This issue features groups of papers on theory of mind and schizophrenia, other aspects of schizophrenia, gender and depression, psychoimmunology, antecedents of somatic and psychiatric illness.

We suspect that people have an everyday theory of mind because they explain and frequently talk about the behaviour of others and themselves in terms of beliefs and desires. Having a theory of mind means that we believe that other people have minds like ours and that we understand the behaviour of these others in terms of the contents of their minds: their knowledge, beliefs and desires. But how can we demonstrate experimentally that people are using their theory of mind to predict the behaviour of others. This problem is particularly acute in the case of animals or young human children when they do not have language. Dennett (1978) discussing Premack & Woodruff's (1978) seminal paper ‘Does the chimpanzee have a theory of mind?’, suggested that the use of false beliefs to explain behaviour would provide convincing evidence. When their belief is true (i.e. corresponds to the actual state of the world) we can explain peoples' behaviour on the basis of the state of the world without needing to know about their beliefs. This ambiguity does not arise when the belief is false. The first experiment to use this approach was published by Wimmer & Perner (1983). They showed that at around 4 years of age a child knows that Maxi will look for his chocolates where Maxi believes them to be, even though the child knows that this belief is false because he has seen Maxi's mother moving the chocolates. In the English-speaking world the task involving Maxi and the chocolates has become the Sally-Anne task (see this issue, Lee et al. 2004).

Background. A better understanding of the neural basis of social cognition including mindreading (or theory of mind) and empathy might help to explain some deficits in social functioning in people with schizophrenia. Our aim was to review neuroimaging and neuropsychological studies on social cognition, as they may shed light on the neural mechanisms of social cognition and its dysfunction in patients with schizophrenia.

Method. A selective literature review was undertaken.

Results. Neuroimaging and neuropsychological studies suggest convergence upon specific networks for mindreading and empathy (the temporal cortex, amygdala and the prefrontal cortex). The frontal lobe is likely to play a central role in enabling social cognition, but mindreading and empathic abilities may require relatively different weighting of subcomponents within the same frontal-temporal social cognition network.

Conclusions. Disturbances in social cognition may represent an abnormal interaction between frontal lobe and its functionally connected cortical and subcortical areas. Future studies should seek to explore the heterogeneity of social dysfunction within schizophrenia.

Background. Having a ‘theory of mind’ (ToM) means that one appreciates one's own and others' mental states, and that this appreciation guides interactions with others. It has been proposed that ToM is impaired in schizophrenia and experimental studies show that patients with schizophrenia have problems with ToM, particularly during acute episodes. The model predicts that communicative problems will result from ToM deficits.

Method. We analysed 35 encounters (>80 h of recordings) between mental health professionals and people with chronic schizophrenia (out-patient consultations and cognitive behaviour therapy sessions) using conversation analysis in order to identify how the participants used or failed to use ToM relevant skills in social interaction.

Results. Schizophrenics with ongoing positive and negative symptoms appropriately reported first and second order mental states of others and designed their contributions to conversations on the basis of what they thought their communicative partners knew and intended. Patients recognized that others do not share their delusions and attempted to reconcile others' beliefs with their own but problems arose when they try to warrant their delusional claims. They did not make the justification for their claim understandable for their interlocutor. Nevertheless, they did not fail to recognize that the justification for their claim is unconvincing. However, the ensuing disagreement did not lead them to modify their beliefs.

Conclusions. Individuals with schizophrenia demonstrated intact ToM skills in conversational interactions. Psychotic beliefs persisted despite the realization they are not shared but not because patients cannot reflect on them and compare them with what others believe.

Background. Recent reviews of randomized controlled trials have concluded that cognitive behaviour therapy (CBT) is effective, as an addition to standard care, in the treatment of people suffering from schizophrenia. Most of the trials have been conducted with stabilized out-patients. The aim of this trial was to evaluate the effectiveness of CBT for in-patients suffering acute psychotic episodes, when delivered under conditions representative of current clinical practice.

Method. Consecutive admissions meeting criteria were recruited. After screening, 43 were assigned at random to a treatment-as-usual (TAU) control group and 47 were assigned to TAU plus CBT. At baseline, 6 months and 12 months, patients were rated on symptoms and social functioning. CBT (maximum 25 sessions) began immediately after baseline assessment.

Results. The CBT group gained greater benefit than the TAU group on symptoms and social functioning. A larger proportion of the CBT group (60%) than the TAU group (40%) showed reliable and clinically important change, and none of them (v. 17%) showed reliable deterioration compared with baseline.

