A sample of 1111 survivors from a population aged 75 years and over completed the Mini-Mental State Examination (MMSE) twice, separated by 28 months on average. There was a mean decline of 1·3 points in MMSE score. With increasing age, mean drop in score also increased. The proportion at each age identified as newly cognitively impaired according to any standard cut-point on MMSE rose markedly. Mean decline was greater in women than men even after adjustment for age. Cognitive change on the MMSE was approximately unimodally and normally distributed. This distribution was a marked contrast to the distribution of MMSE scores themselves, which was skewed due to truncation of scores at the maximum. The decline was not due to the inclusion of individuals with physical impairment. These findings indicate that cognitive decline, like dementia, becomes increasingly common with advancing age, and suggest that dementia may be regarded as one extreme of the continuum of cognitive decline.

The cognitive performance of 47 elderly psychotic patients with onset of symptoms in late life (late paraphrenia) was compared to that of 33 controls matched for age, sex, ethnic origin, number of years of education, and pre-morbid IQ as measured by the NART. Neuropsychological indices of general cognitive functioning (MMSE, CAMCOG, WAIS-R verbal and performance scores) showed that patients were performing the tasks at a significantly lower level than controls. Patients also showed a trend to have a lower span capacity than controls, particularly at the spatial span subtest. There was no obvious impairment of learning as measured by the digit and spatial recurring span tasks nor of simultaneous matching-to-sample ability. However, patients' performance on a delayed-matching-to-sample procedure was significantly worse than that of controls. In addition, patients performed worse than controls on the Recognition Memory Test for Faces, but not for Words. Finally, the performance of patients on tests assessing executive functioning (Verbal Fluency Test, Computerized Extra and Intra-Dimensional Shift Task, Computerized Spatial Working Memory Task, and Computerized Tower of London Task) was consistently worse than that of controls. These results suggest that psychotic states arising in late life are predominantly associated with a decline on measures of general cognitive ability and executive functioning. The neuropsychological meaning of these findings is discussed in the light of cognitive models of psychotic symptoms, as well as of schizophrenia and dementia research. We concluded that the lack of a clear pattern of impairment among these patients may be the result of their clinical and cognitive diversity.

This study aimed to explore the heterogeneity of paranoid psychosis with onset in late life by using cognitive factors in a centroid method of cluster analysis. Forty-seven subjects were allocated to two different clusters, the first with 24 (51·1 %) and the second with 23 (48·9 %) patients. Their cognitive attainment was evaluated against the performance of 33 elderly controls, all groups being matched for age, sex, and the numbers of years of education. Patients in cluster 2 showed a pattern of widespread cognitive impairment, which involved general measures of cognitive performance (MMSE, CAMCOG, WAIS-R verbal and performance scores), memory (digit and spatial span, delayed matching-to-sample, recognition memory for words and faces), and executive functions (verbal fluency, extra and intra-dimensional shift ability, spatial working memory, and planning). In contrast, patients in cluster 1 were only impaired on their extra-dimensional set shift and planning abilities, suggesting a more specific and restricted executive functioning deficit. We also analysed the impact that the use of antipsychotic medication could have had on patients' cognitive performance, which was shown to be negligible. In addition, there was no difference between the clusters with regard to the number of patients using neuroleptics, suggesting that the medication was unlikely to have introduced a performance bias in the two patient clusters. The validity of the subdivision of these patients into two separate groups was further supported by other clinical findings. Patients in cluster 1 exhibited more severe psychotic symptoms, as measured by the SAPS, than their counterparts in cluster 2, and were also more likely to display first-rank symptoms of Schneider. Conversely, cluster 2 membership was strongly associated with the presence of neurological signs and negative symptoms. We suggest that psychotic states arising in late life are a heterogeneous condition that may be best divided in two: ‘type A’, including patients with a wide range of psychotic symptoms, mild increase in the frequency of neurological signs, and cognitive deficits restricted to executive functions, and ‘type B’, which includes patients with less complex psychotic symptoms associated with a marked increase in the frequency of neurological signs and generalized cognitive impairment. The basis for this subdivision and the prospect for future studies are discussed.

