The lead papers in this issue are two meta-analyses of controlled trials in a recently very active area: psychological treatments for schizophrenia. The findings of Pilling and colleagues are clear-cut. There is good evidence of worthwhile benefit from two forms of treatment. Family therapy delivered to people with schizophrenia who are in contact with carers, and particularly in single family rather than group approaches, lowers relapse rates and improves medication compliance. Cognitive therapy improves mental states and may be particularly useful for those with resistant symptoms. By contrast two other psychological treatments, social skills training and cognitive remediation, have failed to show evidence of benefit in controlled trials. The findings of these review articles have important implications for treatment.

Background. While there is a growing body of evidence on the efficacy of psychological interventions for schizophrenia, this meta-analysis improves upon previous systematic and meta-analytical reviews by including a wider range of randomized controlled trials and providing comparisons against both standard care and other active interventions.

Method. Literature searches identified randomized controlled trials of four types of psychological interventions: family intervention, cognitive behavioural therapy (CBT), social skills training and cognitive remediation. These were then subjected to meta-analysis on a variety of outcome measures. This paper presents results relating to the first two.

Results. Family therapy, in particular single family therapy, had clear preventative effects on the outcomes of psychotic relapse and readmission, in addition to benefits in medication compliance. CBT produced higher rates of ‘important improvement’ in mental state and demonstrated positive effects on continuous measures of mental state at follow-up. CBT also seems to be associated with low drop-out rates.

Conclusions. Family intervention should be offered to people with schizophrenia who are in contact with carers. CBT may be useful for those with treatment resistant symptoms. Both treatments, in particular CBT, should be further investigated in large trials across a variety of patients, in various settings. The factors mediating treatment success in these interventions should be researched.

Background. Social skills training and cognitive remediation are psychological techniques with considerable face validity for the treatment of negative symptoms of schizophrenia and their consequences. This paper provides a meta-analytical review of these treatments. It includes an appreciable number of randomized controlled trials, using comparisons against both standard care and other active interventions. However, the assessment of particular outcomes sometimes had to be based on single studies.

Method. A detailed search strategy was used to identify randomized controlled trials of social skills training and cognitive remediation, primarily employing electronic databases. Randomized controlled trials (RCTs) that met predefined criteria were then subjected to meta-analysis on a variety of outcome measures.

Results. There was no clear evidence for any benefits of social skills training on relapse rate, global adjustment, social functioning, quality of life or treatment compliance. Cognitive remediation had no benefit on attention, verbal memory, visual memory, planning, cognitive flexibility or mental state.

Conclusions. Social skills training and cognitive remediation do not appear to confer reliable benefits for patients with schizophrenia and cannot be recommended for clinical practice.

Background. Somatic and psychiatric morbidity may cluster because of reciprocal effects between them but also as a result of common underlying factors.

Methods. The data come from the 1946 MRC birth cohort (N = 5362). Clustering of 20 chronic medical conditions at the participants' 43rd year was analysed using multi-morbidity coefficients. Associations of somatic and psychiatric morbidity at 43 years, with temperament and behaviour, assessed from adolescence to early adulthood, and background variables like paternal social class, were examined using structural equation modelling. The focus was on whether links applied to both morbidity types or one only, and were direct or were indirect, mediated by prior morbidity.

Results. Reported chronic medical conditions clustered strongly. Somatic multi-morbidity and psychiatric ill-health at 43 years were associated with temperamental and behavioural features assessed between the subjects' 13th and 26th birthday, like neuroticism and aggression, as well as with external variables like parental death before the participants' 16th birthday. However, only neuroticism holds direct links with somatic as well as with psychiatric ill-health, 28% of the former and 52% of the latter association being independent of the simultaneous presence of the other morbidity type and of participants' health status 7 years earlier.

