Dementia scores in the population of very old subjects (70 to > 95) do not demonstrate an obviously bimodal distribution. Heterogeneity analysis shows that the assumption of two distributions explains the data significantly better than a one-distribution model. The first distribution component can be regarded as representing the normal range of scores and the second the pathological range. An additional finding shows the normal range distribution shifting to the pathological range with increasing age.

The purpose of this study was to evaluate whether childhood and adolescent premorbid asociality differed in neuroleptic-responsive and neuroleptic-resistant schizophrenia. Premorbid asociality was assessed with the Pre-morbid Asociality Adjustment Scale in 411 patients meeting DSM-III-R criteria for chronic schizophrenia or schizoaffective disorder categorized as being either neuroleptic-responsive or neuroleptic-resistant. Patterns of childhood and adolescent asociality were found to be different in neuroleptic-resistant and neuroleptic-responsive patients. Pre-morbid asociality during the pre-adult years was not consistently worse in patients with poor response to neuroleptic treatment. Greater impairment in late adolescent psychosexual functioning was predictive of poor outcome with regard to neuroleptic treatment.

This study reports the results of a comparison of DSM-III-R and ICD-10 personality disorder criteria by application of both sets of criteria to the same group of patients. Despite the clinical relevance of these disorders and the need for reliable diagnostic criteria, such a comparison has not previously been reported. DSM-III-R and ICD-10 have converged in their classification of personality disorders, but some important differences between the two systems remain. Personality disorder diagnoses from both systems were obtained in 52 out-patients, using the Standardized Assessment of Personality (SAP), a brief, informant-based interview which yields diagnoses in both DSM-III-R and ICD-10. For individual personality disorder diagnoses, agreement between systems was limited. Thirty-four subjects received a personality disorder diagnosis that had an equivalent form in both systems, but only 10 subjects (29%) received the same primary diagnosis in each system. There was a difference in rate of diagnosis, with ICD-10 making significantly more personality disorder diagnoses. The lower diagnostic threshold of the ICD-10 contributed most of this effect. Further modifications in ICD-10 Diagnostic Criteria for Research (DCR) and DSM-IV to the personality disorder category have been considered. The omission in DSM-IV of three categories unique to that system and the raising of the threshold in ICD-10 DCR, do seem to have been helpful in promoting convergence.

Patients suffering from persecutory delusions exhibit information processing and social reasoning biases that have been hypothesized to have a self-protective function. In a test of this hypothesis, patients suffering from persecutory delusions who were also depressed and non-depressed deluded subjects were compared with depressed and normal controls on two indirect assessments of self-schemata: the Dysfunctional Attitudes Scale (DAS) and incidental recall of negative and positive trait words that had previously been judged to be self-descriptive or not self-descriptive. Both the depressed subjects and the deluded subjects, whether or not they were depressed, scored highly on the DAS. Like normals, both depressed and non-depressed deluded subjects endorsed more positive than negative trait words as true of themselves whereas the depressed subjects endorsed as many negative as positive trait works. Like the depressed subjects, both groups of deluded subjects recalled as many of the negative words they had endorsed as positive words, whereas the normals remembered more positive words. No such bias was observed in subjects' recall of unendorsed words. The DAS results are interpreted as clearly consistent with a defensive model of persecutory delusions whereas the incidental recall data were equivocally so.

Thirty-eight subjects identified in a large community survey were found to attribute their fatigue to ‘myalgic encephalomyelitis’ (ME). They were matched randomly to two other groups of subjects who attributed their fatigue to either psychological or social factors. All three groups were followed up 18 months later and were asked to complete a series of questionnaires that examined fatigue, psychological distress, number of symptoms, attributional style and levels of disability. At onset the ‘ME’ group were found to be more fatigued, had been tired for longer but were less psychologically distressed than the other two groups. At follow-up the ‘ME’ group were more handicapped in relation to home, work, social and private leisure activities, even when controlling for both duration of fatigue and fatigue at time 1, but were less psychologically distressed. The relationships between psychological distress, specific illness attributions, attributional style and their effect on the experience of illness and its prognosis are discussed. Attributing fatigue to social reasons appears to be most protective.

