Jealousy is a common emotion which can be considered pathological in some circumstances. The term ‘morbid jealousy’ has been used to signify this abnormal or extreme condition. However, the literature on morbid jealousy is sparse and the empirical data fragmentary. The aims of this paper are to briefly review the concept, to define the dimensions of the disorder and to apply a cognitive-behavioural framework to it. Such a summary paper is timely, to draw together the different aspects of the problem and to provide a theoretical base from which to generate further research.

Advances in genetic linkage strategies, including techniques of molecular genetics, augur well for the discovery of disease-related genes in mental disorders. Recent studies showing linkage of chromosomal loci to bipolar affective illness and schizophrenia attest to the potential in the ‘new genetics'. However, the failure to replicate some of the early findings has led to calls for re-evaluation of the methodology in psychiatric research. Problems in studying complex (psychiatric) disorders include diagnostic uncertainties, unclear mode of transmission, aetiological heterogeneity, cohort effects, and assortative mating. Knowing the potential pitfalls in linkage analysis of mental illness should avert spurious findings and will increase the prospects of success.

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’.

Torture is one of the most important preventable causes of psychological morbidity. Amnesty International (1987) has reported the use of “brutal torture and ill-treatment” in over 90 countries in the 1980s. In some countries torture has been applied on such a widespread scale and in such an arbitrary manner that whole populations are affected. In Kampuchea under the Pol Pot regime, for example, genocide and torture took place on a massive scale; indeed, merely wearing spectacles became for many a capital offence (Amnesty International, 1983). Similar reports abound from many other countries and regions.

Since a previous review (Kellam, 1987), the subject of neuroleptic malignant syndrome (NMS) has continued to cause considerable interest, particularly in the USA where there is still controversy about its frequency, despite two attempts to survey prospectively all cases admitted to two different hospitals. Cases of NMS are now being more widely recognised by non-psychiatrists, especially geriatricians.

There has been great variability and inconsistency in the reported effects of neuroleptic drugs on cognitive and psychomotor function in both patients and normal controls. Experimental design rather than any particular cognitive or psychomotor test appears to have determined the sensitivity of detection of neuroleptic drug effects. In general, sedative phenothiazines have been found to depress psychomotor function and sustained attention, but higher cognitive functions are relatively unaffected. In the majority of studies of schizophrenic patients, both cognitive function and attention improve with neuroleptic treatment, in parallel with clinical recovery. Negative symptoms are not increased and usually show slight improvement with neuroleptic treatment. Controls are more sensitive than schizophrenic patients to neuroleptic drug-induced impairments. Tolerance has been seen in patients but has not been demonstrated in normal volunteers. The way in which neuroleptics produce their beneficial effects in patients remains unknown. Three main hypotheses to replace early arousal theories are proposed: normalisation of attention, facilitated indirectly by suppression of ‘released’ limbic dopamine hyperactivity; normalisation of asymmetrical temporohippocampal function; or direct improvement of attentional processing. Studies of the effects of new antipsychotic drugs with selective actions and the development of more reliable and selective tests of psychomotor and cognitive functions are required.

In the 19th century the triumphs of neuropathology and the clinico-anatomical method led to the evolution of neurology as a separate ‘organically’ based discipline associated with the concept of functional localisation. At the same time the growth of psychodynamic psychiatry contributed to the progressive separation of the two disciplines, with neuropsychiatry sitting uneasily in the middle. Psychiatrists are now showing increasing interest in the structure and function of the nervous system, but are having difficulty in integrating their findings into ‘functional’ diseases. This may be because disorder of function in the nervous system is much more complex than previously envisaged. The function of the nervous system is profoundly affected by psychological and social factors. The view that neurology is wholly ‘organic’ and synonymous with structural disease of the nervous system is fallacious. Neurological patients have complex dynamic disorders of function in the nervous system whether or not structural disease is present.

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.

It has been hypothesised that community cases of depression compared with clinic cases: (a) have fewer symptoms; (b) have milder symptoms; (c) have different symptoms; (d) are of shorter duration; (e) are less incapacitating; (f) are more environmentally and less biologically caused; and (g) respond better to psychological than pharmacological intervention. A review of the literature indicates that some of these hypotheses have not been tested, others have not been adequately tested, and none has been unequivocally confirmed. Further investigations of these important issues are required.

Projective identification is a psychoanalytic concept encompassing functions of defence and communication. It is invaluable in a variety of settings in general psychiatry, including patient assessment, ward management and work with families.

Psychiatry is under threat from developments within mental health care. In educating future psychiatrists, more emphasis should be placed upon: collaborative research; integrated teamwork, without interprofessional rivalry; work in primary care; the non-scientific components of psychiatry, centred upon relationships with patients; less dogmatic attitudes for or against psychoanalysis; psychiatry as a branch of medicine; and modern management and audit methods. Younger psychiatrists should be encouraged to take responsibility for shaping the future of the profession.

Cortical inhibitory neurotransmitters, neuropeptides, dopamine and noradrenaline are probably either not selectively or not critically affected in AD. It is, however, likely that a key change is shrinkage or loss of corticocortical pyramidal neurones, which probably use glutamate as their transmitter. This depletion appears to be circumscribed and clinically relevant.