The heterogeneity of schizophrenia constitutes an impediment in the identification of reliable biological markers of the illness and aetiological factors. The two syndrome concept of the illness has proved a powerful stimulus in this endeavour. There is however evidence now to regard this construct as inadequate and in need of refinement. Using a sample of young patients with early onset of illness who fulfilled the Research Diagnostic Criteria for schizophrenia, we have shown that three rather than two dimensions better describe the pathology of the illness. The results of factor analysis showed these syndromes, termed disorganization, positive, and negative syndromes, to account for 65% of the total variance of the psychopathology of the disorder. The negative syndrome was associated with disturbed pre-morbid functioning while the disorganization syndrome bore significant association with early onset of illness, poorer socio-educational attainment, and impairment on neuropsychological tests, especially those designed to evaluate frontal lobe functioning. The positive syndrome was not associated with any of the assessed variables. These results provide strong support for the validity of the three-syndrome construct even among a sample of non-institutionalized patients.

One hundred and sixteen working-class housewives, part-time and full-time employees were compared on a range of well-being measures in three different lifestages. A group of factory employees was contrasted with a ‘mixed occupation’ group for a comparison of type of employment. The general contention that the association between employment and well-being would vary with position in the life cycle was confirmed for distress, physical illness and some of the satisfaction measures. Only one measure (personal competence) suggested that employment had a positive influence on well-being irrespective of lifestage. Young employees working for longer hours and older housewives were both defined as ‘cases’ by the General Health Questionnaire (GHQ-12). However, their profiles on the other well-being variables were very different.

Great advances have been made during the last 20 years in the development of structured and semi-structured interviews for use with psychiatric patients. However, in the field of child and adolescent psychiatry there have been weaknesses in the specification and definition of both symptoms and the psychosocial impairments resulting from psychiatric disorder. Furthermore, most of the available interviews for use with children have been tied to a single diagnostic system (DSM-III, DSM-III-R, or ICD-9). This has meant that symptom coverage has been limited and nosological comparisons have been inhibited. The Child and Adolescent Psychiatric Assessment (CAPA) represents an attempt to remedy some of these shortcomings. This paper outlines the principles adopted in the CAPA to improve the standardization, reliability and meaningfulness of symptom and diagnostic ratings. The CAPA is an interviewer-based diagnostic interview with versions for use with children and their parents, focused on symptoms occurring during the preceding 3 month period, adapted for assessments in both clinical and epidemiological research.

Seventy-seven 10–18-year-old psychiatric in-patients and out-patients took part in a test-retest study of the Child and Adolescent Psychiatric Assessment (CAPA). They were interviewed on two occasions several days apart. Overall reliability of diagnosis ranged from K = 0·55 (conduct disorder) to 1·0 (substance abuse or dependence). In general, reliability for scale scores of psychopathology was somewhat lower in out-patients than in-patients, though the opposite was the case for anxiety disorders and psychosocial incapacity and the reliability of the diagnosis of conduct disorder – the only individual diagnosis sufficiently common to permit this comparison. Unreliability of reports of behavioural problems was found to be related to admitting to being a liar in the first interview. The implications of these results for the use of the CAPA are discussed.

This study describes a cohort of 23 patients undergoing stereotactic subcaudate tractotomy. Research Diagnostic Criteria indicated that 70% suffered major depressive disorder; the remainder mostly had a bipolar affective disorder. There were serial assessments pre-operatively and at 2 weeks and 6 months post-operatively using the Hamilton Rating Scale for depression, the Present State Examination (PSE), Newcastle Scale, the Beck Depression Inventory, and the Taylor Manifest Anxiety Scale. Neuropsychological assessment included tests thought to be sensitive to frontal lobe dysfunction, as well as tests of general intelligence, attention, memory, language and visuo-spatial function.