Alternative explanations for the changes in thinking associated with depression were examined. Depressive thinking could reflect a generalized increase in accessibility of negative constructs and memories, previously associated with depression. Alternatively, depressive thinking could reflect changes at a more generic level of cognitive representation, related to schematic mental models. To investigate contrasting predictions from these two explanations, depressed patients and non-depressed controls completed sentence stems involving social approval or personal achievement e.g. ‘If I could always be right then others would____me’. Construct accessibility views predict that depression will be associated with more negative completions (e.g. ‘dislike’). By contrast, the schematic model view predicts patients may give more positive completions (e.g. ‘like’). This is because schematic models reflect inter-relationships between constructs, and, it is suggested, depression is associated with use of schematic mental models that imply closer dependence of personal worth/acceptance on success/approval than the models used in the non-depressed state. Predictions from the schematic model view were supported, confirming previous findings. Results suggest that depressive thinking reflects changes in the high level mental models used to interpret experience.

Three hundred and twenty-six consecutively admitted patients with definite or possible functional psychotic illnesses to which no diagnostic classification had been applied were followed up after 2·5 years. In 86 cases symptomatology had been inadequate for the patients to enter the functional psychosis study, and in 75 cases this was because the symptoms were partial or transient. These patients were compared at follow-up with those who fulfilled operational criteria for schizophrenic, affective or schizoaffective psychoses. Differences between the ‘partial’ cases and those fulfilling specific diagnostic criteria were few, but the transient cases fared significantly better. Although the transient illnesses were recurrent, at follow-up at 2·5 years they appeared to have a good outcome in terms of social variables and symptomatology.

This study investigates the basis of individual variation in exposure to stressful life events (SLEs). A population based sample of 547 MZ and 390 DZ female–female twin pairs, aged between 17 and 55 years, were surveyed by two structured interviews, separated by at least 1 year, that enquired about SLEs experienced during the preceding 12 months. Data were analysed with a model that resolves occasion specific (‘random’) versus enduring (‘stable’) influences on SLEs. The latter is partitioned into that due to genetic, familial environmental and unique environmental factors. We demonstrate that both random factors and stable individual differences underlie variation in self-reported exposure to SLEs. For most network events this stable variance makes a relatively small contribution to the total variance in SLEs exposure and is almost entirely due to genetic or familial environmental effects. Stable individual differences are more important determinants of personal SLEs, and these reflect both familial factors as well as previous experiences unshared by relatives.

The aim of this study was to identify underlying dimensions of psychopathology in a cohort of patients with functional psychosis of recent onset, and to examine their prognostic value. Factor analysis of the psychopathological features of 166 consecutively admitted patients with functional psychosis of recent onset revealed seven psychopathological dimensions, which explained 63% of the variance. Five of these seven syndromes bore differential associations with subsequent treatment and illness course, independent of: (i) associations with DSM-III-R diagnosis; (ii) associations with other prognostic factors; and (iii) associations with the baseline values of outcome variables. The most striking associations were shown for an early and insidious onset syndrome with affective flattening, which predicted a more disabled course of illness on three of four outcome dimensions, and which was more common in males and unmarried individuals. A second syndrome, characterized by bizarre behaviour, inappropriate affect, catatonia, and poor rapport showed similar, slightly less striking, associations with illness course, as well as with poor pre-morbid social functioning. A third syndrome, characterized by positive psychotic symptoms was to a lesser degree associated with poorer outcome, whereas a fourth syndrome distinguished by manic symptomatology predicted a more benign illness course. A fifth syndrome identified by lack of insight predicted more time in hospital and admission under a section of the Mental Health Act during the follow-up period.

A further finding was that dimensional representations of psychopathological features were considerably more useful than categorical representations (DSM-III-R and ICD-10) as predictors of illness course and treatment decisions.

The paper reports the profile of impairment across a variety of cognitive functions with special emphasis on tests sensitive to frontal lobe dysfunction, in 24 elderly depressed patients during and on recovery from mood disorder, compared with 15 age- and sex-matched controls. Traditional neuropsychological tests and a recently developed battery of computerized tests (CANTAB) were used. Impairments were found in the depressed group compared to controls and to themselves on recovery across all domains examined. The depressed group showed deficits on visuospatial recognition memory, attentional shifting at the extra-dimensional shift stage and in measures of both processing and motor speed without impaired accuracy in a visual search task. Impairments were also found on a planning task with disproportionately increased numbers of moves needed for more difficult problems and evidence of both slowed motor response and increased processing time once the task was commenced.

Performance on recovery improved across all tasks. Comparisons were made with the performance of patients suffering from dementia of the Alzheimer type (DAT) and Parkinson's disease on similar tests. Response latencies in test performance were found to correlate with the number of episodes of depression suffered and with ventricular size on CT scan, as measured by computerized planimetry. On recovery, residual depression scores correlated with latency of test performance and with ventricular brain ratio. The results, thus, show that depression in the elderly is associated with a significant degree of deficit on tests sensitive to frontostriatal dysfunction. Some of the deficits appear specific to depression and some do not remit following clinical recovery. However, these impairments have to be interpreted in the context of a broad profile of cognitive deficit.

