People with psychoses often report fixed, delusional beliefs that are sustained even in the presence of unequivocal contrary evidence. Such delusional beliefs are the result of integrating new and old evidence inappropriately in forming a cognitive model. We propose and test a cognitive model of belief formation using experimental data from an interactive ‘Rock Paper Scissors’ (RPS) game.

Participants (33 controls and 27 people with schizophrenia) played a competitive, time-pressured interactive two-player game (RPS). Participants' behavior was modeled by a generative computational model using leaky integrator and temporal difference methods. This model describes how new and old evidence is integrated to form a playing strategy to beat the opponent and to provide a mechanism for reporting confidence in one's playing strategy to win against the opponent.

People with schizophrenia fail to appropriately model their opponent's play despite consistent (rather than random) patterns that can be exploited in the simulated opponent's play. This is manifest as a failure to weigh existing evidence appropriately against new evidence. Furthermore, participants with schizophrenia show a ‘jumping to conclusions’ (JTC) bias, reporting successful discovery of a winning strategy with insufficient evidence.

The model presented suggests two tentative mechanisms in delusional belief formation: (i) one for modeling patterns in other's behavior, where people with schizophrenia fail to use old evidence appropriately, and (ii) a metacognitive mechanism for ‘confidence’ in such beliefs, where people with schizophrenia overweight recent reward history in deciding on the value of beliefs about the opponent.

People with psychosis demonstrate impaired response inhibition on the Stop Signal Task (SST). It is less clear if this impairment extends to reflection impulsivity, a form of impulsivity that has been linked to substance use in non-psychotic samples.

We compared 49 patients with first-episode psychosis (FEP) and 30 healthy control participants on two forms of impulsivity measured using the Information Sampling Test (IST) and the SST, along with clinical and IQ assessments. We also compared those patients who used cannabis with those who had either given up or never used.

Patients with FEP had significantly greater impairment in response inhibition but not in reflection impulsivity compared with healthy controls. By contrast, patients who reported current cannabis use demonstrated greater reflection impulsivity than those that had either given up or never used, whereas there were no differences in response inhibition.

These data suggest that abnormal reflection impulsivity is associated with substance use in psychosis but not psychosis itself; the opposite relationship may hold for response inhibition.

It has been argued that sleep disturbances are a risk factor for depression but previous longitudinal studies have had limitations and not addressed alternative explanations. The aim of this study was to examine the longitudinal association between sleep disturbances and depressive symptoms in a nationally representative sample.

Data from the 18-month follow-up of the UK National Psychiatric Morbidity survey were used (n = 2406). Sleep disturbances, depressive and other psychiatric symptoms (fatigue, concentration problems, irritability, anxiety and pain symptoms) were assessed using the Revised Clinical Interview Schedule (CIS-R). The bidirectional association between symptoms was investigated with logistic regression analyses and path analysis.

Sleep disturbances and depressive symptoms were correlated with each other cross-sectionally (r = 0.52, p < 0.001). In the longitudinal analysis, sleep disturbances at baseline did not predict depressive symptoms at follow-up [odds ratio (OR) 1.27, 95% confidence interval (CI) 0.51–3.19] and the same was observed for the reciprocal association (OR 0.87, 95% CI 0.56–1.35). In the path analysis, the reciprocal model did not have a better fit compared to the simpler first-order model without cross-lagged paths. The path from sleep disturbances at baseline to depressive symptoms at follow-up had a minimal contribution to the explained variance of the latter (<1%).

Previous studies may have overestimated the importance of sleep disturbances as an independent risk factor of depression. The strong cross-sectional association is compatible with sleep disturbances being either a prodromal or a residual symptom of depression and this may have implications for recognition and treatment of depression.

Given the important role of the default mode network (DMN) in cognitive function and the well-known neurocognitive deficit in schizophrenia, it is intriguing to examine systematically the relationship between neurocognitive dysfunction and aberrant intrinsic activities, and also functional connectivity, of the DMN in patients with schizophrenia.

