Sleep paralysis

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The Nightmare, by Henry Fuseli (1781) is thought to be one of the classic depictions of sleep paralysis perceived as a demonic visitation.

Sleep paralysis is a phenomenon in which people, either when falling asleep or wakening, temporarily experience an inability to move. It is a transition state between wakefulness and rest characterized by complete muscle atonia (muscle weakness). It can occur at sleep onset or upon awakening, and it is often associated with terrifying visions, such as an intruder in the room, to which one is unable to react due to paralysis. It is believed to be a result of disrupted REM sleep, which is normally characterized by complete muscle atonia that prevents individuals 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] When linked to another disorder, sleep paralysis commonly occurs in association with the neurological sleep disorder narcolepsy.[2]

Classification[edit]

The two major classifications of sleep paralysis are isolated sleep paralysis (ISP) and recurrent isolated sleep paralysis (RISP). Of these two types, ISP is much more common than RISP.[2] ISP episodes are infrequent and of short duration, approximately one minute. Sleep paralysis might even only occur once in an individual's lifetime.[2] As the name suggests, recurrent isolated sleep paralysis is a chronic condition. The individual suffers from frequent episodes throughout their lifetime.[2] One of the major differences between ISP and RISP is duration. 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 hallucinations. RISP episodes can, however, persist for up to half an hour.[2] With RISP the individual can also suffer back to back episodes of sleep paralysis in the same night while this 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 on awakening.[3]

Signs and symptoms[edit]

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

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. When it occurs upon falling asleep, the person remains aware while the body shuts down for REM sleep, and it is 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 entirely 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]

Hypnagogic and hypnopompic hallucinations are symptoms commonly experienced during episodes of sleep paralysis. Some scientists have proposed this condition as an explanation for reports of alien abductions and ghostly encounters.[7] Some suggest that reports of alien abductions are related to sleep paralysis rather than to temporal lobe lability.[8] There are three main types of these hallucinations that can be linked to pathologic neurophysiology.[9] These include the belief that there is an intruder in the room, the incubus, and vestibular motor sensations.[10]

Many people that experience sleep paralysis are struck with a deep sense of terror, because they sense a menacing presence in the room while paralyzed—hereafter referred to as the intruder. This phenomenon is believed to be the result of a hyper vigilant state created in the midbrain.[9] More specifically, the emergency response activates in the brain when individuals wake up paralyzed and feel vulnerable to attack.[10] This helplessness can intensify the effects of the threat response well above the level typical to normal dreams; this could explain why hallucinations during sleep paralysis are so vivid.[10] Normally the threat activated vigilance system is a protective mechanism the body uses to differentiate between dangerous situations and determine whether the fear response is appropriate.[10] This threat vigilance system is evolutionarily biased to interpret ambiguous stimuli as dangerous, because "erring on the side of caution" increases survival chances.[10] This could explain why those who experience sleep paralysis generally believe the presence they sense is evil.[10] The amygdala is heavily involved in the threat activation response mechanism, which is implicated in both intruder and incubus SP hallucinations.[3] The specific pathway the threat-activated vigilance system acts through is not perfectly understood. It is believed that either the thalamus receives sensory information and sends it on the amygdala, which regulates emotional experience—or that the amygdaloid complex, anterior cingulate, and the structures in the pontine tegmentum interact to create the hallucination.[9] 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 area, which lets it integrate the different sensations and emotions we experience.[9] The amygdaloid complex helps us interpret emotional experience and act appropriately.[11] Most importantly, it helps us direct our attention to the most pertinent stimuli in a potentially dangerous situation and act appropriately.[11] Proper amygdaloid complex function requires input from the thalamus. This creates a thalamoamygdala pathway capable of bypassing intense scrutiny of incoming stimuli, which allows for quick responses in a potentially life-threatening situation.[9][11]

Typically these pathways let us quickly disregard non-threatening situations. In sleep paralysis, however, these pathways become over-excited and move into a state of hypervigilance where the mind perceives every external stimulus as a threat. The individual can create endogenous stimuli that contribute to the perceived threat.[9] A similar process occurs in the incubus hallucination, with slight variations.

The incubus hallucination is associated with the subject's belief that an intruder is attempting to suffocate them, usually by strangulation.[10] It is believed that the incubus hallucination is a combination of the threat vigilance activation system and the muscle paralysis associated with sleep paralysis that removes voluntary control of breathing.[10] Several features of REM breathing patterns exacerbate the feeling of suffocation.[10] These include shallow rapid breathing, hypercapnia, and slight blockage of the airway, a symptom prevalent in sleep apnea patients.[9] Attempts at breathing deeply fail, and give the individual a sense of resistance, which the threat-activated vigilance system interprets as someone sitting on their chest, suffocating them.[9] The sensation of entrapment causes a feedback loop that involves the threat-activated vigilance system: fear of suffocation increases as a result of continued helplessness, which makes the individual struggle to end the SP episode.[10] The intruder and incubus hallucinations highly correlate with one another, and moderately correlate with the third type of hallucination, vestibular-motor hallucination, also known as out-of-body experiences.[10]

The third hallucination type differs from the other two in that it involves the brainstem, cerebellar, and cortical vestibular centers—not the threat activation 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.[9] In sleep paralysis, these mechanisms—which usually coordinate body movement and provide information on body position—activate and, because there is no actual movement, become confused and induce a floating sensation.[10] The vestibular nuclei in particular has been identified as being closely related to dreaming during the REM stage of sleep.[9] Unlike the other two types of hallucinations, vestibular-motor experiences arise from completely endogenous sources of stimuli.[10]

Pathophysiology[edit]

The pathophysiology of sleep paralysis has not been concretely identified, although there are several theories about what causes an individual to develop sleep paralysis. The first of these stems from the understanding that sleep paralysis is a parasomnia resulting from inappropriate overlap of the REM and waking stages of sleep.[12] Polysomnographic studies found that individuals with sleep paralysis had 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 bodies that regulate sleep are out of balance in such a way that allows for the different sleep states to overlap.[9] In this case, cholinergic sleep on neural populations are hyper activated and the serotonergic sleep off neural populations are under-activated.[9] 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.[9] Normally during REM sleep the threshold for a stimulus capable of causing arousal is greatly elevated; however, in individuals with SP there is almost no blocking of exogenous stimuli, which means it is much easier for the individual to be aroused by a stimulus.[9] 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 have come to the conclusion that there is a dissociative state in sleep paralysis. Sleep paralysis in narcolepsy: more than just a motor dissociative phenomenon[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[edit]

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[edit]

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 to be 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[edit]

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[edit]

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

Epidemiology[edit]

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[edit]

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 to be 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 part in 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[edit]

Folklore[edit]

East Asia[edit]

South-East Asia[edit]

South Asia[edit]

Middle-East, Western and Central Asia[edit]

Africa[edit]

Europe[edit]

Americas[edit]

See also[edit]

References[edit]

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  27. ^ ผีอำ
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External links[edit]