I am deeply conscious of the high honour which has been bestowed on me in having been granted the privilege of delivering this year's Maudsley Lecture. It is an honour which I value very highly, and I trust that the subject I have chosen for your consideration may prove in some degree worthy of the occasion.

Pelizaeus (1885) described a family of which five members exhibited a rather uniform clinical symptomatology, consisting of tremor of the head, nystagmus, spastic paraplegia, etc. He thought he was dealing with an atypical familial form of disseminated sclerosis. Twenty-five years later Merzbacher (1910) investigated the same family and found the symptoms in twelve members, representing four generations. Symptomatology and clinical course of the condition was, in all patients, approximately identical: onset within the first months of life, rapid progression within the first six years, slowing down later considerably, death after twenty to thirty years due to intercurrent disease. The symptoms were tremor of the head, nystagmus; later paraplegia, ataxia, visual and auditory disturbances, involuntary movements, etc. The emotional and intellectual sphere remained comparatively unimpaired. The heredity was found to be recessive: the mothers, though themselves spared by the disease, pass it on to their sons (though among the twelve cases of Merzbacher there were also two females). In the one case investigated histopathologically by Merzbacher a diffuse demyelinization was found, particularly marked within the occipital region, distributed symmetrically in both the hemispheres and characterized by the persistence of myelin islands, often around vessels, which gave the condition the appearance of a tiger's skin. Merzbacher thought he was dealing with an hereditary aplasia of axis cylinders and myelin fibres, and called the condition aplasia axialis extra-corticalis congenita.

The opportunity I have of speaking to you is for me both a pleasure and a privilege, but it is also, I fully appreciate, a responsibility.

The field of psychiatry to-day is not unfruitful and not a few discoveries of lasting worth appear to have been made, while certainly claims to progress of more doubtful value, both as regards letiology and even more with regard to treatment, are so numerous as to be rather bewildering, particularly when they become the subject of articles in the popular press, whereby relatives are enabled to make a diagnosis and decide on a line of treatment without any reference to the medical man.

Truant is an old French word meaning “vagrant”, and the term “truancy” means “unlawful absence”. The study of truancy in children is chiefly concerned with wandering, staying out from home, and staying away from, and refusing to go to school.

Ladies and Gentlemen,—I have to acknowledge with grateful appreciation the honour you have done me in electing me to the Presidency of this Section.

I recall that my immediate predecessor, in his learned address from this chair, deplored the slow progress of psychiatry in the last half century. He stressed the necessity for intensive research in many directions. As I listened to him I felt that there was one supreme need in psychiatry, and that need was the co-ordination of biological and psychological views. As it seems to me, we have an increasing volume of research proceeding on these two lines, yet the lines never seem to meet. The psychologists pour out an incessant stream of literature, equalled only by the joint efforts of histologists, biochemists, neurologists and the rest. But what psychopathologist would bring himself to refer to Alzheimer cells, or what biochemist could make mention of an Œdipus complex? Yet in some of our patients—perhaps in most, if not in' all—such factors co-exist. I venture to express the hope that during this session our discussions may elaborate the leitmotif of synergic ietiology.

The insulin treatment of schizophrenia has been practised at Hatton since June, 1937. The Vienna technique has been employed, with certain modifications described in a recent paper in this journal by Gillman and Parfitt.

From the use of insulin in the treatment of schizophrenia much has been learned about hypoglycæmia, but nevertheless the physiopathology of the subject remains obscure. The intricacies of the ætiology of hypoglycæmia are well illustrated by Martin and Hellmuth's (1) study of 404 patients uninfluenced by insulin. The blood sugar in the majority of these cases was found at some time to be below 70 mgrm. %, and only in about one-third was an organic basis ascertained. Only 9% had definite symptoms of hypoglycæmia, 71% were asymptomatic and 20% were suggestive. The blood-sugar levels at which symptoms occurred differed in different individuals. Those showing symptoms at comparatively high levels belonged mainly to a group described as “symptomatic functional hypoglycæmia “, and those showing symptoms at lower levels were mostly suffering from psychoneurotic disorders. Martin and Hellmuth consider that few of these cases should be diagnosed as suffering from “hyperinsulinism” as described by Seal Harris (2) and Ross and Josephs (3).

The concept of accident-proneness is by no means a new one; but the term has passed into popular use, and although the colloquial usage of the term is frequently incorrect, yet the idea that some people are more liable to sustain accidents than their more fortunate fellows is now widely accepted. Of late years psychologists have made it their business to inquire into the nature of this susceptibility to accidents, and have found that whilst mankind in general is characterized by this proneness, there are individual differences in the degree to which it is possessed. In any sufficiently large observational group it is usually found that most of the accidents are sustained by a minority of the members of that group, and it is obviously of importance to discover what are the personal qualities or lack of abilities which make this minority specially accident-prone.

On the subject of the correlation of neurological lesions with psycho-pathological phenomena, two eminent neuro-histologists, the Werthams, have recently written: “It must be pointed out that in proportion to the extraordinary complexity and differentiation of the finer functions mediated by the central nervous system, histological lesions are very gross. However we may conceive of the functional processes going on in the central nervous system—physiological, physico-chemical, metabolic, electrical, etc.—it should be obvious that only the grossest miscarriages and defects would become morphologically visible. Structural lesions are the effect of functional reactions that are not histologically demonstrable. Physico-chemical changes, metabolic processes, functional changes of blood-vessels, and similar biological phenomena that cannot be micro-histologically demonstrated, precede the anatomically visible lesions which occur only where the processes have attained a certain intensity. What we can demonstrate histologically in the nervous parenchyma is not by any means an adequate basis for the understanding of the quality, intensity or normality of nervous functions. In a patient who dies in the convulsions of tetanus, the anterior horn-cells may reveal nothing abnormal. Even the most minute and complete histological examination of the central nervous system in a case may fail to reveal any evidence of an existing profound disorder of brain function. There are cases of idiocy of the severest type in which no significant histological changes may be demonstrable in the brain.”

In any search for enteric carriers the patient with a positive blood-agglutination must be regarded as suspect. Earlier workers were of opinion that the converse of this was true—that a negative agglutination reaction implied that the case was not a carrier. It is true that McCowan and Mann (1925) described a series of nine carriers, of whom two showed a negative agglutination reaction during the clinical attack of typhoid fever, but the subsequent history of the agglutination reactions is not given. Ashby (1931) indicates in his series the prevailing belief that carriers show significant alterations in their agglutination reactions. Although repeatedly controverted in the medical literature by the publication of small groups of cases where the carrier state has been accompanied by negative blood-agglutination reactions, this view dies hard, and was revived during the recent discussions centring around the Croydon typhoid epidemic.