A comprehensive semi-structured questionnaire was administered to 100 psychotic patients who had experienced auditory hallucinations. The aim was to extend the phenomenology of the hallucination into areas of both form and content and also to guide future theoretical development. All subjects heard ‘voices’ talking to or about them. The location of the voice, its characteristics and the nature of address were described. Precipitants and alleviating factors plus the effect of the hallucinations on the sufferer were identified. Other hallucinatory experiences, thought insertion and insight were examined for their inter-relationships. A pattern emerged of increasing complexity of the auditory–verbal hallucination over time by a process of accretion, with the addition of more voices and extended dialogues, and more intimacy between subject and voice. Such evolution seemed to relate to the lessening of distress and improved coping. These findings should inform both neurological and cognitive accounts of the pathogenesis of auditory hallucinations in psychotic disorders.

In health, acute administration of glucocorticoids, such as dexamethasone (DEX), leads to growth hormone (GH) secretion. Depression is characterized by blunted DEX/GH responses. In order to determine the specificity of this test for depression we administered 4 mg of oral DEX, to patients with a DSM-III-R diagnosis of depression, schizophrenia, mania and alcohol dependency syndrome. Samples for GH estimation were taken at − 15 min, 0 min, +60 min, +180 min, +240 min and +300 min. GH responses were attenuated to a similar degree in depression and mania. Less marked attenuation was seen in schizophrenia while those with alcohol dependency syndrome had GH responses indistinguishable from normal volunteers. Overall, we conclude that subnormal DEX/GH secretion is not specific to depression.

A cognitive science analysis of the interaction between psychosocial stress and the neurobiology of affective illness highlights a number of mechanisms relevant to the study of recurrence in major depressive disorder. It builds on observations previously offered by Post (1992) regarding the importance of kindling and sensitization effects in determining activation of neural structures, and proposes a model of knowledge structure activation that follows similar parameters. Vulnerability to depressive relapse/recurrence is determined by the increased risk of particular negative patterns of information processing being activated in depressed states. As is found in studies of kindling and behavioural sensitization, the likelihood of cognitive patterns being activated is dependent on the frequency of past usage, and increased reliance on these patterns of processing makes it easier for their future activation to be achieved on the basis of increasingly minimal cues. This model suggests that the processes related to relapse/recurrence and episode onset may not be isomorphic and, as such, treatments that emphasize relapse prevention strategies should take this distinction into account.

The paper of Anderson et al. (1993), based on cross-sectional data, showed that minor psychiatric disorder in a population is linearly related to the mean number of psychiatric symptoms in the population. The present investigation asks whether the same relationship holds longitudinally as well as cross-sectionally. Data from a 7-year follow-up of a general population sample demonstrate, for the first time, that a relationship exists between changes in prevalence of psychiatric disorder and changes in the mean number of psychiatric symptoms in a given population. Moreover, the relationship is linear; a one-point decrease in mean scores on the GHQ-30 is associated with a 6% decrease in prevalence of disorder.

There is controversy over how best to classify eating disorders in which there is recurrent binge eating. Many patients with recurrent binge eating do not meet diagnostic criteria for either of the two established eating disorders, anorexia nervosa or bulimia nervosa. The present study was designed to derive an empirically based, and clinically meaningful, diagnostic scheme by identifying subgroups from among those with recurrent binge eating, testing the validity of these subgroups and comparing their predictive validity with that of the DSM-IV scheme.

A general population sample of 250 young women with recurrent binge eating was recruited using a two-stage design. Four subgroups among the sample were identified using a Ward's cluster analysis. The first subgroup had either objective or subjective bulimic episodes and vomiting or laxative misuse; the second had objective bulimic episodes and low levels of vomiting or laxative misuse; the third had subjective bulimic episodes and low levels of vomiting or laxative misuse; and the fourth was heterogeneous in character. This cluster solution was robust to replication. It had good descriptive and predictive validity and partial construct validity.

The results support the concept of bulimia nervosa and its division into purging and non-purging subtypes. They also suggest a possible new binge eating syndrome. Binge eating disorder, listed as an example of Eating Disorder Not Otherwise Specified within DSM-IV, did not emerge from the cluster analysis.