Conclusions. Personality traits like neuroticism not only raise the risk of psychiatric disorder but also, irrespective of whether manifest psychiatric disorders have developed, of a broad spectrum of chronic somatic diseases. This suggests that clinicians and researchers should focus not only on the psychiatric disorders associated with such personality traits but also on their medical consequences.

Background. Exposure to an ill parent in childhood may be a risk factor for adult somatization. This study examines the hypothesis that somatizing adults are more likely to have been exposed to illness as a child and that in turn, their children are more likely to report ill health and to have more contact with medical services than children of other mothers.

Method. A cross-sectional comparative investigation of three groups of mothers and their children of 4–8 years of age: (i) 48 mothers suffering from chronic somatization; (ii) 51 mothers with chronic ‘organic’ illness; and (iii) 52 healthy mothers was carried out.

Results. Somatizing mothers were more likely than other women to report exposure to childhood neglect and to physical illness in a parent (OR 2·9; 95% CI 1·4–6·1). The children of these somatizing mothers were more likely to have health problems than were the children of organically ill or healthy women and had more consultations with family doctors (average annual rates: somatizers 4·9 (S.D. 3·8), organic 3·0 (S.D. 3·5) and healthy 2·8 (S.D. 2·6)). Multivariate modelling of consultation rates among children found significant main effects for maternal somatization, maternal childhood adversity, the child's tendency to worry about health and a two-way interaction of maternal childhood adversity and her somatization status.

Conclusions. The hypotheses are broadly supported. However, it is important to emphasize the extent to which these findings are based on maternal reports.

Background. Although genes are known to influence the aetiology of ADHD, the impact of exposure to parental ADHD has received limited scientific scrutiny. This study investigated the impact of exposure to parental ADHD on clinical features and dysfunction in offspring.

Methods. We studied 1099 offspring (53% male, mean age 12·4 years) of non-ADHD, remitted ADHD, and persistent ADHD parents, using structured diagnostic interviews and a battery of cognitive and psychosocial measures. Offspring across these three groups were compared on clinical, cognitive and psychosocial outcomes, adjusting for exposure to other parental psychopathology, offspring ADHD status and social class.

Results. Parental ADHD was associated with an increased risk for ADHD in offspring relative to no parental ADHD, but no significant differences were found between children of remitted versus persistent ADHD parents. Exposure to parental ADHD predicted higher levels of family conflict and lesser levels of family cohesion relative to families without parental ADHD, independent of other psychopathological conditions in parents or ADHD status. Significant interactions were detected in which parental ADHD had a deleterious impact on measures of school performance in offspring without ADHD but not in those with the disorder.

Conclusions. These results find no support for the hypothesis that exposure to parental ADHD increases the risk for ADHD in children beyond that conveyed by the liability associated with the diagnosis in the parent. However, since exposure to parental ADHD was associated with a disruptive family environment, the identification and treatment of adults with ADHD may be an important component of the treatment plan of youth with ADHD.

Background. Psychiatric diagnoses obtained at personal interview are only moderately reliable and depend critically on accurate self-observation. Reports by family members provide additional information but may be biased. It is unclear how best to combine these two sources of diagnostic data.

Methods. Using complete data on lifetime prevalence for six disorders in ∼1200 male–male twin pairs from a population based registry, we first applied a standard bivariate twin model – which treats self-diagnoses and informant-diagnoses as separate phenotypes – and then examined a ‘multiple-rater’ model – which assumes that self-report and co-twin-report are fallible indices of one underlying disease liability. Best-fit models were chosen using Akaike's information criterion.

Results. Standard bivariate analyses indicated that the same genetic factors accounted for variation in self-reported and co-twin-reported diagnoses. The multiple-rater model produced a substantial decrease in variance attributed to individual-specific environment and a proportional increase in heritability of liability for major depression, generalized anxiety disorder, alcohol dependence and adult antisocial behaviour, but not for drug abuse/dependence or regular tobacco use. The best-fit model consistently included either a ‘bias’ or a ‘correlated error’ path. No evidence for family environmental risk factors was found for any disorder.

