A single small aperture connecting each lateral ventricle with the dorsocephalic portion of the third ventricle provides the sole means of escape for cerebro-spinal fluid, and consequently it follows that any interference with its patency will seriously retard the outward flow of ventricular fluid. Complete, or even partial, closure of the foramen leads to a rapid increase in the volume and pressure of imprisoned ventricular fluid so that a condition of internal hydrocephalus is soon established. Usually both foramina are occluded, the hydrocephalus being therefore bilateral and the ventricles more or less symmetrically enlarged. In rare instances, however, only one foramen is obstructed, in which case the dilatation will, of course, be confined to the ipsilateral ventricle. Unilateral hydrocephalus of this obstructive type is commonly caused by inflammatory conditions in the neighbourhood of the foramen, or by pedunculated tumours attached to the choroid plexus which enjoy a degree of movement sufficient to permit intermittent or permanent blockage of the foramen of Monro. It is, however, possible to find examples of unilateral hydrocephalus in which the outflow of cerebro-spinal fluid through the foramen of Monro is unimpeded, and in these the cause of the ventricular dilatation is to be sought in some diseased condition of the cerebral wall which has become so weakened as to be unable to resist even normal ventricular pressure. Such expansion may be either limited to one part of the lateral ventricle, or general, involving the entire body with its horns.

The object of this paper is to test the following two hypotheses:

1. 1. That the physique of female adults can be regarded as the resultant of two independent modes of variation, one determining differences in size or bulk, and the other determining differences in proportion or type.

2. 2. That a relation exists between schizophrenia and manic-depres sion, on the one hand, and differences in physical proportion or type, on the other.

In a study on chorea, tics and compulsive utterances, Creak and Guttmann (1) discussed some problems of the inter-relation of organic neurological and neurotic symptoms. They showed that residuals, latent or manifest, of neurological diseases of the motor system may be instrumental in shaping the clinical picture of neuroses. There is generally no difficulty in demonstrating such interrelations, if the neurological anomalies are of a well-known type and clear cut in onset. Pareses, peripheral or central, or aphasic disorders, are generally not difficult to recognize where they are the nucleus of a neurotic picture, and not much objection is encountered if one tries to assess their importance, pathogenetic or pathoplastic, in a given clinical picture. This, however, is difficult where less well known syndromes are concerned, such as apraxic or agnosic pictures, or where beginning or end are gradual and the whole picture less clearly defined, as in disturbances of the extra-pyramidal motor system. To recognize an early stage of Parkinsonianism within a depression or other “neurotic” illness is not easy. The same is true of mild extra-pyramidal hyperkinetic states, partly because they may be so similar to normal movements (pseudo-purposeful), and partly because the milder anomalies as seen in early or later stages (and in abortive cases) are little known.

The problem of the differentiation between neurosis and psychosis has given rise to much confused literature and discussion. This is particularly true of those cases in which anxiety or depression is the outstanding feature of the illness, and which do not show any gross symptoms of psychotic illness. Such confusion as exists appears to be due to a variety of causes. For example, the social implications of psychotic illness tend to favour a diagnosis of neurosis in many of the milder cases. Again, the same diagnostic terms are often used with quite different meanings by different workers. An even more potent cause of difficulty is the temptation to search for fixed disease entities in psychiatry which can be sharply separated one from the other.

The nature of the action of insulin in producing cure in cases of schizophrenia is still quite obscure. One of the most striking features of insulin hypoglycaemia is the occurrence of phenomena pointing to disturbance of the autonomic nervous system, and many authors on this subject have expressed the belief that insulin produces cure by virtue of its action on the autonomic nervous system. There is, however, extensive contradiction in the literature as to what actually are the changes which take place in autonomic functions during hypoglycaemia. Some authors say that hypoglycaemia produces a generalized sympathetic stimulation, some say a generalized parasympathetic activity and others that there is dissociation of action of the two systems. Sakel (1) appears to believe that hypoglycaemia produces a vagotonia which underlies the curative effects of his treatment; Hadorn (2), that small doses of insulin stimulate the vagus, and large doses cause a primary secretion of adrenaline; Beno (3), that changes on the vegetative system cannot be sufficient to allow a reasonable understanding of the results; Pfister (4), that hypoglycaemia produces beneficial effects in schizophrenia because it damps the sympathetic; Wespi (5), that dissociation appears to prevail in the autonomic regulation; Gellhorn (6), that the treatment is successful because it leads to excitation of the sympathetico-adrenal apparatus through hypoglycaemia of the brain; and lastly, Heilbrunn (7), that his experiments are in favour of a sympatheticotonia.

It is generally agreed that there are many objections to the use of cardiazol and azoman (triazol) as convulsants. The treatment is generally disliked and the injections are attended by much apprehension. There is frequently amnesia, though usually of a temporary nature. There may be some actual damage to the brain, fractures are not infrequent, and other complications sometimes occur. Old tuberculous lesions have been reactivated and deaths have occurred in status epilepticus from the use of azoman.

I am presenting to you in this paper my own views and experience in a practical psychotherapeutic approach to psychotics. I am aware—acutely aware—that I am speaking, with only two or three years' experience behind me, to distinguished psychiatrists. I cannot bring myself to apologize for having definite views on so short an experience; they are views that struck me before I had been employed in a mental hospital for a week, and I have had no occasion to change them since. I am not even sufficiently well up in the subject to know if they are peculiar to me.

The senile psychoses are in regard to their origin an unsolved problem. Much valid work has been done in the field of anatomy and histology in approaching this problem, but as the mental diseases of old age cannot be separated from the growing old of body and mind generally, this problem is more or less a biological one. The borderline between old age and senile dementia is not a sharp one. In brains of old people without clinical symptoms of dementia there have been found histological changes, such as are usually found in cases of senile dementia. This makes it probable that the extent of degeneration of brain cells alone is not decisive for the appearance of senile psychoses. The finding of the characteristic plaques in the brain of senile psychoses may give evidence of the extent of the process and the severity of clinical symptoms, but it does not tell us anything about their nature and origin. Whether a constitutional factor is decisive or whether the histological changes are a reaction to an unknown noxa is undecided. Heredity may have its share too.

This subject has a moderately extensive literature and examples have been recorded by various authors for some years. Most of the cases, however, have been the subjects of some pathological lesion, either congenital or acquired. Perhaps the earliest authentic case is the one originally described by Rosinius Lentilius in 1698, and quoted by Critchley, of a female, presumably young, epileptic sinistrad. The sex is not as important as the other factors, but it is a pity that there is no reference to the intellectual capacity. It is, if nothing else, a pointer to the usual type of case studied. In the adults, hemiplegics seem to have proved the most fruitful source for those collecting examples of this phenomenon, although a full list of causes is well known.

Meduna and Rohny (1939) have recently commented on the rise of sugar and lactic acid in the blood of schizophrenic patients following therapeutic cardiazol fits. Insulin causes a lowering of the blood sugar, but later the resting level becomes higher than before treatment. Hence they suggest that the alteration of carbohydrate metabolism in the direction of diabetes may be the common mechanism underlying both forms of treatment, and this hypothesis is supported by Nyiro's observation (quoted by Meduna and Rohny) that diabetes is rare amongst patients with schizophrenia.