Conclusions. CBT for patients suffering acute psychotic episodes can produce significant benefits when provided under clinically representative conditions.

Background. Carers' satisfaction with psychiatric services related to information and advice is generally poor. This may be particularly true for services trying to meet the needs of ethnically diverse communities. It is important that services attempt to ameliorate carers' concerns as early as possible. The authors aimed to assess the impact of a brief educational and advice support service on carers of patients with a first episode of psychotic illness.

Method. Carers of all patients identified with a first episode of psychosis in a defined psychiatric catchment area of North London were invited to participate. Following consent from patients and relatives, relatives were randomly allocated to receive (in addition to usual services) a brief intervention comprising education and advice about the disorder from a support team or to usual care from community psychiatric services.

Results. One hundred and six carers were recruited to the study. Take-up of the intervention was less than expected and the intervention had little impact. The authors found no differences over time between the randomized arms for relatives' satisfaction (F=2·3, p=0·14, df=1) or number of days spent by patients in hospital over nine months from entry to the trial (F=1·7, p=0·18, df=1).

Conclusions. It was found that the support and advice intervention for families had little impact on their satisfaction or on patients' outcomes. However, failure to take up the intervention threatens the conclusions as the power to show an effect was reduced. Although family interventions, in general, are considered an important adjunct to the treatment of patients with chronic psychosis, there may be difficulties in providing an educational and support intervention shortly after first onset. How and when psychiatric services provide information and advice to carers of people newly diagnosed with a psychosis requires further study.

Background. While men with schizophrenia are at higher risk of displaying homicidal behaviours compared with the general population, very little is known about the circumstances related to the triggering of such violent acts among offenders with schizophrenia. The main goal of the present investigation was to describe the surrounding context, psychotic symptoms, target characteristics and other circumstantial factors associated with homicidal acts committed by men with schizophrenia, with or without an additional antisocial personality disorder (APD).

Method. Comprehensive clinical and research interviews, as well as multiple sources of information including reports from social workers and police officers, criminal records, witness statements and questionnaires completed by friends, acquaintances and family members were used to determine specific characteristics surrounding the homicidal acts.

Results. Overall, a significant majority of homicides were considered as the consequence of psychotic symptoms; they mostly involved someone who knew the offender; and they usually occurred in a private residence. However, the subgroup of offenders with both schizophrenia and APD were less likely to be judged as responding to psychotic symptoms; they assaulted a non-relative more frequently, and they were more likely to have used alcohol and to be involved in an altercation with the victim prior to the incident than offenders without APD.

Conclusion. Even for such extreme acts as homicides, the circumstances affecting the occurrence of violence among offenders with schizophrenia may differ when an additional APD diagnosis is present, which would have important implications for prevention and treatment programmes.

Background. Clinical studies suggest that psychotic and paranoid states in late life are associated with cognitive dysfunction. However, it is not clear whether this finding would be observed in general population samples of non-demented elderly, particularly after adjustment for potential confounding factors.

Method. A representative sample of non-demented 85-year-olds living in the community or in institutions in Göteborg, Sweden (N=347) was examined using a psychiatric and physical examination (including a medical history), key-informant interview, psychometric testing and review of medical records. Individuals with psychotic symptoms and paranoid ideation were compared with the mentally healthy regarding tests of verbal ability, inductive logical reasoning, spatial ability, perceptual speed, basic arithmetic, primary memory and secondary memory.

Results. Non-demented 85-year-olds with psychotic symptoms or paranoid ideation performed specifically worse on tests measuring verbal ability, logical reasoning and two tests of spatial ability after adjustment for sex, education, hearing impairment, visual deficits, somatic disorders, depression, 3-year-mortality rate and incident dementia.

Conclusions. Psychotic symptoms and paranoid ideation were associated with lower performance on cognitive tests related to verbal ability, logical reasoning and spatial ability in non-demented 85-year-olds after adjustment for potential confounders.

Background. In schizophrenia, affective disorders, and obsessive–compulsive disorder (OCD) dysfunction of frontal neuronal circuits has been suggested. Such impairments imply corresponding oculomotor deficits.

Method. Eye movement response to foveofugal and foveopetal step–ramp stimuli was recorded within the same study design in patients with schizophrenia (N=16), affective disorder (N=15), and OCD (N=18) and compared with controls (N=23) using infra-red reflection oculography.