First-episode, treatment-naive patients with schizophrenia (FES) (n = 115) and healthy controls (n = 113) underwent resting-state functional magnetic resonance imaging (fMRI) scans and neurocognitive tests. Intrinsic neural activities evaluated by using the fragment amplitude of low-frequency fluctuations (fALFF) and the resting-state functional connectivity assessed by seed-based correlational analysis were compared between patients and controls. Aberrant intrinsic activities and DMN connectivity in patients were then correlated to neurocognitive performance and clinical symptoms.

Compared to controls, patients with FES showed decreased fALFF in the bilateral medial prefrontal cortex (MPFC) and the orbitofrontal cortex (OFC), and increased fALFF in the bilateral putamen. Increased functional connectivity with the DMN was observed in the left insula and bilateral dorsolateral PFC (DLPFC) in patients with FES. In patients, aberrant fALFF in the bilateral OFC were correlated with cognitive processing speed; fALFF in the left OFC and right putamen were correlated with the clinical factors excited/activation and disorganization; and increased DMN functional connectivity in the left insula was correlated with the clinical factors positive, excited/activation, disorganization and neurocognitive deficit in the domain of sustained attention.

These associations between neurocognitive dysfunction and aberrant intrinsic activities, and also functional connectivity, of the DMN in patients with schizophrenia may provide important insights into the neural mechanism of the disease.

Schizophrenia is associated with lower pre-morbid intelligence (IQ) in addition to (pre-morbid) cognitive decline. Both schizophrenia and IQ are highly heritable traits. Therefore, we hypothesized that genetic variants associated with schizophrenia, including copy number variants (CNVs) and a polygenic schizophrenia (risk) score (PSS), may influence intelligence.

IQ was estimated with the Wechsler Adult Intelligence Scale (WAIS). CNVs were determined from single nucleotide polymorphism (SNP) data using the QuantiSNP and PennCNV algorithms. For the PSS, odds ratios for genome-wide SNP data were calculated in a sample collected by the Psychiatric Genome-Wide Association Study (GWAS) Consortium (8690 schizophrenia patients and 11 831 controls). These were used to calculate individual PSSs in our independent sample of 350 schizophrenia patients and 322 healthy controls.

Although significantly more genes were disrupted by deletions in schizophrenia patients compared to controls (p = 0.009), there was no effect of CNV measures on IQ. The PSS was associated with disease status (R2 = 0.055, p = 2.1 × 10−7) and with IQ in the entire sample (R2 = 0.018, p = 0.0008) but the effect on IQ disappeared after correction for disease status.

Our data suggest that rare and common schizophrenia-associated variants do not explain the variation in IQ in healthy subjects or in schizophrenia patients. Thus, reductions in IQ in schizophrenia patients may be secondary to other processes related to schizophrenia risk.

In the present study we investigated whether SCP predicted fatigue and pain over a 14-day period in a sample of 90 CFS patients using a diary method approach. After completing the Depressive Experiences Questionnaire (DEQ) as a measure of SCP, patients were asked each day for 14 days to complete Visual Analogue Scales (VAS) of fatigue, pain and severity of depression. Data were analysed using multilevel analysis.

The results from unconditional models revealed considerable fluctuations in fatigue over the 14 days, suggesting strong temporal variability in fatigue. By contrast, pain was relatively stable over time but showed significant inter-individual differences. Congruent with expectations, fixed-effect models showed that SCP was prospectively associated with higher daily fatigue and pain levels over the 14-day period, even after controlling for levels of depression.

This is the first study to show that SCP predicts both fatigue and pain symptoms in CFS in the daily course of life. Hence, therapeutic interventions aimed at targeting SCP should be considered in the treatment of CFS patients with such features.

Depression frequently co-occurs with somatization, and somatic complaints have been reported as a vulnerability marker for affective disorders observable before disease onset. Somatization is thought to result from an increased attention to somatic sensations, which should be reflected in long-latency somatosensory evoked electroencephalogram (EEG) potentials (SSEPs) at the physiological level. Previous studies revealed that SSEPs are altered in depressed patients and suggested late SSEP components as vulnerability markers for affective disorders. Neurotransmitters such as serotonin, γ-aminobutyric acid (GABA) and the neuropeptide substance P may play an important role for both affective disorders and somatosensory processing.

