Attention was first drawn to the importance of this topic by Schneider (1957) when he proposed that some of his first-rank symptoms could be grouped together under the concept of ‘permeability’ of the barrier between the individual and his/her environment — the ‘loss of ego boundaries’. Similarly, in a recent series of papers (Strauss et al, 1987), the essence of schizophrenia was conceptualised in the processes of interaction between biology, behaviour, and environment. The two main syndromes — acute and chronic — can each be precipitated or made worse by environmental factors, and although most patients with the negative syndrome appear to show some irreducible impairment, poverty of the social environment has been found to worsen their condition, while on the other hand, a moderate degree of social stimulation promotes relative improvement (Wing, 1987).

The hypothesis of a neurodevelopmental aetiology of manic-depressive psychosis and schizophrenia is based on the relation between onset of puberty and the final regressive events in the central nervous system (elimination of 40% of neuronal synapses), and the discrepancy in body build in the two disorders which is similar to that between early- and late-maturing individuals. The marked rise in manic–depressive psychoses and decline in schizophrenia, particularly the non-paranoid categories, accompanying the decline in mean pubertal age by some four years during the past hundred years are taken as evidence that manic–depressive psychosis affects early maturers and schizophrenia particularly affects late maturers. Gender differences and social differentials accord with this theory. Redundancy of neuronal synapses characterises manic-depressive psychosis, and reduced density of synapses is a characteristic of schizophrenia, whereas ‘normality’, with optimal synaptic density, is in between.

Of five patients with pervasive developmental disorders (PDDs), four developed psychotic illnesses in adult life. The other was treated with antipsychotic medication for many years following a mistaken diagnosis of schizophrenia.

Musical hallucinations had caused an 86-year-old deaf woman to become anxious and depressed. She was admitted, and tranquillising and hypnotic drugs afforded some slight improvement. The use of her hearing aid to increase ambient noise levels reduced the intensity of the hallucinations, and the patient improved.

Twenty Asian psychiatric patients suffering from neurotic illness completed the Urdu version of the HAD Scale. The results were compared with the Clinical Interview Schedule. Somatic symptoms were significantly related to various measures of anxiety but not to those of depression. This finding contradicts the previously held view of linking somatic symptoms with the presentation of depression.

Aggression and anxiety are among the most common phenomena needing medical control, especially in acute mental disorders. Today we can choose from a confusingly large array of drugs which can quickly control these two kinds of emotional and behavioural disorders. Everyday practice shows that these two groups of symptoms, seemingly so different from one another, can be treated with the same drugs. If we probe more deeply into the matter, we find that the similarities in these effects include not only inhibition of aggressiveness and anxiety but also their enhancement, activation, and provocation. These effects seem to form a regular pattern: those that increase aggressiveness (sympathicomimetics, catecholamines, ‘activating’ antidepressants, psychostimulants, and anti-Parkinsonics (cholinolytics)) also tend to increase anxiety, while those that decrease aggressiveness (beta-blockers, neuroleptics (major tranquillisers), ‘sedative’ antidepressants, minor tranquilisers, hypnotics, analgesics, and anticonvulsants) also tend to decrease anxiety.

Before a drug trial, researchers reasonably plan that participants will remain ignorant of which drug each patient is taking, reflected in the use of allegedly identical preparations. However, only rarely is this plan subjected to systematic scrutiny after the event, and our point of view is that this is unsatisfactory.

The research question of which mediating factors influence the long-term course of schizophrenia was not asked until recently because the expectation has been of uniformly poor outcome (Kraepelin, 1902; American Psychiatric Association, 1980). However, anecdotal clinical knowledge about heterogeneity in the long-term course of this severe illness has been firmly supported in the last 15 years by six recent longitudinal studies in Europe, Asia, and the USA (Blueler, 1972; Ciompi & Müller, 1976; Huber et al, 1979; Tsuang et al, 1979; Harding et al, 19876; Ogawa et al, 1987). Each of these studies, more methodologically rigorous than those of the past, has found multiple indices of wide heterogeneity in the long-term outcome of schizophrenia with trends toward significant improvement or recovery demonstrated in over half of each cohort.

