The current characterisation of dementia as a state of global cognitive failure (DSM-III-R, 1987) cannot differentiate it reliably, in cross-sectional diagnosis, from other states of compromised cognition. This is likely to contribute to both the over- and under-diagnosis of dementia in clinical practice (Marsden & Harrison, 1972; Fleminger, 1975; Ron et al, 1979; Smith & Kiloh, 1981; Garcia et al, 1984; Klein et al, 1985). However, diagnostic discrimination between true dementia and its behavioural phenocopies (e.g. depressive pseudo-dementia, quiet delirium, etc.) can be improved in a number of ways. One such is the longitudinal assessment of symptom-clusters (e.g. those related to memory, personality, and cortical syndromes); another is the inclusion of new symptoms into the definition of dementia. The first of these strategies has been given more attention than the second.

Obsessive-compulsive disorders (OCDs) (ICD-9 = 300.3) (ICD-9, 1978) remain an obscure, heterogeneous, and often unmanageable collection of interfering and repetitive experiences and actions which may interrupt, and occasionally obliterate the flow of behaviour (Beech, 1974; Rachman & Hodgson, 1980; Berrios, 1985; Jenike et al, 1986). Considered during the 19th century as a form of psychosis, OCDs were incorporated at the turn of the century into the psychodynamically redefined class of the ‘neuroses’ (Berrios, 1985). However, this newly gained identity has proved to be heuristically sterile as well as delaying research.

This paper gives a brief outline of the present state of development of the psychiatric chapter of the tenth revision of the International Classification of Diseases (ICD-10). It is written from the point of view of one of the many consultants to the Division of Mental Health, World Health Organization (WHO), Geneva, and thus is not an authoritative or official statement on behalf of WHO. The responsibility for decisions about ICD-10 Chapter V (F) rests with Dr Norman Sartorius, Director of the Division of Mental Health, though many psychiatrists in many countries have contributed to ICD-10 Chapter V (F), and will continue to do so, since much work is still to be done before the final form is officially agreed and published in about 1990. Before he left WHO, Geneva in September, 1986, Dr Assen Jablensky also carried a great deal of responsibility for the arrangements necessary for the production of the drafts of ICD-10 Chapter V (F) that are now being developed.

‘Hypochondria’, ‘hypochondriasis’, and ‘somatisation’ are terms long used to characterise individuals who display unrelenting somatic symptoms that cannot be medically explained. A psychiatric aetiology for such phenomena is often assumed on the basis of potential psychological gain, the presence of ‘stressors’, the co-existence of unexplained somatic symptom and symptoms of depression or anxiety, or merely the absence of a medical explanation.

The classification of anxiety disorders is a controversial subject, and this controversy is reflected in the differences between the systems adopted in DSM-III-R and in the draft of ICD-10. The scheme in ICD-10 is the simpler: anxiety disorders are divided into phobic disorders and other anxiety disorders, and each is divided further into three subgroups. The three phobic disorders are: agoraphobia, social phobia, and specific phobia. The three subgroups of ‘other anxiety disorders’ are panic disorder, generalised anxiety disorder, and mixed anxiety and depressive disorder. The subdivisions of phobic disorder are those now generally adopted in most countries, and are uncontroversial. The subdivisions of generalised anxiety disorder, and mixed anxiety depressive disorder are also widely accepted, the latter group being particularly frequent among patients seen in general practice and not referred on to psychiatrists. Only the category of panic disorder is controversial. In addition to these categories which are specifically allocated to anxiety disorders, two others are relevant: ‘reactions to severe stress and adjustment disorders’, and anxious personality disorder.

Psychiatric diagnosis tests the hypothesis that particular signs and symptoms, when regularly found together, belong to a particular class. The class concerned, in turn, is usually part of a taxonomic system, and which system one chooses will depend on the aim and function of diagnosis (treatment, research, administration, etc.). Diagnosis and classification involve a loss of information, the magnitude of which is determined by both the use to which the diagnosis has been put and the assumptions and theoretical orientation of the clinicians involved in the exercise.

Criticism of the validity of traditional psychiatric diagnosis include concerns about its inability to capture both the meaning of the patient's problems, and the factors involved in the gestation of disorder, as well as its limited usefulness with regard to prognosis and treatment. However, the main drawback of traditional diagnosis seems to be that it leads to treating the disease rather than the individual. Against these fears, the role of diagnosis has been emphasised in enhancing communication among professionals, organising clinical experiences, planning services, building scientific theories, and pointing to new research directions (Kendell, 1975).

The facts that neither the International Classification of Diseases (ICD) nor any other major standard diagnostic system have offered a full definition of psychiatric illness and that earnest definitional attempts reported in the literature (e.g. Spitzer & Endicott, 1978) have not received wide acceptance, have led distinguished nosologists (e.g. Kendell, 1985) to suggest that all we can say about psychiatric classifications is that they are classifications of kinds of problems which psychiatrists currently deal with. However, one immediate difficulty with this characterisation is that it is based on what psychiatrists do, when in fact psychiatric problems are dealt with also by other professionals of various types and levels of training. Another difficulty is that it implies that there is not even an approximate common denominator or core concept underlying the various forms of psychiatric disorder listed in the ICD or other standard diagnostic systems.

