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Sleep Paralysis: Pathogenesis, Clinical Manifestations, and Treatment Strategies.

Yi'an Wang, Qi Li, Zhijun Zhong, Qian Ouyang, Xueliang Zou, Kaiyu Yue, Dongyuan Yao

Journal of Integrative Neuroscience August 25, 2025 DOI: 10.31083/jin38979 (opens in new tab) via PubMed

Summary

AI-generated from the abstract

Sleep paralysis is a temporary inability to move or speak while falling asleep or waking up, caused by REM-sleep muscle atonia persisting into wakefulness. The brain's subcoeruleus nucleus (or sublaterodorsal nucleus in rats) primarily induces this paralysis. The condition appears in the International Classification of Sleep Disorders as a REM-sleep parasomnia, either isolated or narcolepsy-associated. This article systematically reviews the neural circuits controlling REM sleep, predisposing factors, clinical features, and treatments for sleep paralysis, compares isolated and narcolepsy-associated forms, and speculates on microsleep's role.

Study at a glance

Characteristics Systematic review Peer reviewed
Keywords Rem sleep Mechanism Narcolepsy Parasomnia Sleep disorder
Key finding Sleep paralysis results from the inability to immediately restore muscle tone during the transition from sleep to wakefulness, with the subcoeruleus nucleus as the primary brain region responsible for inducing muscle paralysis during REM sleep.

Abstract

Sleep paralysis, colloquially known as "ghost pressing" is a state of momentary bodily immobilization occurring either at the onset of sleep or upon awakening. It is characterized by atonia during rapid eye movement (REM) sleep that continues into wakefulness, causing patients to become temporarily unable to talk or move but possessing full consciousness and awareness of their surroundings. Sleep paralysis is listed in the International Classification of Sleep Disorders, 3rd Edition (ICSD-3) as a parasomnia occurring during REM sleep that be classified as either isolated or narcolepsy-associated. Several brain areas, including the forebrain, hypothalamus, and brainstem, as well as several neurotransmitters and modulators, are involved in the control of REM sleep. The primary brain region responsible for inducing muscle paralysis during REM sleep is the subcoeruleus nucleus, also known as the sublaterodorsal (SLD) nucleus in rats. Sleep paralysis results from the inability to immediately restore muscle tone during the transition from sleep to wakefulness. In this article, we systematically review the neural circuit that controls REM sleep and the underlying mechanisms, predisposing factors, clinical characteristics, and treatments for sleep paralysis. We also compare isolated sleep paralysis (ISP) and narcolepsy-associated sleep paralysis and speculate upon the role of microsleep in sleep paralysis.

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