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.

Background. Generalized anxiety disorder is a common condition of excessive worry and tension which tends to run a chronic course associated with significant psychiatric and medical problems. Cognitive behaviour therapy (CBT) has been shown to be of clinical value in about 50% of cases with treatment gains maintained over follow-up periods ranging from 6 to 12 months. The potential value of CBT over the longer term has not been subject to rigorous investigation.

Method. Results are reported of 8–14 year follow-up of two randomized controlled trials of cognitive-behaviour therapy for generalized anxiety disorder employing structured interview with an assessor blind to initial treatment condition. Comparison groups included medication and placebo in one study based in primary care, and analytical psychotherapy in the other based in secondary care. Follow-up samples (30% and 55% of trial entrants) were broadly representative of the original cohorts.

Results. Overall, 50% of participants were markedly improved of whom 30–40% were recovered (i.e. free of symptoms). Outcome was significantly worse for the study based in secondary care in which the clinical presentation of participants was more complex and severe. For a minority (30–40%), mainly from the secondary care study, outcome was poor. Treatment with CBT was associated with significantly lower overall severity of symptomatology and less interim treatment, in comparison with non-CBT conditions, but there was no evidence that CBT influenced diagnostic status, probability of recovery or patient perceptions of overall improvement.

Conclusions. Both CBT and the complexity and severity of presenting problems appear to influence the long-term outcome of GAD.

Background. The rate of binocular rivalry has been reported to be slower in subjects with bipolar disorder than in controls when tested with drifting, vertical and horizontal gratings of high spatial frequency.

Method. Here we assess the rate of binocular rivalry with stationary, vertical and horizontal gratings of low spatial frequency in 30 subjects with bipolar disorder, 30 age- and sex-matched controls, 18 subjects with schizophrenia and 18 subjects with major depression. Along with rivalry rate, the predominance of each of the rivaling images was assessed, as was the distribution of normalized rivalry intervals.

Results. The bipolar group demonstrated significantly slower rivalry than the control, schizophrenia and major depression groups. The schizophrenia and major depression groups did not differ significantly from the control group. Predominance values did not differ according to diagnosis and the distribution of normalized rivalry intervals was well described by a gamma function in all groups.

Conclusions. The results provide further evidence that binocular rivalry is slow in bipolar disorder and demonstrate that rivalry predominance and the distribution of normalized rivalry intervals are not abnormal in bipolar disorder. It is also shown by comparison with previous work, that high strength stimuli more effectively distinguish bipolar from control subjects than low strength stimuli. The data on schizophrenia and major depression suggest the need for large-scale specificity trials. Further study is also required to assess genetic and pathophysiological factors as well as the potential effects of state, medication, and clinical and biological subtypes.

Background. Current knowledge about associations between psychosocial factors and non-psychotic symptoms provide little information about their relationship to specific types of neurotic symptoms such as symptoms of fatigue, worry, phobic anxiety and obsessional symptoms.

Method. The British National Survey of Psychiatric Morbidity was based on a cross-sectional random sample of 10108 householders. Neurotic symptoms were established by lay interviewers using the revised fully structured Clinical Interview Schedule (CIS-R). Subjects were asked about perceived social support, the size of their close primary social network and sociodemographic attributes. To assess possible associations between specific types of neurotic symptoms and psychosocial risk factors multivariate Huber logistic models (a modified form of repeated measures design modelling) was used taking account of correlation between symptom types and sampling design including clustering.

Results. After controlling for sociodemographic factors the risk of having a high total CIS-R score ([ges ]12) was approximately doubled for both types of poor social functioning. Specific types of neurotic symptoms were associated both with a small primary group and with inadequate perceived social support. Depression, depressive ideas and panic symptoms had a higher prevalence in multivariate models. Poverty was associated with low support.

Conclusions. Associations with deficiencies in social support and self-reported neurotic symptoms are better explained by symptom type and in particular by depression than by the total number of symptoms. If confirmed by longitudinal study findings this knowledge could be used to inform the development of interventions to improve social support in order to reduce specific neurotic symptom types.

Background. Many people who are depressed do not receive any professional help and their beliefs about the helpfulness of treatment do not always correspond with those of health professionals. To facilitate choices about treatment, the present study examined the effects of providing depressed people in the community with evidence on whether various treatment options work.

Method. A randomized controlled trial was carried out with 1094 persons selected at random from the community who screened positive for depressive symptoms and agreed to participate. Participants were mailed either an evidence-based consumer guide to treatments for depression or, as a control, a general brochure on depression. Outcomes were the rated usefulness of the information provided, changes in attitudes to depression treatments, actions taken to reduce depression, and changes in depressive symptoms, anxiety symptoms and disability.

