Background. The long-term outcome of major depression is often unfavorable, and because most cases of depression are managed by general practitioners (GPs), this places stress on the need to improve treatment in primary care. This study evaluated the long-term effects of enhancing the GP's usual care (UC) with three experimental interventions.

Method. A randomized controlled trial was conducted from 1998 to 2003. The main inclusion criterion was receiving GP treatment for a depressive episode. We compared: (1) UC (n=72) with UC enhanced with: (2) a psycho-educational prevention (PEP) program (n=112); (3) psychiatrist-enhanced PEP (n=37); and (4) brief cognitive behavioral therapy followed by PEP (CBT-enhanced PEP) (n=44). We assessed depression status quarterly during a 3-year follow-up.

Results. Pooled across groups, depressive disorder-free and symptom-free times during follow-up were 83% and 17% respectively. Almost 64% of the patients had a relapse or recurrence, the median time to recurrence was 96 weeks, and the mean Beck Depression Inventory (BDI) score over 12 follow-up assessments was 9·6. Unexpectedly, PEP patients had no better outcomes than UC patients. However, psychiatrist-enhanced PEP and CBT-enhanced PEP patients reported lower BDI severity during follow-up than UC patients [mean difference 2·07 (95% confidence interval (CI) 1·13–3·00) and 1·62 (95% CI 0·70–2·55) respectively] and PEP patients [2·37 (95% CI 1·35–3·39) and 1·93 (95% CI 0·92–2·94) respectively].

Conclusions. The PEP program had no extra benefit compared to UC and may even worsen outcome in severely depressed patients. Enhancing treatment of depression in primary care with psychiatric consultation or brief CBT seems to improve the long-term outcome, but findings need replication as the interventions were combined with the ineffective PEP program.

Background. Vascular depression is regarded as a subtype of depression, especially in, but not entirely restricted to, the elderly, characterized by a specific clinical presentation and an association with (cerebro)vascular risk and disease. It could have major implications for treatment if subjects at risk for such a depression could be easily identified by their clinical presentation in general practice.

Method. We studied the symptom profile of depression in subjects with and without vascular risk factors in two large Dutch community-based studies, the Rotterdam Study and the Amsterdam Study of the Elderly (AMSTEL).

Results. We could not confirm the specific symptom profile in depressed subjects with vascular risk factors in either of the two cohorts. Depressed subjects with vascular risk factors showed more loss of energy and more physical disability than those without vascular risk factors. However, presumed specific symptoms of vascular depression, namely psychomotor retardation and anhedonia, were not significantly associated with any of the vascular risk indicators. Loss of energy was significantly associated with myocardial infarction and peripheral arterial disease.

Conclusions. In these two large community-based studies we identified some differences between vascular and non-vascular depressed subjects but found no evidence for a specific symptom profile of vascular depression as previously defined.

Background. There is increasing evidence that subthreshold forms of psychopathology are both common and clinically relevant. To enable classification of these subthreshold forms of psychopathology, it may be useful to distinguish not only a threshold for illness but also for health. Our aim was to investigate this with regard to panic.

Method. Data were derived from the Netherlands Mental Health Survey and Incidence Study (NEMESIS), which is based on a large representative sample of the adult general population (18–65 years) of The Netherlands (n=7076). The Composite International Diagnostic Interview was used as a diagnostic instrument. By defining two thresholds, three groups were formed: panic disorder, subthreshold panic disorder and no-panic. These groups were compared using multinomial regression analysis, χ2 and analysis of variance.

Results. The 12-month prevalence of panic disorder was 2·2% while that of subthreshold panic disorder was 1·9%. Symptom profiles and risk indicators associated with panic disorder and subthreshold panic disorder were similar, and half of the risk indicators were more strongly associated with panic disorder than with subthreshold panic disorder. Subthreshold panic disorder occupied an intermediate position between panic disorder and no-panic with regard to the number of symptoms, the percentage of subjects with co-morbidity, and functioning.

