Background. Major depression is a prevalent mental disorder in the general population, with a multi-factorial etiology. However, work stress as a risk factor for major depression has not been well studied.

Method. Using a longitudinal study design, this analysis investigated the association between the levels of work stress and major depressive episode(s) in the Canadian working population, aged 18 to 64 years. Data from the longitudinal cohort of the Canadian National Population Health Survey (NPHS) were used (n=6663). The NPHS participants who did not have major depressive episodes (MDE) at baseline (1994–1995 NPHS) were classified into four groups by the quartile values of the baseline work stress scores. The proportion of MDE of each group was calculated using the 1996–1997 NPHS data.

Results. The first three quartile groups had a similar risk of MDE. Those who had a work stress score above the 75th percentile had an elevated risk of MDE (7·1%). Using the 75th percentile as a cut-off, work stress was significantly associated with the risk of MDE in multivariate analysis (odds ratio=2·35, 95% confidence interval 1·54–3·77). Other factors associated with MDE in multivariate analysis included educational level, number of chronic medical illnesses and child and adulthood traumatic events. There was no evidence of effect modification between work stress and selected sociodemographic, clinical and psychosocial variables.

Conclusions. Work stress is an independent risk factor for the development of MDE in the working population. Strategies to improve working environment are needed to keep workers mentally healthy and productive.

SYNOPSIS Experimental data on the location in the brain of electrode sites supporting electrical self-stimulation are reviewed. All previous studies are in agreement that the behaviour is most easily elicited from lateral hypothalamic sites corresponding approximately to the fibre pathways known as the ‘medial forebrain bundle’. Some brainstem electrode sites will support self-stimulation. Experiments are summarized which indicate that there is a correlation between the sites of electrode tips positive for self-stimulation and the location of catecholamine-containing neurones in two regions: (1) in the region of the dopamine-containing cells in the ventral mesencephalon (cell-body groups A9 and AIO of Dahlstr¨m and Fuxe, 1964), and (2) in the region of the noradrenaline-containing cells of the locus coeruleus (A6 group). These two cell-body groups give rise to axons which pass through the medial forebrain bundle to form terminal systems with a widespread distribution in the prosencephalon. The hypothesis is advanced that electrical self-stimulation results in the majority of cases from activation of one or both of these catecholamine-containing systems.

Background. A portion of the genetic risk factors for the personality trait neuroticism (N) may also increase risk for major depression (MD). Females have both higher levels of N and higher rates of MD than males, suggesting that these traits may be more genetically correlated in females.

Methods. Structured interviews, including a lifetime assessment for MD by DSM-III-R criteria, were administered to 863 male–male MZ (monozygotic), 649 male–male DZ (dizygotic), 506 female–female MZ, 345 female–female DZ, and 1408 opposite-sex twin pairs. N was assessed using the short-form of the Eysenck Personality Questionnaire. A sex-limited Cholesky model was fitted which allowed us to decompose into additive genetic, common environmental, and individual-specific environmental components two main classes of correlations: within-sex between-variable and between-sex within-variable.

Results. Our best-fitting model contained only additive genetic and individual-specific environmental factors for both N and MD. The within-sex genetic correlations between N and MD were estimated at +0·68 in men and +0·49 in women. This model fitted only slightly better than one in which the N–MD within-sex genetic correlation was constrained to be equal across the sexes, and estimated at +0·55. There may be sex-specific genes influencing both N and MD.

Conclusion. Our best-fitting model failed to establish a significant sex difference in the genetic correlation between N and MD. These results, as well as evidence for sex-specific genetic factors for both traits, have implications for the diagnosis, classification, and treatment of the affective disorders, and molecular genetic approaches to the study of these traits.

The interaction of physical and mental vulnerability and environmental constraints is thought to foster the development of psychiatric disorders such as major depressive disorder (MDD). A central factor in the development of psychopathology is mental stress. Despite some evidence for parasympathetic withdrawal and sympathetic overactivity in MDD, the psychophysiological response to stress in depression is not clear-cut. Given the growing interest in heart rate and heart rate variability as indicators for remote monitoring of patients, it is important to understand how patients with MDD react to stress in a laboratory-controlled environment. We conducted a systematic review of studies using electrocardiography to derive heart rate and heart rate variability during stress in patients with clinical depression. We focused on well-validated stress tasks- the mental arithmetic stress task, the Trier social stress task and public speaking task- to minimize confounding effects due to the nature of the stressor. The majority of studies found hypo-reactivity during stress as a hallmark of depression as evidenced by lower fluctuation in heart rate and heart rate variability in the high-frequency band. We address the potential underlying biological mechanisms, the influence of covariates on these measures and briefly discuss the specificity and potential for remote monitoring by using these variables.

