Editing Rapid eye movement sleep (section)

== Physiology ==

=== Electrical activity in the brain===
[[File:Sleep EEG REM.png|thumb|right|300px|[[Polysomnography|Polysomnographic]] record of REM Sleep. [[EEG]] highlighted by red box. Eye movement highlighted by red line.]]
REM sleep is called "paradoxical" because of its similarities to [[wakefulness]]. Although the body is paralyzed, the brain acts as if it is somewhat awake, with [[Cerebral cortex|cerebral]] neurons firing with the same overall intensity as in wakefulness.<ref name=MatarazzoEtAl2011>{{cite book | vauthors = Matarazzo L, Foret A, Mascetti L, Muto V, Shaffii A, Maquet P, Morrison AR, Mallick BN, McCarley RW, Pandi-Perumal SR | chapter = A systems-level approach to human REM sleep. | veditors = Mallick BN, Pandi-Perumal SR, McCarley RW, Morrison AR | title = Rapid Eye Movement Sleep: Regulation and Function | date = July 2011 | pages = 71 | publisher = Cambridge University Press | isbn = 978-1-139-50378-5 | chapter-url = https://books.google.com/books?id=yajLoMNSJUwC&pg=PA71 }}</ref><ref name="myers7e">{{cite book | vauthors = Myers D |author-link=David Myers (academic) |title=Psychology |edition=7th |year=2004 |publisher=Worth Publishers |location=New York |isbn=978-0-7167-8595-8 |page=[https://archive.org/details/psycholo2004myer/page/268 268] |url=https://archive.org/details/psycholo2004myer |url-access=registration |access-date=2010-01-09}}</ref> [[Electroencephalography]] during REM sleep reveals fast, low amplitude, desynchronized [[neural oscillation]] (brainwaves) that resemble the pattern seen during wakefulness, which differ from the slow [[delta waves|δ (delta) waves]] pattern of NREM deep sleep.<ref name=BrownMcCarley>{{cite book | vauthors = Brown RE, McCarley RW | date = 2008 | chapter = Neuroanatomical and neurochemical basis of wakefulness and REM sleep systems | title = Neurochemistry of Sleep and Wakefulness | veditors =  Monti J, Pandi-Perumal SR, Sinton CM | location = Cambridge | publisher = Cambridge University Press | isbn = 978-0-521-86441-1 }}</ref><ref name="Steriade_2013">{{cite book | vauthors = Steriade MM, McCarley RW | title = Brainstem control of wakefulness and sleep | publisher = Springer Science & Business Media | date = March 2013 | isbn = 978-1-4757-4669-3 }}</ref>{{rp|§1.2 7–23}} An important element of this contrast is the 3–10 [[Hertz|Hz]] [[theta rhythm]] in the [[hippocampus]]<ref name="Steriade_2013" />{{rp|§7.2–3 206–208}} and 40–60&nbsp;Hz [[gamma waves]] in the [[Cerebral cortex|cortex]]; patterns of EEG activity similar to these rhythms are also observed during wakefulness.<ref name="Horne2013">{{cite journal | vauthors = Horne J | title = Why REM sleep? Clues beyond the laboratory in a more challenging world | journal = Biological Psychology | volume = 92 | issue = 2 | pages = 152–68 | date = February 2013 | pmid = 23174692 | doi = 10.1016/j.biopsycho.2012.10.010 | s2cid = 206109082 }}</ref> The cortical and [[Thalamus|thalamic]] neurons in the waking and REM sleeping brain are more depolarized (fire more readily) than in the NREM deep sleeping brain.<ref name="Steriade_2013" />{{rp|§8.1 232–243}} Human theta wave activity predominates during REM sleep in both the hippocampus and the cortex.<ref name="pmid26441373">{{cite journal | vauthors = Lomas T, Ivtzan I, Fu CH | title = A systematic review of the neurophysiology of mindfulness on EEG oscillations | journal = Neuroscience and Biobehavioral Reviews | volume = 57 | pages = 401–410 | date = October 2015 | pmid = 26441373 | doi = 10.1016/j.neubiorev.2015.09.018 | s2cid = 7276590 | url = http://roar.uel.ac.uk/4509/1/A%20systematic%20review%20of%20the%20neurophysiology%20of.pdf }}</ref><ref name="pmid24596562">{{cite journal | vauthors = Hinterberger T, Schmidt S, Kamei T, Walach H | title = Decreased electrophysiological activity represents the conscious state of emptiness in meditation | journal = Frontiers in Psychology | volume = 5 | pages = 99 | year = 2014 | pmid = 24596562 | pmc = 3925830 | doi = 10.3389/fpsyg.2014.00099 | doi-access = free }}</ref>

