Sleep paralysis

Sleep paralysis

The Nightmare, by Henry Fuseli (1781) is thought to be one of the classic depictions of sleep paralysis perceived as a demonic visitation.
Classification and external resources
Specialty Sleep medicine
DiseasesDB 12182
MeSH D020188

Sleep paralysis is a phenomenon in which a person either during falling asleep (hypnagogia) or awakening (hypnopompia), temporarily experiences an inability to move, speak, or react.

It is a transitional state between wakefulness and sleep, characterized by muscle atonia (muscle weakness). It is often accompanied by terrifying hallucinations (such as an intruder in the room) to which one is unable to react due to paralysis, and physical experiences (such as strong current running through the upper body).

One hypothesis is that it results from disrupted REM sleep, which normally induces complete muscle atonia to prevent sleepers from acting out their dreams. Sleep paralysis has been linked to disorders such as narcolepsy, migraines, anxiety disorders, and obstructive sleep apnea; however, it can also occur in isolation.[1][2]

Classification

The two major classifications of sleep paralysis are isolated sleep paralysis (ISP) and the significantly rarer recurrent isolated sleep paralysis (RISP).[2] ISP episodes are infrequent, and may occur only once in an individual's lifetime,[2] while recurrent isolated sleep paralysis is a chronic condition, and can recur throughout a person's lifetime.[2] RISP episodes can last for up to an hour or longer, and have a much higher occurrence of perceived out of body experiences, while ISP episodes are generally short (usually no longer than one minute) and are typically associated with the intruder and incubus visitations. With RISP the individual can also suffer back-to-back episodes of sleep paralysis in the same night, which is unlikely in individuals who suffer from ISP.[2]

It can be difficult to differentiate between cataplexy brought on by narcolepsy and true sleep paralysis, because the two phenomena are physically indistinguishable.[2] The best way to differentiate between the two is to note when the attacks occur most often. Narcolepsy attacks are more common when the individual is falling asleep; ISP and RISP attacks are more common upon awakening.[3]

Signs and symptoms

A notable depiction of a Succubus-like vision, in contrast to the Incubus. My Dream, My Bad Dream, 1915, by Fritz Schwimbeck

Physiologically, sleep paralysis is closely related to REM atonia, the paralysis that occurs as a natural part of REM (rapid eye movement) sleep. Sleep paralysis occurs either when falling asleep, or when awakening from sleep. When it occurs upon falling asleep, the person remains aware while the body shuts down for REM sleep, a condition called hypnagogic or predormital sleep paralysis. When it occurs upon awakening, the person becomes aware before the REM cycle is complete, and it is called hypnopompic or postdormital.[4] The paralysis can last from several seconds to several minutes, with some rare cases being hours, "by which the individual may experience panic symptoms"[5] (described below). 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.[6]

Le Cauchemar (The Nightmare), by Eugène Thivier (1894)

Hypnagogic and hypnopompic visions and hearing a demonic voice when resistance is attempted are symptoms commonly experienced during episodes of sleep paralysis. Some scientists have proposed this condition as an explanation for reports of ghost parasites and alien visits.[7][8] Some suggest that reports of extraterrestrial involvements are related to sleep paralysis rather than to temporal lobe lability.[9] There are three main types of these visions that can be linked to pathologic neurophysiology: the belief that there is an intruder in the room, the incubus, and vestibular motor sensations.[7][10]

Many people who experience sleep paralysis are struck with a deep sense of terror when they sense a menacing presence in the room while paralyzed—hereafter referred to as the intruder. A neurological interpretation of this phenomenon is that it results from a hyper-vigilant state created in the midbrain.[10] More specifically, the emergency response is activated in the brain when individuals wake up paralyzed and feel vulnerable to attack.[7] 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.[7] Normally the threat-activated vigilance system is a protective mechanism to differentiate between dangerous situations and to determine whether the fear response is appropriate.[7] Some hypothesize that the threat vigilance system is evolutionarily biased to interpret ambiguous stimuli as dangerous, because "erring on the side of caution" increases survival chances.[7] This hypothesis could account for why the threatening presence is perceived as being evil.[7] The amygdala is heavily involved in the threat activation response mechanism, which is implicated in both intruder and incubus SP visions.[3]

