It is now generally accepted that stressful life events and chronic difficulties can trigger the onset of depression in predisposed individuals. However, although much is known of the neurobiology of stress, few attempts have been made to provide a biological explanation for the mechanisms whereby life events might trigger depression. Enough is now known of the central control of hypothalamic pituitary adrenal (HPA) function and its response to stress to permit an examination of its role in the neurobiology of the triggering of depression by stress. This evidence is reviewed, and the proposal explored that stress triggers depression by a genomic action of corticosteroids.

Pre-natal infection with polioviruses could contribute to the subsequent development of schizophrenia. The hypothesis draws support from the declining incidence of schizophrenia, the excess of schizophrenic winter births, and the increased rates of schizophrenia among West Indian immigrants. There are parallels with other late sequelae of poliovirus infections. These postulations generate a testable hypothesis of a genetic link between schizophrenia and susceptibility to poliomyelitis.

The delineation of panic disorder as a distinct diagnostic entity has provided renewed impetus for research into panic. This review describes and examines the range of neurobiological theories of panic attacks. It illustrates the diversity of mechanisms that have been invoked to explain the production of panic attacks, and which have influenced much of the current thinking about the neurochemistry of anxiety.

We examined the relationship between the dates of births of schizophrenic patients admitted to hospitals for the first time in England and Wales between 1970 and 1979, and the occurrence of influenza epidemics between 1939 and 1960. Our results indicate that exposure to influenza epidemics between the third and seventh month of gestation is associated with schizophrenia in adult life. The hypothesis that maternal viral infection is an important cause of schizophrenia can explain many aspects of the enigmatic epidemiology of the condition.

Post-traumatic stress disorder (PTSD) is a recently introduced diagnosis. The disorder is quite common, yet often unrecognised, and leads to significant morbidity or mortality. Effective treatment often entails use of psychotropic medication. Only recently has this become apparent, and awareness of the role of drug therapy in PTSD remains limited. A number of studies have indicated efficacy for antidepressant, mood-stabilising, anticonvulsant and antianxiety medications. This review describes the role of pharmacotherapy, by examining issues of diagnosis and recognition of PTSD, the theoretical basis for drug use, goals of drug treatment, dose ranges, and clinical application of psychotropic drugs.

Full neuropharmacological understanding of the atypical antipsychotic agent clozapine remains elusive. Antidopaminergic actions of most neuroleptics probably contribute to their antipsychotic benefits, but also to neurological side-effects. Clinical evidence of abnormalities of dopamine (DA) and serotonin (5-HT) in psychotic disorders is inconsistent, but there is substantial metabolic and post-mortem evidence for hyperactivity of noradrenalin (NA). Clozapine is only weakly antidopaminergic but is a potent antagonist at brain α1-adrenergic, 5-HT2-serotonergic, and muscarinic receptors. Its apparent limbic-over-extrapyramidal neuro-physiological selectivity can be mimicked by combining a typical neuroleptic with a central α1 antagonist. Clozapine strongly upregulates α1, but not DA, receptor abundance, and may supersensitise α1 but not DA receptors in rat brain. Clozapine also selectively increases activity of NA neurons and metabolic turnover in NA more than DA areas of rat brain, and also increases NA, but not DA or 5-HT, metabolites in human CSF. Potential psychotropic effects of selective central antiadrenergic agents may deserve reconsideration.

Within the context of marked increases in suicide rates in the UK among men between 1974 and 1988, the rate among those aged 15–24 years rose more than that of any other age band. The UK suicide rate among young men also worsened compared with those of most other countries in the EC. Rises in the general male suicide rate were statistically associated with rises in unemployment in most of the EC.

The range of interventions available for the treatment of erectile failure has increased in the past ten years. A significant development is intracavernosal injection of vasoactive drugs, but this treatment is far from ideal. Other, less invasive, pharmacological interventions are being investigated; as yet, none of these appear effective enough to have any significant clinical impact. External vacuum devices are a viable option for some patients, and penile prostheses have become increasingly sophisticated, although research examining their benefits has not. The range of available treatment methods and the growing complexity of the assessment for erectile problems demands an eclecticism of approach which can best be provided by multidisciplinary clinics specialising in sexual dysfunctions.