During REM sleep, [[Brain connectivity estimators|electrical connectivity among different parts of the brain]] manifests differently than during wakefulness. Frontal and posterior areas are less [[Corticocortical coherence|coherent]] in most frequencies, a fact which has been cited in relation to the chaotic experience of dreaming. However, the posterior areas are more coherent with each other; as are the right and left hemispheres of the brain, especially during [[lucid dream]]s.<ref>{{cite book | vauthors = Gackenbach J | chapter = Interhemispheric EEG coherence in REM sleep and meditation: The lucid dreaming connection. | veditors = Antrobus JS, Bertini M | title = The neuropsychology of sleep and dreaming | date = January 2013 | pages = 265–288 | location = New York | publisher = Psychology Press | isbn = 978-0-203-77254-6 }}</ref><ref name=EPS2011>{{cite book | vauthors = Pace-Schott EF | chapter = REM sleep and dreaming. | veditors = Mallick BN, Pandi-Perumal SR, McCarley RW, Morrison AR | title = Rapid Eye Movement Sleep: Regulation and Function. | publisher = Cambridge University Press | location = Cambridge | date = July 2011 | pages = 8–20 | isbn = 978-1-139-50378-5 | chapter-url = https://books.google.com/books?id=yajLoMNSJUwC&pg=PA8 }}</ref>

Brain energy use in REM sleep, as measured by oxygen and glucose metabolism, equals or exceeds energy use in waking. The rate in non-REM sleep is 11–40% lower.<ref name=HobsonEtAl2000 />

==== Brain stem ====
Neural activity during REM sleep seems to originate in the [[brain stem]], especially the [[pontine tegmentum]] and [[locus coeruleus]]. REM sleep is punctuated and immediately preceded by [[PGO waves|PGO (ponto-geniculo-occipital) waves]], bursts of electrical activity originating in the brain stem.<ref name="Steriade_2013" />{{rp|§9.1–2 263–282}} (PGO waves have long been measured directly in cats but not in humans because of constraints on experimentation; however, comparable effects have been observed in humans during "phasic" events which occur during REM sleep, and the existence of similar PGO waves is thus inferred.)<ref name=EPS2011 /> These waves occur in clusters about every 6 seconds for 1–2 minutes during the transition from deep to paradoxical sleep.<ref name="Steriade_2013" /> They exhibit their highest amplitude upon moving into the [[visual cortex]] and are a cause of the "rapid eye movements" in paradoxical sleep.<ref name=Datta>{{cite book | vauthors = Datta S | chapter = PGO Wave Generation: Mechanism and functional significance | title = Rapid Eye Movement Sleep | date = 1999 | pages = 91–106 }}</ref><ref name=ErmisEtAl /><ref name=HobsonEtAl2000 /> Other muscles may also contract under the influence of these waves.<ref name=Siegel2009 />

==== Forebrain ====

Research in the 1990s using [[positron emission tomography]] (PET) confirmed the role of the brain stem and suggested that, within the [[forebrain]], the [[limbic]] and [[paralimbic cortex|paralimbic]] systems showed more activation than other areas.<ref name=MatarazzoEtAl2011 /> The areas activated during REM sleep are approximately inverse to those activated during non-REM sleep<ref name=HobsonEtAl2000 /> and display greater activity than in quiet waking. The "anterior paralimbic REM activation area" (APRA) includes areas linked with [[emotion]], memory, fear and sex, and may thus relate to the experience of dreaming during REMS.<ref name=EPS2011 /><ref>{{cite journal | vauthors = Nofzinger EA, Mintun MA, Wiseman M, Kupfer DJ, Moore RY | title = Forebrain activation in REM sleep: an FDG PET study | journal = Brain Research | volume = 770 | issue = 1–2 | pages = 192–201 | date = October 1997 | pmid = 9372219 | doi = 10.1016/s0006-8993(97)00807-x | s2cid = 22764238 }}</ref> More recent PET research has indicated that the distribution of brain activity during REM sleep varies in correspondence with the type of activity seen in the prior period of wakefulness.<ref name=MatarazzoEtAl2011 />

