1848, as every student of history knows, was a revolutionary year in Europe. During that year, a minor, long forgotten revolution occurred in London medical circles when a physician, John Elliotson, published a paper entitled ‘Cure of a true cancer of the female breast with mesmerism’ (Elliotson, 1848). It is, as far as I can ascertain, the first recorded case of its kind. The author hypnotized his patient, a 42-year-old single woman, for “5 years and upwards … and for the greater part of the period three times a day”; during that time, Elliotson observed a ‘cancerous tumour’ in her right breast shrink away completely. No less than seven physicians and surgeons independently attested to the diagnosis of breast cancer, but no pathological examination was carried out. Elliotson was roundly abused, not for using hypnosis to treat cancer, but for using hypnosis at all—a practice condemned by certain physicians of fervid imagination as “indecent, disgraceful … liable to excite lascivious passions … an infernal system … the workings of Satan” (Elliotson, 1848).

One hundred and sixteen patients with major depressive disorder were asked for details of headaches during a depressive episode and during a nondepressed period. They experienced a headache rate similar to controls during the nondepressed period, but had an increased headache rate during depression (P <.02). Patients with an increase in depressive headaches were younger, had more somatic complaints, and experienced more hypersomnia than other depressives.

The aetiological model proposed by Brown and Harris was examined in a sample of 110 working class women with children in Oxford. Using the same methodology as Brown and Harris, the role of provoking agents in the onset of affective disorder was found to be very similar to that which they originally described. Lack of an intimate relationship with a husband or boyfriend was found to act as a vulnerability factor, increasing the risk of psychiatric disorder in the face of a provoking agent. There was a trend for women with three or more children aged 14 or under to have an increased vulnerability. However, unemployment was not found to be a vulnerability factor. These results provide general support for Brown and Harris's causal model.

Forty male patients with bipolar affective illness were examined for factors correlating with dangerous inpatient behaviour. It was found that 63 per cent of the variance for inpatient assaults could be accounted for by a combination of a history of severe childhood discipline, a manic state, the degree of psychosis and a record of violence prior to admission. Such information may be of use in the clinical prediction of violent acts by bipolar patients, as well as suggesting ways of preventing them.

Three groups of 114 depressed patients admitted to hospital in Edinburgh, one in the year 1892, one in 1942–3 and one in 1981–2, were studied. The occurrence and content of depressive delusions were recorded. A significantly higher proportion of depressives had delusions in 1892 than in 1942–3, but there was no significant decline between 1942–3 and 1981–2. It is concluded that this decline in the proportion of depressives having delusions since 1892 probably does not reflect a genuine decline in the prevalence of depressive illness with delusions. The content of delusions differs between the years and between the sexes, and these differences are discussed.

All ‘new chronics' (N = 571), defined as patients aged 18–64 years in hospital more than one but less than six years, were identified in 14 psychiatric hospitals serving 56 per cent of the Scottish population. The bed occupancy was 20/100,000 of the general population (range between hospitals 12–29/100,000). First admissions (5.8 beds/100,000) were clearly distinguished from re-admissions. Although for the whole group schizophrenia was the most common diagnosis the majority of first admissions had organic brain disease. First admissions were more disabled and most were well placed in hospital. Thirty-eight per cent of all patients did not need inpatient care; 20 per cent could have been accommodated in staffed hostels. Widespread differences, especially in numbers, found between hospitals may have been due in part to different attitudes among staff towards the prospect of patients' discharge.

Family data from schizophrenic and control probands were analyzed using a descriptive analysis and multiple threshold models to determine whether a given group of diagnoses made in accordance with ICD–9 was aetiologically related to schizophrenia. The proportion of relatives receiving any psychiatric diagnosis, other than schizophrenia and affective disorder, was essentially the same between the two study groups. Furthermore, the data did not fit the multiple threshold model tested. Thus, the hypothesis that schizophrenia and a spectrum of disorders defined according to ICD–9 have a common familial aetiology was not accepted.