The Psychological Impairments Rating Schedule (PIRS) was originally designed by the WHO (Jablensky, 1978; see also Biehl et al this volume) and was used as a supplement to the Present State Examination (PSE) (Wing et al, 1974) in a number of collaborative WHO studies. It was mainly designed for assessing selected areas of psychological and behavioural impairments (or deficits) in patients who have suffered, or are suffering, from functional psychotic disorders. It comprised items and scales for rating observed behaviour and was filled in immediately or soon after a psychiatric or PSE interview. Raters were encouraged to take note of a subject's current behaviour and function both before and after the interview proper. The first two sections of PIRS included all behavioural items of PSE (ninth edition). Sections 18–20 as well as a number of items taken from other psychopathological rating scales and items formulated de novo.

Trichotillomania is reported in a 33-year-old female victim of incest, with a possible causal connection.

Epileptic automatism and violence are seldom found among temporal lobe epileptics. The case of a 19-year-old girl who killed a 20-month-old child during an epileptic attack is described, and the literature and medico-legal issues are briefly reviewed.

A number of recent studies (Leff & Vaughn, 1985; Nuechterlein et al, 1986; Jenkins et al, 1986; Mintz et al, 1987) have indicated that attitudes of family members towards a relative with schizophrenia (termed High Epressed Emotion (EE)), are predictive of the short-term course of the patient's disorder. The measure used to define EE status of a relative is a semi-structured interview, the Camberwell Family Interview (CFI) (Vaughn & Leff, 1976), which is usually administered shortly after the patient is admitted to hospital for an index episode of the disorder.

The case of a man presenting with paedophilia who has found to be hyperprolactinaemic is described. There is possibly a link between paedophilia and endocrine disorders.

An evaluation of 15 patients treated by subcaudate stereotactic tractotomy (SST) for treatment-resistant unipolar affective disorder was made for frequency and severity of recurrence of illness. One-third had died by the time of assessment, but none by suicide. Two-thirds of the sample experienced a reduction in the severity of depressive episodes after the operation; only one-third reported a reduction in frequency of episodes.

A 39-year-old man had his pathological jealousy successfully treated with pimozide. It is suggested that pimozide might be considered the drug of choice in all the monodelusional disorders.

Consider:

1. (i) the most striking characteristics of the subject in general appearance and gait;

2. (ii) conforming to social routines and conventions;

3. (iii) physical appearance;

4. (iv) skills in presenting a favourable façade of own personality and concealing unfavourable aspects.

“A study was conducted to investigate a novel approach to the prophylaxis of schizophrenic relapse. The treatment strategy comprised brief intermittent courses of neuroleptic agents begun as soon as non-psychotic symptoms believed to be early signs of relapse appeared. Fifty four stable, remitted outpatients meeting the American Psychiatric Association's DSM–III criteria for schizophrenia were randomised double blind to receive brief intermittent treatment with either active or placebo depot neuroleptic injections. Only three patients given placebo injections and two controls were admitted to hospital during one year of follow up. Eight (30%) of the patients given placebo injections and only 2 (7%) of the controls, however, had a recurrence of schizophrenic symptoms. Patients given placebo injections experienced fewer extrapyramidal side effects and showed a trend towards a reduction in tardive dyskinesia. Dysphoric and neurotic symptoms were identified before eight out of 11 relapses, and these symptoms were more frequent in patients given placebo depot injections. These results suggest a viable but not necessarily better alternative to continuous oral or depot treatment for less ill, chronic, stabilised schizophrenics based on the early treatment of putative prodromal symptoms of relapse.”

Three schizophrenic patients who had transient recurrence of auditory hallucinations during acute dystonia precipitated by neuroleptic medication are reported. If it is accepted that psychotic symptoms result from dopaminergic overactivity, such phenomena suggest that acute dystonia might also have been caused by increased dopaminergic neurotransmission in these cases.

An individual with agenesis of the corpus callosum associated with recurrent severe sweating and hypothermia developed a social phobia. Phobias may be adaptations to real and potentially dangerous physiological events.