A one-sided approach to any question, which is always suspect, becomes a very real danger when it concerns medicine. It is the purpose of this paper to draw attention to certain half-truths which have arisen in this way in connection with fear. Fear, like pain, is a danger-signal, called into existence to draw to the individual's notice the presence of some threat to his welfare. It has, therefore, ultimately a protective purpose with a direct relation to self-preservation.

Since the passing of the Mental Treatment Act of 1930 the use made of Section 5, dealing with temporary treatment without certification, has varied considerably in different areas, and has, in general, been much less than had been hoped for. In a discussion of this section of the Act held at a quarterly meeting of the Royal Medico-Psychological Association on November 20, 1934, Sir Hubert Bond stated that, while in the opinion of the Board of Control temporary patients should form 15% of the admissions to a mental hospital, in 1933 the proportion of such patients to total admissions was 6·5% in registered hospitals and licensed houses, and only 1·8% in the public mental hospitals.

The improvement of general paralysis by treatment with malaria is known to be accompanied by—and may be said to be due to—the disappearance of the spirochætes from the brain. The problem of the mode of action of this therapy therefore is centred in the question to what factor the antispirochætal effect of malaria is due.

One of the greatest problems facing the psychiatrist of to-day is the ætiology of schizophrenia, particularly that of the catatonic variety. Our ignorance in this respect is reflected by the number of hypotheses which have been put forward by the various schools of thought. It would be a task beyond the scope of this paper to attempt to summarize or criticize these theories, but for the sake of clarity a brief survey may here be made. The ætiological hypotheses fall into three main groups:

The observations I wish to make in this paper are based upon some work which my colleagues at Cardiff and I have carried out, and which has a bearing on the question of prognosis in the manic-depressive psychoses.

This series of investigations originated in a study of the Necker cube. It has been suggested that the fluctuation-rate of this and similar ambiguous bodies will serve to differentiate between the introvert and the extravert. While this assertion was being investigated, it was found that those patients who were depressed showed a slow fluctuation-rate. It was decided to investigate the question whether or not the fluctuation varied with the degree of depression. Since the fluctuation-rate is known to vary considerably from person to person, it was decided to study a group of depressives over a long period of time, if possible until recovery. The stability of the fluctuation-rate in the same person from day to day is considerable. Guilford and Braby report a coefficient of reliability of ·96.

The theme of this essay is not new. It is humbly suggested that the method involved in it, while not original, is not usual. We have employed no original technique and formulated no new doctrine. We claim to have approached the subject in the appropriate, inevitably laborious fashion.

Carriers of the enteric group of organisms are apt to be a source of some administrative difficulty in mental hospitals. The Infectious Diseases Sub-Committee have therefore attempted to estimate the value of cholecystectomy in this condition.

The objects of this paper are twofold: they are, on the one hand, to give a straightforward description of psycho-therapeutic procedure for those who are unfamiliar with its more technical aspects, and, on the other, to discuss specific problems which have arisen in the course of clinical work, and which might be of interest to other therapists.

The problem of the relationship of the endocrine system to personality and its disorders has long been an intriguing one. The literature abounds with the views of the psychiatrist, physiologist, pathologist and endocrinologist, and still there remains a multitude of challenging questions unanswered. The ætiology of personality disorders, that of the psychoses, and the true function of the endocrines and their working mechanism have never been satisfactorily determined. To establish scientifically any ætiological factor in medicine one must make a definite diagnosis of the entity, identify the ætiological factor, the specific pathological picture, and the influence of specific therapy.

The somatic symptoms found in anxiety states are referable mainly to imbalance of the autonomic nervous system; correction of this imbalance might theoretically be expected to improve the patient's condition. It is almost impossible accurately to assess the autonomic status of any patient, but subjective and objective clinical data together with pharmaco-dynamic reactions, reflex reactions and sugar-tolerance curves collectively represent a sufficiently comprehensive picture to justify some conclusions being drawn as to the state of the patient's autonomic nervous system.

Originally used to describe any case of dementia with chronic excitement, the term “chronic mania” has been limited in its application to a group of cases described by Schott and others during this century. In the main, they apply it to cases of mania developed after the age of 40, and differing from an acute attack chiefly in their long duration. In the cases I describe I have confined myself to this usage, and have not included constitutional fluctuating hypomanics who have manifested this after their youth onwards, nor do I include prolonged manic phases in circular manic-depressive cases.

The contractile response of the anterior abdominal wall to the stimulus of a scratch or stroke has become an observation of great value in the routine examination of the nervous system.

It was in 1923 that J. Capgras (1) first described the syndrome of non-recognition which has since come to be associated with his name.

Investigations into the possible causes of toxic symptoms arising during the course of prolonged somnifaine narcosis showed that a fall in serum calcium occurred during the course of the treatment (1). Previous investigations on blood calcium (3, 4, 5, 6, 15) made it clear that during barbiturate narcosis there was a fall of 10–20% of the normal value. Observations, however (7, 8, 9, 10), that therapeutic exhibition of insulin resulted in an increase in serum calcium suggested that no gross abnormality in calcium level was to be expected during the modified somnifaine-insulin-glucose treatment (2) practised in this hospital. The investigations here reported were undertaken to determine what fall in serum calcium occurred during this modified treatment, and to determine whether this fall was sufficient to cause toxic symptoms. If so the advisability of taking steps to avoid them could then be considered. The investigations showed a definite lowering in serum calcium during the course of treatment of psychotic patients by this method, and they suggested that somnifaine and insulin are only pseudo-antagonistic in their effect upon calcium metabolism. In the ten cases reported, a fall in serum calcium of from 3–20% has invariably been observed, the maximum being reached four to seven days after the beginning of the treatment.

The investigations on which is based the form of therapy presented in this paper being partly several years old, and partly published in Scandinavian languages, it will be of advantage to review them briefly.