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Sleep seems like one of those things that’s impossible to get right. It’s supposed to be the time when we get much needed rest and our brains restore themselves so that we can arise the following day fresh as a daisy. But when you start looking into it, sleep is fraught with all sorts of problems, mysteries, and counter-intuitive facts. Did you know, for instance, that too much sleep may decrease your life span?……..Continue reading….
The main symptom of sleep paralysis is being unable to move or speak 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. It has also been known that one may feel pressure on their chest and intense pain in their head during an episode.
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 hallucinations, such as an intruding presence or dark figure in the room, suffocating or the individual feeling a sense of terror, accompanied by a feeling of pressure on one’s chest and difficulty breathing.
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.
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. 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. 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 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 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. Although the core features of sleep paralysis (e.g., atonia, a clear sensorium, and frequent hallucinations) appear to be universal, the ways in which they are experienced vary according to time, place, and culture.
Over 100 terms have been identified for these experiences.Some scientists have proposed sleep paralysis as an explanation for reports of paranormal and spiritual phenomena such as ghosts, alien visits, demons or demonic possession, alien abduction experiences, the night hag and shadow people haunting.
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