|The Nightmare, by Henry Fuseli (1781) is thought to be one of the classic depictions of sleep paralysis perceived as a demonic visitation.|
|Similar conditions||Nacrolepsy, atonic seizure, hypokalemic periodic paralysis|
Sleep paralysis is a phenomenon in which an individual, either during falling asleep or awakening, briefly experiences an inability to move, speak, or react. It is sometimes accompanied by frightening hallucinations to which one is unable to react due to paralysis and perceived physical experiences, such as a strong current running through the upper body. Sleep paralysis poses no immediate risk to those who experience it, and it lasts from several seconds to several minutes.
Genetics and sleep deprivation are a major cause of sleep paralysis, and it has also been linked to disorders such as narcolepsy, migraines, stress, anxiety disorders, and obstructive sleep apnea. Sleeping in a fixed supine position increases the chance of sleep paralysis. The underlying mechanism is believed to result from disrupted REM sleep, when there should be a general inability to move muscle to prevent the sleeper from acting out their dreams.
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.
Signs and symptomsEdit
Humming, hissing, static, zapping and buzzing noises are reported during sleep paralysis. Imagined sounds (voices, whispers and roars) are also experienced. These symptoms are usually accompanied by intense emotions: such as fear, and panic. People also have sensations of being dragged out of bed or of flying, and feelings of electric tingles or vibrations running through their body.
Sleep paralysis may include hallucinations, such as a supernatural creature suffocating or terrifying the individual, accompanied by a feeling of pressure on one's chest and difficulty breathing. Another example of a hallucination involves a menacing shadowy figure entering one's room or lurking outside one's window, while the subject is paralyzed.
The body image distortion (affecting parietal regions and the temporoparietal junction) may result in the sleeper having bodily hallucinations, such as llusory limbs and out-of-body experiences. The content and interpretation of these hallucinations are driven by fear, somatic sensations, REM induced sexual arousal, and REM mentation which are embedded in the sleeper's cultural narrative.
REM sleep physiology and somatic symptoms coupled with the awareness that one is paralyzed, can generate a variety of psychological symptoms during sleep paralysis, including fear and worry that are aggravated by catastrophic cognitions about the attack. This can activate a fight-flight reaction and panic-like arousal. Consequently, when the person attempts to escape the paralysis, somatic symptoms and arousal are exacerbated, as execution of motor programs in the absence of dampening proprioceptive feedback can lead to heightened sensations of bodily tightness and pressure, and even pain and spasms in limbs.
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. 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. 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.
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. In this case, cholinergic sleep on neural populations are hyper activated 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, cortical, thalamic, and cerebellar centers coordinate things such as head and eye movement, and orientation in space.
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. There may also be a problem with the regulation of melatonin, which under normal circumstances regulates the serotonergic neural populations. Melatonin is typically at its lowest point during REM sleep. 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. The vestibular nuclei in particular has been identified as being closely related to dreaming during the REM stage of sleep. According to this hypothesis, vestibular-motor disorientation, unlike hallucinations, arise from completely endogenous sources of stimuli.
This could explain why the REM and waking stages of sleep overlap during sleep paralysis, and definitely explains the muscle paralysis experienced on awakening. 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. 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.
Research has found a genetic component in sleep paralysis. 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. 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. 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.
Three examples of hallucinations can be linked to pathologic neurophysiology: the belief that there is an intruder in the room, the incubus, and vestibular motor sensations. 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.
A neuroscientific explanation claims that hallucinations arise due to a functional disturbance in the multisensory processing of body and self at the temporoparietal junction (TPJ). During sleep paralysis there is a desynchrony between motor-execution and feedback from limbs (proprioception) which results in massive deafferentation (conflicting efferent and afferent neural conduction).
The parietal lobes are likely to play a pivotal role in this body image distortion during sleep paralysis. Especially the right superior parietal lobule (SPL) is involved in the construction of a neural representation of the body. This is broadly consistent with the laboratory finding that causing a functional disturbance in the TPJ through electric stimulation can induce an illusory shadow-like person mimicking one’s body postures.
The intruder and incubus hallucinations highly correlate with one another, and moderately correlate with the third hallucination, vestibular-motor disorientation, also known as out-of-body experiences, which differ from the other two in not involving the threat-activated vigilance system.
A hyper-vigilant state created in the midbrain may further contribute to hallucinations. 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.
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. This hypothesis could account for why the threatening presence is perceived as being evil. The amygdala is heavily involved in the threat activation response mechanism, which is implicated in hallucinations.
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. 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.
The amygdaloid complex helps us interpret emotional experience and act appropriately. 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. 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. 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. 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 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. Several features of REM breathing patterns exacerbate the feeling of suffocation. These include shallow rapid breathing, hypercapnia, and slight blockage of the airway, which is a symptom prevalent in sleep apnea patients.
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. 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.
Sleep paralysis is mainly diagnosed by ruling out other potential sleep disorders that could account for the feelings of paralysis. 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. 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. If the two descriptions match and no other sleep disorder can account for the symptoms, the patient is diagnosed with sleep paralysis.