Results. Participants rated the evidence-based consumer guide as more useful than the control brochure. Attitudes to some treatments changed. Improvements in symptoms and disability did not differ significantly between interventions.

Conclusion. Providing people who are depressed with evidence on which treatments work produces some changes in attitudes and behaviour. However, this intervention may need to be enhanced if it is to produce symptom change.

Background. Discontinuation of benzodiazepine (BZ) treatment results in a well-characterized withdrawal syndrome in 40–50% of anxious patients. While numerous studies have established the role of BZ dose, treatment duration, half-life, potency, rate of withdrawal and severity of underlying anxiety disorder in predicting severity of withdrawal symptoms, fewer studies have examined the role of psychological and personality factors.

Method. In 123 panic disorder patients undergoing gradual tapered discontinuation of alprazolam in conjunction with pre-treatment with carbamazepine or placebo, the relationship between measures of ‘symptom sensitivity’ and ‘harm avoidance’, and severity of withdrawal symptoms measured as peak severity of symptoms, time before taper needed to be slowed due to symptoms, and ability to complete taper, was examined.

Results. After controlling for the less substantial effects of dose, treatment duration, pre-taper anxiety and panic attack frequency, measures of symptom sensitivity and harm avoidance accounted for an additional 3–6% of withdrawal variance.

Conclusions. These results show an effect of symptom sensitivity and harm avoidance on BZ withdrawal symptoms, comparable to prior findings linking dependent personality characteristics to withdrawal severity. Failure to show the expected effect on ability to complete taper may be due to either the more symptomatic nature of the patients in this study.

Background. Previous research has yielded conflicting evidence regarding the long-term cognitive outcome of depression. Some studies have found evidence for a higher incidence of subsequent cognitive impairment or dementia, while others have refuted this.

Method. Depression, neuropsychological performance, functional ability and clinical variables were assessed in a sample of patients who had been hospitalized for depression 25 years previously.

Results. Data were available on 71 depressed patients (10 of whom were deceased) and 50 surgical controls. No significant differences were found between depressed subjects and controls on any neuropsychological measure. Ten depressed patients but no controls were found to have dementia at follow-up (continuity corrected χ2=5·93, P<0·01). Presence of dementia was predicted by older age at baseline. Vascular dementia was the most common type.

Conclusions. We conclude that this study did not find evidence that early onset depression is a risk factor for Alzheimer's disease, but that for a small subgroup there appears to be a link with vascular dementia. Several plausible explanations for this link, such as lifestyle factors, require further investigation.

Background. We tested the hypotheses that the addition of medication to psychotherapy enhances participation in the latter by: (1) speeding the acquisition of the psychotherapy's targeted skill; and (2) facilitating higher skill level acquisition.

Method. Participants were 431 chronically depressed patients who received Cognitive Behavioral Analysis System of Psychotherapy (CBASP), alone (N=214) or in combination with nefazodone (N=217), as part of a randomized chronic depression study (Keller et al. 2000). CBASP, developed specifically to treat chronic depression, uses a specific procedure, ‘situational analysis’ to help patients engage in more effective goal-oriented interpersonal behaviours. At the end of each session, therapists rated patients on their performance of situational analysis. Outcome on depressive symptoms was assessed with the 24-item Hamilton Rating Scale for Depression.

Results. Although reductions in depression were significantly greater in combined treatment compared to CBASP alone, there were no between-group differences in either the rate of skill acquisition or overall skill level at the end of treatment. Proficiency in the use of the main skill taught in psychotherapy at treatment midpoint predicted outcome independently of medication status and of baseline depressive severity.

Conclusions. Effective participation in CBASP, as reflected by proficiency in the compensatory skill taught in psychotherapy, is not enhanced by the addition of medication and does not mediate the between-group difference in depression outcome.

Background. Prior research on work-related factors in the aetiology of psychiatric disorders has been concentrated on job control, job demands and social support. To broaden the view to managerial procedures, we examined whether the extent to which employees are treated with equity in the workplace predicts their mental health. Organizational equity refers to decision-making procedures, which are consistently applied, open, correctable and include input from affected parties (procedural justice). It also refers to respectful and considerate treatment of individuals by supervisors (relational justice).

Method. A cohort of 1786 female hospital employees with no psychiatric disorder at baseline responded to a questionnaire on organizational equity. From the responses, both an individual score and a work unit mean score were assigned to each participant. The outcome was new reports of doctor-diagnosed psychiatric disorders during the 2-year follow-up. Odds ratios and 95% confidence intervals were corrected for clustering of the data.