The concept of reactive or psychogenic psychoses has had a peculiar fate. Especially at the beginning of the century, under the influence of the writings of Jaspers (Jaspers, 1913) which included definitions of ‘psychogenic’ and ‘psychoses’, the term ‘psychogenic psychoses’ came into common use in European psychiatry. In Scandinavia, this trend was greatly reinforced by August Wimmer's monograph in 1916 on the subject. In the later editions of Kraepelin's standard textbook, the concept appeared quite frequently, and the same was the case in other leading textbooks, for instance in the Soviet Union and Japan.

In a survey of authoritative psychiatric texts, inconsistent, sometimes contradictory use can be found of the terms ‘affect’, ‘mood’, and ‘emotion’. There is some consensus that these terms deal with subsets of the larger domain of feelings, but many authorities, explicitly or implicitly, treat them as at least partially interchangeable. Others see the terms as referring to different phenomena, but disagree on how they differ. In lay usage, feelings are primarily subjective experiences, but the term is used here in a more encompassing, generic sense. In the psychiatric texts, some attributes are frequently used to distinguish among feelings. These include the duration of the phenomena; whether they are subjective, objective or both; the relative involvement of cognition; and whether they are clinically observable or rather reflect the patient's potential for response. Some examples of current usage will be considered before alternative formulations are suggested.

Several attempts have been made to relate subtypes of schizophrenia to dopaminergic status. For example, Crow's hypothesis states that Type I schizophrenia is characterised by positive symptoms, increased activity of the dopaminergic system, good response to neuroleptics, and no brain structural changes; and Type II by negative symptoms, reduced dopaminergic activity, poor response to neuroleptics, and brain structural changes. Testing of this hypothesis has, however, been inconclusive, and it seems more likely that both types are inter-related.

Coping strategies to adapt to environmental and psychological contingencies have been well studied in the human subject. The typical individual is known to have response patterns that permit automatic, and often unconscious adjustment to changing conditions. Psychological (defence) mechanisms facilitate adaptation to new situations or interactions, and when successful, no additional coping mechanisms need to be invoked. However, situations may arise when such mechanisms are insufficient: this may result from developmental failure, personality factors, inordinate levels of stress, or combinations thereof.

Insights into the cellular and molecular mechanisms of action of anti-depressant drugs have led to the study of possible dysfunctions of monoamine neurotransmitter receptors in endogenous depression. Presynaptic receptors play an important role in the regulation of transmitter release from neurons. The major mechanism that regulates the release of noradrenaline appears to be feedback inhibition by the neurotransmitter located in the synaptic cleft. This inhibition is mediated by stimulation of a presynaptic autoreceptor, the inhibitory α2-adrenoceptor. When this is stimulated, further release of noradrenaline is inhibited; therefore, increased autoreceptor sensitivity could result in insufficient neuronal release of noradrenaline, and lead to depression.

An important topic in the neurobiology of the affective disorders relates to changes in the metabolism of neurotransmitters. Since the early 1960s, the ‘serotonergic’ hypothesis (Coppen et al, 1972) has been supported by findings such as a low concentration of 5-hydroxy-indoleacetic acid (5-HIAA) in the cerebro-spinal fluid (CSF) of patients with melancholic depression and/or suicidal behaviour (Banki & Arato, 1983; Åsberg et al, 1984; Banki et al, 1984; López-Ibor, Jr et al, 1985; Korpi et al, 1986) as well as the efficacy of serotonin precursors, when combined with MAOIs, in the treatment of depressed patients (Coppen et al, 1963; Glassman & Platman, 1969; Ayuso et al, 1971; López-Ibor, Jr et al, 1976).

Normal-pressure hydrocephalus (NPH) was described in 1964 (Adams, 1965; Hakim, 1965) and defined by the symptom triad: dementia, motor disturbance, and sphincter disturbance. The original publication by Adams already contained a reference to psychiatric symptoms: depression, slowness, hallucinations, and apathy. Rice & Gendelman (1973) reported five cases, and commented on the development of both early cognitive impairment and behavioural regression, suggesting that personality factors might play a role in the appearance of latter symptoms. Trevor et al (1977) described a case suffering from psychotic depression, paranoid symptoms, inadequate affect, and self-destructive behaviour.

Freud's Three Essays on the Theory of Sexuality (1905) made possible the understanding of the concept of perversion as a form of psychic conflict resulting from both constitutional and acquired factors. He stated (as against earlier views) that sexual deviations could not be separated from ‘normal’ sexual behaviour, on the grounds that both sprang from a common source (infantile sexuality). In the first essay, Freud classified sexual deviations into two groups, depending on whether the aim (e.g. sadism and masochism) or the object of the instinct (e.g. homosexuality and paedophilia) were displaced. In the second essay he characterised infantile sexuality as a collection of partial instincts and erotogenic zones, on which both the source and the object of the instinct converged. He also stated that infantile sexuality was auto-erotic, implying that the sexual object was contingent.