Conclusions. Subthreshold panic disorder is common, and seems clinically relevant, but is milder than panic disorder. These results thus support the use of a double threshold in panic. Further research should focus on the positioning of the thresholds, the course of subthreshold panic disorder and its treatment options.

Background. Impairments in verbal learning and memory, executive functions and attention are manifest in some euthymic patients with bipolar disorder (BPD). However, evidence is sparse on their putative role as aetiologically important genetic vulnerability markers for the disorder. This population-based study examined the cognitive functions of affected and unaffected individuals in families with BPD. The aim was to discover whether any cognitive function would indicate genetic liability to the disorder and could thus be regarded as endophenotypes of BPD.

Method. A diagnostic interview and a neuropsychological test battery were administered to 32 familial bipolar I disorder patients, 40 of their unaffected first-degree relatives and 55 controls, all representing population-based samples.

Results. Unaffected first-degree relatives showed impairment in psychomotor performance speed and slight impairment in executive function. Bipolar patients were impaired in verbal learning and memory compared with unaffected relatives and controls. They also differed from controls in tasks of executive functions. There were no difference between the groups in simple attention and working memory tasks.

Conclusions. Impaired psychomotor performance speed and executive function may represent endophenotypes of BPD, reflecting possible underlying vulnerability to the disorder. Verbal memory impairments appear to be more related to the fully developed disorder.

Background. Poor clinician-rated parenting outcome and observed interactive deficits in mothers with schizophrenia admitted to a psychiatric mother and baby unit (MBU) reflect continuing concerns over the parenting capacity of this group. However, little is known about whether interaction deficits are accounted for by severity of illness or adverse social circumstances typically experienced by these mothers.

Method. Thirty-eight women with severe perinatal illness (schizophrenia n=13; affective disorders n=25) and their infants were observed in play interaction a week prior to MBU discharge. Clinical and sociodemographic data were also obtained.

Results. Mothers with schizophrenia and their infants were rated to have poorer interactive behaviour than the affective disorders group. Infant avoidance of the mother was associated with a lack of maternal sensitivity and responsiveness. The deficits in mother–infant interaction found in the schizophrenia group could not be accounted for by our measures of illness severity or factors relating to adverse social circumstances.

Conclusions. The results replicate and extend previous findings showing poor interactive behaviours in mothers with schizophrenia, their infants, and in the dyad, in a range of areas following clinical recovery. The findings suggest that factors other than illness duration, dose of medication, marital status and occupational status are explanatory for the interactive deficits associated with maternal schizophrenia. Parenting interventions that aim to improve maternal sensitivity need to be developed specifically for this group.

Background. Neuroticism is widely used as an explanatory concept in etiological research of psychopathology. In order to clarify what neuroticism actually represents, we investigated the genetic association between neuroticism and cardiovascular measures.

Method. In 125 female twin pairs (18–30 years), electrocardiogram and continuous finger blood pressure were assessed during two rest and two mental stress conditions. Mean values for baroreflex sensitivity (BRS), heart rate variability (HRV) and inter-beat interval (IBI) were calculated for each condition. Neuroticism was assessed by multiple questionnaires. Multivariate genetic model-fitting analyses were used to investigate the genetic correlation between latent neuroticism and the cardiovascular autonomic nervous system (ANS) measures.

Results. Neuroticism was negatively correlated to BRS and HRV. Neuroticism was not correlated to IBI. For BRS, this phenotypical relation was entirely determined by shared genetic influences. For HRV, the genetic contribution to the phenotypical correlation was not significant, but the proportions of explained covariance showed a trend of more genetic than environmental influences on the phenotypical relationship.

Conclusions. High neuroticism is associated with a deregulated ANS. Pleiotropic genetic effects may be partly responsible for this effect.