Results. In the foveofugal task steady-state velocity was lower in all patient groups compared with controls. Post-saccadic eye velocity was also decreased in patients with schizophrenia and affective disorder. In the foveopetal stimulus steady-state velocity was reduced in schizophrenic patients, only. Changes of saccadic latencies or position errors were not found in any of the patient groups. Also, pursuit latency was unchanged and initial eye acceleration was not decreased.

Conclusions. Unaltered saccadic parameters indicate intact motion perception in cortical visual area V5. Therefore, the observed deficit of pursuit maintenance implies a dysfunction of frontal networks in all patient groups including the pursuit region of the frontal eye field (FEF). In patients with schizophrenia and affective disorder reduced post-saccadic pursuit initiation may indicate an impaired interaction between the pursuit and the saccadic system.

Background. While a female preponderance in unipolar depression is a consistent finding in community-based studies, determinants remain speculative. This study aimed to examine whether a female preponderance in certain anxiety disorders drives a gender difference in depression.

Method. The relevant data from the National Comorbidity Study (NCS) are analysed.

Results. We observed a biphasic pattern in the emergence of a female preponderance in the depressive and anxiety disorders, with an initial pre-pubertal or early adolescent onset, and after attenuation in early to middle adulthood, re-emergence in mid- to late-adulthood. Analyses focused on determinants of the initial female preponderance. Female gender, presence of an anxiety disorder and variable ages of onset in the anxiety disorder all contributed to the increased chance of an initial depressive episode. Some specificity in linking the onset of depressive temporally in early adolescence with two anxiety disorders was demonstrated, specifically generalized anxiety disorder and panic disorder.

Conclusions. The separate anxiety disorders and their age of onset had variable links with depression, but female gender remained a significant predictor of depression after accounting for the effects of prior anxiety.

Background. The present study aimed to investigate the relative importance of genetic and environmental influences on depressive symptoms in the elderly.

Methods. Depressive symptoms were assessed through the Center for Epidemiological Studies – Depression (CES-D) scale. The CES-D scale was administered to 959 twin pairs (123 female MZs, 90 male MZs, 207 same-sex female DZs, 109 same-sex male DZs and 430 opposite-sex DZs) aged 50 years or older (mean age 72 years). A dichotomous depressed state variable was constructed based on CES-D cut-offs and self-reported use of antidepressant medication. Structural equation models were fitted to the data to dissect genetic and environmental variance components.

Results. The sex-specific heritability estimates for depressive symptoms were 14% for males and 29% for females and 23% when constrained to be equal for men and women. The prevalence of clinically significant depressive symptoms was 16% for men and 24% for women. Heritability estimates for the dichotomous depressed state measure were 7% for males and 49% for females in the full model and 33% when constrained to be equal.

Conclusion. Our results suggest that depressive symptoms in the elderly are moderately heritable, with a higher heritability for women than men, although differences in heritability estimates were not statistically significant.

Background. There is evidence that depression impairs natural killer cell activity (NKA); this could have implications for anti-tumour immunity. Our aim was to examine the role of the hypothalamic–pituitary–adrenal (HPA) axis in suppressing NKA in a population of patients with early breast cancer, screened for depression. Secondary aims were to study the relationship between psychological, endocrine and immune variables and baseline tumour characteristics.

Methods. A cross-sectional population of female patients (n=55) with early breast cancer was sampled prior to primary surgery. Structured interview and psychometric instruments measured psychological distress. Flow cytometry was used to enumerate NK cells and lymphocytes were cryopreserved for use in a 51Cr-release assay, to estimate NKA. Midnight and three early morning saliva samples were collected to measure free cortisol levels. Tumour characteristics were obtained from hospital laboratory data.

Results. A high rate of psychological morbidity (40%) was observed in the population. NKA was reduced in those with past or current psychiatric illness compared to those without (344 v. 553 LU20 and 455 v. 569 LU20 respectively, p<0·05 for both). Cortisol was not related to psychological status but was modestly positively correlated to NKA. A positive correlation was observed between the Fighting Spirit subscale of the Mental Adjustment to Cancer Scale and tumour size (r=0·383, p=0·012)

Conclusions. Our data support the evidence that psychological morbidity is associated with immune dysfunction; however, the most obvious candidate mediator of this effect, the HPA axis, does not appear responsible for this effect. Possible reasons for this are discussed.