Conclusion. The genetic factors that influence self-report psychiatric illness also influence psychiatric illness as described by relatives. For many psychiatric disorders, incorporation of self-report and family history data in a single model may reduce measurement error and increase estimates of heritability. However, account must be taken of the fact that family history reports are systematically biased. While promising, these results are preliminary and require replication.

Background. A self-rated measure of health anxiety should be sensitive across the full range of intensity (from mild concern to frank hypochondriasis) and should differentiate people suffering from health anxiety from those who have actual physical illness but who are not excessively concerned about their health. It should also encompass the full range of clinical symptoms characteristic of clinical hypochondriasis. The development and validation of such a scale is described.

Method. Three studies were conducted. First, the questionnaire was validated by comparing the responses of patients suffering from hypochondriasis with those suffering from hypochondriasis and panic disorder, panic disorder, social phobia and non-patient controls. Secondly, a state version of the questionnaire was administered to patients undergoing cognitive-behavioural treatment or wait-list in order to examine the measure's sensitivity to change. In the third study, a shortened version was developed and validated in similar types of sample, and in a range of samples of people seeking medical help for physical illness.

Results. The scale was found to be reliable and to have a high internal consistency. Hypochondriacal patients scored significantly higher than anxiety disorder patients, including both social phobic patients and panic disorder patients as well as normal controls. In the second study, a ‘state’ version of the scale was found to be sensitive to treatment effects, and to correlate very highly with a clinician rating based on an interview of present clinical state. A development and refinement of the scale (intended to reflect more fully the range of symptoms of and reactions to hypochondriasis) was found to be reliable and valid. A very short (14 item) version of the scale was found to have comparable properties to the full length scale.

Conclusions. The HAI is a reliable and valid measure of health anxiety. It is likely to be useful as a brief screening instrument, as there is a short form which correlates highly with the longer version.

Background. Much of the difficulty in helping the homeless mentally ill arises as a consequence of their resistance to engagement. A refused intervention can seldom influence a client's problems and engagement status can be argued as being an important independent predictor of outcome. No instrument could be identified which systematically measured the factors involved. This paper describes the development and psychometric properties of a new scale, the Homeless Engagement and Acceptance Scale (HEAS).

Method. Staff from an established project for the homeless mentally ill helped to identify relevant questions used to develop a five-item rating scale for completion by an informant. After piloting, the instrument was tested in a study in which subjects were assessed twice over 12 months by informants. Item analysis was undertaken and predictive validity was assessed.

Results. Item analysis indicated a good facility index signifying all items were able to differentiate subjects according to the characteristic being measured, and a high discrimination index demonstrating that all items were measuring the same concept. Predictive validity and internal consistency coefficients were both good. The 3 month HEAS score was found to be a significant predictor of accommodation status and adequacy of a support network at 12 months.

Conclusions. The good psychometric properties and predictive validity of the scale suggest the HEAS is likely to be a useful tool in assessing engagement status. One of the five questions (Q4) can be omitted for those who are not homeless and the scale termed the Engagement and Acceptance Scale (EAS).

Background. A key challenge in trauma care is the prevention of psychopathology. However, no definitive method of identifying individuals at risk of developing psychopathology exists. The Aberdeen Trauma Screening Index (ATSI) is a brief screening tool developed for use in a clinical setting by non-mental health professionals to facilitate the early identification of individuals most at risk of psychopathology 3-months post-accident.

Methods. The ATSI derived from a prospective study of a 150 out of an initial pool of 213 consecutive admissions to the Orthopaedic Trauma Unit and the Accident and Emergency Department of Aberdeen Royal Infirmary. Potential predictors were identified by a comprehensive assessment conducted within 1-week post-accident. Outcome at 3-months post-accident was measured using ‘caseness’ according to the General Health Questionnaire (GHQ-28).