We investigated the associations between SSEPs and polymorphisms within candidate genes of the serotonergic, GABAergic as well as the substance P system in subjects at high risk for affective disorders. The sample was composed of high-risk families participating in the Munich Vulnerability Study and genetic association analyses were calculated using qfam (family-based association tests for quantitative traits) implemented in PLINK 1.05.

We observed significant associations (false discovery rate <0.05) withstanding correction for multiple testing between late SSEP components (response strength 170–370 ms after stimulation) and four single nucleotide polymorphisms within the GABA transaminase (ABAT) gene region coding for a protein responsible for GABA degradation. No effects were found with the classical disease trait approach, suggesting SSEP marker specificity of the observed associations.

Our findings point to a possible role of ABAT gene-regulated GABA catabolism for an altered processing of somatosensory stimuli as a potential vulnerability marker for affective disorders.

Bullying victimization may be linked to psychosis but only self-report measures of victimization have been used so far. This study aimed (a) to investigate the differential associations of peer-nominated versus self-reported victim status with non-clinical psychotic experiences in a sample of young adolescents, and (b) to examine whether different types of self-reported victimization predict non-clinical psychotic experiences in these adolescents.

A combination of standard self-report and peer nomination procedures was used to assess victimization. The sample (n = 724) was divided into four groups (exclusively self-reported victims, self- and peer-reported victims, exclusively peer-reported victims, and non-victims) to test for a group effect on non-clinical psychotic experiences. The relationship between types of victimization and non-clinical psychotic experiences was examined by a regression analysis.

Self-reported victims, along with self- and peer-reported victims, scored higher than peer-reported victims and non-victims on non-clinical psychotic experiences. Self-reports of direct relational, indirect relational and physical victimization significantly improved the prediction of non-clinical psychotic experiences whereas verbal and possession-directed victimization had no significant predictive value.

The relationship between victimization and non-clinical psychotic experiences is only present for self-reported victimization, possibly indicative of an interpretation bias. The observed discrepancy between self-report and peer-report highlights the importance of implementing a combination of both measures for future research.

Recent models of major depressive disorder (MDD) have proposed the rostral anterior cingulate (rACC) and dorsomedial prefrontal cortex (dmPFC) as nexus sites in the dysfunctional regulation of cognitive-affective state. Limited evidence from remitted-state MDD supports these theories by suggesting that aberrant neural activity proximal to the rACC and the dmPFC may play a role in vulnerability to recurrence/relapse within this disorder. Here we present a targeted analysis assessing functional activity within these two regions of interest (ROIs) for groups with identified vulnerability to MDD: first, remitted, high predicted recurrence-risk patients; and second, patients suffering observed 1-year recurrence.

Baseline T2* images sensitive to blood oxygen level-dependent (BOLD) contrast were acquired from patients and controls during a Go/No-Go (GNG) task incorporating negative feedback, with 1-year patient follow-up to identify recurrence. BOLD contrast data for error commission (EC) and visual negative feedback (VNF) were used in an ROI analysis based on rACC and dmPFC coordinates from the literature, comparing patients versus controls and recurrence versus non-recurrence versus control groups.

Analysis of patients (n = 20) versus controls (n = 20) showed significant right dmPFC [Brodmann area (BA) 9] hypoactivity within the patient group, co-localized during EC and VNF, with additional significant rACC (BA 32) hypoactivity during EC. The results from the follow-up analysis were undermined by small groups and potential confounders but suggested persistent right dmPFC (BA 9) hypoactivity associated with 1-year recurrence.

Convergent hypoactive right dmPFC (BA 9) processing of VNF and EC, possibly impairing adaptive reappraisal of negative experience, was associated most clearly with clinically predicted vulnerability to MDD.

Hyperprolactinemia is frequent in patients with schizophrenic psychoses. It is usually regarded as an adverse effect of antipsychotics but has recently also been shown in patients without antipsychotic medication. Our objective was to test whether hyperprolactinemia occurs in antipsychotic-naive first-episode patients (FEPs).

In the framework of the European First Episode Schizophrenia Trial (EUFEST), 249 out of 498 FEPs were eligible for this study, of whom 74 were antipsychotic naive. All patients were investigated regarding their serum prolactin levels with immunoassays standardized against the 3rd International Reference Standard 84/500.