The [[superior frontal gyrus]], [[medial frontal gyrus|medial frontal areas]], [[intraparietal sulcus]], and [[superior parietal lobule|superior parietal cortex]], areas involved in sophisticated [[mind|mental]] activity, show equal activity in REM sleep as in wakefulness. The [[amygdala]] is also active during REM sleep and may participate in generating the PGO waves, and experimental suppression of the amygdala results in less REM sleep.<ref>{{cite book | vauthors = Sanford LD, Ross RJ | chapter = Amygdalar regulation of REM sleep. | veditors = Mallick BN, Pandi-Perumal SR, McCarley RW, Morrison AR | title = Rapid eye movement sleep. | publisher = Cambridge University Press | location = Cambridge | date = July 2011 | pages = 110–120 }}</ref> The amygdala may also regulate cardiac function in lieu of the less active [[insular cortex]].<ref name=MatarazzoEtAl2011 />

=== Chemicals in the brain ===

Compared to [[slow-wave sleep]], both waking and paradoxical sleep involve higher use of the neurotransmitter [[acetylcholine]], which may cause the faster brainwaves. The  [[monoamine]] neurotransmitters [[norepinephrine]], [[serotonin]] and [[histamine]] are completely unavailable. Injections of [[acetylcholinesterase inhibitor]], which effectively increases available acetylcholine, have been found to induce paradoxical sleep in humans and other animals already in slow-wave sleep. [[Carbachol]], which mimics the effect of acetylcholine on neurons, has a similar influence. In waking humans, the same injections produce paradoxical sleep only if the monoamine neurotransmitters have already been depleted.<ref name="BrownMcCarley"/><ref name=MallickEtAl>{{cite book | vauthors = Mallick BN, Madan V, Jha S | chapter = Rapid eye movement sleep regulation by modulation of the noradrenergic system. | veditors = Monti J, Pandi-Perumal SR, Sinton CM | title = Neurochemistry of Sleep and Wakefulness. | publisher = Camibridge University Press | location = New York | date = 2008 | pages = 59–81 }}.</ref><ref name=Hobson2009>{{cite journal | vauthors = Hobson JA | title = REM sleep and dreaming: towards a theory of protoconsciousness | journal = Nature Reviews. Neuroscience | volume = 10 | issue = 11 | pages = 803–813 | date = November 2009 | pmid = 19794431 | doi = 10.1038/nrn2716 | s2cid = 205505278 }}</ref><ref name=AstonJonesEtAl>{{cite book | vauthors = Aston-Jones G, Gonzalez M, Doran S | chapter = Role of the locus coeruleus-norepinephrine system in arousal and circadian regulation of the sleep–wake cycle. | veditors =  Ordway GA, Schwartz MA, Frazer A | title = Brain norepinephrine: Neurobiology and therapeutics. | publisher = Cambridge University Press | date = February 2007 | pages = 157–195 | chapter-url = http://academicdepartments.musc.edu/neuromodulation/epapers/Aston-JonesetalLCsleepOrdway07.pdf | archive-url =  https://web.archive.org/web/20111213130015/http://academicdepartments.musc.edu/neuromodulation/epapers/Aston-JonesetalLCsleepOrdway07.pdf | archive-date=2011-12-13}}</ref><ref>{{cite book | vauthors = Siegel JM | date = 2005 | chapter = REM Sleep | title = Principles and Practice of Sleep Medicine | edition = 4th | veditors = Kryger MH, Roth T, Dement WB | publisher = Elsevier | pages = 120–135 }}</ref>

Two other [[Neurotransmitter receptor|neurotransmitters]], [[orexin]] and [[gamma-Aminobutyric acid]] (GABA), seem to promote wakefulness, diminish during deep sleep, and inhibit paradoxical sleep.<ref name=BrownMcCarley /><ref name=LuppiEtAl>{{cite book | vauthors = Luppi PH, Gervasoni D, Verret L, Goutagny R, Peyron C, Salvert D, Léger L, Fort P | date = 2008 | chapter = Gamma-aminobutyric acid and the regulation of paradoxical, or rapid eye movement, sleeps | title = Neurochemistry of Sleep and Wakefulness | veditors =  Monti J, Pandi-Perumal SR, Sinton CM | location = Cambridge | publisher = Cambridge University Press | isbn = 978-0-521-86441-1 | pages = 85–108 }}</ref>

