Jaspers (1946) has pointed out that in the history of psychiatry one can distinguish two main types of psychiatrist. On the one hand there is the describer who depicts a lively clear clinical picture and communicates it to the reader in everyday speech. On the other hand there is the analyst who dissects the clinical picture and tries to obtain clear concepts about the abnormal phenomena. The describer is always popular because little effort is required to understand his views and appreciate his clinical descriptions. However it is much more difficult to understand the analyst as this requires time-consuming preparatory work and an attempt to apply the analyst's views in practice. Thus anyone who wishes to understand the views of Kleist and Leonhard, who are the modern representatives of the great clinical analyst Carl Wernicke, has a difficult task. If therefore this present communication appears to disagree with other work recently published by the author (Fish, 1957b, 1958) then all that can be said in extenuation is that the analysis of clinical pictures is difficult and one can only achieve accuracy in this field by learning from mistakes.

This paper describes an inquiry into the effects of giving oral doses of the narcotic drug variously known as hashish, marihuana and, in South Africa, dagga. The drug is a preparation from the plant Cannabis sativa whose narcotic effect has been known for centuries. The writer's interest in it was inspired by the work in recent years on the mental disturbances produced by the active principles of other plants, e.g. mescaline and lysergic acid. Because of the similarity of these changes to those occurring in conditions such as schizophrenia, some workers have suggested that these “model psychoses” could be used as a research tool in attempts to elucidate the mechanisms and causes of the naturally occurring psychoses. Although there has been a great deal of work on mescaline and lysergic acid, cannabis has not received much attention. This may be because its chemistry is still not fully worked out and preparations of the plant are difficult to standardize and vary in their potency.

The aim of this paper is to show how, in our view, the diagnosis of Pick's pre-senile dementia can be made in some cases during life on clinical grounds alone.

The controlled study of the major physical treatments in schizophrenia (and other psychiatric conditions) has been retarded by the view that it is unethical to withhold treatment from the patient. Although this argument is clearly dubious until a treatment is proved, the number of forward-looking controlled studies of E.C.T., insulin coma therapy and leucotomy may nevertheless be counted on the fingers of two hands. Not all schizophrenics have, however, received every possible treatment, and if it were possible to make comparisons of treated and untreated cases retrospectively, there would be no ethical objection to overcome.

This paper summarizes the main findings of two years' ethno-psychiatric field-work carried out in N.W. Ashanti throughout 1956 and 1957, and later to be published in full detail.

The picture surrounding the rural field-worker is essentially different from that seen by psychiatrists in mental hospitals. In rural districts only homicidal patients are ever referred to a mental hospital, and then only from the police-magistrate's court. All other mental illness is regarded as super-naturally determined and hence outside the province of European medicine.

The increasing importance of properly controlled drug trials in modern medicine has shown the need for further study of the “placebo response” and the effects of “suggestion”, particularly in the evaluation of the results of treatment of the psychoneuroses. Much of the work on the response to placebos has been done on their deleterious side-effects, i.e., the production of symptoms of various kinds, but some recent investigations have clearly demonstrated the amelioration of symptoms by the administration of placebo.

Of all the tranquillizers, it may well be said that benactyzine has had the most chequered history. After its synthesis, a series of most careful experiments on animals demonstrated its ability to reduce or modify behaviour induced by stress. The first clinical trial gave rise to high hopes of its value in treatment but as further trials, more carefully designed, were made the results became increasingly inconclusive.

The assessment of the results of a treatment in any particular disorder is generally a very complicated one, by reason of the fact that the treatment does not usually improve all the manifestations of the disorder, and even when it does so, it does not affect them equally. The case of thyroid medication, which completely eliminates all the manifestations of thyroid deficiency, is an unusual one in medicine. Even where the pathological process may be completely stopped, as in general paresis and pulmonary tuberculosis, the patient may be left with residual loss of function due to irrevocable loss of normal tissue. In some cases the treatment itself may be of such a nature that the patient merely exchanges one disability for another. For example, the treatment of mild diabetes mellitus by a reducing diet may indeed eliminate the diabetes, but only at the cost of replacing it by chronic hunger and social restrictions, which many patients feel are worse than the original disease. In the end, they may give up their treatment. In some cases, the treatment has “complications”, which means to the patient that he merely exchanges one set of symptoms for another. For example, he may exchange the symptoms of duodenal ulcer for those of dumping syndrome.

At a recent court case (40), the plaintiff, who sustained bilateral acetabular fractures following unmodified electroplexy, maintained that the defendants were guilty of negligence by failing to use relaxant drugs to prevent the risks of injury.

In a recent investigation the present author has shown that glucose tolerance (G.T.) was significantly lower in a group of middle-aged mental hospital patients suffering from severe depression, than in a non-psychiatric group of similar age distribution (Pryce, 1958). This observation is similar to many others reported earlier (see review by McFarland and Goldstein, 1939). The cause of this impairment of G.T. is unknown; it cannot be explained by defective absorption of glucose from the alimentary canal since an intravenous G.T. test was employed in the investigation mentioned. Again, defective dietary intake during the days before testing could have contributed to the decreased G.T. in only a few cases; there was also no correlation between G.T. and either general symptomatology or the patients' behaviour during testing. However, it was observed that the group of depressions weighed significantly less than the control group, though again no correlation was found between body weight and G.T. among the depressions themselves. McCowan and Quastel (1931) and others have reported a close parallel between decreased G.T. and “emotional tension”, evidence which favours an emotional cause for the phenomenon, in line with the theories of W. B. Cannon (1911).