Background. Major depressive disorder (MDD) has been associated with alterations in immune function. Suppression of natural killer (NK) cell activity (NKCA) reliably characterizes immunological alterations observed in MDD. Antidepressant pharmacotherapy has been associated with modulation of NKCA. Previous investigations into antidepressant modulation of NKCA have not employed randomized double-blind placebo controlled designs. Thus, it is unknown whether treatment-associated changes in immune function are due to drug, placebo, or spontaneous remission effects. The present investigation examined the effect of antidepressant treatment on NKCA utilizing a randomized double-blind placebo controlled experimental design.

Method. Patients (N=16) met DSM-IV criteria for MDD and were randomly assigned to drug (N=8; citalopram, 20 mg/day) or placebo (N=8) under double-blind conditions. Severity and pattern of depressive symptoms were assessed by the Hamilton Depression Rating Scale (HDRS). NK cell function was measured using a standard chromium-release assay and NK cell number assessed by flow cytometry. HDRS scores, NK cell function, and NK cell numbers were collected at 0, 1, 2 and 4 weeks of treatment.

Results. Clinical response was associated with augmented NKCA independent of treatment condition. Failure to respond to treatment resulted in significantly reduced NKCA over treatment interval.

Conclusions. The present results suggest that alterations in the depressive syndrome, regardless of therapeutic modality, may be sufficient to modulate NKCA during antidepressant trials and thus may significantly impact on co-morbid health outcomes in MDD.

Background. A previous principal components analysis of symptoms occurring after infectious mononucleosis suggested that a discrete fatigue syndrome occurs, which is independent of psychiatric disorder. This work has not been replicated and no latent class analysis of subjects has been published.

Method. We prospectively examined a cohort of 150 American primary care patients 2 and 6 months after the onset of corroborated infectious mononucleosis. A subset of 50 subjects was studied 4 years after onset. We performed principal components analyses of both psychological and somatic symptoms and latent class analyses of subjects.

Results. Principal components analyses consistently delineated two fatigue factors at 2 and 6 months and one fatigue factor at 4 years. These factors were separate from a mixed anxiety and depressive factor. A four-class solution for the latent class analyses consisted of most subjects with few symptoms, a few with many symptoms, a group with predominantly mood symptoms and some subjects with fatigue symptoms.

Conclusions. The symptoms of the principal factors with fatigue were similar to those previously described. Both the factors and classes were independent of an equally delineated mood factor and class. These results support the existence of two discrete chronic fatigue syndromes after infectious mononucleosis, one of which is still demonstrable 4 years after onset.

Background. The goal of this investigation was to determine the association between self-reported childhood trauma and physical disorders among adults in the United States.

Method. Data were drawn from the National Comorbidity Survey (N=S877). Multiple logistic regression analyses were used to determine the associations between childhood physical abuse, sexual abuse, and childhood neglect and the likelihood of specific physical disorders among adults.

Results. Childhood physical abuse, sexual abuse and neglect were associated with a statistically significantly increased risk of a wide range of physical illnesses during adulthood. After adjusting for demographic characteristics, lifetime anxiety and depressive disorders, alcohol and substance dependence, and all types of trauma: results showed that childhood physical abuse was associated with increased risk of lung disease (OR=1·5 (1·1, 2·2)), peptic ulcer (OR=1·5 (1·03, 2·2)) and arthritic disorders (OR=1·5 (1·1, 2·2)); childhood sexual abuse was associated with increased risk of cardiac disease (OR=3·7 (1·5, 9·4)); and childhood neglect was associated with increased risk of diabetes (OR=2·2 (1·1, 4·4)) and autoimmune disorders (OR=4·4 (1·7, 11·6)).

Conclusions. Consistent with previous work, these results suggest that self-reported childhood trauma is associated with increased risk of a range of physical illnesses during adulthood. Future research that includes replication of these findings using prospectively assessed physical and mental disorders with objectively measured biological data using a longitudinal design, including other known risk factors for these diseases and more detailed information on specific forms of abuse, is needed to understand the potential mechanisms of these links.

Background. Neuroticism and somatic complaints are linked, and the aim of this study is to disentangle which mechanisms may be responsible for this association.

Method. In a stratified sample of 7076 adults (18–65 years), neuroticism, 22 self-reported chronic somatic conditions and five broad CIDI-diagnosed psychiatric syndromes were assessed at baseline and, in 3625 (51%) subjects, 3 years later. Using path analysis we examined whether neuroticism has direct links with future somatic morbidity and, conversely, whether morbidity at baseline is linked with higher neuroticism later on.