Results. After adjustment for age and salary, odds ratio of new psychiatric disorders for self-reported low procedural justice was 1·9 (95% CI 1·1 to 3·2). Corresponding odds ratio for low procedural justice, as assessed with work unit mean scores, was 1·7 (95% CI 1·5 to 2·0). These associations remained statistically significant after additional adjustment for mental distress at baseline and job control, job demands and social support. Relational justice did not predict psychiatric disorders.

Conclusion. Research on organizational equity provides new information about potential work-related determinants of mental health. Low procedural justice seems to be an independent risk factor for psychiatric disorders in female employees.

Background. Numerous studies have suggested, via the interpretation of negative priming effects, that subjects with schizophrenia are less able than controls to inhibit irrelevant distracting information. Further issues concerning impairment in inhibitory processes are investigated here. First, recent research has revealed that negative priming (NP) effects can be caused by different processes, distractor inhibition or perceptual review. Therefore, conclusions concerning reduced inhibition in patients with schizophrenia are not possible from previous NP research. Secondly, previous NP studies have required subjects to identify some feature of the target. This is the first study to examine NP that uses a spatial task in patients with schizophrenia.

Method. Twenty-eight subjects with schizophrenia and 28 age and sex matched non-psychiatric control subjects completed a computerized NP task that eliminated the possible contribution of perceptual review.

Results. Subjects with schizophrenia had reduced levels of NP compared to control subjects on this spatial NP task (t=2·46, P<0·02). Current age, positive, negative or total PANNS scores did not correlate with negative priming scores, but post hoc analyses revealed that clozapine-treated patients had significantly greater levels of negative priming than patients receiving typical antipsychotic medications.

Conclusions. The present experiment eliminated the contribution of perceptual review to negative priming and demonstrated that when a pure measure of inhibition is taken on a localization task, patients with schizophrenia were less able to inhibit irrelevant distracting stimuli. The fact that NP was reduced in a spatial task suggested a more diffuse reduction in inhibition than previous studies that examined only identification-based responses.

Objective. The study was designed to determine the association between self-reported asthma and the risk, persistence and severity of panic attacks among adults in the community.

Method. Data were drawn from waves 1 and 2 of the Baltimore site of the Epidemiologic Catchment Area (ECA) Study (N=2768), which included self-report information on asthma, treatment for asthma and panic attacks in 1981 and 1982. Multiple logistic regression analyses were used to calculate odds ratios comparing the prevalence of panic attack at baseline and follow-up by asthma status at baseline. Linear regression analyses were used to examine the relationship between self-reported asthma status and the number of panic symptoms during a panic attack.

Results. Self-report asthma was associated with significantly increased likelihood of having panic attacks at baseline (1981) (12·1% v. 7·3%, P<0·05) and of having panic attacks at both baseline and follow-up (15·9% v. 7·3%, P<0·05), compared to those without asthma at baseline. Adults receiving treatment for asthma at baseline had an increased risk of incident panic attacks at follow-up (OR=2·65 (1·11, 6·34)) and at baseline and follow-up (OR=5.88 (2·21, 15.62)), though untreated asthma did not appear to increase risk of incident panic at follow-up. Similarly, the risk of panic at follow-up was not increased among those with asthma at baseline who did not report asthma at follow-up, compared with those without asthma at baseline. Treated asthma was associated with having more panic symptoms during panic attacks, compared to those without asthma (P<0·001).

Conclusion. These findings are consistent with and extend previous results suggesting that self-reported asthma is associated with an increased risk of panic attacks among adults in the general population, and that there is a consistent relation between severity and persistence of asthma and panic attacks. The lack of association between remitted asthma and panic attack may reveal a need for further research to determine whether asthma may be a causal risk factor for panic attacks, or whether a third factor (genetic or environmental) may be associated with increased risk of the co-occurrence of asthma and panic attacks. Replication of these results using alternative methodology with corroborative data on asthma and panic attacks is needed next.

Background. Motor function is deficient in many patients with obsessive–compulsive disorder (OCD), especially in the face. To investigate subtle motor dysfunction, kinematical analysis of emotional facial expressions can be used. Our aim was to investigate facial movements in response to humorous film stimuli in OCD patients.

