Functional anatomy of non-REM sleep

Abstract

The state of non-REM sleep (NREM), or slow wave sleep, is associated with a synchronized EEG pattern in which sleep spindles and/or K complexes and high-voltage slow wave activity (SWA) can be recorded over the entire cortical surface. In humans, NREM is subdivided into stages 2 and 3–4 (presently named N3) depending on the proportions of each of these polygraphic events. NREM is necessary for normal physical and intellectual performance and behavior. An overview of the brain structures involved in NREM generation shows that the thalamus and the cerebral cortex are absolutely necessary for the most significant bioelectric and behavioral events of NREM to be expressed; other structures like the basal forebrain, anterior hypothalamus, cerebellum, caudal brain stem, spinal cord and peripheral nerves contribute to NREM regulation and modulation. In NREM stage 2, sustained hyperpolarized membrane potential levels resulting from interaction between thalamic reticular and projection neurons gives rise to spindle oscillations in the membrane potential; the initiation and termination of individual spindle sequences depends on corticothalamic activities. Cortical and thalamic mechanisms are also involved in the generation of EEG delta SWA that appears in deep stage 3–4 (N3) NREM; the cortex has classically been considered to be the structure that generates this activity, but delta oscillations can also be generated in thalamocortical neurons. NREM is probably necessary to normalize synapses to a sustainable basal condition that can ensure cellular homeostasis. Sleep homeostasis depends not only on the duration of prior wakefulness but also on its intensity, and sleep need increases when wakefulness is associated with learning. NREM seems to ensure cell homeostasis by reducing the number of synaptic connections to a basic level; based on simple energy demands, cerebral energy economizing during NREM sleep is one of the prevalent hypotheses to explain NREM homeostasis.

The Sleeping Cerebellum

“…This neglect is intriguing, because malfunction of the cerebellum does not only impair motor control and motor memory formation [6][7][8], but it may also lead to changes in the sleep-wake cycle [9,10] and even cause sleep disorders [11]. Furthermore, decades of behavioral and physiological research has shown the positive impact of sleep on episodic memory formation.…”

“…K-complexes are single slow waves occurring typically in NREM2. Spindles are short bursts of activity at a frequency of [10][11][12][13][14][15]. More continuous slow waves occur in what is considered deep sleep, NREM3, or SWS [12].…”

“…Most, if not all, of the monoaminergic systems also have widespread impact on other parts of the brain involved in sleep control. For example, the noradrenergic, serotonergic, and histaminergic neurons control the GABAergic galanin-containing neurons of the ventrolateral and median preoptic nucleus that become active during NREM [3], while orexinergic neurons can stabilize the switch between the wakesleep-promoting networks [3,10] activity. Cerebellar signs of bistability, which is distinct for NREM3, have been studied in animals since the second half of the previous century [39].…”

Spectrum of Sleep Disorders in a Patient with Spinocerebellar Ataxia 13

“…10,13,14,18,19 It must be noted, though, that studies using polysomnography in patients with SCA 3 have failed to show a significantly higher incidence of sleep disordered breathing and a significantly different average respiratory disturbance index (RDI) or average apnea hypopnea index (AHI) in these patients as compared to healthy controls. 9,10 The cerebellum plays an underappreciated role in the sleep wake cycle 20 and breathing, [21][22][23] and its involvement in patients with SCA might lead to some of their sleep and respiratory problems.…”

A Patient with Unusual Electroencephalographic Findings during Rapid Eye Movement Sleep

“…Bazil (2,4). Determining the cause of a seizure in an adult patient can be difficult, and many adults presenting with their first seizure do not have an identifiable cause (5, 6).…”