Twenty-nine (39%) of the 74 antipsychotic-naive patients showed hyperprolactinemia not explained by any other reason, 11 (50%) of 22 women and 18 (35%) of 52 men.

Hyperprolactinemia may be present in patients with schizophrenic psychoses independent of antipsychotic medication. It might be stress induced. As enhanced prolactin can increase dopamine release through a feedback mechanism, this could contribute to explaining how stress can trigger the outbreak of psychosis.

Cognitive impairment is a core feature of schizophrenia. Its relationship with duration of untreated psychosis (DUP), a potentially malleable prognostic factor, has been less studied, with inconsistent findings being observed in the literature. Previous research investigating such a relationship was mostly cross-sectional and none of those prospective studies had a follow-up duration beyond 2 years.

A total of 93 Hong Kong Chinese aged 18 to 55 years presenting with first-episode schizophrenia-spectrum disorder were studied. DUP and pre-morbid adjustment were measured using a structured interview incorporating multiple sources of information. Psychopathological evaluation was administered at intake, after clinical stabilization of the first psychotic episode, and at 12, 24 and 36 months. Cognitive functions were measured at clinical stabilization, and at 12, 24 and 36 months.

DUP exerted differential effects on various cognitive domains, with memory deficits being the most related to DUP even when potential confounders including pre-morbid adjustment and sex were adjusted. Prolonged DUP was associated with more severe impairment in visual memory at clinical stabilization and verbal memory at 24 and 36 months. Further, patients with a long DUP were found to have worse outcomes on negative symptoms at 36 months. The effects of DUP on verbal memory remained significant even when negative symptoms were taken into consideration.

Our findings provided further supportive evidence that delayed treatment to first-episode psychosis is associated with poorer cognitive and clinical outcomes. In addition, DUP may specifically affect memory function and its adverse impact on verbal memory may only become evident at a later stage of the recovery process.

Patients with bipolar disorder exhibit consistent deficits in facial affect identification at both behavioral and neural levels. However, little is known about which stages of facial affect processing are dysfunctional.

Event-related potentials (ERPs), including amplitude and latency, were used to evaluate two stages of facial affect processing: N170 to examine structural encoding of facial features and N250 to examine decoding of facial features in 57 bipolar disorder patients, 30 schizophrenia patients and 30 healthy controls. Three conditions were administered: participants were asked to identify the emotion of a face, the gender of a face, or whether a building was one or two stories tall.

Schizophrenia patients' emotion identification accuracy was lower than that of bipolar patients and healthy controls. N170 amplitude was significantly smaller in schizophrenia patients compared to bipolar patients and healthy controls, which did not differ from each other. Both patient groups had significantly longer N170 latency compared to healthy controls. For N250, both patient groups showed significantly smaller amplitudes compared with controls, but did not differ from each other. Bipolar patients showed longer N250 latency than healthy controls; patient groups did not differ from each other.

Bipolar disorder patients have relatively intact structural encoding of faces (N170) but are impaired when decoding facial features for complex judgments about faces (N250 latency and amplitude), such as identifying emotion or gender.

Although auditory verbal hallucinations (AVH) are a core symptom of schizophrenia, they also occur in non-psychotic individuals, in the absence of other psychotic, affective, cognitive and negative symptoms. AVH have been hypothesized to result from deviant integration of inferior frontal, parahippocampal and superior temporal brain areas. However, a direct link between dysfunctional connectivity and AVH has not yet been established. To determine whether hallucinations are indeed related to aberrant connectivity, AVH should be studied in isolation, for example in non-psychotic individuals with AVH.

Resting-state connectivity was investigated in 25 non-psychotic subjects with AVH and 25 matched control subjects using seed regression analysis with the (1) left and (2) right inferior frontal, (3) left and (4) right superior temporal and (5) left parahippocampal areas as the seed regions. To correct for cardiorespiratory (CR) pulsatility rhythms in the functional magnetic resonance imaging (fMRI) data, heartbeat and respiration were monitored during scanning and the fMRI data were corrected for these rhythms using the image-based method for retrospective correction of physiological motion effects RETROICOR.

