There have been several inquiries into the incidence of various “neuropathic” conditions among the relatives of the mental defective, and it has been found that mental defectives often have relatives who have suffered from such conditions as cerebral hæmorrhage, epilepsy, alcoholism, etc. Thus it has been stated that 80% of mental defectives have a “positive” family history, and it is suggested that this figure (80%) supports the theory that most mental deficiency is due to hereditary factors. Before the significance of such a figure can be discussed we must first know the corresponding figure for the normal population.

The following account is based on the writer's experience of convulsion treatment at centres abroad, on a review of the literature up to the present date, and on three cases recently treated at West Park Hospital, Epsom. It is published at this early stage in order to make a knowledge of the technique and literature of a method which has already proved itself worthy of extensive trial, available to a larger number of workers in this country.

I appreciate very deeply the honour of being invited to deliver this the seventeenth Maudsley Memorial Lecture. I also feel the responsibility of adequately fulfilling a task so well carried out by my predecessors and so brilliantly initiated by Sir James Crichton-Browne. I never had the privilege of knowing Henry Maudsley, but Sir James's description of his fellow York-shireman as having “a dash of Wuthering Heights about him” illuminated him for me as by a flash of lightning. It has been said that his last book, Organic to Human, embodies his philosophy, which may be summed up in the principle of unity of the human organism and its continuity with the rest of Nature's processes. His Pathology of Mind also bears abundant testimony to his deep and life-long interest in the subject on which with some temerity I am venturing to address you. Whether I should have been rash enough to do so in his presence is another matter. I recall the fate of “a certain clergyman” whom Dr. Samuel Johnson blasted into silence by a single thunderbolt, and I fear that Dr. Henry Maudsley's keen and logical mind would pounce on some loose joints in my argument. So I crave your indulgence.

For many years it has been the policy of the London Authority to avoid the certification of patients directly from their own homes, by passing them through an observation ward before making a decision as to their disposal. The system originated partly from the fact that the London Mental Hospitals are some distance from town, and partly from the shortage of accommodation, it being necessary to secure the safe custody of the patients pending their admission. The small scattered wards have now been fused together to form larger and more efficient units, which ensure every case having the fullest consideration and investigation before deciding upon any method of disposal. The various points arising in this paper are illustrated by reference to the work of the largest of these units.

My address to you to-day consists of observations on a number of subjects connected with the care of the insane, which may be of interest to you either because they are specially associated with Scottish administration, or because of their topicality at the present time.

In 1929 Berger (1) discovered that changes of electrical potential in the human brain could be detected through the unopened skull. Since that time the study of electro-encephalography has occupied the attention of many workers, and the literature is already too extensive for adequate review in this place. A brief description of the technique for obtaining an electro-encephalogram, or “EEG”, and a summary of its normal and pathological characters may be found in a communication by one of us (2) on the relation between the EEG and the presence of intracranial neoplasms. The cortex in the region of a tumour was found to produce abnormally slow potential waves, which were provisionally called “delta” (δ) waves to distinguish them from the normal “alpha” (α) waves which are the original “Berger rhythm”. In the same paper a case was reported in which a focus of δ waves was found in the left parieto-occipital region associated with an area of degenerating cortex. The history in this case was of occasional minor attacks and one major fit and an indefinite severe illness in infancy, the only sign being a right homonymous hemianopia in accordance with the left-sided focus. Ether and nitrous oxide anæsthesia are also accompanied by the production of slow waves, but in this condition there is no fixed focus, the whole cortex being engaged in abnormal electrical activity. Since the publication of the above-mentioned results, a case of cerebral abscess has been examined, and the EEG was found to indicate a δ focus similar in character to those which have been found in cases of new growth.

Since the passing of the Mental Treatment Act, 1930, 30 patients have been admitted to St. Ebba's Hospital under Section 5, and it is proposed to analyse the type of case admitted, and to mention some of the difficulties encountered in treating patients on a temporary basis.

The title of this paper will suggest a number of problems which are still the subject of considerable controversy.