Thirty schizophrenic patients (20 medicated, 10 off medication) were compared with 30 normal controls subjects matched for age, sex, handedness and intelligence. During the performance of a frontal activation task, normal subjects showed increased interhemispheric coherence between anterior brain regions. Schizophrenic patients did not show the same amount of bilateral anterior activation. During the performance of right hemisphere cognitive activation tasks, normal subjects and medicated schizophrenic patients showed significantly reduced bilateral interhemispheric coherence patterns, while the drug-free schizophrenic patients showed a trend towards this same pattern. It is suggested that these findings provide additional evidence for an aberrant functional organization of the brain in schizophrenia.

Forty patients with obsessive–compulsive disorder (OCD) were compared to matched healthy controls on neuropsychological tests which are sensitive to frontal lobe dysfunction. On a computerized version of the Tower of London test of planning, the patients were no different from healthy controls in the accuracy of their solutions. However, when they made a mistake, they spent more time than the controls in generating alternative solutions or checking that the next move would be correct. The results suggest that OCD patients have a selective deficit in generating alternative strategies when they make a mistake. In a separate attentional set-shifting task, OCD patients were impaired in a simple discrimination learning task and showed a continuous cumulative increase in the number who failed at each stage of the task, including the crucial extra-dimensional set shifting stage. This suggests that OCD patients show deficits in both acquiring and maintaining cognitive sets.

The cognitive deficits in OCD may be summarized as: (i) being easily distracted by other competing stimuli; (ii) excessive monitoring and checking of the response to ensure a mistake does not occur; and (iii) when a mistake does occur, being more rigid at setting aside the main goal and planning the necessary subgoals. Both studies support the evidence of fronto-striatal dysfunction in OCD and the results are discussed in terms of an impaired Supervisory Attentional System.

While the relationship of life events to depression onset has occupied researchers for almost a quarter of a century, few studies have attempted to account for either the temporal patterning of events relative to episode onset, or, the effect of multiple events in a study period. In this report, we attempt to address the issues of timing of events, multiple events (both positive and negative) and multiple aspects (both positivity and negativity) of single events on latency time to depression onset, while simultaneously accounting for possible decay in the effects of events over time. We use the proportional hazards approach to model the effects of life events and consider modelling the change in impact of events with the passage of time.

After interviewing 142 recurrent unipolar patients using the Life Events and Difficulties Schedule, we rated severity and positivity of life events reported during the 6-month period prior to onset. As we hypothesized, additional life events occurring after an initial provoking agent level event significantly alter the risk of illness onset. Additional severely threatening events decrease the time to onset, but positive events do not appear to delay onset. Interestingly, seemingly neutral events had a highly significant effect in shortening the time to onset. We note the many limitations imposed on the interpretation of these findings related to the selected group of subjects studied and encourage those who have more generalizable data to apply these methods of analysis.

Until recently, life events were considered as chance occurrences. However, there is now increasing evidence that reported life events, at least in adult life are not random. Life events not only tend to cluster in families but also appear to be influenced by genetic factors. The aim of this study was to investigate whether genetic factors also influence reported life events in childhood using a systematically ascertained sample of 376 twin pairs aged 8 to 17. Overall, reported life events in this younger population were found to be heritable. However, the degree of genetic and environmental influence appeared to vary across the sexes, at least for parent-rated life events and according to whether life events were rated by the parents or the children themselves. Genetic influences appeared to be more important for self reports, suggesting that individual differences in cognition play a role in reporting life events.

We describe the results of our follow-up magnetic resonance imaging (MRI) study of underweight patients with anorexia nervosa, using rigorous methodology to control for head position across time. All subjects first underwent an initial scan and rescan to verify that our computerized three-dimensional co-planar grid method for volume measurement was reliable and accurate, regardless of head positioning. After a period of several months, subjects had a follow-up scan to assess for changes that may have occurred following significant weight gain.

Ventricular and total brain volume measurements from the initial scans were compared with the scans from an age- and sex-matched normal control group to determine whether we could replicate previous findings of ventricular enlargement compared with controls and whether brain volume is reduced compared with controls. Anorexic subjects had significantly larger ventricles when compared with normal controls but did not differ significantly in total brain volume. Using a repeated measures analysis of variance, a priori contrasts compared the initial/rescan pair volumes with each other and the initial/rescan pair volumes with the follow-up volume. These analyses showed that ventricular and total brain volumes derived from the initial/rescan pair were nearly identical, but that at follow-up ventricular volume decreased significantly and total brain volume increased significantly after weight gain.