The Sleeping Brain

Sleep is not one state but a sequence. Loomis, Harvey, and Hobart (1937) first divided the night by the electroencephalogram into stages of deepening slow waves; Aserinsky and Kleitman (1953) found the periods of rapid eye movement that the scheme had missed, and Rechtschaffen and Kales (1968) fixed the scoring rules that stood for forty years. The adult night runs in cycles of about ninety minutes: light sleep (N1, N2), deep slow-wave sleep (N3), then REM, with the slow-wave sleep concentrated in the first cycles and the REM periods lengthening towards morning from a few minutes to half an hour or more.

REM sleep is a third state of the brain, as distinct from non-REM sleep as either is from waking (Jouvet, 1959, 1962): the cortex is as active as in waking, the eyes move in bursts, breathing and heart rate are irregular, the penis and clitoris engorge, body temperature regulation stops, and the skeletal muscles are paralysed by a brainstem circuit so that the dream is not acted out. Jouvet cut that circuit in cats and watched them stalk and pounce in their sleep. In people the same failure, REM sleep behaviour disorder, was described by Schenck in 1986 and is the earliest known sign of Parkinson’s disease and the related synucleinopathies: in long follow-up most patients convert (Postuma et al., 2019, 1,280 patients, 6.3 per cent a year).

The chemistry switches with the state. In REM the cholinergic neurons of the pons fire and the noradrenaline and serotonin neurons fall silent, which Hobson and McCarley (1975) modelled as a reciprocal oscillator; the silence of noradrenaline is one reason the dream is so poorly remembered, since that system is what consolidates memory in waking. The waves that precede each burst of eye movement (PGO waves, from pons to geniculate to occipital cortex) were, for Hobson, the random signals the dreaming cortex made sense of.

Deep slow-wave sleep is the opposite picture: the cortex fires in synchronised slow oscillations, the thalamus gates out the senses, and growth hormone is secreted. It is in this stage that night terrors and sleepwalking occur, in the first third of the night, with no dream to report; and it is the stage in which the hippocampus replays the day’s learning to the cortex (Wilson and McNaughton, 1994), which is one half of the account of why we sleep. Whether dreaming in non-REM sleep is the same process at lower intensity, or a different one, is the open question that Siclari’s posterior hot zone (2017) began to answer, since it predicts the dream in both states.

Sources

• Loomis, A. L., Harvey, E. N., and Hobart, G. A. (1937). “Cerebral states during sleep, as studied by human brain potentials.” Journal of Experimental Psychology 21.
• Jouvet, M. (1962). “Recherches sur les structures nerveuses et les mécanismes responsables des différentes phases du sommeil physiologique.” Archives Italiennes de Biologie 100.
• Rechtschaffen, A., and Kales, A., eds. (1968). A Manual of Standardized Terminology, Techniques and Scoring System for Sleep Stages of Human Subjects. NIH.
• Hobson, J. A., McCarley, R. W., and Wyzinski, P. W. (1975). “Sleep cycle oscillation: reciprocal discharge by two brainstem neuronal groups.” Science 189.
• Postuma, R. B., et al. (2019). “Risk and predictors of dementia and parkinsonism in idiopathic REM sleep behaviour disorder: a multicentre study.” Brain 142.
• Wilson, M. A., and McNaughton, B. L. (1994). “Reactivation of hippocampal ensemble memories during sleep.” Science 265.

A review of the literature for readers; not medical advice.