Thus, some authorities appear to uphold the general proposition that there is a fundamental and clear-cut distinction between all neuroses (or psychoneuroses) on the one hand, and all psychoses on the other.

Salm (1) has recently described stuporous conditions which developed in schizophrenic patients undergoing the insulin shock treatment. He concludes that such cases constitute a serious problem, because, if they do not yield to the repeated administration of sugar, one is at a loss in regard to specific treatment.

Prof. Golla, in introducing the discussion, said: I do not think there is any subject that is of greater importance at the present moment than the physiology and the pathology of the circulation of the central nervous system. I am dealing now with the physiology, with a view to putting a few facts before you which are fairly well authenticated, and pointing out how very little we know at present. I do not intend to speak of the pathological aspect, but I may remind you, in passing, of such things as the therapeutic effects of amytal and of CO2. Again, in the case of epilepsy, whatever one's ultimate view of epilepsy is, we are all agreed that circulatory disturbance plays a very large part.

The subject of the following record was a married man, aged 40, whose business had brought in an income of about £2,000 per annum. The onset of his illness dated from an accident which was said to have occurred about seven months before he was seen by us. According to the history obtained from the wife it appeared that as he was passing a building in course of erection a fairly large piece of iron fell from the scaffolding and struck him on the left side of the head. He did not fall, but picked up the piece of iron, walked into the building and interviewed the foreman. He then went home, his only complaint being of headache. The wife said she noticed a swelling on the scalp, but as there was no bleeding or wound she did not send for a doctor immediately. The patient was put to bed and is said to have been sick on two occasions. As he did not improve, he was taken, after six days, to the out-patients’ department of a general hospital, where the doctor who saw him attributed the condition to concussion. He was admitted four days later and remained for three weeks. The report from the hospital stated that the patient complained of headaches, became easily irritable and lost all power of control. He is said to have been sleepless, but no sickness had occurred. There was no mention of any external damage to the head, and X-ray examination of the skull revealed no injury. The blood Wassermann reaction was negative and the blood precipitation test was normal. No physical signs of disease were discovered. The wife stated that while in this hospital the patient chased one of the doctors down the stairs. Soon afterwards he ran away from the hospital, telephoned to his wife and was taken back by her, remaining a further week. He then returned home, and after a few days’ rest resumed work. He was unable to continue as he became excitable and irritable, and on one occasion “smashed his office up”. He was seen by his own doctor, who expressed the opinion that the accident had undoubtedly caused a hæmorrhage inside the skull, and that the clot so formed was responsible for the patient's mental disability. Ten days later he was examined by a distinguished neurologist, who also expressed the opinion that a blood tumour from bleeding within the membranes of the brain was the cause of the symptoms. The patient gradually lost interest in his work, stayed at home and spent most of the day in bed, preferring to be left alone. He became violent and on more than one occasion attacked his wife.

This paper is a preliminary report of some investigations we are now making into the pathology of mental deficiency, mainly from the histological point of view. We have so far examined 22 cases, comprising 7 low-grade defectives showing gross neurological lesions, chiefly of extrapyramidal character, 6 microcephalics with spastic diplegia and severe mental defect, 2 able-bodied microcephalics without gross neurological signs, 1 simple able-bodied idiot and 6 mongols. In this short paper it is impossible to give even the slightest indication of the wealth of pathological material found in such a variety of widely differing conditions. A full description of our findings, together with a more detailed discussion, must be left to further papers dealing with individual groups of cases. The purpose of making a short note at this stage is to draw attention to one particular finding which struck us by its surprising constancy, i.e., a proliferation of the fibrous glia, particularly pronounced within the cerebral and often also the cerebellar white matter. In many of the cases the cortical changes were slight compared with the intense lesions of the white matter. In none of them was demyelinization a well-marked feature, nor did its severity approach that of the glial proliferation; in many it was negligible, and there were none of the fatty breakdown products, characteristic of the demyelinizing disease of the white matter called after Schilder. The gliosis was either diffused or patchy, and was often markedly perivascular; even stripe-like scars, as described by Hallervorden (10), were to be seen, although, contrary to this author's observation, there was, as a rule, no corresponding myelin defect.