Editing Sleep paralysis (section)

== Pathophysiology ==
The pathophysiology of sleep paralysis has not been concretely identified, although there are several theories about its cause.<ref name=":0">{{cite book|title=Unusual and rare psychological disorders: a handbook for clinical practice and research|last=A.|first=Sharpless, Brian|isbn=978-0-19-024586-3|oclc=952152912|date = 2016-11-15|publisher=Oxford University Press }}</ref> The first of these stems from the understanding that sleep paralysis is a [[parasomnia]] resulting from dysfunctional overlap of the REM and waking stages of sleep.<ref name=Goldstein>{{cite journal|last=Goldstein |first=K. |title=Parasomnias|journal=Disease-a-Month|year=2011|volume=57 |pages=364–88|doi=10.1016/j.disamonth.2011.04.007 |pmid=21807161 |issue=7}}</ref> Polysomnographic studies have found that individuals who experience sleep paralysis have shorter REM sleep latencies than normal along with shortened NREM and REM sleep cycles, and fragmentation of REM sleep. This study supports the observation that disturbance of regular sleeping patterns can precipitate an episode of sleep paralysis, because fragmentation of REM sleep commonly occurs when sleep patterns are disrupted and has now been seen in combination with sleep paralysis.<ref name="Walther">{{cite journal |last1=Walther |first1=B. |last2=Schulz |first2=H. |year=2004 |title=Recurrent isolated sleep paralysis: Polysomnographic and clinical findings |journal=Somnologie – Schlafforschung und Schlafmedizin |volume=8 |issue=2 |pages=53–60 |doi=10.1111/j.1439-054X.2004.00017.x |s2cid=143146512}}</ref>

Another major theory is that the neural functions that regulate sleep are out of balance, causing different sleep states to overlap. In this case, cholinergic sleep "on" [[neural population]]s are hyperactivated and the serotonergic sleep "off" neural populations are under-activated. As a result, the cells capable of sending the signals, that would allow for complete arousal from the sleep state, the serotonergic neural populations, have difficulty in overcoming the signals sent by the cells that keep the brain in the sleep state. During normal REM sleep, the threshold for a stimulus to cause arousal is greatly elevated. Under normal conditions, medial and [[vestibular nuclei]], [[Cortex (anatomy)|cortical]], [[thalamic]], and [[cerebellar]] centers coordinate things such as head and eye movement, and orientation in space.<ref name=Cheyneninenine />

In individuals reporting sleep paralysis, there is almost no blocking of exogenous stimuli, which means it is much easier for a stimulus to arouse the individual. The [[vestibular nuclei]] in particular has been identified as being closely related to dreaming during the REM stage of sleep.<ref name=Cheyneninenine /> According to this hypothesis, vestibular-motor disorientation, unlike hallucinations, arise from completely endogenous sources of stimuli.<ref name="Cheynetwothree">{{cite journal |last=Cheyne |first=J. |year=2003 |title=Sleep Paralysis and the Structure of Waking-Nightmare Hallucinations |journal=[[Dreaming (journal)|Dreaming]] |volume=13 |issue=3 |pages=163–179 |doi=10.1023/A:1025373412722 |s2cid=145006406}}</ref>

If the effects of sleep "on" neural populations cannot be counteracted, characteristics of REM sleep are retained upon awakening. Common consequences of sleep paralysis include headaches, muscle pains or weakness or paranoia. As the correlation with REM sleep suggests, the paralysis is not complete: use of [[EOG]] traces shows that eye movement is still possible during such episodes; however, the individual experiencing sleep paralysis is unable to speak.<ref>Hearne, K. (1990). ''The Dream Machine: Lucid dreams and how to control them'', p. 18. {{ISBN|0-85030-906-9}}.</ref>

Research has found a genetic component in sleep paralysis.<ref>(Sehgal 2011)</ref> The characteristic fragmentation of REM sleep, [[hypnopompic]], and [[Hypnagogia|hypnagogic]] hallucinations have a heritable component in other parasomnias, which lends credence to the idea that sleep paralysis is also genetic. Twin studies have shown that if one twin of a monozygotic pair ([[Twin#Monozygotic (identical) twins|identical twins]]) experiences sleep paralysis that the other twin is very likely to experience it as well.<ref name="Sehgal">{{cite journal |last1=Sehgal |first1=A. |last2=Mignot |first2=E. |year=2011 |title=Genetics of Sleep and Sleep Disorders |journal=Cell |volume=146 |issue=2 |pages=194–207 |doi=10.1016/j.cell.2011.07.004 |pmc=3153991 |pmid=21784243}}</ref> The identification of a genetic component means that there is some sort of disruption of a function at the physiological level. Further studies must be conducted to determine whether there is a mistake in the signaling pathway for arousal as suggested by the first theory presented, or whether the regulation of melatonin or the neural populations themselves have been disrupted.

===Hallucinations===
[[File:Fritz Schwimbeck - My Dream, My Bad Dream. 1915.jpg|thumb|upright=1.3|A picture of a [[succubus]]-like vision. ''My Dream, My Bad Dream'', 1915, by Fritz Schwimbeck]]

Several types of hallucinations have been linked to sleep paralysis: the belief that there is an intruder in the room, the feeling of a presence, and the sensation of floating. One common hallucination is the presence of an [[incubus]]. A neurological hypothesis is that in sleep paralysis the [[cerebellum]], which usually coordinates body movement and provides information on body position, experiences a brief myoclonic spike in brain activity inducing a [[floating (psychological phenomenon)|floating]] sensation.<ref name=Cheynetwothree />

The [[trespasser|intruder]] and incubus hallucinations highly correlate with one another, and moderately correlated with the third hallucination, vestibular-motor disorientation, also known as [[out-of-body experience]]s,<ref name=Cheynetwothree /> which differ from the other two in not involving the threat-activated vigilance system.<ref name=FISP />

=== Threat hyper-vigilance ===
A [[Hypervigilance|hyper-vigilant]] state created in the [[midbrain]] may further contribute to hallucinations.<ref name="Cheyneninenine" /> More specifically, the emergency response is activated in the brain when individuals wake up paralyzed and feel vulnerable to attack. This helplessness can intensify the effects of the threat response well above the level typical of normal dreams, which could explain why such visions during sleep paralysis are so vivid. The threat-activated vigilance system is a protective mechanism that differentiates between dangerous situations and determines whether the fear response is appropriate.<ref name="Cheynetwothree" />

The hyper-vigilance response can lead to the creation of endogenous stimuli that contribute to the perceived threat.<ref name=Cheyneninenine /> A similar process may explain hallucinations, with slight variations, in which an evil presence is perceived by the subject to be attempting to suffocate them, either by pressing heavily on the chest or by strangulation. A neurological explanation holds that this results from a combination of the threat vigilance activation system and the muscle paralysis associated with sleep paralysis that removes voluntary control of breathing. Several features of REM breathing patterns exacerbate the feeling of suffocation.<ref name=Cheynetwothree /> These include shallow rapid breathing, [[hypercapnia]], and slight blockage of the airway, which is a symptom prevalent in [[sleep apnea]] patients.<ref name=Cheyneninenine />

According to this account, the subjects attempt to breathe deeply and find themselves unable to do so, creating a sensation of resistance, which the threat-activated vigilance system interprets as an unearthly being sitting on their chest, threatening suffocation.<ref name=Cheyneninenine /> The sensation of entrapment causes a feedback loop when the fear of suffocation increases as a result of continued helplessness, causing the subjects to struggle to end the SP episode.<ref name=Cheynetwothree />