Abstract
A discontinuity characterizes the sleep process: the steady unfolding of quiet sleep (non-rapid eye movement sleep, NREMS) is periodically interrupted by active sleep episodes (rapid eye movement sleep, REMS). The state change from NREMS to REMS has best been described as switching from a homeostatic to a non-homeostatic condition [1]; in the latter the physiological control loops are affected by disturbances (neural discharges in sensory systems and efferent pathways) of central origin locked to the sleep process. Not all the control loops are equally affected, and “central commands” and set point values may also be perturbed; at any rate, a condition of physiological instability appears to be the cardinal feature of REMS. This “physiological risk” [2] may be related to the high incidence of acute cardiovascular disease in the early morning hours of higher REMS density [3–5]. The substantial overlap of neural circuits in the brain stem responsible for controlling both cardiovascular regulation and REMS phasic events gives a “structural” foundation to cardiovascular instability during REMS [6] (Fig. 1).
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Lenzi, P., Zoccoli, G., Franzini, C. (1997). Regulation of Cerebral and Extracerebral Circulation During the Wake-Sleep Cycle. In: Lugaresi, E., Parmeggiani, P.L. (eds) Somatic and Autonomic Regulation in Sleep. Springer, Milano. https://doi.org/10.1007/978-88-470-2275-1_2
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