Slow-wave sleep

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Slow-wave sleep (SWS), often referred to as deep sleep, consists of stages three and four of non-rapid eye movement sleep, according to the Rechtschaffen & Kales (R&K) standard of 1968.^[1] As of 2008, the American Academy of Sleep Medicine (AASM) has discontinued the use of stage 4,^[2][3][4] such that the previous stages 3 and 4 now are combined as stage 3. An epoch (30 seconds of sleep) which consists of 20% or more slow wave (delta) sleep, now is considered to be stage 3.

The highest arousal thresholds (e.g. difficulty of awakening, such as by a sound of a particular volume) are observed in deep sleep. A person will typically feel more groggy when awoken from slow-wave sleep, and indeed, cognitive tests administered after awakening then indicate that mental performance is somewhat impaired for periods up to 30 minutes or so, relative to awakenings from other stages. This phenomenon has been called "sleep inertia."

After sleep deprivation there is a sharp rebound of SWS, suggesting there is a "need" for this stage.

The major factor determining how much slow-wave sleep is observed in a given sleep period is the duration of preceding wakefulness, likely related to accumulation of sleep-promoting substances in the brain. Some of the few factors known to increase slow-wave sleep in the sleep period that follows them include body heating (as by immersion in a hot tub), high carbohydrate ingestion, and intense prolonged exercise. The latter probably exerts its influence by increasing body temperature.^{[citation needed]}

In addition to these factors, the duration of SWS periods can be increased by ingestion of alcohol, THC, SSRIs, and other drugs.^{[citation needed]} In instances such as these, TST (Total Sleep Time) is often unaffected due to circadian rhythms and/or a person's alarm clock and early morning obligations. This increase of SWS can lead to increased REM latency and a decrease in REM period durations. If the total time spent in REM is decreased long enough and repeatedly over a substantial number of nights a "REM rebound" will occur in response to removal of its inhibitor. An increase in REM is believed to produce symptoms of depression and bipolar disorder in many patients for an amount of time relative to the severity of the previous "REM suppression". It is debatable whether or not this could explain the return in symptoms of depression disorder after removal of SSRI medications.

Certain substances, such as benzodiazepines (e.g. Ativan, Valium, Klonopin) seem to have the reverse effect on the time spent in SWS. Instead of lengthening SWS (as do the substances mentioned above), they are known to shorten the time. While these sedatives can increase sleep duration or shorten the time it takes before sleep-onset occurs, they tend to deprive patients of deep sleep.

The chemical GHB is known to promote SWS.^{[citation needed]} In the United States, the Food and Drug Administration permits the use of GHB under the trade name Xyrem to reduce cataplexy attacks and excessive daytime sleepiness in patients with narcolepsy.

Electroencephalographic characteristics

Polysomnogram demonstrating SWS, stage 4.
High amplitude EEG is highlighted in red.

Large 75 microvolt (0.5 - 2 Hz) delta waves predominate the electroencephalogram (EEG). Stage N3 is defined by the presence of 20% delta waves in any given 30 second epoch of the EEG during sleep, by the current 2007 AASM guidelines.^[4]

Longer periods of slow-wave sleep occur in the first part of the night, primarily in the first two sleep cycles (roughly 3 hours). Children and young adults will have more total slow-wave sleep in a night than older adults. The elderly may not go into slow-wave sleep at all during many nights of sleep.

Slow-wave sleep (SWS) is an active phenomenon probably brought about by the activation of serotonergic neurons of the raphe system.

The slow wave seen in the cortical EEG is generated through thalamocortical communication through the thalamocortical neurones. In the TC neurones this is generated by the 'slow oscillation' and is dependent on membrane potential bistability, a property of these neurones due to an electrophysiological component known as I t Window. I t Window is due to the overlap underneath activation/inactivation curves if plotted for T-type calcium channels (inward current). If these two curves are multiplied, and another line superimposed on the graph to show a small Ik leak current (outward), then the interplay between these inward (It Window) and outward (small Ik leak), three equilibrium points are seen at -90, -70 and -60mv, -90 and -60 being stable and -70 unstable. This property allows the generation of slow waves due to an oscillation between two stable points. It is important to note that in vitro, mGluR must be activated on these neurones to allow a small Ik Leak, as seen in vivo situations.

See also

• Non-rapid eye movement sleep (NREM)
• Sleep and learning
• Preconscious
• Unconscious mind
• Subconscious

References

Further reading

• M. Massimini, G. Tononi, et al., “Breakdown of Cortical Effective Connectivity During Sleep,” Science, vol. 309, 2005, pp. 2228–32.
• P. Cicogna, V. Natale, M. Occhionero, and M. Bosinelli, “Slow Wave and REM Sleep Mentation,” Sleep Research Online, vol. 3, no. 2, 2000, pp. 67–72.
• D. Foulkes et al., “Ego Functions and Dreaming During Sleep Onset,” in Charles Tart, ed., Altered States of Consciousness, p. 75.
• Rock, Andrea (2004). The Mind at Night. 
• Warren, Jeff (2007). "The Slow Wave". The Head Trip: Adventures on the Wheel of Consciousness. ISBN 978-0679314080.