Background. Cognitive behavioural therapy (CBT) has been implemented in bipolar (BP) disorder with varying degrees of success. The link between CBT for BP disorder and underlying theory is not clear. There have been attempts to identify a unique style of dysfunctional thinking in BP disorder analogous to that in unipolar (UP) disorder but this has suffered from a dearth of prospective studies controlling for mood and phase of illness. In this prospective study, we have examined whether dysfunctional thinking and the (dys)regulation of traumatic memories are trait vulnerability factors in BP versus UP mood disorders.

Method. BP-1 and UP groups were followed-up from acute episode to recovery, and compared with a healthy control group. Measures of dysfunctional thinking and linked personality dimensions were taken, together with measures assessing autobiographical memory retrieval (AMT). The presence and control of intrusive memories of traumatic events in BP and UP disorder were assessed.

Results. Controlling for mood symptoms and phase of illness, the BP (but not the UP) group was largely indistinguishable from controls on dysfunctional thinking. Intrusive memories of traumatic events were present in 45% of the BP and 48% of the UP groups; and those without intrusions were more overgeneral on the AMT in all phases of illness.

Conclusion. These findings are in line with the ‘affect regulation’ hypothesis for UP disorder and deliberate self-harm. This may help in understanding the mode of action of CBT in BP disorder and to further improve the therapy, primarily through the promotion of affective regulation, which is one component of the complex CBT intervention for BP disorder.

Background. A long-standing debate concerns whether dysfunctional cognitive processes and content play a causal role in the etiology of depression or more simply represent correlates of the disorder. There has been insufficient appreciation in this debate of specific predictions afforded by cognitive theory in relation to major life stress and changes in cognition over time. In this paper we present a novel perspective for investigating the etiological relevance of cognitive factors in depression. We hypothesize that individuals who experienced a severe life event prior to the onset of major depression will exhibit greater changes in dysfunctional attitudes over the course of the episode than will individuals without a severe life event.

Method. Fifty-three participants diagnosed with major depression were assessed longitudinally, approximately 1 year apart, with state-of-the-art measures of life stress and dysfunctional attitudes.

Results. Depressed individuals with a severe life event prior to episode onset exhibited greater changes in cognitive biases over time than did depressed individuals without a prior severe event. These results were especially pronounced for individuals who no longer met diagnostic criteria for major depression at the second assessment.

Conclusions. Specific patterns of change in cognitive biases over the course of depression as a function of major life stress support the etiological relevance of cognition in major depression.

Background. Past research has demonstrated that depression is associated with dysfunctional processing of emotional information. Recent studies demonstrate that a bias in the attentional processing of negative information may be an important cognitive vulnerability factor underlying the onset and maintenance of depression. However, to date, the nature of this attentional bias is still poorly understood and further exploration of this topic to advance current knowledge of attentional biases in depression seems imperative.

Method. This study examined attentional biases for angry facial expressions presented for 1000 ms in 20 patients with major depressive disorder (MDD) and 20 non-depressed control participants (NC) matched for age and gender using an emotional modification of the Exogenous Cueing task.

Results. Patients with MDD showed maintained attention for angry faces compared with neutral faces. In comparison with non-depressed participants they showed a stronger attentional engagement for angry faces. In contrast, the NC group directed attention away from angry faces, more rapidly disengaging their attention compared with neutral faces.

Conclusions. This pattern of results supports the assumption that MDD is characterized by deficits in the attentional processing of negative, interpersonal information and suggests a ‘protective’ bias in non-depressed individuals. Implications in relation to previous research exploring cognitive and interpersonal functioning in depression are discussed.

Background. Identify a group of adults with ‘undiagnosed’ attention deficit hyperactivity disorder (ADHD) and compare their personal and family medical histories, psychosocial profiles, functional impairment and quality of life with non-ADHD controls. Additionally, compare adults with undiagnosed and diagnosed ADHD to investigate possible reasons why the undiagnosed avoid clinical detection.