In comparison with the control group, non-psychotic individuals with AVH showed increased connectivity between the left and the right superior temporal regions and also between the left parahippocampal region and the left inferior frontal gyrus. Moreover, this group did not show a negative correlation between the left superior temporal region and the right inferior frontal region, as was observed in the healthy control group.

Aberrant connectivity of frontal, parahippocampal and superior temporal brain areas can be specifically related to the predisposition to hallucinate in the auditory domain.

Several cognitive biases are related to psychotic symptoms, including auditory verbal hallucinations (AVH). It remains unclear whether these biases differ in voice-hearers with and without a ‘need-for-care’.

A total of 72 healthy controls, 72 healthy voice-hearers and 72 clinical voice-hearers were compared on the Cognitive Biases Questionnaire for psychosis (CBQp), which assesses ‘intentionalizing’, ‘jumping to conclusions’, ‘catastrophizing’, ‘dichotomous thinking’ and ‘emotional reasoning’ in vignettes characterized by two themes, ‘threatening events’ and ‘anomalous perceptions’.

Healthy voice-hearers scored intermediately on total CBQp between the control and clinical groups, differing significantly from both. However, on four out of five biases the scores of the healthy voice-hearers were comparable with those of the healthy controls. The only exception was ‘emotional reasoning’, on which their scores were comparable with the clinical group. Healthy voice-hearers demonstrated fewer biases than the psychotic patients on the ‘threatening events’, but not the ‘anomalous perceptions’, vignettes. CBQp scores were related to both cognitive and emotional, but not physical, characteristics of voices.

Most cognitive biases prevalent in clinical voice-hearers, particularly with threatening events themes, are absent in healthy voice-hearers, apart from emotional reasoning which may be specifically related to the vulnerability to develop AVH. The association between biases and both beliefs about voices and distress/emotional valence is consistent with the close links between emotions and psychotic phenomena identified by cognitive models of psychosis. The absence of reasoning biases might prevent the formation of threatening appraisals about anomalous experiences, thereby reducing the likelihood of distress and ‘need for care’.

Abnormalities in incentive decision making, typically assessed using the Iowa Gambling Task (IGT), have been reported in both schizophrenia (SZ) and bipolar disorder (BD). We applied the Expectancy–Valence (E–V) model to determine whether motivational, cognitive and response selection component processes of IGT performance are differentially affected in SZ and BD.

Performance on the IGT was assessed in 280 individuals comprising 70 remitted patients with SZ, 70 remitted patients with BD and 140 age-, sex- and IQ-matched healthy individuals. Based on the E–V model, we extracted three parameters, ‘attention to gains or loses’, ‘expectancy learning’ and ‘response consistency’, that respectively reflect motivational, cognitive and response selection influences on IGT performance.

Both patient groups underperformed in the IGT compared to healthy individuals. However, the source of these deficits was diagnosis specific. Associative learning underlying the representation of expectancies was disrupted in SZ whereas BD was associated with increased incentive salience of gains. These findings were not attributable to non-specific effects of sex, IQ, psychopathology or medication.

Our results point to dissociable processes underlying abnormal incentive decision making in BD and SZ that could potentially be mapped to different neural circuits.

Several studies have reported weak associations between religious or spiritual belief and psychological health. However, most have been cross-sectional surveys in the USA, limiting inference about generalizability. An international longitudinal study of incidence of major depression gave us the opportunity to investigate this relationship further.

Data were collected in a prospective cohort study of adult general practice attendees across seven countries. Participants were followed at 6 and 12 months. Spiritual and religious beliefs were assessed using a standardized questionnaire, and DSM-IV diagnosis of major depression was made using the Composite International Diagnostic Interview (CIDI). Logistic regression was used to estimate incidence rates and odds ratios (ORs), after multiple imputation of missing data.

The analyses included 8318 attendees. Of participants reporting a spiritual understanding of life at baseline, 10.5% had an episode of depression in the following year compared to 10.3% of religious participants and 7.0% of the secular group (p < 0.001). However, the findings varied significantly across countries, with the difference being significant only in the UK, where spiritual participants were nearly three times more likely to experience an episode of depression than the secular group [OR 2.73, 95% confidence interval (CI) 1.59–4.68]. The strength of belief also had an effect, with participants with strong belief having twice the risk of participants with weak belief. There was no evidence of religion acting as a buffer to prevent depression after a serious life event.