Results. The ATSI is based on a final model comprising only seven variables with a sensitivity of 79% and specificity of 65%. A predictive index score (0–100) was produced to ensure the practical utility of the ATSI in a clinical setting. A ROC curve was constructed to illustrate the relationship between sensitivity and the specificity values with their corresponding threshold scores. On the basis of a prevalence rate of 55% ‘caseness’, as identified in the present study, a cut-off point of 45 provides the optimal outcome with a sensitivity value of 70% and a specificity value of 71%.

Conclusions. The ATSI can accurately identify those most at risk of developing psychopathology 3-months post-accident in a sample of accidentally injured adult subjects recruited as consecutive admissions to an urban hospital in the North East of Scotland. However, to establish the generalizability of these findings, it is important that the ATSI be validated in both similar and diverse populations.

Background. Although cases of early onset anorexia nervosa have been described, there has been no systematic comparison of early onset cases with classic cases of later onset, or with other forms of early onset eating disturbance.

Method. A consecutive series of patients referred to two specialist child and adolescent eating disorder services with a clinical diagnosis of eating disorder (N = 126) was systematically assessed using a child version of the Eating Disorder Examination (EDE) and the K-SADS interview.

Results. Of 86 patients with a diagnosis of eating disorder of early onset, 38 received a clinical diagnosis of anorexia nervosa (AN). The remainder were mainly diagnosed as having food avoidance emotional disorder (25 patients) and selective eating (17 patients). Six received other diagnoses (bulimia nervosa, or functional dysphasia). These 48 patients were combined to form a group of early onset non-AN eating disturbance. In terms of specific eating disorder psychopathology and general psychopathology, the early onset AN group was very similar to the late onset AN sample. When the two early onset groups were compared, there was a marked difference between them in terms of eating disorder psychopathology. A discriminant function analysis using the EDE information produced a clear discrimination, with the EDE restraint and shape concern subscales doing most of the discrimination work.

Conclusions. The specific psychopathology of AN of early onset is very similar to that of classic adolescent onset AN. Other forms of early onset eating disorder do not evidence this specific psychopathology.

Background. Chronic fatigue syndrome and fibromyalgia continue to be perplexing conditions of unknown validity. Aetiological and symptomatic heterogeneity is likely and the distinctiveness of these disorders remains unclear. Our aims were to investigate empirically symptomatic heterogeneity in chronic fatigue syndrome and fibromyalgia.

Methods. Latent class analysis was applied to data from 646 patients who met accepted criteria for chronic fatigue syndrome and/or fibromyalgia who were systematically evaluated at a specialist fatigue clinic. Thirty-two symptoms commonly found in chronic fatigue syndrome and fibromyalgia were entered into the latent class analysis.

Results. We chose to interpret a four class solution. The classes appeared to differ in a graded fashion (rather than qualitatively) for symptom endorsements, pre-morbid characteristics, and co-morbidity with panic disorder and major depression.

Conclusions. These results were unexpected given the usual assumption of the distinctiveness of chronic fatigue syndrome and fibromyalgia. These results support a conceptualization of chronic fatigue syndrome and fibromyalgia as being characterized by greater similarities than differences.

Background. Screening surveys of depressive symptoms were conducted among primary care patients at six sites in different countries. The LIDO Study was designed to assess quality of life and economic correlates of depression and its treatment in culturally diverse primary health care settings. This paper describes: (1) the association between depressive symptoms and functional status, global health-related quality of life (QoL), and use of general health services across different cultural settings; and (2) among subjects with depressive symptoms, the factors associated with recent treatment for depression.

Methods. Subjects aged 18 to 75 were recruited from participating primary care facilities in Be'er Sheva (Israel), Porto Alegre (Brazil), Melbourne (Australia), Barcelona (Spain), St Petersburg (Russian Federation) and Seattle (USA). Depressive symptoms were measured using the CES-D. Also administered were the SF-12, global questions on QoL, selected demographic and social measures, and questions on recent treatment for depression, use of health care services, and lost workdays.

