraphobia rated the intensity of each of the ten DSM-IV bodily symptoms during a typical panic attack. The factor structure of these data was investigated with nonlinear confirmatory factor analysis (CFA). The identified bodily symptom dimensions were related to panic cognitions, anxiety sensitivity and fear of suffocation by means of nonlinear structural equation modelling (SEM).

CFA indicated a respiratory, a vestibular/mixed somatic and a cardiac dimension of the bodily symptom criteria. These three factors were differentially associated with specific panic cognitions, different anxiety sensitivity facets and suffocation fear.

Taking into account the dimensional structure of panic attack symptoms may help to increase the specificity of the associations between the experience of panic attack symptoms and various panic related constructs.

Depression is known to run in families, but the effects of parental history of other psychiatric diagnoses on depression rates are less well studied. Few studies have examined the impact of parental psychopathology on depression rates in older age groups.

We established a population-based cohort including all individuals born in Denmark after 1954 and alive on their 10th birthday (N = 29 76 264). Exposure variables were maternal and paternal history of schizophrenia, bipolar disorder, depression, anxiety or ‘other’ psychiatric diagnoses. Incidence rate ratios (IRRs) were estimated using Poisson regressions.

Parental history of any psychiatric diagnosis increased incidence rates of outpatient (maternal: IRR 1.88, p < 0.0001; paternal: IRR 1.68, p < 0.0001) and inpatient (maternal: IRR 1.99, p < 0.0001; paternal: IRR 1.83, p < 0.0001) depression relative to no parental history. IRRs for parental history of non-affective disorders remained relatively stable across age groups, while IRRs for parental affective disorders (unipolar or bipolar) decreased with age from 2.29–3.96 in the youngest age group to 1.53–1.90 in the oldest group. IRR estimates for all parental diagnoses were similar among individuals aged ⩾41 years (IRR range 1.51–1.90).

Parental history of any psychiatric diagnosis is associated with increased incidence rates of unipolar depression. In younger age groups, parental history of affective diagnoses is more strongly associated with rates of unipolar depression than non-affective diagnoses; however, this distinction disappears after age 40, suggesting that parental psychopathology in general, rather than any one disorder, confers risk for depression in middle life.

Neurocognitive deficits are important aspects of schizophrenic disorder because they have a strong impact on social and vocational outcomes. Previously it was assumed that cognitive abilities progressively deteriorate with illness onset. However, recent research results have contradicted this with observations of continuous or even improved performance in individuals at risk for psychosis or manifest schizophrenia. The objective of our longitudinal study was to examine neurocognitive functioning in help-seeking individuals meeting basic symptoms or ultra-high-risk criteria for schizophrenic psychosis (HRSchiz) or risk criteria for affective psychosis (HRBip). The progression of cognitive functioning in individuals converting to psychosis was compared with that of at-risk individuals who did not convert during the follow-up period.

Data were available from 86 study participants who completed neurocognitive and clinical assessments at baseline and, on average, 12.8 (s.d. = 1.5) months later. Neurocognitive measures were grouped according to their load in factor analysis to five cognitive domains: speed, attention, fluency, learning and memory, and working memory.

Neurocognitive functioning in HRSchiz and HRBip individuals generally improved over time. Subjects converting to manifest psychosis displayed a stable neurocognitive profile from baseline to follow-up. Compared with non-converters, they had already demonstrated a significantly lower level of performance during their baseline examinations.

Our data provide no evidence for a progressive cognitive decline in individuals at risk of psychosis. In line with the neurodevelopmental model, our findings suggest that cognitive deficits are already present very early, before or during the prodromal stage of the illness.

Cognitive behaviour therapy (CBT) for chronic fatigue syndrome (CFS) leads to a significant decrease in CFS-related symptoms and disability. The primary objective of this study was to explore whether partners’ solicitous responses and patients’ and partners’ perceived relationship satisfaction had an effect on treatment outcome.

The treatment outcome of a cohort of 204 consecutively referred patients treated with CBT was analysed. At baseline, CFS patients completed the Maudsley Marital Questionnaire. The Checklist Individual Strength subscale Fatigue and the Sickness Impact Profile total scores completed by CFS patients post-treatment were used as measures of clinically significant improvement. Partners completed the Family Response Questionnaire, the Maudsley Marital Questionnaire, the Brief Illness Perception Questionnaire, and the Causal Attribution List. Logistic regression analyses were performed with clinically significant improvement in fatigue and disability as dependent variables and scores on questionnaires at baseline as predictors.

Solicitous responses of the partner were associated with less clinically significant improvement in fatigue and disability. Partners more often reported solicitous responses when they perceived CFS as a severe condition. Patients’ relationship dissatisfaction was negatively associated with clinically significant improvement in fatigue.

Partners’ solicitous responses and illness perceptions at the start of the therapy can negatively affect the outcome of CBT for CFS. We emphasize the importance of addressing this in therapy.