WHY the similar visions, the evil presence?
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 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.
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-activated 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.