The cloze procedure was used to examine predictability in speech samples from schizophrenic, depressive, manic, schizoaffective and normal subjects. Each speech sample was also rated for particular indices of thought disorder using the Andreasen Scale for the Assessment of Thought, Language and Communication. Schizophrenics were found to be less predictable than other patient groups or normals. Depressives were found to be the most predictable. Correlational analyses of cloze scores and specific thought disorder ratings suggest that reduced predictability is associated with traditional indicators of thought disorder.

In this double-blind, four-week study, 28 chronic schizophrenic patients receiving neuroleptic medication plus the antiparkinsonian drug, benztropine mesylate, were either switched to placebo or maintained on benztropine. Patients withdrawn from benztropine reliably increased their overall scores on the Wechsler Memory Scale in comparison with the drug group. Sub-test scores suggest that deficits in attention and concentration were induced by treatment with benztropine. Psychotio decompensation appeared to develop simultaneously with extrapyramidal symptoms (EPS) in some patients, but only 14.2 per cent of the placebo group experienced extrapyramidal symptoms severe enough to require resumption of benztropine therapy. It is suggested that antiparkinsonian agents should be prescribed only if and when EPS occur.

This is an attempt to evaluate the results of planned changes on a long-stay rehabilitation ward in a traditional mental hospital in England. The ward was housing a mixture of groups of patients of differing types and needs. The results of our study suggest that it is possible to improve patient care and staff morale on similar wards without extra staff, money or structural changes. Good planning, collaborative teamwork and dedication were the main tools.

From a prospective study of tardive dyskinesia (TD), psychiatric patients with neuroleptically—induced “persistent” TD were contrasted with controls on a neuropsychological measure of abstracting ability. A significant association is demonstrated between impaired cognitive performance and TD, even when the neuropsychological measure was obtained in advance of TD onset.

Two hundred inpatients suffering from primary depressive illness were studied. Seventy eight of the patients were treated by electroconvulsive therapy (ECT) and 122 patients received antidepressant medication. Response to ECT and antidepressant medication at 4 weeks showed a curvilinear relationship to Newcastle scores. Patients with Newcastle scores in the middle range (4–8) showed significantly higher percentage improvement than those with low (0–3) and high (9–12) scores. Ninety five patients with unipolar depression who received lithium therapy for one year were also studied. Response to lithium showed a linear relationship to Newcastle scores in these patients. It is suggested that these differences in response to antidepressant therapies reflect the heterogeneity of depressive illness.

Two groups of normal volunteers had regional cerebral blood flow (rCBF) measured, by the 133Xenon inhalation technique, before and 30 minutes after 250 mg or 500 mg caffeine given orally. rCBF was measured in a third group of subjects, twice, at a similar interval under identical laboratory conditions. Subjects who received caffeine showed significant decreases in rCBF while the others showed no rCBF change from the first to the second measurement. However, the two caffeine groups did not differ in degrees of rCBF reduction. There were no regional variations in the post-caffeine decrease in cerebral blood flow. The three groups did not show significant changes in end-tidal carbon dioxide, pulse rate, blood pressure, forehead skin temperature and respiratory rate.

A treatment trial comparing cognitive therapy and pharmacotherapy, alone and in combination, in depressed out-patients, indicated that outcome on cognitive variables was similar to outcome on mood and severity measures, pharmacotherapy being less effective than cognitive therapy or the combined treatment in a hospital and a general practice sample. While combined treatment was superior to cognitive therapy in the hospital outpatients, the two treatments were equivalent in the general practice. Significant effects were obtained on measures of views of self, the world and the future, whose validity was demonstrated. The pattern of change through treatment showed the same order of progress for responders, while non-responders to cognitive therapy tended to do worst. The specificity of treatment effect is discussed.

Prolactin, Cortisol, growth hormone and TSH serum levels (before and 15 minutes after treatment) were measured in 62 patients with endogenous depression randomly allocated to real or pseudo-ECT. Prolactin increased significantly more in those receiving real ECT than in those receiving pseudo-ECT, but the size of this effect had diminished by the time of the last (8th) treatment in the trial. Cortisol secretion was also significantly increased following the first treatment by real ECT, but this increase was of significantly smaller size in patients with delusions. Tolerance to the effects of ECT on Cortisol secretion was not observed. No effects of ECT on growth hormone or TSH secretion were detected, and no clear evidence was obtained that endocrine responses can be used as a predictor of response to ECT.