Periodic physiological dissolution of consciousness: sleep and coma

Etymologically, coma means sleep, and for a long time coma has been regarded as a very deep sleep. One is then entitled to wonder whether some forms of coma are not due to the exaggeration of the normal sleep mechanism. This seems unlikely for the following reasons which we shall discuss briefly:

(1) Lesions of the sleep systems in animals result in a state of prolonged insomnia, without disorders of perceptivity.

(2) Stimulation of the sleep systems will induce a reversible sleep, but never causes prolonged loss of consciousness.

Structures responsible for the states of sleep. Two forms of sleep are recognized: one which is characterized by slow, or synchronized, cortical activity, with maintenance of some muscle tone: "slow sleep"; the second is accompanied by a higher frequency cortical activity of low voltage (similar to that in the waking state), complete loss of muscle tone, and rapid eye movements: this is "paradoxical sleep" (Jouvet 1967). This second sleep occurs periodically during physiological sleep and constitutes about 20 % of normal sleeping time. It corresponds in man to oneiric activity.

It has been shown that these states of sleep are the result of an active process of inactivation of the waking system. The theory according to which sleep is due to passive inactivation of the activating reticular system has now been abandoned. It is in fact possible to induce prolonged insomnia by destroying the hypnogenic systems. These are situated in the lower part of the brainstem (pons and medulla) and there appear to be two distinct systems: one, situated at the level of the nuclei of Raphé, which is associated with slow sleep, and one situated in the laterodorsal part of the pontine tegmentum which is associated with paradoxical sleep.

Destruction of these systems causes elective suppression of the sleeping states. But this lesion, which causes considerable prolongation of the waking state, induces no disturbances of perceptivity or of reactivity in animals.

It is possible on the other hand, to bring on one or the other form of sleep by stimulating, under well defined conditions either the sleep centres or some of their afferent or efferent connections. The sleep induced in this way is always short-lasting and is always easily reversed by external stimu lation. Prolonged loss of consciousness has never been induced experimentally in animals by stimulation of the sleep systems.

Although a priori it may seem possible that certain inflammatory processes (Von Economo's epidemic encephalitis) might lead to chronic excitation of the hypnogenic structures, it seems unlikely that hypersomnia and encephalitic le thargy are due to lesions of these structures. In animals at least, reversible hypersomnia and irre versible coma have always been induced by lesions of the waking system.

This observation leads to the following corollaries which may be of some practical interest:

- (irreversible) coma must not be identified with sleep;

- some forms of coma (due to an organic or functional lesion of the waking system) can there fore be actively modulated by activation of the two hypnogenic systems which, under normal conditions, are responsible for slow and paradoxical sleep respectively. This modulation ex plains the various degrees of loss of perceptivity or reactivity observed in certain patients at different times, and which might be due to the fact that the few structures concerned with waking spared by the lesion are periodically submitted to an active process of inactivation from the sleep systems. Finally, total muscular atony such as is found in paradoxical sleep, may occur periodically in states of rigidity due to decortication or to decerebration. This explains the fluctuations in muscle tone encountered during continuous poly graphic recordings (Jouvet et al. 1961) (Fig.2).

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