Cognitive models of the positive symptoms of psychosis specify the cognitive, social and emotional processes hypothesized to contribute to their occurrence and persistence, and propose that vulnerable individuals make characteristic appraisals that result in specific positive symptoms.

We describe cognitive models of positive psychotic symptoms and use this as the basis of discussing recent relevant empirical investigations and reviews that integrate cognitive approaches into neurobiological frameworks.

Evidence increasingly supports a number of the hypotheses proposed by cognitive models. These are that: psychosis is on a continuum; specific cognitive processes are risk factors for the transition from subclinical experiences to clinical disorder; social adversity and trauma are associated with psychosis and with negative emotional processes; and these emotional processes contribute to the occurrence and persistence of psychotic symptoms. There is also evidence that reasoning biases contribute to the occurrence of delusions.

The benefits of incorporating cognitive processes into neurobiological research include more sophisticated, bidirectional and interactive causal models, the amplification of phenotypes in neurobiological investigations by including emotional processes, and the adoption of more specific clinical phenotypes. For example, there is potential value in studying gene×environment×cognition/emotion interactions. Cognitive models and their derived phenotypes constitute the missing link in the chain between genetic or acquired biological vulnerability, the social environment and the expression of individual positive symptoms.

The effectiveness of a psychosocial skills training (PSST) approach applied to chronic out-patients with schizophrenia was examined. We hypothesized that the PSST programme, which included treatment as usual (TAU), PSST and family therapy (FT), would reduce positive and negative symptoms, prevent relapse and rehospitalization, and improve psychosocial functioning (PSF), global functioning and treatment adherence.

Eighty-two patients were randomly assigned to receive either TAU [antipsychotic medication (AP); n=39] or the PSST approach (TAU+PSST+FT; n=43). The two groups were assessed at intake and after completion of 1 year of treatment.

There were statistically significant differences between the two groups. Patients in the PSST group improved their symptomatology, psychosocial and global functioning (symptoms and psychological, social and occupational functioning), showed lower relapse, rehospitalization and drop-out rates, a higher level of compliance with AP medication, and a high level of therapeutic adherence in comparison with TAU patients, whose symptoms also improved although they showed no improvement in any of the clinical or psychosocial variables. A comparison of the standardized effect sizes showed a medium and a large effect size of PSF and global functioning for the PSST group and a non-effect size for the TAU group.

A higher level of effectiveness was demonstrated when combining TAU, PSST and FT in comparison with AP medication alone. The PSST approach should be recommended for clinical practice.

A form of confabulation has been documented in schizophrenia and appears to be related to the symptom of thought disorder. It is unclear whether it is associated with the same pattern of neuropsychological deficits as confabulation in neurological patients.

Thirty-four patients with chronic schizophrenia, including those with and without thought disorder, and 17 healthy controls were given a fable recall task to elicit confabulation. They were also examined on a range of executive, episodic and semantic memory tests.

Confabulation was seen at a significantly higher rate in the schizophrenic patients than the controls, and predominated in those with thought disorder. Neuropsychologically, it was not a function of general intellectual impairment, and was not clearly related to episodic memory or executive impairment. However, there were indications of an association with semantic memory impairment.

The findings support the existence of a form of confabulation in schizophrenia that is related to thought disorder and has a different neuropsychological signature to the neurological form of the symptom.

The incidence of schizophrenia varies by individual-level characteristics and neighbourhood-level attributes. Few specific socio-environmental risk factors (SERFs) have been identified at the neighbourhood level. Cross-level interactions are poorly understood. We investigated these issues using data from the Aetiology and Ethnicity in Schizophrenia and Other Psychoses (AESOP) study.

All incidence cases of ICD-10 schizophrenia (F20) and other non-affective psychoses (F21–29), aged 16–64 years, across 33 wards in Southeast London were identified over a 2-year period (1997–1999). Census data provided the denominator for each ward. Multilevel Poisson regression simultaneously modelled individual- and neighbourhood-level SERFs, including socio-economic deprivation, voter turnout (proxy for social capital), ethnic fragmentation (segregation) and ethnic density.

A total of 218 subjects were identified during 565 576 person-years at risk. Twenty-three per cent of variance in incidence of schizophrenia across wards could be attributed to neighbourhood-level risk factors [95% confidence interval (CI) 9·9–42·2]. Thus, 1% increases in voter turnout [incidence rate ratio (IRR) 0·95, 95% CI 0·92–0·99] and ethnic segregation (IRR 0·95, 95% CI 0·92–0·99) were both independently associated with a reduced incidence of 5%, independent of age, sex, ethnicity, deprivation and population density. This was similar for other non-affective psychoses. There was some evidence that ethnic minority individuals were at greater risk of schizophrenia in areas with smaller proportions of minority groups (p=0·07).

SERFs at individual and neighbourhood levels were implicated in the aetiology of psychosis, but we were unable to determine whether these associations were causal. Individual risk may be mediated by social capital, which could operate as a protective factor, perhaps moderating social stress in the onset of psychoses.