Results. Neuroticism at baseline is associated with psychiatric and somatic morbidity at follow-up after 3 years (31% and 24%, respectively, are direct associations, i.e. unmediated by each other or neuroticism at follow-up and independent of morbidity at baseline). Conversely, somatic and psychiatric morbidity at baseline are associated with increased neuroticism at follow-up (27% and 15%, respectively, are direct associations).

Conclusions. Neuroticism raises risk for psychiatric and somatic morbidity but also results from them. It represents a central nexus in the process of morbidity accumulation.

Background. Studies have been fairly consistent in finding a relationship between social support and depression. However, little is known about the relationship between depression and social support in the context of treatment for depression. This study examined the effects of treatment for depression on social support among patients with multiple sclerosis (MS).

Method. Sixty-three moderately depressed MS patients received 16 weeks of cognitive behaviour therapy (CBT), supportive expressive group psychotherapy (SEGP) or sertraline. Depression was measured using the Beck Depression Inventory and social support was measured using Arizona Social Support Interview Schedule.

Results. Treatment for depression was associated with significant increases in perceived social support, utilized social support and satisfaction with support, as well as reduction in need for emotional support. There were no significant changes in structural support or need for physical support. There were also no differences in change in social support across treatments. All changes in social support were fully explained by depression. Improvements in utilized social support and satisfaction with social support were fully mediated by improvements in depression. Baseline depression predicted improvements in perceived support and need for emotional support.

Conclusions. These findings suggest that improvements in social support among MS patients during treatment for depression can be explained by depression. However, different domains of social support may be differentially sensitive to changes in depression.

Background. We examined whether, in the UK, there is an increased risk of autism (AD) following exposures, in early life, to: (1) wild measles; (2) live attenuated measles, alone or in combination as MMR; and (3) the alteration of the mumps strain within MMR.

Method. We conducted time trend analyses of 2407 AD subjects born between 1959–93; and for comparison, 4640 Down's syndrome (DS) subjects born between 1966–93. Between 1968–86, we correlated variations in AD and DS births with wild measles incidence. Between 1959–93, we tested for abrupt changes in the long-term AD birth trend for the effects of introducing: (1) monovalent measles vaccines in 1968; (2) MMR immunization in 1988; and (3) the ‘overnight switch’ from mixed use of Urabe MMR to exclusive use of Jeryl–Lynn MMR in 1992. Incidence rate ratios (IRRs) were used as measures of association.

Results. We found no significant association between AD births and exposure (prenatal and post-natal up to 18 months age) to population rates of measles infections, and no ‘step-up’ increase in AD births associated with the introduction of monovalent measles and MMR vaccines, and changing mumps strain. An unexpected reduction in AD births of 21% (95% CI 6·9–33·3%; P=0·005) among the post-1987 birth cohorts was detected.

Conclusion. No increased risk of AD following exposures to wild measles and vaccinations with monovalent measles, and Urabe or Jeryl–Lynn variants of MMR was detected. The precise meaning of the detected AD births reduction is unclear. Our study cannot exclude rare complications of MMR, given its correlational design.

Background. Little is known about how continuation and maintenance cognitive-behavioural therapy (CBT) influences important psychological constructs that may be associated with long-term outcome of major depressive disorder. The goal of this study was to examine whether CBT would help maintain attributional style changes experienced by patients during acute phase fluoxetine treatment.

Method. Three hundred and ninety-one patients with major depressive disorder were enrolled in an open, fixed-dose 8 week fluoxetine trial. Remitters to this acute phase treatment (N=132) were randomized to receive either fixed-dose fluoxetine (meds only) or fixed-dose fluoxetine plus cognitive-behavioural therapy (CBT+meds) during a 6-month continuation treatment phase. The Attributional Style Questionnaire (ASQ) was completed by patients at three time points – acute phase baseline, continuation phase baseline and continuation phase endpoint. Analysis of covariance was used to compare continuation phase ASQ composite score changes between groups.

Results. Patients in both treatment groups experienced significant gains in positive attributional style during the acute phase of treatment. Continuation phase ASQ composite change scores differed significantly between treatment groups, with the CBT+meds group maintaining acute phase positive attributional style changes, and the meds only group exhibiting a worsening of attributional style. The two treatment groups did not significantly differ in rates of relapse and final continuation phase visit HAMD-17 scores.

Conclusions. In this sample, the addition of CBT to continuation psychopharmacological treatment was associated with maintenance of acute treatment phase attributional style gains. Further research is needed to evaluate the role of such gains in the long-term course of depressive illness.