Although anorexia nervosa may vary widely in its severity and outcome, it is usually regarded as an illness in its own right, as patients do not display major changes in the form of the illness over time (Russell, 1970). It readily lends itself to being accorded clear-cut diagnostic criteria (Russell, 1977) and this is reflected in ICD–10 (World Health Organization, 1987). However, the nosological independence of anorexia nervosa has undergone vigorous assault since its classic description by William Gull (1874). For example, the psychological nature of anorexia nervosa was obscured for 30 years by Simmond's (1914) description of anterior pituitary lesions and cachexia, and Kay & Leigh's (1954) influential study of anorexia nervosa concluded with their doubts about its status as a ‘psychiatric entity’.

Neurotic syndromes are defined by characteristic patterns of symptoms, but the validity of the distinction between one syndrome and another depends on associations between the syndromes and clinical history, or treatment response factors that are independent of the defining phenomena. In both a group of twin volunteers and a group of patients with panic disorder/agoraphobia, the lifetime experience of more than one diagnosis of a neurotic syndrome was common but there was no evidence of patterns of co-occurrence of diagnoses being associated with particular syndromes. Receiving a diagnosis was associated with abnormal scores on measures of neuroticism and locus of control, the extent of the abnormality increasing with the number of different diagnoses satisfied. It is argued that the concept of a general neurotic syndrome depends in part on the presence of such predisposing personality factors, and that reduction in this predisposition to neurosis should be the focus of treatment.

Patients diagnosed in the late 1960s as suffering from either endogenous or neurotic depression, or as presenting with depression but discharged with another neurotic diagnosis, were followed for 15 years. Diagnosis at index admission did not predict overall outcome, but patients with endogenous depression, an apparently stable diagnosis, had longer index admissions, were readmitted sooner, but spent less time ill than patients in either of the neurosis groups. Personality abnormality accounted for 20% of the variance in outcome in the neurotic groups and only 2% of the variance in the endogenous group. Thus there is evidence that endogenous and neurotic depression are two illnesses and that, in the neuroses particularly, prognosis will depend on the extent to which these personality abnormalities are modified by treatment.

In 1965/66, a consecutive series of 89 in-patients with depression were interviewed, given two personality tests (the EPI and LOI), and were accorded a score on a neurotic-psychotic continuum (Dl). Eighteen years later, the series was followed up and the predictive power of the original data was determined. High neuroticism scores on the EPI on recovery and particularly when ill but referring to the pre-morbid state were associated with poor overall outcome and chronicity. High obsessional interference scores on the LOI on recovery were also associated with poor long-term outcome, impaired social adjustment, more time spent in hospital, and with the subsequent development of schizophrenic or schizoaffective episodes. High psychotic scores on the Dl were also associated with poor long-term outcome, a greater length of time spent in hospital, and with bipolar affective disorder, and this effect was independent of the personality measures.

A review of the evidence shows that there is no convincing support for a separate clinical diagnosis of ‘cannabis psychosis'. Cannabis can, however, produce brief acute organic reactions and, in moderate to heavy doses, psychotic episodes in clear consciousness. Ingestion in naive users or increasingly heavy use in habitual users can precipitate a schizophreniform episode. Heavy users may have an increased risk of developing schizophrenia in the subsequent 15 years. Well controlled, longitudinal studies are required to explore these associations further and their possible aetiological significance.

Supervised administration of disulfiram is one of the very few treatments that can significantly reduce alcohol consumption, yet it is rarely used, despite being simple and cheap. Disulfiram is not ‘aversion therapy‘, but a technique for facilitating exposure and response prevention, and it fits comfortably into a behavioural, social-learning model of addiction (or dependence) and its treatment. The availability of other effective antagonists, notably to opiates, suggests that an approach that is demonstrably effective in alcohol dependence may be helpful in treating other addictions. The reasons for the unpopularity of this approach appear to be largely ideological.

Two studies are reported. In the first, of 62 schizophrenic patients, no correlation between negative symptom scores (rated blindly) and any measure of positive symptoms was found. This independence was confirmed by factor and cluster analyses, which left the question of a third ‘disorganisation’ class of schizophrenic symptoms open. In the second study, of 80 patients, formal thought disorder separated unequivocally into ‘positive formal thought disorder’ and ‘alogia’ syndromes on the basis of correlations with positive and negative symptoms. Catatonic motor disorder also showed evidence of a corresponding positive: negative division, although this only emerged when severity or chronicity of illness was controlled for. Cognitive impairment showed a broad range of affiliations and its particular correlation with negative symptoms was perhaps artefactual.

The ability to shift cognitive set, which is probably subserved, at least in part, by the pre-frontal cortex, was determined for schizophrenic, bipolar (manic) and control subjects, using the Wisconsin Card Sorting Test (WCST). The schizophrenic and manic subjects both demonstrated poor performance on the WCST, suggesting that cognitive inflexibility and/or pre-frontal dysfunction, is not specific to schizophrenia (although laterality differences could exist). Moderate levels of poor performance in the non-psychiatric control group suggest the need for a review of the cut-off figures in the WCST currently used for predicting ‘brain damage’ and ‘focal frontal involvement‘, especially given the trend for the increasing use of cognitive assessment and rehabilitation in the major psychoses.

The possibility that separation of a categorical depressive disease (‘melancholia’) from remaining depressive disorders can be improved by assessment of mental state signs was examined in patients treated by representative Sydney psychiatrists and patients referred to a specialised mood disorders unit. A set of signs, principally assessing retardation, was derived within the two samples by principal-components and latent-class analyses. Scores were significantly correlated with clinical, DSM–III, and RDC diagnoses, and appeared independent of severity, suggesting that melancholia can be defined phenomenologically. Scores were also associated with several ‘validating’ factors. Comparative analyses of a refined list of melancholia symptoms suggested that ratings of defined signs are likely to have greater capacity than symptom ratings to differentiate melancholia from residual depressive disorders.

