This paper presents a new hypothesis as to the function of the claustrum. Our basic premise is that the claustrum functions as a detector and integrator of synchrony in the axonal trains in its afferent inputs. In the first place an unexpected stimulus sets up a processed signal to the sensory cortex that initiates a focus of synchronized gamma oscillations therein. This focus may then interact with a general alerting signal conveyed from the reticular formation via cholinergic mechanisms, and with other salient activations set up by the stimulus in other sensory pathways that are relayed to the cortex. This activity is relayed from the cortex to the claustrum, which then processes these several inputs by means of multiple competitive intraclaustral synchronized oscillations at different frequencies. Finally it modulates the synchronized outputs that the claustrum distributes to most cortical and many subcortical structures, including the motor cortex. In this way, during multicenter perceptual and cognitive operations, reverberating claustro-cortical loops potentiate weak intracortical synchronizations by means of connected strong intraclaustral synchronizations. These may also occur without a salient stimulus. By this mechanism, the claustrum may play a strong role in the control of interactive processes in different parts of the brain, and in the control of voluntary behavior. These may include the neural correlates of consciousness. We also consider the role of GABAergic mechanisms and deafferentation plasticity.

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Mr. Gladstone, with that candour which a great Statesman can afford, once said, “Government is a rough business, and the results are most unsatisfactory.” Unfortunately no great psychiatrist has described the present state of our knowledge and treatment of schizophrenia in an equally robust phrase; but surely, “rough business and unsatisfactory results” would not be an unfair summing up ?We have now known of this illness for nearly half a century, and yet our understanding of it is slight and our useful information scanty. This is not because we have been idle, but because our efforts have been poorly rewarded. Thousands of papers are written every decade; tens of thousands of observations are made; there is no lack of opportunity for studying patients when about one hospital bed in five in this country is occupied by a schizophrenic, yet we are still entirely ignorant of the cause of this disease. There are, it is true, numerous theories, but none is generally accepted. We have one form of treatment, deep insulin, which produces remission of symptoms in some cases and what seems to be a cure in others, but even the value of this treatment is hotly disputed. Because deep insulin is a purely empirical procedure the psychiatrist is always tempted to become preoccupied with details of technique so that he forgets, or at least becomes less aware of our fundamental ignorance.

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About one year ago, with the encouragement of the Editor-in-Chief, a short paper appeared in this Journal entitled “Schizophrenia; A New Approach” (18). In this paper it was noted that mescaline and adrenaline have a similar biochemical structure. It was suggested that one of the aetiological agents in schizophrenia might be a substance or substances lying between these two; with the psychological properties of mescaline but effective in concentrations nearer those of adrenaline. Dr. Harley Mason elaborated this suggestion from the biochemical standpoint. For convenience these hypothetical substances were called, collectively, M substance. If M substance occurred in the body, it would account for the group of illnesses usually referred to as schizophrenia better than any hypothesis so far advanced. It has been the good fortune of the co-authors of that first paper (J. R. S. and H. O.) to be able to join forces with the third author of this paper (A. H.) to test the hypothsis. It is with the efforts of the last year that this paper is concerned.

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