Method. Kinematical analysis of facial movements was performed. Ultrasound markers at defined points of the face provided exact measurement of facial movements, while subjects watched a humorous movie (‘Mr Bean’). Thirty-four OCD patients (19 male, 15 female; mean (S.D.) age: 35·8 (11·5) years; mean (S.D.) total Y-BOCS score: 25·5 (5·9)) were studied in unmedicated state and after a 10-week treatment with the SSRI sertraline. Thirty-four healthy controls (19 male, 15 female; mean (S.D.) age: 37·5 (13·1) years) were also investigated.

Results. At baseline, OCD patients showed significantly slower velocity at the beginning of laughing than healthy controls and a reduced laughing frequency. There was a significant negative correlation between laughing frequency and severity of OCD symptoms. Ten weeks later a significant increase of laughing frequency and initial velocity during laughing was found.

Conclusions. Execution of adequate facial reactions to humour is abnormally slow in OCD patients. Susceptibility of OCD patients with regard to emotional stimuli is less pronounced than in healthy subjects. This phenomenon is closely correlated to OCD symptoms and is state-dependent.

Background. Visual masking tasks assess the earliest stages of visual processing. This study was conducted to address: (1) whether schizophrenia patients show masking deficits after controlling for sensory input factors; (2) whether patients have relatively intact forward masking (when the mask precedes the target) compared with backward masking (when the mask follows the target); and (3) whether the masking deficits in schizophrenia reflect an accelerated age-related decline in performance.

Method. A staircase method was used to ensure that the unmasked target identification was equivalent across subjects to eliminate any confounding due to differences in discrimination of simple perceptual inputs. Three computerized visual masking tasks were administered to 120 schizophrenia patients (ages 18–56) and 55 normal comparison subjects (ages 19–54) under both forward and backward masking conditions. The tasks included: (1) locating a target; (2) identifying a target with a high-energy mask; and (3) identifying a target with a low-energy mask.

Results. Patients showed deficits across all three masking tasks. Interactions of group by forward versus backward masking were not significant, suggesting that deficits in forward and backward masking were comparable. All three conditions showed an age-related decline in performance and rates of decline were comparable between patients and controls. Two of the masking conditions showed increased rates of decline in backward, compared to forward, masking.

Conclusions. We found age-related decline in performance that was comparable for the two groups. In addition, we failed to find evidence of a relative sparing of forward masking in schizophrenia. These results suggest that: (1) early visual processing deficits in schizophrenia are not due to a simple perceptual input problem; (2) sustained channels are involved in the masking deficit (in addition to transient channels); and (3) for the age range in this study, these deficits in schizophrenia are not age-related.

Background. The present study attempted to extend previous research on source monitoring deficits in schizophrenia. We hypothesized that patients would show a bias to attribute self-generated words to an external source. Furthermore, it was expected that schizophrenic patients would be over-confident regarding false memory attributions.

Method. Thirty schizophrenic and 21 healthy participants were instructed to provide a semantic association for 20 words. Subsequently, a list was read containing experimenter- and self-generated words as well as new words. The subject was required to identify each item as old/new, name the source, and state the degree of confidence for the source attribution.

Results. Schizophrenic patients displayed a significantly increased number of source attribution errors and were significantly more confident than controls that a false source attribution response was true. The latter bias was ameliorated by higher doses of neuroleptics.

Conclusions. It is inferred that a core cognitive deficit underlying schizophrenia is a failure to distinguish false from true mnestic contents.

Background. Published studies of emotional processing and cognitive style in bipolar disorders tend to have small sample sizes or use non-clinical samples. Larger clinically representative studies are needed.

Method. Self-esteem, dysfunctional attitudes and personality style were compared in unipolar (N=16) and bipolar disorder (N=77); and then investigated in the different phases of bipolar disorder (remitted=26; depressed=38; hypomanic=13). One-year outcome was assessed in 36 bipolar subjects.

Results. Unipolar subjects and bipolar subjects differed significantly in their mean levels of negative self-esteem (unipolar=15·5; bipolar=12·7; P<0·05). Bipolar subjects with hypomania reported mean levels of dysfunctional beliefs that were higher than individuals in remission but lower than depressed subjects (remitted=136·7; depressed=153·8; hypomanic=144·8; P<0·05). Hypomanic subjects recorded the highest levels of negative as well as positive self-esteem. In the exploratory analysis of outcome, negative self-esteem (Exp [B] 1·91; 95% CI 1·11 to 3·32; P<0·05) was the most robust predictor of relapse.

Conclusions. There are similarities in the cognitive style of individuals with unipolar as compared to bipolar disorders. Cognitive style in hypomania represents a phase between remission and depression rather than the polar opposite of depression. The implications of these findings are considered for psychological and neural network models.