This article addresses the issues of recognition and labelling of psychological disorders (PDs) by general practitioners (GPs), and he association of recognition with management and outcome. Nearly 2000 attenders of 25 GPs were screened with the GHQ and a stratified sample of 296 patients was examined twice, using the Present State Examination (PSE) and Groningen Social Disability Schedule (GSDS).

Prevalence rates of PDs according to the GHQ, GP and PSE were 46%, 26% and 15% respectively. For the 1450 ‘new’ patients, i.e. patients who had no PD diagnosed by their GP in the 12 months prior to the enrolment visit, these rates were 38%, 14%, and 10%. GPs missed half of the PSE cases and typically assigned non-specific diagnoses to recognized cases. Depressions were more readily recognized than anxiety disorders, and the detection rates for severe disorders were higher than those for less severe disorders.

Recognition was strongly associated with management and outcome. Recognized as compared to non-recognized cases were more likely to receive mental health interventions from their GP and had better outcomes in terms of both psychopathology and social functioning. Initial severity, psychological reasons for encounter, recency of onset, diagnostic category, and psychiatric comorbidity were related to both better recognition and outcome. However, these variables could not account for the association of recognition with management and outcome, but some did modify the association. A causal model of the relationships is presented and possible reasons for non-recognition and for the beneficial effects of recognition are discussed.

Autistic and non-autistic mentally retarded adolescents and young adults were individually matched for age and verbal ability and were given tasks in which they chose photographs of faces for emotionally expressive voices, and photographs of non-emotional things or events to accompany recorded sounds. The results were that relative to control subjects, autistic individuals performed less well on the emotion tasks than on the non-emotion tasks. The findings suggest that autistic individuals have a disability in recognizing bodily expressions of emotion, and that there is a degree of task-specificity to this impairment.

Background. Several previous studies have indicated high rates of schizophrenia in African-Caribbeans in the UK compared to White population.

Method. All people aged 18 to 64 years residing in two health districts in London who made contact with hospital or community services over a 1-year (Whites) or 2-year (ethnic minorities) period were screened for psychotic symptoms.

Results. One hundred and twenty-three patients passed the screen, of whom 100 were assigned a schizophrenic class by the CATEGO program. Of these, 38 were White, 38 African-Caribbean and 24 Asian. The incidence rate for broad schizophrenia was significantly higher for African-Caribbeans than for Whites. Asians showed a high rate among people age 30 and over, particularly women. Poor outcome at 1-year follow-up was significantly more common for African-Caribbeans than for the other two groups. The proportion of African-Caribbeans with a poor outcome was two and a half times greater than that of Whites. On a range of seven socio-demographic variables, African-Caribbeans differed from the other two groups only on unemployment.

Conclusions. A multitide of factors play a role in the aetiology of schizophrenia. Comparison of environmental factors in these groups may identify factors that contribute to the aetiology of schizophrenia.

Fifty-seven chronic agoraphobic outpatients were treated by 12 hours of exposure in vivo on four days over two weeks to check the effects of oral diazepam versus placebo during group exposure, group versus individual exposure, and high versus medium anxiety arousal during individual exposure. The controlled parallel design allowed comparative evaluation of each treatment condition to six months follow-up. Assessment was blind with respect to drug and psychological treatment. Patients in all treatment conditions improved significantly in phobias and in related life areas.

Outcome to group exposure on phobias and other measures was similar in all three drug conditions (placebo, waning diazepam, peak diazepam) with no significant differences between them. Diazepam patients had significantly less discomfort than placebo patients during group exposure treatment. Group exposure patients improved slightly but significantly more than individual exposure patients on non-phobic measures, though group exposure was accompanied by more panics during treatment yet was easier to run by the therapist. Individual exposure under high anxiety arousal was no more therapeutic than with lower anxiety. Diazepam is a mild palliative during group exposure but does not facilitate outcome to treatment. Group exposure in vivo is mildly facilitatory for outcome compared with individual exposure. Anxiety evocation during treatment was not therapeutically helpful.

