Despite being raised Roman Catholic, I never believed in the “devil” or demons. However, I can attest to the fact that there was unequivocally a “presence” during these episodes. The “visitations” occurred 9 times over the course of 13 years. These were not dreams, I was fully awake during each incident.
Although the entity was present every time the sleep paralysis befell me, I only saw this creature once. The most significant occurrence happened when I was 9 years old. Robed in darkness, the faceless hooded being was lurking beside my bed. There was a sound emitting from him, not like breathing, it’s not a sound I can describe, it was more like a frequency, nor can I explain how I knew “it” was a he/alpha.
Unable to move or speak, I dared not fall into sleep, eyes wide open until dawn. As the sun rose he melted into the ground, or under my bed I thought, but when his image dissolved, I was released from the grip of paralysis. Exhausted, as if I had a stroke, I thought this “fearsome entity” was out to possess my soul or was trying to crush or smother my life force.
This strange experience in the middle of the night, as you just come out of sleep, can be downright terrifying.
I know now there is NO sinister menacing intruder watching me, but as a child, it felt very real.
Sleep paralysis is a phenomenon in which a person, either when falling asleep or awakening, temporarily experiences an inability to move. It is a transitional state between wakefulness and sleep characterized by complete muscle atonia (muscle weakness). It is often associated with terrifying visions, such as an intruder in the room, to which one is unable to react due to paralysis, from which the term “nightmare” is derived. One theory is that it results from disrupted REM sleep, which is normally characterized by complete muscle atonia to prevent the sleeper from acting out his or her 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. When linked to another disorder, sleep paralysis commonly occurs in association with the neurological sleep disorder narcolepsy.
The two major classifications of sleep paralysis are Isolated sleep paralysis (ISP) and the significantly rarer Recurrent Isolated Sleep Paralysis (RISP). 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 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.
Signs and symptoms
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, 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. The paralysis can last from several seconds to several minutes, with some rare cases being hours, “by which the individual may experience panic symptoms” (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.
Hypnagogia and Hypnopompic visions 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. Some suggest that reports of alien abductions are related to sleep paralysis rather than to temporal lobe lability. There are three main types of these visions that can be linked to pathologic Neurophysiology. These include the belief that there is an intruder in the room, the incubus, and vestibular motor sensations.
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. 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. Normally the threat-activated vigilance system is a protective mechanism to differentiate between dangerous situations and to determine 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 both intruder and incubus SP visions. 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 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. 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 breath 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.
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, which differ from the other two in not involving the threat activation vigilance system. Under normal conditions, medial and vestibular nuclei, cortical, thalamic, and cerebellar centers coordinate things such as head and eye movement, and orientation in space. 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. 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 the intruder and incubus experiences, arise from completely endogenous sources of stimuli.
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. 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. 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.
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.
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.
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.