Unlike the abrupt transitions in electrical patterns, the chemical changes in the brain show continuous periodic oscillation.<ref name=McCarley2007>{{cite journal | vauthors = McCarley RW | title = Neurobiology of REM and NREM sleep | journal = Sleep Medicine | volume = 8 | issue = 4 | pages = 302–30 | date = June 2007 | pmid = 17468046 | doi = 10.1016/j.sleep.2007.03.005 }}</ref>

==== Models of REM regulation ====

According to the [[activation-synthesis hypothesis]] proposed by [[Robert McCarley]] and [[Allan Hobson]] in 1975–1977, control over REM sleep involves pathways of "REM-on" and "REM-off" neurons in the brain stem. REM-on neurons are primarily cholinergic (i.e., involve acetylcholine); REM-off neurons activate serotonin and noradrenaline, which among other functions suppress the REM-on neurons. McCarley and Hobson suggested that the REM-on neurons actually stimulate REM-off neurons, thereby serving as the mechanism for the cycling between REM and non-REM sleep.<ref name=BrownMcCarley /><ref name=MallickEtAl /><ref name=AstonJonesEtAl /><ref name=HobsonMcCarley1977>{{cite journal | vauthors = Hobson JA, McCarley RW | title = The brain as a dream state generator: an activation-synthesis hypothesis of the dream process | journal = The American Journal of Psychiatry | volume = 134 | issue = 12 | pages = 1335–48 | date = December 1977 | pmid = 21570 | doi = 10.1176/ajp.134.12.1335 }}</ref> They used [[Lotka–Volterra equation]]s to describe this cyclical inverse relationship.<ref name="Steriade_2013" />{{rp|§12.2 369–373}}  Kayuza Sakai and Michel Jouvet advanced a similar model in 1981.<ref name=LuppiEtAl /> Whereas acetylcholine manifests in the cortex equally during wakefulness and REM, it appears in higher concentrations in the brain stem during REM.<ref>{{cite book | vauthors = Lydic R, Baghdoyan HA | chapter = Acetylcholine modulates sleep and wakefulness: a synaptic perspective | veditors = Monti J, Pandi-Perumal SR, Sinton CM | title = Neurochemistry of Sleep and Wakefulness | date = 17 January 2008 | publisher = Cambridge University Press | isbn = 978-1-139-46789-6 }}</ref> The withdrawal of orexin and GABA  may cause the absence of the other excitatory neurotransmitters;<ref name = "Parmeggiani_2011">{{cite book | vauthors = Parmeggiani PL | date = 2011 | title = Systemic Homeostasis and Poikilostasis in Sleep: Is REM Sleep a Physiological Paradox? | location = London | publisher = Imperial College Press | isbn = 978-1-84816-572-4 }}</ref>{{rp|16}} researchers in recent years increasingly include GABA regulation in their models.<ref>{{cite book | vauthors = McKenna JT, Chen L, McCarley RW | chapter = Neuronal models of REM-sleep control: evolving concepts. | veditors = Mallick BN, Pandi-Perumal SR, McCarley RW, Morrison AR  | title = REM sleep: regulation and function | date = July 2011 | pages = 285–299 | publisher = Cambridge University Press| location = Cambridge }}</ref>

=== Eye movements ===
Most of the [[eye movements]] in "rapid eye movement" sleep are in fact less rapid than those normally exhibited by waking humans. They are also shorter in duration and more likely to loop back to their starting point. About seven such loops take place over one minute of REM sleep. In slow-wave sleep, the eyes can drift apart; however, the eyes of the paradoxical sleeper move in tandem.<ref name="Steriade_2013" />{{rp|§10.7.2 307–309}} These eye movements follow the ponto-geniculo-occipital waves originating in the brain stem.<ref name=Datta /><ref name=ErmisEtAl /> The eye movements themselves may relate to the sense of vision experienced in the dream,<ref>{{cite journal | vauthors = Andrillon T, Nir Y, Cirelli C, Tononi G, Fried I | title = Single-neuron activity and eye movements during human REM sleep and awake vision | journal = Nature Communications | volume = 6 | issue = 1038 | pages = 7884 | date = August 2015 | pmid = 26262924 | pmc = 4866865 | doi = 10.1038/ncomms8884 | bibcode = 2015NatCo...6.7884A }}</ref> but a direct relationship remains to be clearly established. Congenitally blind people, who do not typically have visual imagery in their dreams, still move their eyes in REM sleep.<ref name=HobsonEtAl2000 /> An alternative explanation suggests that the functional purpose of REM sleep is for procedural memory processing, and the rapid eye movement is only a side effect of the brain processing the eye-related procedural memory.<ref>{{cite book | vauthors = Zhang J |year=2005 |title=Continual-activation theory of dreaming, Dynamical Psychology |url= http://www.goertzel.org/dynapsyc/2005/ZhangDreams.htm }}</ref><ref>{{cite book | vauthors = Zhang J |year=2016 |title=Towards a comprehensive model of human memory |doi=10.13140/RG.2.1.2103.9606 |url=https://www.researchgate.net/publication/304604880}}</ref>