The introduction of neuroimaging techniques for the study of brain structure and function has revolutionised the endeavour to elucidate the pathology of psychiatric disorder, the Holy Grail in psychiatry (Krishnan, 1990). Emil Kraepelin discovered the two major mental disorders, dementia praecox and manic-depression, and conceived their aetiology in brain pathology. It was Alois Alzheimer, however, his most successful student, who discovered the neuropathology of Alzheimer's disease. Sigmund Freud, who started his inquiries in brain science, lost faith and shifted to the study of the mind. Brain science and mind ‘science’ rapidly became odd bed fellows and parted company. The breakdown in communication fostered a mistrust in both parties, aborting endeavours of reconciliation. The evidence for the neuropathology of the ‘functional’ psychoses has, however, been inconclusive. It was the advent of brain-imaging techniques that rejuvenated brain sciences and modern neurosciences. The introduction of neuroimaging techniques, such as the electroencephalogram (EEG) in the 1920s and the whole-brain blood-flow techniques (Berger, 1929; Kety & Schmidt, 1948), antedated the discovery of psychotropic drugs. Pneumoencephalography was also applied to study brain structure in schizophrenia (Storey, 1966). The true methodological leap, however, was the introduction of computerised methods to construct three-dimensional images from two-dimensional data, enabling the development of computerised tomography (CT), magnetic resonance imaging (MRI), positron-emission tomography (PET) and single-photon emission computerised tomography (SPECT).

Eighty-eight in-patients admitted to a psychiatric mother-and-baby unit and 80 randomly selected recently delivered women in the general population were interviewed using the LEDS. Only five of 33 patients (15%) with puerperal psychosis had provoking agents, which is less than the figure for women in the community (36%). Provoking agents were present in only 8 of 25 patients with post-natal depression, but they were present in seven of nine patients with pre-natal depression and eight of nine women in the community with pre-natal depression.

In alcohol withdrawal, abnormalities occur in a number of neurotransmitter systems: there is reduced inhibitory function, and increased activity of excitatory systems. The former, indicated by reduced GABA and alpha-2-adrenoceptor activity, acts in conjunction with, and is exacerbated by, the latter, which itself may be due to the potentiation of NMDA activity by depletion of magnesium, and overactivity of catecholaminergic and CRF neurones. These dysfunctions produce immediate effects and may also contribute to the long-term changes in brain excitability by a kindling-like process. It is possible that early and active treatment may oppose this process. Present strategies for treatment of alcohol withdrawal enhance GABA and alpha-2 inhibitory, or reduce excitatory, mechanisms. Future possibilities include the use of CRF and/or NMDA antagonists.

Many of the functions of large psychiatric hospitals were those of asylum. As the structure of services has changed and the role of the large hospital has diminished, the necessity to continue to cover their functions has tended to be forgotten, partly because it has been thought that, even at best, they were purely protective. Such a point of view cannot be sustained. The functions of asylum have always been both refuge and recuperation. ‘Community care’ will come to deserve the odium now attached to the worst practices of former times if the tradition of asylum practised in the best of the large hospitals is not (with appropriate modification) acknowledged, properly placed in the psychiatric curriculum, and given high priority in service planning.

The outcome at two years of patients who were eligible for a study of first schizophrenic episodes was assessed in terms of occupation (n = 237) and in terms of number of days spent as an in-patient from the time of first admission (n = 252), and was related to social, behavioural, mental state and neurological measures during the initial admission. Poor outcome was in general associated with more social withdrawal, inactivity and abnormal social presentation and with more ‘neurological soft signs'. Good occupational outcome in patients with a relatively short pre-treatment duration of illness was associated with the prescription of placebo medication during the follow-up period.

The planning of long-term care in the community as an alternative to in-patient care requires accurate information on the likely expense of altering the balance of provision. Unfortunately, as very few long-stay psychiatric hospitals have yet closed, the planning of these resource requirements has had to proceed in a vacuum. By examining the costs of community reprovision for the first 136 people to leave Claybury and Friern Hospitals, a prediction equation has been estimated from existing data which links the hospital-assessed characteristics (including psychiatric symptoms and behavioural problems) of these people to the subsequent cost of community care. About a third of the observed variation in these costs can be explained statistically by these ‘baseline’ characteristics. However, the first cohorts exhibit fewer behavioural problems and other symptoms of mental illness, they have been in hospital for shorter lengths of time, and they are younger. The prediction equation for the leavers is thus used to extrapolate community costs for those hospital residents yet to leave. It is found that community costs are lower than hospital costs, not just for the first cohorts of leavers, but for the full populations of the two hospitals scheduled to close.

The development of the non-invasive technique of computerised tomography (CT) in the mid-1970s revolutionised the clinician's ability to visualise brain structures in vivo. The main use of the CT scan was to exclude intracranial mass lesions such as cerebral tumours and haematomas. This remains its principal application in neurology and neurosurgery, but in psychiatry additional features such as cerebral infarctions, regional cerebral atrophy, ventricular enlargement and white-matter changes have provoked interest. This review outlines the technique of CT scanning, discusses its use in the differential diagnosis of dementia of the Alzheimer type (DAT), and comments on the relative contributions of cortical atrophy and ventricular enlargement to the clinical picture of DAT.