A 2¼-year prospective study of children suffering head injury is described. Three groups of children were studied: (a) 31 children with ‘severe’ head injuries resulting in a post-traumatic amnesia (PTA) of at least 7 days; (b) an individually matched control group of 28 children with hospital treated orthopaedic injuries; and (c) 29 children with ‘mild’ head injuries resulting in a PTA exceeding 1 hour but less than 1 week. Individual psychological testing was carried out as soon as the child recovered from PTA, and then again 4 months, 1 year, and 2¼ years after the injury. A shortened version of the Wechsler Intelligence Scale for Children (WISC), the Neale Analysis of Reading Ability and a battery of tests of specific cognitive functions were employed. The mild head injury group had a mean level of cognitive functioning below the control group, but the lack of any recovery during the follow-up period indicated that the intellectual impairment was not a consequence of the injury. In the severe head injury group, the presence of cognitive recovery and a ‘dose—response’ relationship with the degree of brain injury showed that the intellectual deficits were caused by brain damage. Some degree of cognitive impairment was common following head injuries giving rise to a PTA of at least 2 weeks. Conversely no cognitive sequelae, transient or persistent, could be detected when the PTA was less than 24 hours. The results were less consistent in the 1-day to 2-week PTA range, but the evidence suggested that a broadly defined threshold for impairment operated at about that level of severity of injury. Timed measures of visuo-spatial and visuo-motor skills tended to show more impairment than verbal skills but otherwise there was no suggestion of a specific pattern of cognitive deficit. Recovery was most rapid in the early months after injury, but substantial recovery continued for 1 year with some improvement continuing in the second year in some children, especially those with the most severe injuries. Age, sex and social class showed no significant effects on the course of recovery.

Background. Hip fracture is common in the elderly. Previous studies suggest that psychiatric illness is common and predicts poor outcome, but have methodological weaknesses. Further studies are required to address this important issue.

Methods. We prospectively recruited 731 elderly participants with hip fracture in two Leeds hospitals. Psychiatric diagnosis was made within 5 days of surgery using the Geriatric Mental State schedule and other standardized instruments, and data on confounding factors was collected. Main study outcomes were length of hospital stay, and mortality over 6 months after fracture.

Results. Fifty-five per cent of participants had cognitive impairment (dementia in 40% and delirium in 15%), 13% had a depressive disorder, 2% had alcohol misuse and 2% had other psychiatric diagnoses. Participants were likely to remain in hospital longer if they suffered from dementia, delirium or depression. The relative risks of mortality over 6 months after hip fracture were increased in dementia and delirium, but not in depression.

Conclusions. Psychiatric illness is common after hip fracture, and has significant effects on important outcomes. This suggests a need for randomized, controlled trials of psychiatric interventions in the elderly hip fracture population.

Background. The dorsolateral prefrontal cortex (DLPFC) is involved in the pathophysiology of major depression. In particular, metabolic (functional hypometabolism) and structural alterations have been described. In this study metabolic changes within the DLPFC of severely depressed patients before and after electroconvulsive therapy (ECT) were evaluated by proton STEAM spectroscopy (1H-MRS).

Method. Twelve severely depressed patients with a diagnosis of major depressive episode, unipolar with melancholic features (DSM-IV), were enrolled, and the left dorsolateral prefrontal cortex (DLPFC) was investigated before and after unilateral ECT by 1H-MRS. Three of the four non-responding patients were remeasured a third time after a combined ECT/antidepressant pharmacotherapy. The results were compared with 12 age- and gender-matched controls.

Results. In depressed patients reduced glutamate/glutamine (Glx) levels were measured pre-ECT; Glx concentrations correlated negatively with severity of depression. After successful treatment, Glx increased significantly and levels no longer differed from those of age-matched controls.

Conclusions. Our results indicate that major depressive disorder is accompanied by state-dependent metabolic alterations, especially in glutamate/glutamine metabolism, which can be reversed by successful ECT.

Background. The usefulness of any diagnostic scheme is directly related to its ability to provide clinically useful information on need for care. In this study, the clinical usefulness of dimensional and categorical representations of psychotic psychopathology were compared.

Method. A total of 706 patients aged 16–65 years with chronic psychosis were recruited. Psychopathology was measured with the Comprehensive Psychopathological Rating Scale (CPRS). Lifetime RDC, DSM-III-R, and ICD-10 diagnoses and ratings of lifetime psychopathology were made using OPCRIT. Other clinical measures included: (i) need for care; (ii) quality of life; (iii) social disability; (iv) satisfaction with services; (v) abnormal movements; (vi) brief neuropsychological screen; and (vii) over the last 2 years – illness course, symptom severity, employment, medication use, self-harm, time in hospital and living independently.

