Nyasaland is a narrow strip of land 40,000 square miles in extent. It lies approximately between latitude S. 9’ 45” and 17’ 15”, and longitude E. 33’ and 36’. It is bounded on the North by Tanganyika Territory, on the East by Lake Nyasa and Portuguese East Africa, and on the West by Northern Rhodesia and Portuguese East Africa.

The material to be presented in this paper is based on the association-motor records of 100 normal controls and 297 psychiatric cases examined by this method during the past three and a half years. The procedure introduced by Luria (1) in 1932, and subsequently modified and adapted by us to meet the expediencies of everyday clinical practice, consists of Jung's word-association technique combined with motor activity.

In dealing with the question of visual impairment in cases of so-called constructional apraxia in a previous paper, I had occasion to discuss arguments put forward by Erich Feuchtwanger, who had proposed to abandon the term “apraxia” for this condition and to call the disturbance “agnosia”. My conclusion was in favour of the original concept of Kleist, who had put the ailment among the apractic syndromes. This, however, makes a detailed analysis of the motor activities and their disturbance in constructional apraxia necessary in order to define its place among the known kinds of apraxia.

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 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.

This case has shown so great an improvement by symptomatic treatment with parasympathetic stimulants and a sympathetic depressant that it seems worthy of record for its own value, apart from the interesting investigations to which it leads.

In the following paper a case of état dysmyélinisé of the globus pallidus, or as it is often synonymously called, “Hallervorden-Spatz disease”, will be presented. Records of thoroughly studied cases of this condition are still rather scanty and there is much need for a systematic extension of experience, the more so since, as Helfand (16, 17) has recently pointed out, progress in the elucidation of the condition has not always been enhanced by generalizations from findings based on too small a case-material. We are happy in having at our disposal the vast resources of the London County Mental Hospitals. It is hoped to follow up this paper by publishing further cases of a rather different nature, though with some characteristics in common with the case described here.

Since we do not yet know the real nature of Schilder's disease nor see a direct way of investigating it, research on this problem can usefully be carried out in two ways: (1) careful description of cases in all possible clinical and pathological detail, and (2) broad comparative studies. That collection of further case-material is still useful was shown, we hope, in the description of a family by one of us (A. M.) in collaboration with Tennent (24). In this family there was a pronounced tendency to gastro-intestinal troubles preceding the nervous symptoms, and the same has been reported by Globus and Strauss (15), Globus (14), and F. Bielschowsky (2). Too much importance must not be attached to such findings, as the onset of the disease just as often follows measles, influenza and other acute infectious conditions; and there is the striking familial taint of tuberculosis in the families described by Symonds (45) and van Bogaert and Scholz (47), and atrophy of the suprarenals was associated with the disease in the latest case reported by R. Pfister (29). The great variety of such preceding illnesses makes us rather chary of regarding them as of direct ætiological or pathogenic significance. It is, on the other hand, of the greatest importance to keep such occurrences carefully in mind, because we do not know yet what common pathogenic factor may lie hidden behind these various initial symptoms. As regards gastro-intestinal troubles, their significance in various avitaminous and other deficiency conditions is generally known, and they have been a very obvious initial symptom in the demyelinizing disease of monkeys, the histopathological kinship of which to Schilder's disease has already been shown in A. Meyer and Tennent's paper, and which will be discussed later in this contribution. This kinship appears to us to be closer than was recognized by Schob (35), Spielmeyer (42), Scherer (33), and Davison (9).