The specific pathway through which the threat-activated vigilance system acts is not well understood. One possibility is that the thalamus receives sensory information and sends it on the amygdala, which regulates emotional experience. Another is that the amygdaloid complex, anterior cingulate, and the structures in the pontine tegmentum interact to create the vision.[10] It is also highly possible that SP hallucinations could result from a combination of these. The anterior cingulate has an extensive array of cortical connections to other cortical areas, which enables it to integrate the various sensations and emotions into the unified sensorium we experience.[10] The amygdaloid complex helps us interpret emotional experience and act appropriately.[11] This is conducive to directing the individual's attention to the most pertinent stimuli in a potentially dangerous situation so that the individual can take self-protective measures.[11]

Proper amygdaloid complex function requires input from the thalamus, which creates a thalamoamygdala pathway capable of bypassing the intense scrutiny of incoming stimuli to enable quick responses in a potentially life-threatening situation.[10][11] Typically, situations assessed as non-threatening are disregarded. In sleep paralysis, however, those pathways can become over-excited and move into a state of hyper-vigilance in which the mind perceives every external stimulus as a threat. The hyper-vigilance response can lead to the creation of endogenous stimuli that contribute to the perceived threat.[10] A similar process may explain the experience of the incubus presence, with slight variations, in which the evil presence is perceived by the subject to be attempting to suffocate them, either by pressing heavily on the chest or by strangulation.[7]

A neurological explanation hold 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.[7] Several features of REM breathing patterns exacerbate the feeling of suffocation.[7] These include shallow rapid breathing, hypercapnia, and slight blockage of the airway, which is a symptom prevalent in sleep apnea patients.[10] According to this account, the subject attempts to breathe deeply and finds herself unable to do so, creating a sensation of resistance, which the threat-activated vigilance system interprets as an unearthly being sitting on her chest, threatening suffocation.[10] The sensation of entrapment causes a feedback loop when the fear of suffocation increases as a result of continued helplessness, causing the subject to struggle to end the SP episode.[7]

The intruder and incubus experiences highly correlate with one another, and moderately correlate with the third characteristic experience, vestibular-motor disorientation, also known as out-of-body experiences,[7] which differ from the other two in not involving the threat-activated vigilance system.[3] Under normal conditions, medial and vestibular nuclei, cortical, thalamic, and cerebellar centers coordinate things such as head and eye movement, and orientation in space.[10] A neurological hypothesis is that in sleep paralysis, these mechanisms—which usually coordinate body movement and provide information on body position—become activated and, because there is no actual movement, induce a floating sensation.[7] The vestibular nuclei in particular has been identified as being closely related to dreaming during the REM stage of sleep.[10] According to this hypothesis, vestibular-motor disorientation, unlike the intruder and incubus experiences, arise from completely endogenous sources of stimuli.[7]

Pathophysiology

The pathophysiology of sleep paralysis has not been concretely identified, although there are several theories about its etiology. 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.[12] Polysomnographic studies 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.[13] This study supports the observation that disturbance of regular sleeping patterns can instigate 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.[13]

Another major theory is that the neural functions that regulate sleep are out of balance in such a way that causes different sleep states to overlap.[10] In this case, cholinergic sleep on neural populations are hyper activated and the serotonergic sleep off neural populations are under-activated.[10] 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.[10] During normal REM sleep, the threshold for a stimulus to cause arousal is greatly elevated. However, in individuals with SP, there is almost no blocking of exogenous stimuli, which means it is much easier for a stimulus to arouse the individual.[10] There may also be a problem with the regulation of melatonin, which under normal circumstances regulates the serotonergic neural populations.[2] Melatonin is typically at its lowest point during REM sleep.[2] Inhibition of melatonin at an inappropriate time would make it impossible for the sleep off neural populations to depolarize when presented with a stimulus that would normally lead to complete arousal.[2] This could explain why the REM and waking stages of sleep overlap during sleep paralysis, and definitely explains the muscle paralysis experienced on awakening.[2] If the effects of sleep on neural populations cannot be counteracted, characteristics of REM sleep are retained upon awakening. Common consequences of sleep paralysis includes headaches, muscle pains or weakness and/or paranoia.

