Background. This report attempted to replicate and extend prior work examining social phobia (SP), co-morbid psychiatric illnesses, and the risk of suicidal ideation and suicide attempts incurred by their adolescent sufferers.

Methods. SP, alcohol dependence (ALD) and major depressive disorder (MDD) diagnoses, and suicide-related symptoms, were assessed in a population-based adolescent female twin sample. The differentiation of risks as a function of co-morbidity was explored. A trivariate model was fitted to estimate sharing of genetic and environmental vulnerability between SP and co-morbid disorders.

Results. The lifetime prevalence of SP was 16·3%. Significant risk for co-morbid MDD (OR = 3·2) and ALD (OR = 2·1) was observed. Strong evidence for shared genetic vulnerability between SP and MDD (respective heritabilities 28%, 45%; genetic r = 1·0) was observed with moderate support noted for similar sharing between SP and ALD (genetic r = 0·52, heritability for ALD 63%). SP with co-morbid MDD was associated with elevated risk for ALD and for suicide-related symptoms.

Conclusions. SP is a common illness often followed by co-morbid MDD and ALD. SP with co-morbid MDD predicts a substantially elevated risk of ALD and suicide-related symptoms, stressing the need for early SP detection.

The goal of much observational research is to identify risk factors that have a causal effect on health and social outcomes. However, observational data are subject to biases from confounding, selection and measurement, which can result in an underestimate or overestimate of the effect of interest. Various advanced statistical approaches exist that offer certain advantages in terms of addressing these potential biases. However, although these statistical approaches have different underlying statistical assumptions, in practice they cannot always completely remove key sources of bias; therefore, using design-based approaches to improve causal inference is also important. Here it is the design of the study that addresses the problem of potential bias – either by ensuring it is not present (under certain assumptions) or by comparing results across methods with different sources and direction of potential bias. The distinction between statistical and design-based approaches is not an absolute one, but it provides a framework for triangulation – the thoughtful application of multiple approaches (e.g. statistical and design based), each with their own strengths and weaknesses, and in particular sources and directions of bias. It is unlikely that any single method can provide a definite answer to a causal question, but the triangulation of evidence provided by different approaches can provide a stronger basis for causal inference. Triangulation can be considered part of wider efforts to improve the transparency and robustness of scientific research, and the wider scientific infrastructure and system of incentives.

Large amount of data have been published on non-psychotic depression (NPD), schizophrenia (SZ), and bipolar disorder, while psychotic depression (PD) as an own entity has received much smaller attention. We performed a systematic review and meta-analyses on epidemiology, especially incidence and prevalence, risk factors, and outcomes of PD. A systematic search to identify potentially relevant studies was conducted using four electronic databases and a manual search. The search identified 1764 unique potentially relevant articles, the final study included 99 articles. We found that the lifetime prevalence of PD varies between 0.35% and 1%, with higher rates in older age. Onset age of PD was earlier than that of NPD in younger samples, but later in older samples. There were no differences in gender distribution in PD v. NPD, but higher proportion of females was found in PD than in SZ or in psychotic bipolar disorder (PBD). Risk factors have rarely been studied, the main finding being that family history of psychosis and bipolar disorder increases the risk of PD. Outcomes of PD were mostly worse when compared with NPD, but better compared with SZ and schizoaffective disorder. The outcome compared with PBD was relatively similar, and somewhat varied depending on the measure of the outcome. Based on this review, the amount of research on PD is far from that of NPD, SZ, and bipolar disorder. Based on our findings, PD seems distinguishable from related disorders and needs more scientific attention.

Background. Past studies have found inconsistent evidence that substance use disorders are related to earlier onset of schizophrenia or more severe symptoms. This study examines prevalence and severity of current substance use disorders and onset of psychotic illness in a multi-facility sample.

Methods. Data are from the Suffolk County Mental Health Project, an epidemiological study of first admission psychosis. The SCID and instruments measuring symptomatology, personality and background characteristics were administered. Respondents were stratified into three groups: (a) no life-time substance diagnosis; (b) in remission or reporting current mild use at admission; and (c) current moderate–severe substance abuse at admission.

Results. Using the SCID severity rating, 17·4% of males and 6·2% of the females had moderate or severe current substance abuse, while 41·5% of males and 68·2% of females had no lifetime substance diagnosis. In almost all cases categorized as moderate–severe, the substance diagnosis predated onset of psychosis. Females categorized as moderate–severe had an earlier age of onset of psychosis than did females in the other groups. There were only slight differences in symptom severity among the groups but more marked antisocial behaviour in the moderate–severe group. Variables discriminating the moderate–severe from non-abuse groups were BPRS thought disturbance, adult anti-social behaviour and current cigarette smoking for males and adult antisocial behaviour and child–teen antisocial behaviour for females.

Conclusions. Severity of substance abuse does not appear to be a pivotal correlate of the early features of psychotic illness.

Background. There have been few large-scale epidemiological studies which have examined the prevalence of bipolar disorder. The authors report 12-month prevalence data for DSM-IV bipolar disorder from the Australian National Survey of Mental Health and Well-Being.

Method. The broad methodology of the Australian National Survey has been described previously. Ten thousand, six hundred and forty-one people participated. The 12-month prevalence of euphoric bipolar disorder (I and II) – similar to the euphoric-grandiose syndrome of Kessler and co-workers – was determined. Those so identified were compared with subjects with major depressive disorder and the rest of the sample, on rates of co-morbidity with anxiety and substance use disorders as well as demographic features and measures of disability and service utilization. Polychotomous logistic regression was used to study the relationship between the three samples and these dependent variables.