Estrogen has been hypothesized to have a protective and antipsychotic-like effect in women at risk for schizophrenia. The aim of the present study was to evaluate the association between menstrual cycle and/or estrogen levels and psychotic symptoms in a sample of women with schizophrenia.

One hundred and twenty-five premenopausal women with schizophrenia and regular menses were examined. The levels of 17β-estradiol and other hormones of the gonadal axis were assessed in the follicular, peri-ovulatory, and luteal phases of the menstrual cycle. The effects of the menstrual cycle phase and/or the estradiol level on the Positive and Negative Syndrome Scale (PANSS) and the Brief Psychiatric Rating Scale (BPRS) scores were calculated by means of regression analyses.

Significant improvement in psychotic, but not depressive, symptoms was observed during the luteal phase, compared with other days of the menstrual cycle.

The present findings indicate that estradiol may have specific antipsychotic-like effects on the symptoms of schizophrenia. Thus further investigation into the therapeutic effect of estrogen may be worthwhile.

The DSM-IV definition of post-traumatic stress disorder (PTSD) requires that the syndrome cause clinically significant distress or impairment. The impact of the clinical significance criterion on the lifetime prevalence of PTSD among civilian victims of traumatic events has not been evaluated.

Data from two community-based samples were examined, the 1996 Detroit Area Survey of Trauma (n=2181) and the Mid-Atlantic Urban Youth Study (n=1698). The World Health Organization Composite International Diagnostic Interview (WHO CIDI) was used to ascertain DSM-IV PTSD.

The inclusion of the clinical significance criterion in DSM-IV reduces the conditional probability of PTSD given exposure to trauma by approximately 30%. Cases with clinically significant syndrome showed more pervasive and persistent disturbance and an excess in impaired activity days.

The consistency of the findings between the two studies strengthens the evidence on the impact of the clinical significance criterion in the diagnosis of PTSD, and the construct validity of its measurement. There is a need for greater research effort on the definition and measurement of the clinical significance criterion.

From a cognitive neuroscience perspective, the emotional attentional bias in post-traumatic stress disorder (PTSD) could be conceptualized either as emotional hyper-responsiveness or as reduced priming of task-relevant representations due to dysfunction in ‘top-down’ regulatory systems. We investigated these possibilities both with respect to threatening and positive stimuli among traumatized individuals with and without PTSD.

Twenty-two patients with PTSD, 21 trauma controls and 20 non-traumatized healthy participants were evaluated on two tasks. For one of these tasks, the affective Stroop task (aST), the emotional stimuli act as distracters and interfere with task performance. For the other, the emotional lexical decision task (eLDT), emotional information facilitates task performance.

Compared to trauma controls and healthy participants, patients with PTSD showed increased interference for negative but not positive distracters on the aST and increased emotional facilitation for negative words on the eLDT.

These findings document that hyper-responsiveness to threat but not to positive stimuli is specific for patients with PTSD.

Some studies suggest that early psychological treatment is effective in preventing chronic post-traumatic stress disorder (PTSD), but it is as yet unclear how best to identify trauma survivors who need such intervention. This prospective longitudinal study investigated the prognostic validity of acute stress disorder (ASD), of variables derived from a meta-analysis of risk factors for PTSD, and of candidate cognitive and biological variables in predicting chronic PTSD following assault.

Assault survivors who had been treated for their injuries at a metropolitan Accident and Emergency (A&E) Department were assessed with structured clinical interviews to establish diagnoses of ASD at 2 weeks (n=222) and PTSD at 6 months (n=205) after the assault. Candidate predictors were assessed at 2 weeks.

Most predictors significantly predicted PTSD status at follow-up. Multivariate logistic regressions showed that a set of four theory-derived cognitive variables predicted PTSD best (Nagelkerke R2=0·50), followed by the variables from the meta-analysis (Nagelkerke R2=0·37) and ASD (Nagelkerke R2=0·25). When all predictors were considered simultaneously, mental defeat, rumination and prior problems with anxiety or depression were chosen as the best combination of predictors (Nagelkerke R2=0·47).

Questionnaires measuring mental defeat, rumination and pre-trauma psychological problems may help to identify assault survivors at risk of chronic PTSD.

Injured survivors of individual and mass trauma are at risk for developing post-traumatic stress disorder (PTSD). Few investigations have assessed PTSD after injury in large samples across diverse acute care hospital settings.

A total of 2931 injured trauma survivors aged 18–84 who were representative of 9983 in-patients were recruited from 69 hospitals across the USA. In-patient medical records were abstracted, and hospitalized patients were interviewed at 3 and 12 months after injury. Symptoms consistent with a DSM-IV diagnosis of PTSD were assessed with the PTSD Checklist (PCL) 12 months after injury.

