Slow-wave sleep

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Ostriches sleeping, with REM and slow-wave sleep phases.[1]

Slow-wave sleep (SWS), often referred to as deep sleep, consists of stage 3 and 4 of non-rapid eye movement sleep, according to the Rechtschaffen & Kales (R & K) standard of 1968.[2] As of 2008, the American Academy of Sleep Medicine (AASM) has discontinued the use of stage 4,[3][4][5] 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.

Slow-wave sleep is considered important to consolidate new memories.[6]

Sleep deprivation studies with humans suggest that the primary function of slow-wave sleep may be to allow the brain to recover from its daily activities. Glucose metabolism in the brain increases as a result of tasks that demand mental activity.[7] Other functions slow-wave sleep can affect include the secretion of growth hormone. It is always greatest during this stage.[8] It is also thought to be responsible for a decrease in sympathetic and increase in parasympathetic neural activity.[8]


The highest arousal thresholds (i.e. 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 of 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, that is, the following bout of sleep will include more and deeper SWS than normal.The duration of slow-wave sleep is determined by the previous duration of this stage as well as the duration of prior wakefulness.[8]

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[citation needed], and intense prolonged exercise. Studies have shown, slow-wave sleep is enabled when brain temperature surpasses a certain threshold. It is hypothesized that the threshold is regulated by circadian and homeostatic processes.[9] In healthy, good sleepers, the very low carbohydrate diet over the short-term promotes increases in the percentage of SWS (deep sleep stage 4) and a reduction in the percentage of REM sleep ('dreaming' sleep) compared to the control mixed diet - the sleep changes may be linked to the metabolism of the fat content of the very low carbohydrate diet. [10]

In addition to these factors, the duration of SWS periods can be increased by the ingestion of THC,[11][unreliable source?] certain SSRIs, and other antidepressants.[citation needed] In instances such as these, TST (Total Sleep Time) is often unaffected due to circadian rhythms 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 duration. 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.[citation needed] 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 gamma-Hydroxybutyric acid (GHB) is known to promote SWS.[12] 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.

Reduced slow wave sleep (SWS) may predict high blood pressure in older men. [13]

A study from the Department of Endocrinology at Boston Children's Hospital, an affiliate of Harvard Medical School, indicated that regular deep sleep in children is helpful in triggering the steady release of the hormones that cause puberty.[14]

Problems associated with Slow-Wave Sleep[edit]

Bedwetting, night terrors, and sleep-walking are all common behaviors that can occur during stage 3 of sleep. These occur most frequently amongst children, who then generally outgrow them.[7] Another problem that may arise is sleep-related eating disorder. An individual will sleep-walk leaving his or her bed in the middle of the night seeking out food, and will eat not having any memory of the event in the morning.[7] Sleep-related eating disorder can usually be treated with dopaminergic agonists, or topiramate which is an anti-seizure medication. Heredity may be a potential cause of this disorder.[7]

Electroencephalographic characteristics[edit]

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

Large 75-microvolt (0.5–3 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.[5]

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 neurons.[15] In the TC neurons this is generated by the "slow oscillation" and is dependent on membrane potential bistability, a property of these neurons 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 (I t Window) and outward (small Ik leak), three equilibrium points are seen at −90, −70 and −60 mv, −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 in vitro, mGluR must be activated on these neurons to allow a small Ik leak, as seen in in vivo situations.

See also[edit]



  1. ^ Lesku, J. A.; Meyer, L. C. R.; Fuller, A.; Maloney, S. K.; Dell'Omo, G.; Vyssotski, A. L.; Rattenborg, N. C. (2011). "Ostriches Sleep like Platypuses". In Balaban, Evan. PLoS ONE 6 (8): e23203. doi:10.1371/journal.pone.0023203. PMC 3160860. PMID 21887239.  edit
  2. ^ Rechtschaffen, A; Kales, A (1968). A Manual of Standardized Terminology, Techniques and Scoring System For Sleep Stages of Human Subjects. US Dept of Health, Education, and Welfare; National Institutes of Health. 
  3. ^ Schulz, Hartmut (2008). "Rethinking sleep analysis. Comment on the AASM Manual for the Scoring of Sleep and Associated Events" (Full text). J Clin Sleep Med (American Academy of Sleep Medicine) 4 (2): 99–103. PMC 2335403. PMID 18468306. Retrieved 2009-01-04. "Although the sequence of non-REM (NREM) sleep stages 1 to 4 (R&K classification) or N1 to N3 (AASM classification) fulfills the criteria..." 
  4. ^ "Glossary. A resource from the Division of Sleep Medicine at Harvard Medical School, Produced in partnership with WGBH Educational Foundation". Harvard University. 2008. Retrieved 2009-03-11. "The 1968 categorization of the combined Sleep Stages 3 - 4 was reclassified in 2007 as Stage N3." 
  5. ^ a b Iber, C; Ancoli-Israel, S; Chesson, A; Quan, SF. for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. Westchester: American Academy of Sleep Medicine; 2007.
  6. ^
  7. ^ a b c d Carlson, Neil R. (2012). Physiology of Behavior. Pearson. p. 297-298. ISBN 0205239390. 
  8. ^ a b c Slow-Wave Sleep: Beyond Insomnia. Wolters Kluwer Pharma Solutions. ISBN 978-0-9561387-1-2. 
  9. ^ McGinty, Dennis; Ronald Szymusiak (1990). "Keeping cool: a hypothesis about the mechanisms and functions of slow-wave sleep". Science Direct. Trends in Neuroscience 13 (12): 480–487. 
  10. ^ Afaghi A, O'Connor H, Chow CM. (August 2008). "Acute effects of the very low carbohydrate diet on sleep indices". Nutr Neurosci. 11 (4): 146–54. doi:10.1179/147683008X301540. PMID 18681982. 
  11. ^ "Marijuana and Sleep". 2012-11-03. Retrieved 2012-11-21. 
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  15. ^ Williams SR, Tóth TI, Turner JP, Hughes SW, Crunelli W (1997) The window component of the low threshold Ca2+ current produces input signal amplification and bistability in cat and rat thalamocortical neurones. J Physiol 505:689–705.

Further reading