Sleep paralysis and “the bedroom intruder”: The role of the right superior parietal, phantom pain and body image projection

Sleep paralysis and “the bedroom intruder”: The role of the right superior parietal, phantom... Background</h5> During sleep paralysis (SP)—either predormital or postdormital—the sleeper experiences a transient period of gross motor paralysis while the sensory system is clear and ocular and respiratory movements intact [1] . SP is one of the typical symptoms of narcolepsy, a chronic autoimmune sleep disorder characterized by excessive daytime sleepiness, cataplexy (sudden progressive loss of muscle tone), hypnogogic and hypnopompic hallucinations, and disrupted nocturnal sleep [2] . Narcolepsy—genetically associated with HLA DQB1 ∗ 06:02 (HLA) and the T-cell receptor (TCR)—is caused by the autoimmune destruction of neurons in the hypothalamus that produce the peptide hypocretin (orexin) (hormones that regulate the sleep cycle) [2–5] . Narcolepsy is rare, occurring in less than one percent of the general population [6] .</P>SP often occurs without narcolepsy (referred to as “isolated” sleep paralysis). Unlike narcolepsy, SP is a common condition with prevalence rates as high as 18–40 percent in the general population [7] . The vast majority of SP episodes are unrelated to sleep pathology and are not autoimmune in nature. The events occur when a person’s sleep pattern is dysregulated (e.g., jet lag, naps); that is, the perceptual and motor aspects of rapid eye movement (REM) sleep sometimes decouple such that http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Medical Hypotheses Elsevier

Sleep paralysis and “the bedroom intruder”: The role of the right superior parietal, phantom pain and body image projection

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Publisher
Elsevier
Copyright
Copyright © 2014 Elsevier Ltd
ISSN
0306-9877
eISSN
1532-2777
D.O.I.
10.1016/j.mehy.2014.10.002
Publisher site
See Article on Publisher Site

Abstract

Background</h5> During sleep paralysis (SP)—either predormital or postdormital—the sleeper experiences a transient period of gross motor paralysis while the sensory system is clear and ocular and respiratory movements intact [1] . SP is one of the typical symptoms of narcolepsy, a chronic autoimmune sleep disorder characterized by excessive daytime sleepiness, cataplexy (sudden progressive loss of muscle tone), hypnogogic and hypnopompic hallucinations, and disrupted nocturnal sleep [2] . Narcolepsy—genetically associated with HLA DQB1 ∗ 06:02 (HLA) and the T-cell receptor (TCR)—is caused by the autoimmune destruction of neurons in the hypothalamus that produce the peptide hypocretin (orexin) (hormones that regulate the sleep cycle) [2–5] . Narcolepsy is rare, occurring in less than one percent of the general population [6] .</P>SP often occurs without narcolepsy (referred to as “isolated” sleep paralysis). Unlike narcolepsy, SP is a common condition with prevalence rates as high as 18–40 percent in the general population [7] . The vast majority of SP episodes are unrelated to sleep pathology and are not autoimmune in nature. The events occur when a person’s sleep pattern is dysregulated (e.g., jet lag, naps); that is, the perceptual and motor aspects of rapid eye movement (REM) sleep sometimes decouple such that

Journal

Medical HypothesesElsevier

Published: Dec 1, 2014

References

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