Approximately 23% of injury survivors had symptoms consistent with a diagnosis of PTSD 12 months after their hospitalization. Greater levels of early post-injury emotional distress and physical pain were associated with an increased risk of symptoms consistent with a PTSD diagnosis. Pre-injury, intensive care unit (ICU) admission [relative risk (RR) 1·17, 95% confidence interval (CI) 1·02–1·34], pre-injury depression (RR 1·33, 95% CI 1·15–1·54), benzodiazepine prescription (RR 1·46, 95% CI 1·17–1·84) and intentional injury (RR 1·32, 95% CI 1·04–1·67) were independently associated with an increased risk of symptoms consistent with a PTSD diagnosis. White injury survivors without insurance demonstrated approximately twice the rate of symptoms consistent with a diagnosis of PTSD when compared to white individuals with private insurance. By contrast, for Hispanic injury survivors PTSD rates were approximately equal between uninsured and privately insured individuals.

Nationwide in the USA, more than 20% of injured trauma survivors have symptoms consistent with a diagnosis of PTSD 12 months after acute care in-patient hospitalization. Coordinated investigative and policy efforts could target mandates for high-quality PTSD screening and intervention in acute care medical settings.

Traumatic memory is a key symptom in psychological trauma victims and may remain vivid for several years. Psychotherapy has shown that neither the psychopathological signs of trauma nor the expression of traumatic memories are static over time. However, few studies have investigated the neural substrates of psychotherapy-related symptom changes.

We studied 16 subthreshold post-traumatic stress disorder (PTSD) subjects by using a script-driven symptom provocation paradigm adapted for single photon emission computed tomography (SPECT) that was read aloud during traumatic memory retrieval both before and after exposure-based and cognitive restructuring therapy. Their neural activity levels were compared with a control group comprising 11 waiting-list subthreshold PTSD patients, who were age- and profile-matched with the psychotherapy group.

Significantly higher activity was observed in the parietal lobes, left hippocampus, thalamus and left prefrontal cortex during memory retrieval after psychotherapy. Positive correlations were found between activity changes in the left prefrontal cortex and left thalamus, and also between the left prefrontal cortex and left parietal lobe.

Neural mechanisms involved in subthreshold PTSD may share neural similarities with those underlying the fragmented and non-verbal nature of traumatic memories in full PTSD. Moreover, psychotherapy may influence the development of a narrative pattern overlaying the declarative memory neural substrates.

Although the effectiveness of cognitive behavioural therapy (CBT) in the management of panic disorder (PD) is now well established, there have been few studies of predictors of outcome with this patient group using clinical effectiveness trial data, a hypothesis-testing model, and a dependent measure of clinically significant change.

The data for this study came from a randomized controlled trial of three forms of CBT delivery for PD with and without agoraphobia (two 6-week CBT programmes, one of which was computer assisted, and one therapist-directed 12-week CBT programme), comprising a total of 186 patients across two sites. Based on previous related research, five hypothesized predictors of post-treatment and follow-up outcome were identified and examined, using a series of bivariate and multivariate analyses.

The results in general supported the hypotheses. Strength of blood/injury fears, age of initial onset of panic symptoms, co-morbid social anxieties and degree of agoraphobic avoidance were predictive of both measures of post-treatment outcome. Degree of residual social difficulties and the continued use of anxiolytics at post-treatment were also shown to predict poor outcome at the 6-month follow-up. However, strength of continuing dysfunctional agoraphobic cognitions by the end of active treatment did not predict outcome at follow-up for the sample as a whole.

The identification of consistent predictors of outcome with CBT has many clinical and research benefits. As CBT, however, is being delivered increasingly in a variety of brief formats, further research is required to identify moderators of response to these ‘non-standard’ treatment formats.

Despite the growth of reduced therapist-contact cognitive behavioural therapy (CBT) programmes, there have been few systematic attempts to determine prescriptive indicators for such programmes vis-à-vis more standard forms of CBT delivery. The present study aimed to address this in relation to brief (6-week) and standard (12-week) therapist-directed CBT for panic disorder (PD) with and without agoraphobia. Higher baseline levels of severity and associated disability/co-morbidity were hypothesized to moderate treatment effects, in favour of the 12-week programme.

Analyses were based on outcome data from two out of three treatment groups (n=72) from a recent trial of three forms of CBT delivery for PD. The dependent variables were a continuous composite panic/anxiety score and a measure of clinical significance. Treatment×predictor interactions were examined using multiple and logistic regression analyses.

As hypothesized, higher baseline severity, disability or co-morbidity as indexed by strength of dysfunctional agoraphobic cognitions; duration of current episode of PD; self-ratings of panic severity; and the 36-item Short Form Health Survey (SF-36) (Mental component) score were all found to predict poorer outcome with brief CBT. A similar trend was apparent in relation to baseline level of depression. With high and low end-state functioning as the outcome measure, however, only the treatment×agoraphobic cognitions interaction was found to be significant.

While there was no evidence that the above variables necessarily contraindicate the use of brief CBT, they were nevertheless associated with greater overall levels of post-treatment improvement with the 12-week approach.