=== Circulation, respiration, and thermoregulation ===

Generally speaking, the body suspends [[homeostasis]] during paradoxical sleep. [[Heart rate]], cardiac pressure, [[cardiac output]], [[Blood pressure|arterial pressure]], and [[respiratory rate|breathing rate]] quickly become irregular when the body moves into REM sleep.<ref name = "Parmeggiani_2011" />{{rp|12–15}} In general, respiratory reflexes such as response to [[Hypoxia (medical)|hypoxia]] diminish. Overall, the brain exerts less control over breathing; electrical stimulation of respiration-linked brain areas does not influence the lungs, as it does during non-REM sleep and in waking.<ref name = "Parmeggiani_2011" />{{rp|35–15}}

[[Erection]]s of the [[penis]] ([[nocturnal penile tumescence]] or NPT) normally accompany REM sleep in rats and humans.<ref name = "Jouvet_1999">{{cite book | vauthors = [[Michel Jouvet|Jouvet M]] | date = 1999 | title = The Paradox of Sleep: The Story of Dreaming | translator-last1= Garey |translator-first1= Laurence | name-list-style = vanc | location = Cambridge | publisher = MIT Press | isbn = 0-262-10080-0 }}</ref>{{rp|169–173}} If a male has [[erectile dysfunction]] (ED) while awake, but has NPT episodes during REM, it would suggest that the ED is from a psychological rather than a physiological cause. In females, erection of the [[clitoris]] ([[nocturnal clitoral tumescence]] or NCT) causes enlargement, with accompanying vaginal blood flow and transudation (i.e. lubrication). During a normal night of sleep, the penis and clitoris may be erect for a total time of from one hour to as long as three and a half hours during REM.<ref>{{cite journal | vauthors = Brown RE, Basheer R, McKenna JT, Strecker RE, McCarley RW | title = Control of sleep and wakefulness | journal = Physiological Reviews | volume = 92 | issue = 3 | pages = 1087–1187 (1127) | date = July 2012 | pmid = 22811426 | pmc = 3621793 | doi = 10.1152/physrev.00032.2011 }}</ref>

Body temperature is not well regulated during REM sleep, and thus organisms become more sensitive to temperatures outside their [[thermoneutral zone]]. Cats and other small furry mammals will [[shiver]] and [[tachypnea|breathe faster]] to regulate temperature during NREMS—but not during REMS.<ref name = "Parmeggiani_2011" />{{rp|12–13}} With the loss of muscle tone, animals lose the ability to regulate temperature through body movement. (However, even cats with pontine lesions preventing muscle atonia during REM did not regulate their temperature by shivering.)<ref name = "Parmeggiani_2011" />{{rp|51–52}} Neurons that typically activate in response to cold temperatures—triggers for neural thermoregulation—simply do not fire during REM sleep, as they do in NREM sleep and waking.<ref name = "Parmeggiani_2011" />{{rp|51–52}}

Consequently, hot or cold environmental temperatures can reduce the proportion of REM sleep, as well as amount of total sleep.<ref>{{cite book | vauthors = Szymusiak R, Alam MN, McGinty D | date = 1999 | chapter = Thermoregulatory Control of the NonREM-REM Sleep Cycle | title = Rapid Eye Movement Sleep | publisher = CRC Press | veditors = Mallick BN, Inoué S | isbn = 978-0-8247-0322-6 }}</ref><ref name = "Parmeggiani_2011" />{{rp|57–59}} In other words, if at the end of a phase of deep sleep, the organism's thermal indicators fall outside of a certain range, it will not enter paradoxical sleep lest deregulation allow temperature to drift further from the desirable value.<ref name = "Parmeggiani_2011" />{{rp|45}} This mechanism can be 'fooled' by artificially warming the brain.<ref name = "Parmeggiani_2011" />{{rp|61}}