Fluctuating asymmetry provides a measure of an organism's capacity to buffer adverse factors that could disturb its development. It is estimated from the differences between theoretically identical right- and left-sided structures. Dermatoglyphic fluctuating asymmetry has been recently used to investigate developmental disorders. Fingerprints and palm prints of schizophrenic patients, which had been the subjects of an earlier report of conventional dermatoglyphic trait frequencies, were reanalysed to determine their level of fluctuating asymmetry. A review of the diagnostic protocols and clinical records used in the original study indicated that most of the 482 subjects would have met DSM–III–R criteria for schizophrenia. The schizophrenic sample had significantly higher levels of fluctuating asymmetry on four dermatoglyphic traits, the finger-ridge counts, fingerprint patterns, the palmar atd angles and palmar a-b ridge counts, than controls. This finding supports the results of two earlier studies, and its relevance to the roles of genetics, foetal insults, and developmental anomalies of the brain in the aetiology of schizophrenia is discussed.

The fragile-X syndrome accounts for up to 10% of individuals with mental handicap, and 50% of cases of X-linked mental retardation. Knowledge of the genetic basis of mental functioning, psychopathology, and neuropsychology is being furthered by this recently recognised condition. The disorder has considerable significance for psychiatrists, particularly, but by no means exclusively, those working in the field of mental handicap and with children. This review outlines the slow clarification of this complex and important behavioural phenotype and the implications of these advances for identification, diagnosis, genetic counselling and a wide range of management interventions.

Clozapine's clinical profile is unique among antipsychotic drugs. What makes it different? For almost two decades researchers have been attempting to answer this question. Based on various data, many hypotheses have been proposed. Using electrophysiological techniques we have found that clozapine, like typical antipsychotic drugs, inactivates most midbrain dopamine cells secondary to the induction of depolarisation block. However, unlike classical antipsychotic drugs, clozapine does not inactivate the nigrostriatal dopamine system. Based on these and other findings the hypothesis of ‘depolarisation block‘ is reviewed and presented as an explanation for clozapine's unique clinical profile. Research data both for and against the hypothesis are then discussed.

The pituitary—adrenal axis participates in the diurnal response of the organism to the environment and in its response to stress. Circulating glucocorticoid and mineralocorticoid hormones act on cells in the brain via Type I and Type II receptors, which operate at the level of gene regulation, and mediate various feedback effects of adrenal steroids on brain chemistry and structure, including the operation of second-messenger generating systems, levels of structural proteins of glial cells, and the death and survival of neurons. The hippocampus is prominent in these effects, and it also displays the highest level of Type I receptors of any brain region. New concepts point to a special role of the hippocampus, a nexus of cognition and emotion, in the feedback actions of adrenal steroids during the diurnal rhythm, and in response to stress. The hippocampus is, therefore, a prime target area for investigation of the events which accompany stress, and which may be related to the maladaptive state that results in depressive illness. Initial studies are described which investigate the effects of tianeptine on pituitary—adrenal function, hippocampal morphology and Type I and Type II receptor levels.

General practitioners were trained in the recognition and treatment of suicide risk either by written text alone or combined with a seminar meeting. They filled in questionnaires before and after training. In the seminar group, knowledge and attitudes changed significantly, while those doctors receiving written material only had similar results to those without training.

Expressed emotion (EE) has substantial scientific support as a predictor of relapse of positive symptoms. The median relapse rate in a high-EE environment is 48%, compared with 21% in a low-EE environment. This effect does not seem to be due to confounding with other variables, but it is subject to limitations in its scope of application. EE probably determines relapse through its effect on emotions and symptom control. A stress-vulnerability model of relapse is advanced that incorporates biological factors as well as cycles of mutual influence between symptomatic behaviour, life events, and EE. Aversive types of behaviour in patients and their relatives are seen as understandable reactions to stress that are moderated by social perceptions and coping skills. Families have made positive achievements, including the provision of non-invasive support.