Results. A total of 18489 patients were screened, of whom 37% overall (range 24–55%) scored [ges ]16 on the CES-D and 28% (range 17–42%) scored [ges ]20. Overall, 13% reported current treatment for depression (range 4 to 23%). Patients with higher depressive symptom scores had worse health, functional status, QoL, and greater use of health services across all sites. Among those with a CES-D score [ges ]16, subjects reporting treatment for depression were more likely than those reporting no treatment to be dissatisfied with their health (except in St Petersburg), and to have higher depressive symptom scores.

Conclusions. Higher depressive symptom scores in primary care patients were consistently associated with poorer health, functional status and QoL, and increased health care use, but not with demographic variables. The likelihood of treatment for depression was associated with perceptions of health, as well as severity of the depression.

Background. Several examinations have detected a relation between depressive symptoms and medical utilization. However, selection biases have been involved in most previous examinations. We sought to test the association between depressive symptoms and prospective, increased medical care utilization, in a population-based Canadian sample, while controlling for utilization due to medical illness and controlling for selection bias.

Methods. Data from the Nova Scotia Health Survey 1995, an age- and sex-stratified random sampling of 3227 Nova Scotian adults, included the Center for Epidemiological Studies-Depression scale and items assessing chronic medical conditions and current limitations in daily activities resulting from medical illness. We linked survey data with medical care utilization measures for the year following the survey, including out-patient visits, reimbursement for out-patient services, hospitalizations, and hospitalization days.

Results. After controlling for age, sex, count of medical diagnoses and current medical severity, those with a greater level of depressive symptoms were at greater risk of having increased medical care utilization in the following year. These results remained after removing mental health care utilization costs.

Conclusions. In a population-based sample, depressive symptoms predicted greater medical care utilization, independent of a number of medical severity measures. Whether depressive symptoms are a risk marker or a causal risk factor for increased medical utilization remains to be explored.

Background. Schizophrenic patients generate fewer words than healthy controls during verbal fluency tasks. The structure of output may explain why patients generate fewer exemplars.

Methods. Twenty-four healthy controls and 24 patients with schizophrenia participated in six, 3 min semantic fluency tasks. In a subsequent session, participants were given cards, each printed with one of their own words generated from previous fluency tasks. Participants were to sort the cards into categories (e.g. subcategories of ‘animals’), thus defining their own semantic subcategories of words, and thereby eliminating experimenter assumptions about word relatedness. These clusters were matched with fluency output of each participant. The time spent searching through semantic networks within clusters and switching to other clusters when locating and producing associated words were measured.

Results. Patients produced fewer words and spent more time switching to words within clusters and to different clusters than controls, but otherwise response profiles were similar. Although controls returned more frequently to clusters and consequently made more switches between these clusters than patients, this group difference disappeared when the total number of words produced was covaried.

Conclusions. Consistent with previous literature, patients produced fewer words and made more errors than controls. The absence of a group difference in number of different clusters or mean number of items per cluster suggests that patients are similar to controls with respect to number of ideas in their semantic network. Patients' longer between-cluster switching times indicate a general slowness that may be attributed to difficulties finding new words within a semantic field.

Background. This study examined the effects of psychological stress on platelet α2-adrenergic receptor (α2-AR) binding sites in relation to stress-induced anxiety and changes in the inflammatory response system (IRS).

Methods. The maximum number of binding sites (Bmax) and their affinity (Kd) for [3H]-rauwolscine, a selective α2-AR antagonist, and the stimulated production of tumor necrosis factor-α (TNFα), the Th1-like cytokine, interferon-γ (IFNγ), and the Th2-like cytokines, interleukin-10 (IL-10) and IL-5, were measured in 35 university students a few weeks before (baseline) as well as on the day before a difficult, oral examination (stress condition). The State-Trait-Anxiety Inventory (STAI)- was recorded during both conditions. The Minnesota Multiphase Personality Inventory (MMPI-2TM) was used to assess psychasthenia (Scale 7).