=== Muscle ===

'''REM atonia''', an almost complete paralysis of the body, is accomplished through the inhibition of [[motor neurons]]. When the body shifts into REM sleep, motor neurons throughout the body undergo a process called [[hyperpolarization (biology)|hyperpolarization]]:<ref>{{cite journal | vauthors = Brooks PL, Peever JH | title = Unraveling the mechanisms of REM sleep atonia | journal = Sleep | volume = 31 | issue = 11 | pages = 1492–1497 | date = November 2008 | pmid = 19226735 | pmc = 2579970 | doi = 10.1093/sleep/31.11.1492 }}</ref> their already-negative [[membrane potential]] decreases by another 2–10 [[Volt|millivolts]], thereby raising the threshold which a stimulus must overcome to excite them. Muscle inhibition may result from unavailability of monoamine neurotransmitters (restraining the abundance of acetylcholine in the brainstem) and perhaps from mechanisms used in waking muscle inhibition.<ref name="Steriade_2013" />{{rp|§10.8–9.1 309–324}} The [[medulla oblongata]], located between pons and spine, seems to have the capacity for organism-wide muscle inhibition.<ref name=LaiSiegel>{{cite book | vauthors = Lai YY, Siegel JM | date = 1999 | chapter = Muscle Atonia in REM Sleep | title = Rapid Eye Movement Sleep | publisher = CRC Press | veditors = Mallick BN, Inoué S | isbn = 978-0-8247-0322-6 }}</ref> Some localized twitching and reflexes can still occur.<ref name = "Parmeggiani_2011" />{{rp|17}} Pupils contract.<ref name=Siegel2009>{{cite journal | vauthors = Siegel JM | title = The neurobiology of sleep | journal = Seminars in Neurology | volume = 29 | issue = 4 | pages = 277–296 | date = September 2009 | pmid = 19742406 | pmc = 8809119 | doi = 10.1055/s-0029-1237118 }}</ref>

Lack of REM [[atonia]] causes [[REM behavior disorder]], where those affected physically act out their dreams,<ref name="pmid1620348">{{cite journal | vauthors = Lapierre O, Montplaisir J | title = Polysomnographic features of REM sleep behavior disorder: development of a scoring method | journal = Neurology | volume = 42 | issue = 7 | pages = 1371–1374 | date = July 1992 | pmid = 1620348 | doi = 10.1212/wnl.42.7.1371 | s2cid = 25312217 }}</ref> or conversely "dream out their acts", under an alternative theory on the relationship between muscle impulses during REM and associated mental imagery (which would also apply to people without the condition, except that commands to their muscles are suppressed).<ref name="Steriade_2013" />{{rp|§13.3.2.3 428–432}} This is different from conventional [[sleepwalking]], which takes place during slow-wave sleep, not REM.<ref name = "Jouvet_1999" />{{rp|102}} [[Narcolepsy]], by contrast, seems to involve excessive and unwanted REM atonia: [[cataplexy]] and [[excessive daytime sleepiness]] while awake, [[hypnagogic hallucinations]] before entering slow-wave sleep, or [[sleep paralysis]] while waking.<ref name="Steriade_2013" />{{rp|§13.1 396–400}} Other psychiatric disorders including depression have been linked to disproportionate REM sleep.<ref name="Steriade_2013" />{{rp|§13.2 400–415}} Patients with suspected sleep disorders are typically evaluated by [[polysomnogram]].<ref>{{cite journal | vauthors = Koval'zon VM | title = [Central mechanisms of sleep-wakefulness cycle] | journal = Fiziologiia Cheloveka | volume = 37 | issue = 4 | pages = 124–134 | date = Jul–Aug 2011 | pmid = 21950094 }}</ref><ref>{{cite web |title=Polysomnography |url= https://www.nlm.nih.gov/medlineplus/ency/article/003932.htm |access-date=2 November 2011 | work = Medline Plus | publisher = U.S. National Library of Medicine }}</ref>

Lesions of the pons to prevent atonia have induced functional "REM behavior disorder" in animals.<ref name = "Parmeggiani_2011" />{{rp|87}}