Positron emission tomography was used to study the relationship between rCBF and symptom profiles in 30 schizophrenic patients. Factor analysis confirmed that the symptoms segregated into three syndromes – psychomotor poverty, disorganisation, and reality distortion – described previously. Analysis of the correlations between syndrome scores and rCBF revealed that each syndrome was associated with a specific pattern of perfusion in paralimbic and association cortex, and in related subcortical nuclei. The study confirmed predictions that psychomotor poverty and disorganisation are associated with altered perfusion at different loci in the pre-frontal cortex, and reality distortion with altered perfusion in the medial temporal lobe. The perfusion patterns suggest that the abnormalities of brain function underlying each of the three syndromes are not confined to single loci, but involve distributed neuronal networks.

The profile and prevalence of a syndrome of somaticised anxiety associated with education in Africa was explored by survey of 2040 senior secondary school students in different types of school: rural, urban, and elite. Response to two different screening methods, an open question to elicit symptoms spontaneously, and the SRQ-24, was compared. Symptom prevalence was higher in rural schools, 34%, than periurban, 22%, and elite, 6%, but the central urban school serving a shanty town was also high at 35%. Three categories of the culturally relevant symptoms were identified - somatic, cognitive and ‘spiritual’ - with affective symptoms sparsely represented in the cultural idiom. The SRQ-24 items screening for psychosis were associated with a range of spontaneous symptoms representing anxiety. This ‘spiritual’ expression of neurosis reflects the world views and beliefs of the culture. Intensification under stress could produce the picture of transient reactive psychosis.

Clozapine has an affinity for the dopamine (DA) D2 receptor which is relatively weak but is in line with its average clinical dose when compared with typical neuroleptic drugs. A few atypical antipsychotic drugs may have high absolute affinities for the D2 receptor, but most are weak D2 blockers. The atypical antipsychotic drugs also differ from the typical antipsychotic drugs by a relatively high affinity for the serotonin (5-HT2) receptor. This is evident on both in vitro and in vivo binding to cortical 5-HT2 receptors. The atypical antipsychotics are best distinguished from the typical antipsychotics on the basis of the relationship between strong 5-HT2 and weak D2 affinities. High D1 receptor binding is not characteristic of the group of atypical drugs. A new group of putative atypical antipsychotic drugs with high affinities for 5-HT2 compared to D2 receptors is under study.

Thirty-four schizophrenic patients in an acute in-patient hospital were compared with 24 in-patients with major affective disorder and 19 non-patient controls on a role-play test of social skills and a test of affect perception. The role-play test consisted of 12 simulated conversations in which the subject was confronted by parents and friends expressing high-EE criticism or non-critical dissatisfaction. Schizophrenic patients lacked assertiveness and social skills in all conditions, but they did not show any differential impairment when presented with high EE. They consistently lied and denied errors rather than responding assertively or apologising, whether confronted with high-EE or benign criticisms. On the affect perception test, schizophrenic patients consistently underestimated the intensity or negativeness of negative emotions, but they were not deficient in perception of positive emotional displays. The data do not support the hypothesis that schizophrenic patients are poor at dealing with high-EE behaviours, but do indicate that their ability to cope with even mild negative affect is impaired. Possible explanations for this impairment include limited attentional capacity, a neurologically based perceptual deficit, and a self-protective mechanism to reduce or avoid stress.

The practice of ECT has been surveyed by visits to all 35 NHS hospitals and five private clinics where it is used in the North East Thames and East Anglian Regions, and observation of ECT administration in 29 NHS and two private clinics. Since 1981 there has been much improvement in the physical conditions in which ECT is given and in anaesthetic practice. Nursing is good or excellent in a majority. About half the clinics have the most effective Ectron constant-current series 5 apparatus; the rest have older models with which ‘missed’ fits and undertreatment are frequent. Stimulus-dosing is usually by habit rather than rational strategy, and routine instrument settings differ fourfold between clinics. Most hospitals have nominated consultants in charge of ECT, but few of these are closely involved and little has changed in the unsatisfactory training and supervision of those who give the treatment. The use of ECT has fallen by 55% in North East Thames Region since 1979, but has risen by 20% in the East Anglian Region. There are up to 12–fold differences in usage between districts.

The psychiatric status of 70 homeless women from two direct-access hostels in inner-London was assessed. Detailed sociodemographic, psychiatric and physical illness data were also collected, and where possible, verified from psychiatric and general hospital sources. Forty-five women met DSM–III–R criteria for schizophrenia, but few were in contact with the psychiatric services or in receipt of any treatment.