Method. ICD-9 codes for ADHD in administrative claims records and responses to a telephone-administered adult ADHD screener [the Adult ADHD Self-Report Scale (ASRS)] were used to classify approximately 21000 members of two large managed health-care plans as ‘undiagnosed’ (no coded diagnosis; ASRS positive) or ‘non-ADHD’ controls (no coded diagnosis; ASRS negative). Patients identified as ‘undiagnosed’ ADHD were compared with samples of non-ADHD controls and ‘diagnosed’ ADHD patients (ICD-9 coded ADHD diagnoses) on the basis of demographics, socio-economic status, past and present mental health conditions, and self-reported functional and psychosocial impairment and quality of life.

Results. A total of 752 ‘undiagnosed’ ADHD subjects, 199 ‘non-ADHD’ controls and 198 ‘diagnosed’ ADHD subjects completed a telephone interview. Overall, the ‘undiagnosed’ ADHD cohort demonstrated higher rates of co-morbid illness and greater functional impairment than ‘non-ADHD’ controls, including significantly higher rates of current depression, and problem drinking, lower educational attainment, and greater emotional and interpersonal difficulties. ‘Undiagnosed’ ADHD subjects reported a different racial composition and lower educational attainment than ‘diagnosed’ ADHD subjects.

Conclusion. Individuals with ‘undiagnosed’ ADHD manifest significantly greater functional and psychosocial impairment than those screening negative for the disorder, suggesting that ADHD poses a serious burden to adults even when clinically unrecognized.

Background. Although communication disturbances (CD) have been associated with poor cognitive control, it is unclear whether they are associated specifically with poor cognitive control or with poor cognition in general. The current research examined whether (a) two specific components of cognitive control, working memory and interference resolution, were associated with CD, and (b) associations between CD and cognitive control could be accounted for by generalized poor cognitive performance.

Method. In this study, as healthy volunteers spoke, the level of cognitive demands was experimentally increased, thereby simulating cognitive deficits (i.e. a reduction in the degree to which certain types of cognitive processes could be used for speech). Hence, this research examined whether simulated cognitive deficits would cause an increase in CD. Participants also completed separate cognitive tasks that assessed working memory, interference resolution and general cognitive ability.

Results. An increase in working memory demands caused an increase in CD. Moreover, working memory demands interacted with interference resolution demands, with the greatest amount of CD caused by both high working memory and high interference resolution demands. By contrast, increasing another cognitive demand, sustained attention, did not increase CD. Furthermore, performance on separate working memory and interference resolution tasks interacted to predict CD on the experimental speech task. However, performance on a psychometrically matched cognitive task did not predict CD.

Conclusion. Overall, the current study provides evidence that working memory and interference resolution may be specifically associated with CD and that manipulations of these cognitive control processes can cause an increase in CD.

Background. Aggressive behaviour is increased among those with schizophrenia but less is known about those with affective psychoses. Similarly, little is known about aggressive behaviour occurring at the onset of illness.

Method. The main reasons for presentation to services were examined among those recruited to a UK-based first episode psychosis study. The proportion of individuals presenting with aggressive behaviour was determined and these individuals were compared to those who were not aggressive on a range of variables including sociodemographic, clinical, criminal history, service contact, and symptom characteristics. Among the aggressive group, those who were physically violent were distinguished from those who were not violent but who were still perceived to present a risk of violence to others.

Results. Almost 40% (n=194) of the sample were aggressive at first contact with services; approximately half of these were physically violent (n=103). Younger age, African-Caribbean ethnicity and a history of previous violent offending were independently associated with aggression. Aggressive behaviour was associated with a diagnosis of mania and individual manic symptoms were also associated with aggression both for the whole sample and for those with schizophrenia. Factors differentiating violent from non-violent aggressive patients included male gender, lower social class and past violent offending.

Conclusions. Aggressive behaviour is not an uncommon feature in those presenting with first episode psychosis. Sociodemographic and past offending factors are associated with aggression and further differentiate those presenting with more serious violence. A diagnosis of mania and the presence of manic symptoms are associated with aggression.