Post-operatively, depression rating scale scores decreased significantly but most patients continued to exhibit a number of PSE syndromes. Depression rating scale scores were correlated with 1 year global outcome: there was no significant correlation except for the 6 month assessment when lower Hamilton scores were found to be associated with better global outcome. Correlations between the neuropsychological tests and the Hamilton and Beck depression scales at 2 weeks post-operatively suggested that an improvement in psychiatric condition was associated with greater efficiency on some tests of attention and verbal recall, as well as faster performance on a sorting task. By contrast, the changes at 6 months suggested an association between improvement in psychiatric condition and less efficient performance on certain neuropsychological tests including verbal recognition memory, attention and two tests of frontal lobe dysfunction.

The prescription pattern of antidepressants was reviewed in a large sample of psychiatric out-patients in the Region of Piedmont. Antidepressants were administered to 780 patients; most were diagnosed with mood disorders (62% of prescriptions) and anxiety disorders (34%), the rest with other diagnoses. The mean prescribed dose of antidepressants was at the lower end of, or below, the recommended range for out-patients, with the exception of amineptine and mianserin. The administered dose of tricyclic antidepressants was significantly associated with sex and diagnosis: female patients received a daily dose that was significantly lower than that for males, and patients with a diagnosis of mood disorders received significantly more medication than those with other diagnoses.

The prevalence rate of subjective memory impairment (SMI) and its value as a predictor of future depression or dementia was studied in a community sample of elderly residents in one electoral ward using the short-CARE. SMI was found to be common, occurring in 25% of subjects. Subjects with SMI were more likely to be suffering from either dementia or depression than those without the complaint, although 60% of subjects with SMI did not have evidence of either disorder. When followed up over a 2-year period, subjects with SMI were found to be at four-fold greater risk of developing future dementia and two-fold greater risk of developing a depression compared with those without SMI. The SMI scale was not found to be useful as a population screen for dementia or depression, although two of the nine items might have value as screening questions in clinical circumstances to determine those with memory complaints at risk for dementia.

Bipolar disorder and alcoholism are familial disorders. The familial–genetic relationship between both is controversial and has received insufficient study. This study explores whether bipolar disorder and alcoholism share familial risk factors, and whether the co-occurrence of lifetime diagnosis of bipolar disorder and alcoholism is familial. We report on first-degree relatives of 146 consecutively admitted patients with either bipolar disorder or/and alcoholism; relatives of the patients (in total 728 relatives directly interviewed) were compared with first-degree relatives of 109 general population probands (320 relatives directly interviewed). Overlap between the familial components underlying bipolar disorder and alcoholism was not observed if the analysis was restricted to ‘pure’ diagnostic groups. Excess comorbidity between bipolar disorder and alcoholism was observed in relatives. Multiple sources for this excess of comorbidity between major affective disorders and alcoholism in families of probands with bipolar disorder are likely; in particular, we found evidence for a distinct subgroup of comorbid cases with familial comorbidity; however, excess comorbidity was also found in absence of familial loading with alcoholism.

Subjects who meet the criteria for an affective syndrome possibly are aetiologically heterogeneous. An approach to this possibility involves examining affectively ill subjects obtained by different methods of ascertainment. This study compares depressed and manic subjects who are related to affectively ill probands with affectively ill subjects who were obtained from a study of a control population, and, therefore, were less likely to be familial. The subjects were identified in a large collaborative study of depression where both family members as well as controls were personally interviewed and followed up for 6 years after admission to the study. Data were obtained on subtypes of affective disorder using the Research Diagnostic Criteria and information was gathered about psychiatric hospitalizations, suicide attempts, alcoholism and psychological functioning prior to admission. Similar assessments were made for the comparison groups for the 6 year period between intake and follow-up. Relatives of bipolar I/schizoaffective manic probands were more likely to show mania than affectively ill controls or relatives of unipolar/schizoaffective depressed probands. Affectively ill controls were less likely to be hospitalized and less likely to suffer from an incapacitating depression. They were also likely to have functioned in a more healthy fashion than the affectively ill relatives of the bipolars and unipolars, in the 5 years before admission to the study. In the 6 year follow-up, both the subjects themselves and raters assessed the depressed controls as functioning better than the affectively ill relatives of the probands. Further, assessment of global adjustment during the 6 year period was worse for the relatives of affectively ill probands than for the depressed controls. Length of major depression was longer in relatives of bipolar and unipolar probands than in controls. Though all of the subjects in this study met research criteria for an affective illness, there were marked differences in the qualitative aspects of these illnesses with the relatives of affectively ill probands, who functioned less well and had longer and more severe episodes and more hospitalizations.