In a previous study (Kornetsky, Humphries and Evarts, 1957) it was found that the impairment of a variety of psychological processes caused by 200 mg. of chlorpromazine was not significantly less than the impairment produced by 200 mg. of secobarbital. It was also shown that the effects of drugs on psychological performance in man are related not only to the specific pharmacological activity of the drug, but also to the specific reactivity of the subject. It appeared that there was something unique to the individual which accounted for a significant portion of the effect of a drug. The present study was designed to extend these observations by reducing the number of drugs tested (in the previous study four drugs were used) and increasing the number of times a subject received each drug. It was hoped that this would give a better estimate of the effect of a specific dose of a specific drug and thus decrease the error of measurement and increase the reliability of the correlation between drugs.

There is hardly any field of natural science where development is so erratic as that of the physiology of the brain. It is true that perhaps no branch of science develops quite evenly. Very often the domination of old and deeply-rooted theories is so strong that they cannot easily be removed under the pressure of new facts, and consequently they may hamper the progress of science in the given field for many years. But generally the development of natural science is straightforward in the sense that its every stage is a logical consequence of the previous stages, and that particular lines of investigation tend to complement each other and eventually to merge into a single whole.

In a previous study of the efficacy of a vitamin-preparation (Krawiecki, Couper and Walton, 1957), the Wechsler Memory Scale Form I (1945) was administered on four occasions to each senile psychotic patient in the trial. Although the experiment produced interesting therapeutic results the present paper is not concerned with these but rather with the diagnostic and predictive implications of the Memory Scale changes.

In a previous paper the results of a two-year follow-up study were reported (Walton, 1958). This study showed that when the Wechsler Memory Scale was administered four times to each patient of a series suffering from a memory defect, significant differences emerged between those patients subsequently diagnosed as brain-damaged or as non-brain-damaged, in respect of the degree of improvement in their performance. The results were of considerable diagnostic and predictive importance. In spite of this, however, the method would be an uneconomical method for routine diagnosis. A shorter test involving the same principle of successive opportunities to learn appeared necessary. Additional analysis of the final Memory Scale results also showed that present learning ability was more impaired in the organic group than in the non-brain-damaged group, whilst scores based on retentivity questions produced many misclassifications. The results strongly suggested that a test of dementia should consist of a measure of present learning ability and that opportunities to learn could best be provided by successive repetitions of the particular test.

It has been clinically observed that psychiatric patients in general (6, 11) and schizophrenic patients in particular (1, 4) show abnormalities of mental speed, being “retarded” or slower than normals on many measures. Confirmatory evidence on this point is to be found but much of the early work on speed of schizophrenic reactivity used measures of speed of motor performance (12, 13) or of reaction time under various conditions (6), ignoring more fundamental slowness of thought processes. The present studies are concentrated on the recent finding that schizophrenics show abnormally slow mental speed measured in a problem-solving situation (4, 18, 19). The aim of the investigation was to discover the exact conditions under which this abnormality appears, and, thence, by manipulating the experimental conditions, to be able to bring speed of mental functioning under experimental control. This paper describes the attempt to bring speed under control by means of drugs. A second paper (2) deals with the effect of practice upon mental speed.

In this paper, a further examination is made of the finding that schizophrenics, given a problem-solving task to measure mental speed, showed marked improvements attributable to practice (4).

Preliminary investigation suggested the importance of the effects of both practice and drugs on speed of problem solving. The latter is reported elsewhere (4). There appears in the literature to be agreement that marked improvement is shown by schizophrenic patients after practice, but Huston and Shakow (11, 12) for example, give evidence that this improvement is even more marked for schizophrenics than it is for normals while Hunt and Cofer (9) report the contrary. Huston and Shakow also raise the question of whether or not it is possible, by very extended practice, to bring the performance of schizophrenics to the level of perfection reached by normal subjects after practice. Clarification of these points is necessary.

Hyaluronidase, the “spreading factor” is widely used today to aid the distribution and absorption of fluids injected at various sites into body tissues. It is derived from the head of the male sperm cell which by its action dissolves hyaluronic acid in the “shell” surrounding the female egg cell and thereby allows spermal penetration and conception; generally speaking it dissolves the ground substance between cells. The most remarkable usage is in paediatrics where it allows for quick replacement of lost fluid and salt in gastro-enteritis, obviating the need to find veins, and thereby saving practically all cases from death by dehydration. There are many other uses.

A role in mental illness for an aberrant metabolism of indole compounds was first advanced some sixty years ago, when their alleged toxicity to the nervous system figured prominently in the then current theory of auto-intoxication by bacterial action in the bowel (Herter, 1898, 1907). Although in a modified form it continues to receive the support of Buscaino (1958), auto-intoxication of this nature is now generally rejected as a factor in mental illness (see particularly Alvarez, 1924) and the renewed interest in indoles and brain function of recent years has come from a different standpoint. Thus, study of the central nervous system effects of indoles such as 5-hydroxytryptamine (serotonin) and bufotenin, and of compounds containing an indole group such as lysergic acid and reserpine, has inspired several new theories concerning normal and abnormal roles for indoles in the brain (Woolley and Shaw, 1957; Brodie and Shore, 1957; Hoffer, 1957).

Two earlier studies (Venables and Tizard, 1956a, b) on the reaction time (RT) of schizophrenics have shown that as the intensity of a visual stimulus is increased beyond an optimum point, RT to the stimulus increases. This “paradoxical” increase in RT is not shown by normal subjects, whose RT decreases as the intensity of visual stimulus increases. It was also found that the paradoxical phenomenon with visual stimuli was only shown on an initial occasion of testing. When the experiment was repeated twenty-four hours later, although there was no alteration in the mean level of RT, the pattern of increase in RT with increasing intensity, previously found, was absent.