The two major classifications of sleep paralysis are isolated sleep paralysis (ISP) and the significantly rarer recurrent isolated sleep paralysis (RISP - Recurrent Isolated Sleep Paralysis). ISP episodes are infrequent, and may occur only once in an individual's lifetime, while recurrent isolated sleep paralysis is a chronic condition, and can recur throughout a person's lifetime. 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 hallucinations. 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.
It can be difficult to differentiate between cataplexy brought on by narcolepsy and true sleep paralysis, because the two phenomena are physically indistinguishable. 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.
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, and physical fatigue. 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. Sleeping in the supine position has been found an especially prominent instigator of sleep paralysis.
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. 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.
While many factors can increase risk for ISP or RISP, they can be avoided with minor lifestyle changes. 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. Practicing meditation regularly might also be helpful in preventing fragmented sleep, and thus the occurrence of sleep paralysis. Research has shown that long-term meditation practitioners spend more time in slow wave sleep, and as such regular meditation practice could reduce nocturnal arousal and thus possibly sleep paralysis.
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. The safest treatment for sleep paralysis is for people to adopt healthier sleeping habits. However, in more serious cases tricyclic antidepressants or selective serotonin reuptake inhibitors (SSRIs) may be used. Despite the fact that these treatments are prescribed there is currently no drug that has been found to completely interrupt episodes of sleep paralysis a majority of the time. Anecdotal reports indicate that wiggling fingers or toes upon awareness of the condition may enable the person to move again.
Meditation-relaxation (MR) therapy is a proposed treatment for sleep paralysis. The treatment was partly derived from a suggestion that attempting movement during sleep paralysis (e.g., due to panic-like reactions) can lead to neurological distortions of one's "body image", possibly triggering hallucinations of shadowy human-like figures. The therapy is based on four steps applied during sleep paralysis: (1) reappraisal of the meaning of the attack; (2) psychological and emotional distancing; (3) inward focused-attention meditation; (4) muscle relaxation. There are preliminary case reports supporting this treatment, although no randomized clinical trials.
Sleep paralysis is just as common for males as it is for females. It occurs frequently in about 6% of the rest of the population, and occurs occasionally in 60%. In surveys from Canada, China, England, Japan and Nigeria, 20% to 60% of individuals reported having experienced sleep paralysis at least once in their lifetime. Approximately 36% of the general population that experiences isolated sleep paralysis is likely to develop it between 25 and 44 years of age.
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. 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.
Sleep paralysis could lead the individual to acquire conditioned fear of the experience ("worry attacks"), resulting in more nighttime awakening and fragmented sleep (because of nocturnal arousal and hyper-alertness to symptoms of paralysis), making the person more likely to have sleep paralysis in the future.
Society and cultureEdit
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.
Some scientists have proposed sleep paralysis as an explanation for reports of ghost, parasites, alien visits, demons or demonic possession, alien abduction experiences, the Night Hag and shadow people haunting.
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. Various cultures have various names for this phenomenon and/or supernatural character. For example, sleep paralysis is referred to as a Pandafeche attack in Italy.
Among Italians the Pandafeche may refer to an evil witch, sometimes a ghost-like-spirit or a terrifying cat-like creature. Sleep paralysis among Cambodians is known as, “the ghost pushes you down,” and entails the belief in dangerous visitations from deceased relatives. In Egypt, sleep paralysis is conceptualized as a terrifying Jinn attack. The Jinn (i.e., evil genies) may terrorize and even kill its victims. Sleep paralysis is sometimes interpreted as space alien abduction in the United States.
According to some scientists culture may be a major factor in shaping sleep paralysis. When sleep paralysis is interpreted through a particular cultural filter, it may take on greater salience. For example, if sleep paralysis is feared in a certain culture, this fear could lead to conditioned fear, and thus worsen the experience, in turn leading to higher rates. Consistent with this idea, high rates and long durations of immobility during sleep paralysis have been found in Egypt, where there are elaborate beliefs about sleep paralysis, involving malevolent spirit-like creatures, the Jinn.
Research has found that sleep paralysis is associated with great fear and fear of impending death in 50% of sufferers in Egypt. A study comparing rates and characteristics of sleep paralysis in Egypt and Denmark, found that the phenomenon is three times more common in Egypt versus Denmark. In Denmark, unlike Egypt, there are no elaborate supernatural beliefs about sleep paralysis, and the experience is often interpreted as an odd physiological event, with overall shorter sleep paralysis episodes and fewer people (17%) fearing that they could die from it.
Various forms of magic and spiritual possession were also advanced as causes in literature. 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."
J. M. Barrie, the author of the Peter Pan stories, may have had sleep paralysis. He said of himself ‘In my early boyhood it was a sheet that tried to choke me in the night.’ He also described several incidents in the Peter Pan stories that indicate that he was familiar with an awareness of a loss of muscle tone whilst in a dream-like state. For example, Maimie is asleep but calls out ‘What was that....It is coming nearer! It is feeling your bed with its horns-it is boring for [into] you’. and when the Darling children were dreaming of flying, Barrie says ‘Nothing horrid was visible in the air, yet their progress had become slow and laboured, exactly as if they were pushing their way through hostile forces. Sometimes they hung in the air until Peter had beaten on it with his fists.’ Barrie describes many parasomnias and neurological symptoms in his books and uses them to explore the nature of consciousness from an experiential point of view.
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, the near death experience 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.
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