Research has found a genetic component in sleep paralysis.[14] The characteristic fragmentation of REM sleep, hypnopompic, and hypnagogic hallucinations have a heritable component in other parasomnias, which lends credence to the idea that sleep paralysis is also genetic.[15] Twin studies have shown that if one twin of a monozygotic pair experiences sleep paralysis that other twin is very likely to experience it as well.[15] The identification of a genetic component means that there is some sort of disruption of 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.

Sleep paralysis could also be a part of a larger diagnosis because of the dissociative state seen during sleep paralysis. Like mentioned earlier patients, especially with narcolepsy, seem to have trouble distinguishing between states of wakefulness and sleep. They are unable to tell if what they are experiencing is a dream or if it is reality. Many patients can recall talking to a doctor if they are in the hospital or family and friends but they are uncertain if this memory was from a state of wakefulness or was experienced in REM sleep. Their recall is very similar to patients who suffer from delirium, which is why some experts conclude there is a dissociative state in sleep paralysis.[16]

Another possible cause of sleep paralysis is depression. There is a correlation between depression and sleep disturbances, sleep paralysis being one of them. In people that are depressed there is about an 11% frequency of people that have sleep paralysis. The reasoning behind this is the depression causes disturbances in the REM sleep cycle.[17]

Diagnosis

Sleep paralysis is mainly diagnosed by ruling out other potential sleep disorders that could account for the feelings of paralysis.[12] The main disorder that is checked for is narcolepsy due to the high prevalence of narcolepsy in conjunction with sleep paralysis. The availability of a genetic test for narcolepsy makes this an easy disorder to rule out.[15] Once all other conditions have been ruled out, the description that the patient gives of their episode is compared to the typical experiences of sleep paralysis that have been well documented.[12] If the two descriptions match and no other sleep disorder can account for the symptoms, the patient is diagnosed with sleep paralysis.[12]

Prevention

Several circumstances have been identified that are associated with an increased risk of sleep paralysis. These include insomnia and sleep deprivation, an erratic sleep schedule, stress, overuse of stimulants, physical fatigue, as well as certain medications that are used to treat ADHD.[2] It is also believed that there may be a genetic component in the development of RISP due to a high concurrent incidence of sleep paralysis in monozygotic twins.[15] Sleeping in the supine position has been found an especially prominent instigator of sleep paralysis.[18]

Sleeping in the supine position is believed to make the sleeper more vulnerable to episodes of sleep paralysis because in this sleeping position it is possible for the soft palate to collapse and obstruct the airway.[18] This is a possibility regardless of whether the individual has been diagnosed with sleep apnea or not. There may also be a greater rate of microarousals while sleeping in the supine position because there is a greater amount of pressure being exerted on the lungs by gravity.[18]

While many factors can increase risk for ISP or RISP, they can be avoided with minor lifestyle changes.[12] By maintaining a regular sleep schedule and observing good sleep hygiene, one can reduce chances of sleep paralysis. It helps subjects to reduce the intake of stimulants and stress in daily life by taking up a hobby or seeing a trained psychologist who can suggest coping mechanisms for stress. However, some cases of ISP and RISP involve a genetic factor—which means some people may find sleep paralysis unavoidable.

Treatment

Anecdotal reports indicate that wiggling fingers or toes upon awareness of the condition may enable the sufferer to move again in some cases. Medical treatment starts with education about sleep stages and the inability to move muscles during REM sleep. People should be evaluated for narcolepsy if symptoms persist.[19] The safest treatment for sleep paralysis is for people to adopt healthier sleeping habits. However, in serious cases more clinical treatments are available. The most commonly used drugs are tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs).[20] Despite the fact that these treatments are prescribed for serious cases of RISP, it is important to note that these drugs are not effective for everyone. There is currently no drug that has been found to completely interrupt episodes of sleep paralysis a majority of the time.[20]

Prognosis

Sleep paralysis poses no immediate risk to those who experience it, despite the fact that it can be an intensely terrifying experience.[2]

