Introduction

A brief review of the physiological data relating to the nature of sleep enables us to get an idea of the duality of structures and mechanisms brought into play during this periodic mystery.

Structural duality : Without referring back to the opposition between cerebral and body sleep, it should be remembered simply that Von Economo (1927), basing his findings on clinical and pharmacological facts, had already contrasted the passive character of telencephalic sleep with the active regulating part played by a hypothetical mesodiencephalic centre.

Duality of mechanisms : Is it possible to reconcile, in a single mechanism, Bergson's sleep "désinterêt" with that vItal. need, the lack of which brings death? Is it possible to reconcile, without calling upon two distinct mechanisms, the hypothesis of passive sleep resulting from neuronal fatigue or deafferentation of the ascending activating reticular system (Bremer, 1954) with Pavlov's theory of sleep as a cortical active inhibition phenomenon or with Hess's (1928) hypothesis of the existence of a diencephalic sleep centre which can be brought into play through stimulation ?

Recently, the idea of sleep mechanism duality has found support from EEG analysis. Slow cortical activity was long considered as the only EEG index of sleep in the cat (Rheinberger and Jasper, 1937; Hess, Koella and Akert, 1953) but certain observations have since shown the existence of a rapid cortical activity (Rimbaud et al., 1955), the periodic recurrence of which has been compared by Dement (1958) to "activated sleep", an intermediary state between wakefulness and sleep.

A brief account will now be given of the experimental results (Jouvet, Michel and Courjon, 1959b; Jouvet, 1961) which enables us to contrast sleep accompanied by slow cerebral activity requiring the integrity of the telencephalon to sleep accompanied by rapid cortical activity, which we shall show to be dependent on the intervention of rhombencephalic structures.

Review of methods : The problem of discovering the cerebral formations responsible for the various stages of sleep can be solved only by animal experiments combining nerve destruction and stimulation. Some methods (Bremer, 1935; Batini et al., 1958) are based essentially on cortical EEG records, which are considered as the most reliable evidence of wakefulness level. A "slow" tracing becomes evidence of sleep, a "rapid" tracing of wakefulness. There are, however, many exceptions.

(1) A synchronized or "slow" tracing is not necessarily a sign of physiological sleep. For example, the irreversibility of barbiturate narcosis or coma due to reticular formation destruction enables us to eliminate one phenomenon of sleep.

(2) A "rapid" cortical tracing is not necessarily a sign of wakefulness: ether narcosis, for instance, is accompanied by "cortical activation" and there are sleep phases in the cat with rapid cortical activity.

(3) Last but not least, the study during chronic experiments of an animal whose brain stem has been sectioned between the quadrigeminal bodies results in a cortical tracing which, if considered by itself, would lead to the conclusion that the animal is asleep; in fact it reacts to pain by fleeing movements and miaowing.

The imperative necessity of checking animal sleep behaviour has lead us to record cortical and subcortical electrical activity in relation to the classic somato-vegetative manifestations of sleep (muscular tonic activity, heart beat, respiratory rhythms, etc.). In a brain stem section, the electrical activity of that part of the encephalon which is situatedbehind the lesion (and not only in front of it), and which is therefore linked to the exterior milieu by its main afferent and efferent pathways, was recorded during the periodic behavioural variations of wakefulness. It has been known since the time of Goltz (1892) that a decorticate animal can sleep. The works of Bard and Macht (1958) and Rioch (1954) have also shown that mesencephalic animals showed behavioural altemations of wakefulness and sleep.

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