These results do not support the notion that religious and spiritual life views enhance psychological well-being.

The effectiveness of large-scale interventions to prevent suicide among persons who previously attempted suicide remains to be determined. The National Suicide Surveillance System (NSSS), launched in Taiwan in 2006, is a structured nationwide intervention program for people who survived their suicide attempts. This naturalistic study examined its effectiveness using data from the first 3 years of its operation.

Effectiveness of the NSSS aftercare services was examined using a logistic/proportional odds mixture model, with eventual suicide as the outcome of interest. As well, we examined time until death for those who died and factors associated with eventual suicide.

Receipt of aftercare services was associated with reduced risk for subsequent suicide; for service recipients who eventually killed themselves, there was a prolonged duration between the index and fatal attempts. Elderly attempters were particularly prone to a shorter duration between the index and fatal attempts. Male gender, the lethality potential of the index attempt, and a history of having had a mental disorder also were associated with higher risk.

The structured aftercare program of the NSSS appears to decrease suicides and to delay time to death for those who remained susceptible to suicide.

Attainment of remission is viewed as the optimal outcome of acute antidepressant treatment. However, some patients experience subsyndromal symptoms after they achieve remission. This study examines the prognostic significance of subsyndromal symptoms occurring during the first 6 months after remission of late-life depression.

Older (age 60–89 years) in-patients and out-patients with unipolar major depression were followed until remission (asymptomatic or almost asymptomatic for 3 consecutive weeks). Two hundred and forty-two achieved remission after uncontrolled antidepressant treatment. This analysis focused on remitted patients who had follow-up data over a 2.5-year period (n = 185).

Approximately 18% of patients relapsed. Of the remainder (n = 152), 42.8% had subsyndromal depressive symptoms during the 6 months following remission. Cox's proportional survival analysis demonstrated that longer duration of subsyndromal symptoms [number of weeks with the Longitudinal Follow-up Examination (LIFE) Psychiatric Status Rating Scale (PSR) score of 3 or 4] in the first 6 months after remission was significantly associated with shorter time to recurrence and higher recurrence rate [hazard ratio (HR) 1.16, 95% confidence interval (CI) 1.08–1.24]. Based on our analysis, patients with 0, 4, 8 and 12 weeks of subsyndromal symptoms in the first 6 months after remission have estimated recurrence rates of 28, 45, 66 and 86% respectively during the ensuing 2 years.

These findings highlight the clinical importance of subsyndromal symptoms occurring after remission in late-life depression. They also argue that studies of geriatric depression may complement the definition of remission with information on subsyndromal symptoms occurring after the initial asymptomatic period.

Thought disorder has been proposed as an indicator of schizotypy, which is considered to be necessary but not sufficient for the development of schizophrenia. It is unclear whether thought disorder is an indicator of susceptibility (i.e. an endophenotype) for schizophrenia. The goal of the present study was to elucidate the role of thought disorder in relation to schizotypy by examining its presence in high-risk individuals during mid-childhood.

The sample consisted of 265 subjects drawn from the New York High-Risk Project. Individuals at high risk for schizophrenia (i.e. offspring of parents with schizophrenia) were compared with individuals at low risk for schizophrenia (i.e. offspring of parents with affective disorder or offspring of psychiatrically normal parents). Videotaped interviews were rated for thought disorder using the Scale for the Assessment of Thought, Language, and Communication (TLC). The same subjects were administered diagnostic interviews in late adolescence/early adulthood.

Although positive thought disorder was equally present in subjects with affective and non-affective psychoses, negative thought disorder (namely, poverty of speech and poverty of content of speech) was elevated only in subjects with schizophrenia-related psychosis. Logistic regression analyses revealed that negative thought disorder added to the prediction of schizophrenia-related psychosis outcomes over and above positive thought disorder.

These findings suggest that negative thought disorder may have a specific association with schizotypy, rather than a more general association with psychosis. The findings also support consideration of negative thought disorder as an endophenotypic indicator of a schizophrenia diathesis.