Epidemiology

Isolated sleep paralysis is commonly seen in patients that have been diagnosed with narcolepsy. Approximately 30–50% of people that have been diagnosed with narcolepsy have experienced sleep paralysis as an auxiliary symptom.[1][21] The prevalence of sleep paralysis in the general population is approximately 6.2%. A majority of the individuals who have experienced sleep paralysis have sporadic episodes that occur once a month to once a year. Only 3% of individuals experiencing sleep paralysis that is not associated with a neuromuscular disorder have nightly episodes, as mentioned earlier, these individuals are diagnosed as having RISP.[1] Sleep paralysis is just as common for males as it is for females; however, different age groups have been found to be more susceptible to developing isolated sleep paralysis. Approximately 36% of the general population that experiences isolated sleep paralysis is likely to develop it between 25 and 44 years of age.[1]

History

The original definition of sleep paralysis was codified by Samuel Johnson in his A Dictionary of the English Language as nightmare, a term that evolved into our modern definition. Such sleep paralysis was widely considered the work of demons, and more specifically incubi, which were thought to sit on the chests of sleepers. In Old English the name for these beings was mare or mære (from a proto-Germanic *marōn, cf. Old Norse mara), hence comes the mare in the word nightmare. The word might be etymologically cognate to Greek Marōn (in the Odyssey) and Sanskrit Māra.

Various forms of magic and spiritual possession were also advanced as causes. In nineteenth century Europe, the vagaries of diet were thought to be responsible. For example, in Charles Dickens's A Christmas Carol, Ebenezer Scrooge attributes the ghost he sees to "... an undigested bit of beef, a blot of mustard, a crumb of cheese, a fragment of an underdone potato..." In a similar vein, the Household Cyclopedia (1881) offers the following advice about nightmares:

"Great attention is to be paid to regularity and choice of diet. Intemperance of every kind is hurtful, but nothing is more productive of this disease than drinking bad wine. Of eatables those which are most prejudicial are all fat and greasy meats and pastry... Moderate exercise contributes in a superior degree to promote the digestion of food and prevent flatulence; those, however, who are necessarily confined to a sedentary occupation, should particularly avoid applying themselves to study or bodily labor immediately after eating... Going to bed before the usual hour is a frequent cause of night-mare, as it either occasions the patient to sleep too long or to lie long awake in the night. Passing a whole night or part of a night without rest likewise gives birth to the disease, as it occasions the patient, on the succeeding night, to sleep too soundly. Indulging in sleep too late in the morning, is an almost certain method to bring on the paroxysm, and the more frequently it returns, the greater strength it acquires; the propensity to sleep at this time is almost irresistible."[22]

Society and culture

Main article: Night hag

The night hag is a generic name for a fantastical creature from the folklore of various peoples which is used to explain the phenomenon of sleep paralysis. A common description is that a person feels a presence of a supernatural malevolent being which immobilizes the person as if sitting on his/her chest.[23] Various cultures have various names for this phenomenon and/or supernatural character.

The Nightmare is a 2015 documentary that discusses the causes of sleep paralysis as seen through extensive interviews with participants, and the experiences are re-enacted by professional actors. In synopsis, it proposes that such cultural memes as alien abduction and shadow people can, in many cases, be attributed to sleep paralysis. The "real-life" horror film debuted at the Sundance Film Festival on January 26, 2015 and premiered in theatres on June 5, 2015.[24]