In an open study of 35 depressed patients, psychomotor disturbance, assessed by the CORE rating system, significantly predicted response to ECT in patients with a ‘retarded’ but not those with an ‘agitated’ type of illness. In multivariate analyses, psychomotor disturbance was the sole predictor of response. This preliminary study suggests that the CORE system, which has been shown to differentiate endogenous and non-endogenous depressive disorders, has predictive validity in relation to ECT response.

In a sample of 178 subjects with Alzheimer's disease, diagnosed by clinical criteria (NINCDS/ADRDA), delusions had occurred in 16% of the sample since the onset of the illness and been present within the last 12 months in 11%. Simple delusions of theft and suspicion were the most common types and a greater proportion of men suffered delusions of theft. Subjects with other types of delusion had relatively well preserved lateral ventricular size and basal ganglia calcification. Twenty per cent of the group had experienced persecutory ideation short of delusions since the onset of the illness. Cognitive function at entry to the study and cognitive deterioration over the succeeding 12 months was not influenced by the presence of disorders of thought content.

In a sample of 178 patients with AD, visual hallucinations had been experienced by 13% and auditory hallucinations by 10%. Thirty per cent had misidentification syndromes; these were associated with a younger age and younger age at onset of illness, and proportionally more men than women were affected. There was a reduced 30-month mortality rate in this group. Subjects with hallucinations had a greater deterioration in cognitive function at 12-month follow-up, which could not be accounted for by neuroleptic medication.

Of 178 patients with AD, at least one depressive symptom was reported by 63%, 24% were rated as being depressed by a trained observer, and 43% were considered depressed by their relatives. Ten per cent had a previous history of depression. Elevated mood was rare, occurring in only six patients (3.5%). Subjects with depressive symptoms had less cognitive impairment and less ventricular enlargement on CT compared with those without symptoms. Widening of the interhemispheric fissure was associated with symptoms of mania but was inversely related to presence of depressive symptoms.

Out of a sample of 178 patients with AD, aggression was present in 20%, wandering in 19%, binge-eating in 10%, hyperorality in 6%, urinary incontinence in 48%, and sexual disinhibition in 7%. Behavioural abnormalities were greater in those with more severe dementia. Temporal-lobe atrophy correlated with aggression, and widening of the third ventricle with hyperorality. Features of the Kluver–Bucy syndrome were commonly seen, but the full syndrome occurred in only one subject. Patients with at least one feature of the Kluver–Bucy syndrome had greater temporal-lobe atropy than those without any of the features.

A questionnaire was developed to help the assessment of patients who take overdoses. Twenty-four house physicians in Southampton university hospitals were randomly divided into a group who used the questionnaire and another group who asked whatever questions they felt appropriate. One hundred and fifty patients who had taken overdoses were included in the study. After the house physician's assessment, a research assistant interviewed all of the patients and the two assessments for each patient were then compared. There was greater agreement between the research assistant and the house physicians who used the questionnaire than those who interviewed patients in an unstructured way with respect to assessments of severity of depression, purpose of the act, suicidal intent, diagnosis, and future management.

An investigation in a large mental handicap hospital revealed that 24% of the in-patients were receiving antipsychotic drugs. Chlorpromazine and thioridazine prescriptions accounted for 62% of the total while 10% of patients received depot preparations. Fifty-five per cent of the patients receiving these drugs had no established psychiatric diagnosis; most of these could be categorised as having a behaviour disorder. Patients aged 30–50 received higher doses, and female patients received a significantly higher mean dosage than male ones. In the patients receiving neuroleptic drugs who had also been taking them four years previously, there was a significant reduction in the dosage of the drugs received and the extent of polypharmacy of these agents. A mandatory requirement to review all prescriptions annually, implemented in 1984, may be a reason for this.

The MRI T1 proton relaxation values were assessed in 14 patients with bipolar affective disorder and 10 with a unipolar disorder and a matched normal control group. The T1 values in the frontal white matter of patients significantly exceeded those of the controls. This difference was accounted for by an increase in T1 values in the frontal white matter of unipolar patients: the values for bipolar patients alone did not differ from those for controls. These preliminary findings support a hypothesis of frontal lobe dysfunction mediating pathological changes in mood.

Three aspects of the approach to philosophy advocated by the Oxford philosopher J. L. Austin are outlined: his conception of the nature of philosophical problems, essentially as a mixed bag; his method of linguistic analysis, namely, clarification of our concepts by active observation of the ways in which they are actually used rather than by passive reflection on their meanings; and his views on the organisation of philosophical research, that in some areas it should be pursued rather as a science is pursued, as a corporate rather than merely individual venture. It is suggested that Austin's approach provides the basis for a potentially fruitful two-way relationship between philosophical theory and medical practice.

DSM–III has largely been based upon essentialist notions of increasingly accurate and ‘valid’ definitions of diseases. A nominalist approach would facilitate study of aetiological factors and variables in the natural history of diseases.

When Kraepelin formulated the concept of dementia praecox, he lumped together a number of diagnostic categories. One of his reasons for doing so was that he had seen many patients who ended up in the same kind of demented state, even though their initial symptoms might have been quite different. He noted that even some cases presenting with mania, or melancholia, took the same downhill course as did the more classic cases of dementia praecox. Kraepelin, aware of the striking paradigm of general paresis, stated that “a single morbid process” explained the downhill course (Kraepelin, 1983, p. 68).