Results. There was a 12-month prevalence of 0·5% for bipolar disorder. Compared with subjects with major depressive disorder, those with bipolar disorder were distinguished by a more equal gender ratio; a greater likelihood of being widowed, separated or divorced; higher rates of drug abuse or dependence; greater disability as measured by days out of role; increased rates of treatment with medicines; and higher lifetime rates of suicide attempts.

Conclusions. This large national survey highlights the marked functional impairment caused by bipolar disorder, even when compared with major depressive disorder.

Hysterical symptoms are defined as complaints that are not fully explained by organic or functional neurological disease. Hysterical symptoms are common in neurological practice, accounting for about 1% of neurological diagnoses. Of those with neurological hysterical symptoms, about 80% will not have the hysterical personality, and about 80% will not have Briquet's hysteria. Some 60% will have a physical disease and perhaps as many as 50% will have recognizable psychiatric illness, particularly depression. Others may have unrecognized physical or psychiatric illness. Many hysterical symptoms may be understood in terms of abnormal illness behaviour.

Psychiatry still lives in a Kraepelinian world and scholarship on the work of Kraepelin has consequently been unhistorical. Selective exegesis of the various editions of his textbook has led to a rigid view of his contribution. However, Kraepelin lived and wrote during an important period of European intellectual history and his work can only be understood against this background. This paper analyses the development of his views in terms of the ‘Research Programme’ he planned early in his life and whose objective was the creation of a stable description and classification of the psychoses. This Kraepelin eventually achieved by longitudinally studying patient cohorts in terms of methodological criteria such as illness course and incurability. In the event, this methodology allowed him to identify by correlation ‘clinical pictures’ that both represented the ‘essence’ of the disease and provided a taxonomic criterion. Although avowedly atheoretical, Kraepelin thus managed to construct (influenced by Kahlbaum and Wundt) an empirical support for his Kantian categorization of the psychoses. A discussion of the cultural variables that moulded these ideas is included.

The probenecid technique was used in a study of the central dopamine DA metabolism in patients with depressions, psychotic disorders, and Parkinson's disease. The disturbances found were neither nosologically nor syndromally specific, but appeared to be symptom-specific. Decreased DA turnover was associated with hypomotility, and increased DA turnover with hypermotility. Decreased DA turnover was probably related aetiologically to the hypomotility: the symptoms subsided after replenishment of the DA deficiency. The relation between increased DA turnover and hypermotility is still under investigation. In view of the findings obtained, a plea is made for the development of a functional psychopathology, in which psychiatric syndromes are ‘dissected’ into their constituent psychological dysfunctions. This development is expected to stimulate human brain and behaviour research. It can be achieved only by intensive collaboration between psychiatrists and experimental psychologists.

Background. Cognitive deficits are common in major depressive disorder, but their nature is unclear. The effort hypothesis states that performance on effortful tasks is disproportionately impaired compared with the performance on automatic tasks. The cognitive speed hypothesis states that depression is characterized by cognitive slowness, which is a source of cognitive dysfunctioning. The present study investigated both theories in unmedicated adult depressive patients. It was also investigated whether the cognitive deficits can be attributed to more general physical illness-related factors or specifically to depressive disorder.

Methods. Thirty non-psychotic depressive out-patients were compared with 38 healthy control subjects and 25 patients with severe allergic rhinitis. The effects of group on more automatic and more effortful aspects of cognitive tasks measuring cognitive speed (Concept Shifting Task, Stroop Colour Word Test, Memory Scanning Test) and memory retrieval (Visual Verbal Learning Task, Verbal Fluency Test) were evaluated by MANCOVA. Age, sex, education and pre-morbid intelligence were treated as covariates.

Results. The depressive group had cognitive deficits in the automatic processing subtask of the Stroop, memory scanning and memory span. Performance on more effortful tasks was not impaired.

Conclusions. Our results are more consistent with the cognitive speed hypothesis. Cognitive functioning in depressive disorder seems to be characterized by a reduced speed of information processing in automatic subtasks.

One hundred and two first-year students at an independent college in Taiwan participated in a questionnaire study. Measurements of stressors (major life events, minor daily hassles and perceived university stress), personality (locus of control, extraversion and neuroticism) and mental health (depression, anxiety and somatic symptoms) were taken. Using multivariate analyses, we found that: (1) life events predicted anxiety, while daily hassles predicted depression; (2) locus of control and extraversion correlated negatively, while neuroticism correlated positively with university stress; and (3) neuroticism had a main effect on symptom reportings across the board, while extraversion had a vulnerability effect on somatic symptoms. Relationships between life events and daily hassles, and the roles of personality in the stress process, are discussed.

Background. Post-traumatic stress disorder (PTSD) is a multisystem neurobiological disorder with chronic alterations in various neurochemical systems. Levels of the GABAA – antagonistic neurosteroids plasma dehydroepiandrosterone (DHEA) and its sulphate derivate, dehydro-epiandrosterone sulphate (DHEAS) may be relevant to depressive and anxiety disorders, including PTSD.

Methods. We assessed the circulatory levels of morning plasma DHEA and DHEAS in 21 male out-patients with untreated chronic combat-related PTSD (CR-PTSD), and 18 healthy control male subjects.

Results. Compared with the control subjects, the PTSD patients showed significantly higher plasma DHEA and DHEAS levels.

Conclusions. Chronic CR-PTSD may be associated with increased circulatory level of neuroactive steroids with inhibitory activity at the GABAA receptors. Neurosteroid-induced decreased GABA-ergic tone may be relevant to the symptomatology and pathophysiology of chronic PTSD, as well as to the frequent co-morbidity of PTSD with depression and anxiety disorders.