Results. Principal component factor analysis of the 65 CPRS items on cross-sectional psychopathology yielded four dimensions of positive, negative, depressive and manic symptoms. Regression models comparing the relative contributions of dimensional and categorical representations of psychopathology with clinical measures consistently indicated strong and significant effects of psychopathological dimensions over and above any effect of their categorical counterparts, whereas the reverse did not hold. The effect of psychopathological dimensions was mostly cumulative: high ratings on more than one dimension increased the contribution to the clinical measures in a dose-response fashion. Similar results were obtained with psychopathological dimensions derived from lifetime psychopathology ratings using the OCCPI.

Conclusions. A dimensional approach towards classification of psychotic illness offers important clinical advantages.

The history of neurasthenia is discussed in the light of current interest in chronic fatigue, and in particular the illness called myalgic encephalomyelitis (‘ ME ’). A comparison is made of the symptoms, presumed aetiologies and treatment of both illnesses, as well as their social setting. It is shown that neurasthenia remained popular as long as it was viewed as a non-psychiatric, neurological illness caused by environmental factors which affected successful people and for which the cure was rest. The decline in neurasthenia was related to the changes which occurred in each of these views. It is argued that similar factors are associated with the current interest in myalgic encephalomyelitis. It is further argued that neither neurasthenia nor ‘ ME ’ can be fully understood within a single medical or psychiatric model. Instead both have arisen in the context of contemporary explanations and attitudes involving mental illness. Future understanding, treatment and prevention of these and related illnesses will depend upon both psychosocial and neurobiological explanations of physical and mental fatigability.

Background. The aim of this study was to estimate the extent to which anxiety disorders contribute to an increase in suicidal behaviour after controlling for both observed and non-observed sources of confounding.

Method. Data were collected from the Christchurch Health and Development Study (CHDS), a 25-year longitudinal study of over 1000 participants. Measures of anxiety disorders [phobia, generalized anxiety disorder (GAD), panic disorder], major depression (MD), substance use disorders, conduct/antisocial personality disorder, stressful life events, unemployment, and suicidal ideation/attempts for subjects aged 16–18, 18–21 and 21–25 years were used to fit random and fixed effects regression models of the associations between anxiety disorders and suicidal behaviours.

Results. Anxiety disorders were strongly associated with suicidal ideation/attempts. Any single anxiety disorder increased the odds of suicidal ideation by 7·96 times [95% confidence interval (CI) 5·69–11·13] and increased the rate of suicide attempts by 5·85 times (95% CI 3·66–9·32). Control for co-occurring mental disorders, non-observed fixed confounding factors and life stress reduced these associations [suicidal ideation odds ratio (OR) 2·80, 95% CI 1·71–4·58; suicide attempts incidence rate ratio (IRR) 1·90, 95% CI 1·07–3·39]. Rates of suicidal behaviour also increased with the number of anxiety disorders. Estimates of the population attributable risk suggested that anxiety disorders accounted for 7–10% of the suicidality in the cohort.

Conclusions. Anxiety disorders may be a risk factor for suicidality, even after controlling for confounding, with risks increasing with multiple anxiety disorders. Management of anxiety disorders may be an important component in strategies to reduce population rates of suicide.

Background. Prevalence and co-occurrence of mental disorders is high among patients consulting their family general practitioner (GP) for a new health problem, but data on diagnostics and sociodemographics are sketchy.

Method. A cross-sectional two-phase epidemiological study. A total of 1785 consecutive patients with new complaints, aged 18–65 years, consulting 28 family practices during March–April 2000 in Aarhus County, Denmark were screened, in the waiting room, for mental and somatic symptoms with SCL-8 and SCL-Somatization questionnaires, for illness worry with Whitely-7 and for alcohol dependency with CAGE. In a stratified random sample of 701 patients, physician interviewers established ICD-10 diagnoses using the SCAN interview. Prevalence was calculated using weighted logistic regression, thus correcting for sample skewness.

Results. Half of the patients fulfilled criteria for an ICD-10 mental disorders and a third of these for more than one group of disorders. Women had higher prevalence of somatization disorder and overall mental disorders than men. Men had higher prevalence of alcohol abuse and hypochondriasis than women. Psychiatric morbidity tended to increase with age. Prevalence of somatoform disorders was 35·9% (95% CI 30·4–41·9), anxiety disorders 16·4% (95% CI 12·7–20·9), mood disorders 13·5% (95% CI 11·1–16·3), organic mental disorders 3·1% (95% CI 1·6–5·7) and alcohol abuse 2·2% (95% CI 1·5–3·1). Co-morbidities between these groups were highest for anxiety disorders, where 89% also had another mental diagnosis, and lowest for somatoform disorders with 39%.

Conclusions. ICD-10 mental disorders are very prevalent in primary care and there is a high co-occurrence between most disorders. Somatoform disorders, however, more often than not exist without other mental disorders.