Background. Numerous studies have documented high rates of co-morbidity between major depressive disorder (MDD) and the anxiety disorders (ANX). However, the reason for this is unclear. Family studies provide one potentially useful approach for addressing this issue.

Method. We explored six explanations of the co-morbidity between MDD and ANX using a family study of a large community sample of young adults and their first-degree relatives. Participants included 112 probands with a lifetime history of both MDD and one or more ANX, 290 probands with a history of MDD but no ANX, 43 probands with a history of one or more ANX but no MDD, 352 probands with no lifetime history of either MDD or ANX, and the probands' 2608 first-degree relatives. Probands were assessed using semi-structured diagnostic interviews on two occasions in adolescence and a third time at age 24. Diagnostic data on relatives were collected using both direct and family history interviews.

Results. Compared with controls, MDD aggregated in the families of probands with MDD, whether or not they had co-morbid ANX; ANX aggregated in the families of probands with ANX, regardless of whether they had co-morbid MDD; and co-morbid MDD/ANX aggregated only in the families of probands with both MDD and ANX. The relatives of probands with ANX alone had a significantly higher rate of ANX than the relatives of probands with MDD alone, although none of the other comparisons between the depressed and anxious groups were significant.

Conclusions. This pattern of findings is largely, although not completely, consistent with the view that MDD and ANX are transmitted independently within families, and suggests that the co-morbidity between MDD and ANX is caused by non-familial aetiological factors.

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. Life events (LE) have consistently been found to influence course and outcome of psychotic disorders. However, the mechanism through which they operate is not known. The present study investigated whether LE have their effect by impacting on the emotional sensitivity for daily hassles.

Method. Patients with clinically remitted psychotic illness (N=42) were studied with the Experience Sampling Method (a structured diary technique assessing current context and mood in daily life) to assess: (1) appraised subjective stress related to daily events and activities; and (2) emotional reactivity conceptualized as changes in both negative affect (NA) and positive affect (PA). LE were assessed with the Brown & Harris Life Event and Difficulties Schedule.

Results. Multilevel regression analyses showed that previous exposure to LE influenced the appraised stressfulness of neither daily events nor the activities in which the subjects were involved. However, a history of LE did modify the emotional reaction to daily life stress, both in models predicting NA and in models predicting PA.

Conclusions. By their cumulative effect on emotional reactivity to daily activities and events, LE may render individuals more vulnerable to the onset or persistence of psychotic experiences.

Background. There are few longitudinal studies of patients with medically unexplained symptoms. The aim of this study was to investigate outcome in frequent attenders in secondary care who present repeatedly with medically unexplained symptoms.

Method. Forty-eight patients presenting with medically unexplained symptoms, from a sample of 61, participated in a 3-year follow-up study. Psychiatric morbidity, functional impairment and use of services were evaluated.

Results. At follow-up there was a high prevalence of psychiatric morbidity with 69% having at least one psychiatric diagnosis. The sample continued to be high users of a range of health services and substantial functional impairment was reported.

Conclusion. In this group of frequent attenders with medically unexplained symptoms outcome as measured by psychiatric morbidity, service use and functional impairment remained poor after 3 years.

Background. This study investigates the competence of patients with dementia, depression and schizophrenia to make treatment decisions. The outcome of an objective test instrument is presented and compared with clinical assessment of competence by the attending physician.

Method. The MacArthur Competence Assessment Tool-Treatment (MacCAT-T), a test instrument to assess abilities in different standards of competence, was administered to patients with diagnoses of dementia (N=31), depression (N=35) and schizophrenia (N=43). Statistical significance of group differences in the MacCAT-T results were tested with the chi-square test. The concordance of the test and clinical assessment of competence by the attending physician were evaluated by Cohen's kappa coefficient.

Results. Patients with dementia, as a group, showed significantly more often impaired performance than those with schizophrenia who were still more impaired than depressed patients. Patients were classified as impaired or not depending on the standards used. By combination of all standards substantially more patients were classified as impaired than by clinical assessment (67·7 v. 48·4% of patients with dementia, 20·0 v. 2·9% of patients with depression, 53·5 v. 18·4% of patients with schizophrenia).

Conclusions. Using different standards of competence the study showed substantial differences among patients with dementia, depression and schizophrenia. The high proportion of patients identified as incompetent raises several ethical questions, in particular, those referring to the selection of standards or the definition of cut-offs for incompetence. The discrepancy between clinical and formal evaluations points out the influence of the used procedure on competence judgements.