Most family studies of psychiatric illness ascertain probands through treatment facilities. If psychiatric illness in relatives influences the probability of treatment seeking, then the risk of illness in the relatives of treated probands will not be representative of the risk of illness in all probands. We have investigated this question in a population-based sample of female twins with lifetime history of DSM-III-R defined major depression (MD) (N = 753), 36% of whom reported seeking professional help for their depression. Logistic and Cox regression methods were used. Treatment seeking for MD was significantly associated with age, education, comorbidity with anxiety disorders, degree of impairment and number of symptoms. Controlling for these predictors, treatment seeking was significantly predicted by the presence of one or more relatives with a lifetime diagnosis of MD (OR = 1·62). The probability of treatment seeking for MD in the proband was significantly increased if the affected relative: (i) had an onset of their MD prior that of the proband and; (ii) themselves sought treatment for their depression. Seeking treatment in this epidemiological sample of depressed women was associated with a 32% increase in risk of MD in relatives. Selecting probands for family studies from treated populations may select for families with an increased rate of illness. For MD, this artefact can explain only a modest proportion of the familial aggregation observed in prior family studies that utilized treated probands.

Melancholia is most commonly distinguished from non-melancholic depression by the presence of psychomotor disturbance (PMD) and a set of ‘endogeneity’ symptoms. We examine the capacity of an operationalized clinician-rated measure of PMD (the CORE system) to predict diagnostic assignment to ‘melancholic/endogenous’ classes by the DSM-III-R and Newcastle systems. Examining a pre-established CORE cut-off score (≥ 8) against independent diagnostic assignment, PMD was present in 51% of those assigned as melancholic by DSM-III-R, and 85% of those assigned as endogenous by the Newcastle system, quantifying the extent to which it is ‘necessary’ to the two definitions of ‘melancholia’. Additionally, multivariate analyses established that the addition of a refined set of historically suggested endogeneity symptoms added only slightly to overall discrimination of melancholic and non-melancholic depressives. While only few endogeneity symptoms independent of psychomotor disturbance were suggested, their specific relevance varied against system definition of melancholia (appetite/weight loss and terminal insomnia being identified for DSM-III-R; anhedonia for Newcastle; and diurnal variation in mood and energy for both systems). Results allow consideration of the relative importance of two domains (psychomotor disturbance and ‘endogeneity’ symptoms) to clinical definition of melancholia, and have the potential to assist both classification and pursuit of neurobiological determinants. We interpret findings as suggesting a ‘core and mantle’ model for conceptualizing the clinical features of melancholia, with psychomotor disturbance as the core and with independent endogeneity symptoms as only a thin mantle.

We have attempted to clarify clinical differentiating features of psychotic depression. Forty-six depressed subjects meeting DSM-III-R criteria for major depression with psychotic features were compared with (i) DSM-defined melancholic, (ii) Newcastle-defined endogenous, and (iii) a residual DSM-defined major depressive episode group. Additionally, a ‘bottom up’ latent class analysis (LCA) suggested a larger sample of 82 ‘psychotic depressive’ subjects, and multivariate analyses contrasted these subjects with both LCA-identified melancholic and all residual depressed subjects. Analyses suggested that, in addition to two features with absolute specificity (delusions and hallucinations), both the DSM-defined and LCA-defined ‘psychotic depressive’ subjects were significantly more likely to demonstrate marked psychomotor disturbance, to report two morbid cognitions (feeling sinful and guilty; feeling deserving of punishment), as well as be more likely to report constipation, terminal insomnia, appetite/weight loss and (variable across the defined ‘psychotic depressive’ groups) loss of interest and pleasure. The study identifies a wider set of potentially discriminating clinical variables than previous studies, as well as both indicating the existence and assisting identification of ‘true’ psychotic depression in the absence of formal psychotic features being acknowledged or elicited.

