One of the problems in psychiatric epidemiology is the use of hospital admissions for the study of true morbidity. Clearly this depends upon whether hospitalized cases can be regarded as a representative sample, in other words if admission to hospital varies from one social group to another, from one region to another, etc. Various authors have shown that the duration of hospital stay varies with social status, with marital condition, etc., and such variations in the chances of being discharged suggest similar variations in the probability of being admitted.

The “archetype” is a concept of Jung's which is fairly widely accepted as a valuable one in spheres of art, literature and theology. Few psychiatrists seem to know much about the concept, and of the few who are interested in it, most find little relevance in it for their clinical work.

Toxoplasmosis is an infectious disease caused by a protozoal parasite of worldwide geographic distribution. The organism, Toxoplasma gondii, has been known since 1908, when it was demonstrated in the gondi, a North African rodent, by Nicolle and Manceaux and independently by Splendore in the rabbit in Brazil. Benda quotes Hellbrügge as mentioning that Toxoplasma apparently had been discovered in 1900 by Laveran, in the blood of a bird. It has since been found to be an infective agent in a great variety of species of rodents, mammals and birds from almost any part of the world, providing a large reservoir for human infection.

As Piercy (1959) has pointed out, it is generally agreed that currently available psychological tests for detecting brain damage (Yates, 1954; Meyer, 1957) or early dementia (Shapiro, 1952; Inglis, 1958) are by and large poorly standardized and poorly validated. If the clinical psychologist attempts such detection he can make very few positive statements if all he does is administer those standardized tests which even approximately meet the commonly accepted standards of validity.

Phenelzine, β-phenylethylhydrazine, of structural formula, is regarded as a potent, rapidly acting, long-lasting monoamine oxidase (M.A.O.) inhibitor. The administration of such compounds protects 5-hydroxytryptamine (serotonin) which is destroyed by M.A.O. 5-hydroxytryptamine is believed to act in the brain as a chemical mediator, the function of which is to control the pulsating action of oligodendroglial cells which supply the other brain tissues with nutrient. It has been suggested that a relative 5-hydroxytryptamine deficiency is the fundamental biochemical disorder of severe depressive states and that M.A.O. inhibitors such as phenelzine tend to promote restoration to more normal concentration and activity.

In conducting drug trials nowadays one is aware of at least some of the difficulties that have to be faced and the possible traps lying ahead. It is probably true to say that perfection is unattainable in trials of this nature because of the unpredictability of the human material concerned—both the tested and the observers sharing this common fallibility. It is necessary to attempt so to arrange the experiment that the magnitude of the errors is kept to a minimum and the results remain unobscured.

Addison (1855) in his classical description wrote of the patient's mind “as occasionally wandering” during the final stages of pernicious anaemia. The relative frequency with which different psychiatric syndromes present differs from that recorded by previous writers and is probably due to earlier psychiatric consultation in the present group, though mode of referral may also play a part. Bowman (1935) found organic confusion in 48 per cent., a death rate of 35 per cent. and a red blood cell count of below 4 0 million in 65 per cent. of his 23 cases. Herman, Most and Joliffe (1937) found organic confusion in 35 per cent. compared with the present writer's 5 per cent., a death rate of 22 · 5 per cent. compared with 10 per cent. and a red blood cell count of under 3 · 0 million in 75 per cent. of his 40 cases, compared with 25 per cent. of the present group.

I am glad that the Papers Committee has arranged today's meeting in order to give some emphasis to the international aspects of preventive psychiatry and work for mental health. Faced continually with the pressing needs of our own individual professional tasks, it is wise sometimes to raise our sights and look at some of the problems and activities of our neighbour countries in the world.

For various reasons we became interested in the possibility that nicotinic acid or nicotinamide might be of some benefit to the chronic schizophrenic. Many workers have noticed clinical similarities between the acute schizophrenias and the encephalopathies of nicotinic acid deficiency (4). Nicotinic acid is known to be of value in pellagra (2) and in the treatment of delirium tremens and allied states (1), and Osmond and Hoffer have had promising results with these substances in the treatment of schizophrenia in its acute phase (3). There seemed therefore to be sufficient reason for an investigation of their effects in the schizophrenic in the chronic phase, for, as far as we are aware, the therapeutic possibilities have not been explored. Since patients often respond strikingly to the giving of any tablet, regardless of its contents, we also gave similar tablets of an innocuous substance, here referred to as Placebo. For convenience the three preparations employed will be referred to in future as A (Nicotinic Acid), M (Nicotinamide) or P (Placebo).