Sleep paralysis is when, during waking up or falling asleep, a person is aware but unable to move or speak. During an episode, one may hallucinate (hear, feel, or see things that are not there), which often results in fear. Episodes generally last less than a couple of minutes. It may occur as a single episode or be recurrent.
The condition may occur in those who are otherwise healthy or those with narcolepsy, or it may run in families as a result of specific genetic changes. The condition can be triggered by sleep deprivation, psychological stress, or abnormal sleep cycles. The underlying mechanism is believed to involve a dysfunction in REM sleep. Diagnosis is based on a person’s description. Other conditions that can present similarly include narcolepsy, atonic seizure, and hypokalemic periodic paralysis.
Treatment options for sleep paralysis have been poorly studied. It is recommended that people be reassured that the condition is common and generally not serious. Other efforts that may be tried include sleep hygiene, cognitive behavioral therapy, and antidepressants.
Between 8% and 50% of people experience sleep paralysis at some time. About 5% of people have regular episodes. Males and females are affected equally. Sleep paralysis has been described throughout history. It is believed to have played a role in the creation of stories about alien abduction and other paranormal events.
Signs and symptoms
The main symptom of sleep paralysis is being unable to move during awakening.
Imagined sounds such as humming, hissing, static, zapping and buzzing noises are reported during sleep paralysis. Other sounds such as 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, numbness, and feelings of electric tingles or vibrations running through their body.
Sleep paralysis may include hypnagogic 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 pathophysiology of sleep paralysis has not been concretely identified, although there are several theories about its cause. 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 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.
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 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, cortical, thalamic, and cerebellar centers coordinate things such as head and eye movement, and orientation in space.
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. 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 include 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 (identical twins) 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 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.
Several types of hallucinations have been linked to sleep paralysis: the belief that there is an intruder in the room, the presence of an incubus, and the sensation of floating. A neurological hypothesis is that in sleep paralysis the 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.
The 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 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.
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 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. 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 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. 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.
Sleep paralysis is mainly diagnosed via clinical interview and 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. Several measures are available to reliably diagnose) or screen (Munich Parasomnia Screening) for recurrent isolated sleep paralysis.
Episodes of sleep paralysis can occur in the context of several medical conditions (e.g., narcolepsy, hypokalemia). When episodes occur independent of these condition or substance use, it is termed “isolated sleep paralysis” (ISP). When ISP episodes are more frequent and cause clinically significant distress and/or interference, it is classified as “recurrent isolated sleep paralysis”(RISP). Episodes of sleep paralysis, regardless of classification, are generally short (1–6 minutes), but longer episodes have been documented. 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.
Similar conditions include:
Exploding head syndrome (EHS) potentially frightening parasomnia, the hallucinations are usually briefer always loud or jarring and there is no paralysis during EHS.
Nightmare disorder (ND); also REM-based parasomnia
Sleep terrors (STs) potentially frightening parasomnia but are not REM based and there is a lack of awareness to surroundings, characteristic screams during STs.
Noctural panic attacks (NPAs) involves fear and acute distress but lacks paralysis and dream imagery
Posttraumatic stress disorder (PTSD) often includes scary imagery and anxiety but not limited to sleep-wake transitions
Several circumstances have been identified that are associated with an increased risk of sleep paralysis. These include insomnia, 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, because there is 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 the risk for ISP or RISP, they can be avoided with minor lifestyle changes.
Sleep paralysis is equally experienced in both males and females. Lifetime prevalence rates derived from 35 aggregated studies indicate that approximately 8% of the general population, 28% of students, and 32% of psychiatric patients experience at least one episode of sleep paralysis at some point in their lives. Rates of recurrent sleep paralysis are not as well known, but 15%-45% of those with a lifetime history of sleep paralysis may meet diagnostic criteria for Recurrent Isolated Sleep Paralysis. 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. In general, non-whites appear to experience sleep paralysis at higher rates than whites, but the magnitude of the difference is rather small. 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 is more frequent in students and psychiatric patients