Results. Academic examination stress induced a significant increase in α2-AR density in students whose STAI scores increased in the stress period, in female students and in students who scored higher on psychasthenia. There were significant and positive correlations between stress-induced anxiety and changes in α2-AR density. Stress-induced anxiety was accompanied by a pro-inflammatory and Th1-like response, i.e. increased IFNγ and TNFα production. The stress-induced changes in platelet α2-AR density were significantly and positively related to the production of TNFα, IL-10 and IL-5 and negatively to that of IFNγ.

Conclusions. Subchronic psychological stress in humans induces increased α2-AR density, which is related to stress-induced anxiety, an anxiety-prone constitution and female sex. Increased α2-AR density is accompanied by a Th2-like response and increased TNFα production. The results suggest that: (i) α2-AR density is sensitive to graded differences in stress-induced anxiety; and (ii) psychological stress is accompanied by intertwined responses in the catecholaminergic system, such as α2-ARs, and the IRS, such as Th1/Th2-like functions and the production of TNFα.

Background. Animal studies have shown that neuroactive steroids modulate the activity of the gamma-aminobutyric acid type A/benzodiazepine receptor complex and that these steroids display anxiolytic or anxiogenic activity depending on their positive (e.g. allopregnanolone) or negative allosteric modulation (e.g. dehydroepiandrosterone sulphate) of this receptor. This study compared plasma levels of allopregnanolone, dehydroepiandrosterone sulphate and pregnenolone sulphate in healthy controls and in patients with generalized social phobia, as assessed with the Mini-International Neuropsychiatric Interview.

Methods. Plasma concentrations of allopregnanolone, pregnenolone sulphate, and dehydroepiandrosterone sulphate were measured in 12 unmedicated male patients with generalized social phobia and 12 matched healthy male volunteers.

Results. Concentrations of pregnenolone sulphate were significantly lower in patients with generalized social phobia than in healthy controls. No statistically significant differences were found for the concentrations of allopregnanolone and dehydroepiandrosterone sulphate in plasma.

Conclusions. These results are particularly interesting since we also observed lower pregnenolone sulphate concentrations in male patients suffering from generalized anxiety disorder. Their relevance to the pathophysiology of social anxiety disorder remains to be determined.

Background. A number of challenge studies have reported abnormalities of serotonergic function in borderline personality disorder (BPD). There are, however, problems with the pharmacological probes used in these studies since fenfluramine and m-CPP are not only serotonergic agents but also induce release of catecholamines, particularly dopamine. Therefore, we tested whether subjects with BPD showed a blunted prolactin (PRL) response to flesinoxan, a highly potent and selective 5-HT1A agonist.

Methods. Flesinoxan challenge test was carried out in 20 BPD in-patients and 20 healthy controls matched for gender but not for age. Since 16 BPD in-patients exhibited major depressive co-morbidity, a group of 20 depressed in-patients matched for gender but not for age was also included.

Results. BPD in-patients exhibited blunted PRL responses as compared to controls, whereas depressed in-patients did not differ from controls. Moreover, PRL responses were lower among BPD in-patients than among depressed in-patients. Among the BPD in-patients, PRL responses to flesinoxan were lower in patients with past history of suicide attempts (N = 8) than in those with a negative history.

Conclusions. The results show major involvement of serotonergic function in BPD and are consistent with previous studies linking lower serotonergic activity with impulsivity. More particularly, our data suggest that BPD is characterized by lower 5-HT1A receptor sensitivity. Moreover, the data support the involvement of 5-HT1A activity in suicidal behaviour. However, this conclusion is limited because other hormonal responses such as ACTH and cortisol were not assessed, and because BPD was assessed by a self-report questionnaire and not a structured clinical interview.