We describe the development of a clinical algorithm to differentiate melancholic from non-melancholic depression, using refined sets of ‘endogeneity’ symptoms together with clinician-rated CORE scores assessing psychomotor disturbance. Assignment by the empirically developed algorithm is contrasted with assignment by DSM-III-R and with several other melancholia subtyping indices. Both the numbers of ‘melancholies’ assigned by the several systems and their capacity to distinguish ‘melancholics’ on clinical, demographic and a biological index test (the DST) varied across the systems with the algorithm being as ‘successful’ as several systems that include inter-episode and treatment response variables. Analyses provide information on the criteria set developed for DSM-IV definition of ‘melancholia’.

The objective of this study was to describe over time the course of cognitive function of elderly without cognitive impairment and of elderly with different stages of impairment, and to assess if the change in cognitive function was dependent on the initial level of function. The Mini-Mental State Examination (MMSE) was used at two time points. The first assessment (MMSE-1) was part of a community-based study and was obtained from 871 subjects. For the second assessment (MMSE-2) a sample of 166 subjects was drawn from the subjects alive at follow-up who had an MMSE-1 score. This sample was stratified by MMSE-1 score to avoid oversampling of subjects with high MMSE-1 scores. A second MMSE score was obtained from 134 elderly, whereas 18 subjects refused participation and 14 subjects were not traceable. The median age at first assessment was 89 years (25th percentile 87, 75th percentile 92), the mean follow-up period (S.D.) was 3·3 (0·5) years. The median change in MMSE score was minus 4 points (95% confidence interval (CI) − 7 to − 2) and the slope of the regression line of MMSE-2 on MMSE-1 was 1·1 (95% CI 0·9–1·3). It is likely that the slope was underestimated due to a floor effect, regression to the mean and missing observations. However, the probability of decline decreased if MMSE-1 was higher. Nevertheless, the probability ranged from 27 to 59% for subjects with the highest MMSE-1 scores aged 85 and 95 years respectively. The latter is an argument in favour of a periodical examination of all subjects aged 85 and over to reveal causes of cognitive decline that can be treated or are amenable to prevention.

Current clinical correlates of duration of initially untreated psychotic symptoms were investigated in a cross-sectional analysis followed by a 10-year prospective study among 88 inpatients with a long-standing schizophrenic illness, many of whom had experienced prolonged periods of untreated psychosis due to illness onset and hospital admission in the pre-neuroleptic era. After controlling for the effects of age, and duration and continuity of subsequent neuroleptic treatment, the primary clinical correlate of duration of initially untreated psychosis was muteness. Over the subsequent 10-year-period, no new cases of muteness emerged and some existing cases of muteness partially resolved, though the speech that emerged remained very sparse and revealed generally gross cognitive debility. The pathophysiology underlying active, unchecked psychosis may also constitute an active morbid process that is associated with the further progression of severe negative symptoms and cognitive dysfunction in the long-term.

It has often been assumed that all subjects with schizophrenia will eventually be admitted to hospital and therefore little bias is introduced by restricting research to hospitalized subjects. Using the Lothian Psychiatric Case Register, 66 subjects were identified who had been diagnosed in Edinburgh as suffering from schizophrenia between 1978 and 1989 but had no history of hospital admission by December 1991. This represented an adjusted average of 6·7% of the estimated annual rate of first diagnosis of schizophrenia: the proportion of such patients did not change over the period. Using a case–control design, the index cases were compared with a control group of schizophrenic patients who had been admitted to hospital within 3 months of diagnosis. At the time of diagnosis, the cases were generally less disturbed with lower levels of violent behaviour and less evidence of neglect or hallucinations. They had a longer duration of illness prior to diagnosis, were more often diagnosed by a consultant and unemployed. In a follow-up study of the index cases, 59 (89%) were traced, of whom 6 (10%) were deceased. The outcome of the illness was heterogeneous although the course was often chronic. The general practitioner provided most of the care they received. The small proportion of such patients suggests that their exclusion from most published series does not seriously bias our picture of the natural history of schizophrenia. Moreover, as there was no increase in the proportion over the period, first admission rates for schizophrenia in Scotland are a reasonable approximation to incidence rates.