See also

References

  1. 1 2 3 4 Ohayon, M.; Zulley, J.; Guilleminault, C.; Smirne, S. (1999). "Prevalence and pathologic associations of sleep paralysis in the general population". Neurology 52 (6): 1194–2000. doi:10.1212/WNL.52.6.1194.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 Terrillon, J.; Marques-Bonham, S. (2001). "Does Recurrent Isolated Sleep Paralysis Involve More Than Cognitive Neurosciences?". Journal of Scientific Exploration 15: 97–123.
  3. 1 2 3 Sharpless, B.; McCarthy, K.; Chambless, D.; Milrod, B.; Khalsa, S.; Barber, J. (2010). "Isolated sleep paralysis and fearful isolated sleep paralysis in outpatients with panic attacks". Journal of Clinical Psychology 66 (12): 1292–1306. doi:10.1002/jclp.20724. PMID 20715166.
  4. ↑ "Sleep Paralysis Symptoms, Treatment, and Causes".
  5. ↑ Hersen, Turner & Beidel. (2007) Adult Psychopathology and Diagnosis. p. 380
  6. ↑ Hearne, K. (1990) The Dream Machine: Lucid dreams and how to control them, p18. ISBN 0-85030-906-9
  7. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Cheyne, J. (2003). "Sleep Paralysis and the Structure of Waking-Nightmare Hallucinations". Dreaming 13 (3): 163–179. doi:10.1023/A:1025373412722.
  8. ↑ McNally RJ, Clancy SA. (2005). "Sleep Paralysis, Sexual Abuse, and Space Alien Abduction". Transcultural Psychiatry 42 (1): 113–122. doi:10.1177/1363461505050715. PMID 15881271.
  9. ↑ Blackmore, Susan; Marcus Cox. "Alien Abductions, Sleep Paralysis and the Temporal Lobe". European Journal of UFO and Abduction Studies (1): 113–118. Retrieved 2008-07-26.
  10. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Cheyne, J.; Rueffer, S.; Newby-Clark, I. (1999). "Hypnagogic and Hypnopompic Hallucinations during Sleep Paralysis: Neurological and Cultural Construction of the Night-Mare". Consciousness and Cognition 8 (3): 319–337. doi:10.1006/ccog.1999.0404. PMID 10487786.
  11. 1 2 3 Jolkkonen, E.; Miettinen, R.; Pikkarainen, M.; Pitkänen, A. (2002). "Projections from the amygdaloid complex to the magnocellular cholinergic basal forebrain in rats". Neuroscience 111 (1): 133–149. doi:10.1016/S0306-4522(01)00578-4. PMID 11955718.
  12. 1 2 3 4 5 Goldstein, K. (2011). "Parasomnias". Dis Mon 57 (7): 364–88. doi:10.1016/j.disamonth.2011.04.007. PMID 21807161.
  13. 1 2 Walther, B.; Schulz, H. (2004). "Recurrent isolated sleep paralysis: Polysomnographic and clinical findings". Somnologie – Schlafforschung und Schlafmedizin 8 (2): 53–60. doi:10.1111/j.1439-054X.2004.00017.x.
  14. ↑ (Sehgal 2011)
  15. 1 2 3 4 Sehgal, A.; Mignot, E. (2011). "Genetics of Sleep and Sleep Disorders". Cell 146 (2): 194–207. doi:10.1016/j.cell.2011.07.004. PMC 3153991. PMID 21784243.
  16. ↑ Terzaghi, M., Ratti, P., Manni, F., & Manni, R. (2012). Sleep paralysis in narcolepsy: more than just a motor dissociative phenomenon?. Neurological Sciences
  17. ↑ SZKLO-COXE, M., YOUNG, T., FINN, L., & MIGNOT, E. (2007). "Depression: relationships to sleep paralysis and other sleep disturbances in a community sample". Journal Of Sleep Research
  18. 1 2 3 Cheyne, J. (2002). "Situational factors affecting sleep paralysis and associated hallucinations: position and timing effects". Journal of Sleep Research 11 (2): 169–177. doi:10.1046/j.1365-2869.2002.00297.x. PMID 12028482.
  19. ↑ Wills L, Garcia J. Parasomnias: Epidemiology and Management. CNS Drugs [serial online]. December 2002;16(12):803–810.
  20. 1 2 Stores, G. (2003). "Medication for sleep-wake disorders". Archives of Disease in Childhood 88 (10): 899–903. doi:10.1136/adc.88.10.899. PMC 1719336. PMID 14500311.
  21. ↑ Dauvilliers, Y.; Billiard, M.; Montplaisir, J. (2003). "Clinical aspects and pathophysiology of narcolepsy". Clinical Neurophysiology 114 (11): 2000–2017. doi:10.1016/S1388-2457(03)00203-7. PMID 14580598.
  22. ↑ The Household Cyclopedia – Medicine
  23. ↑ Folklore: An Encyclopedia of Beliefs, Customs, Tales, Music, and Art, Volume 1, edited by Thomas A. Green, p. 588
  24. ↑

External links

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