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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.

Nightmare disorder and recurrent isolated sleep paralysis are rapid eye movement (REM) parasomnias that cause significant distress to those who suffer from them. Nightmare disorder can cause insomnia due to fear of falling asleep through dread of nightmare occurrence. Hyperarousal and impaired fear extinction are involved in nightmare generation, as well as brain areas involved in emotion regulation. Nightmare disorder is particularly frequent in psychiatric disorders and posttraumatic stress disorder. Nonmedication treatment, in particular imagery rehearsal therapy, is especially effective. Isolated sleep paralysis is experienced at least once by up to 40% of the general population, whereas recurrence is less frequent. Isolated sleep paralysis can be accompanied by very intense and vivid hallucinations. Sleep paralysis represents a dissociated state, with persistence of REM atonia into wakefulness. Variations in circadian rhythm genes might be involved in their pathogenesis. Predisposing factors include sleep deprivation, irregular sleep–wake schedules, and jetlag. The most effective therapy consists of avoiding those factors.

Sleep paralysis is a state of involuntary immobility occurring at sleep onset or offset, often accompanied by uncanny “ghost-like” hallucinations and extreme fear reactions. I provide here a neuropharmacological account for these hallucinatory experiences by evoking the role of the serotonin 2A receptor (5-HT 2A R). Research has shown that 5-HT 2A R activation can induce visual hallucinations, “mystical” subjective states, and out-of-body experiences (OBEs), and modulate fear circuits. Hallucinatory experiences triggered by serotonin—serotonergic (“pseudo”) hallucinations, induced by hallucinogenic drugs—tend to be “dream-like” with the experiencer having insight (“meta-awareness”) that he is hallucinating, unlike dopaminergic (“psychotic” and “life-like”) hallucinations where such insight is lost. Indeed, hallucinatory experiences during sleep paralysis have the classic features of serotonergic hallucinations, and are strikingly similar to perceptual and subjective states induced by hallucinogenic drugs (e.g., lysergic acid diethylamide [LSD] and psilocybin), i.e., they entail visual hallucinations, mystical experiences, OBEs, and extreme fear reactions. I propose a possible mechanism whereby serotonin could be functionally implicated in generating sleep paralysis hallucinations and fear reactions through 5-HT 2A R activity. Moreover, I speculate on the role of 5-HT 2C receptors vis-à-vis anxiety and panic during sleep paralysis, and the orbitofrontal cortex—rich with 5-HT 2A receptors—in influencing visual pathways during sleep paralysis, and, in effect, hallucinations. Finally, I propose, for the first time, a drug to target sleep paralysis hallucinations and fear reactions, namely the selective 5-HT 2A R inverse agonist, pimavanserin. This account implicates gene HTR2A on chromosome 13q as the underlying cause of sleep paralysis hallucinations and could be explored using positron emission tomography.

Abstract Narcolepsy type 1 is a disabling disorder with four primary symptoms: excessive-daytime-sleepiness, cataplexy, hypnagogic hallucinations, and sleep paralysis. The later three symptoms together with a short rapid eye movement (REM) sleep latency have suggested impairment in REM sleep homeostatic regulation with an enhanced propensity for (i.e. tendency to enter) REM sleep. To test this hypothesis, we challenged REM sleep homeostatic regulation in a recognized model of narcolepsy, the orexin knock-out (Orex-KO) mice and their wild-type (WT) littermates. We first performed 48 hr of REM sleep deprivation using the classic small-platforms-over-water method. We found that narcoleptic mice are similarly REM sleep deprived to WT mice. Although they had shorter sleep latency, Orex-KO mice recovered similarly to WT during the following 10 hr of recovery. Interestingly, Orex-KO mice also had cataplexy episodes immediately after REM sleep deprivation, anticipating REM sleep rebound, at a time of day when cataplexy does not occur in baseline condition. We then evaluated REM sleep propensity using our new automated method of deprivation that performs a specific and efficient REM sleep deprivation. We showed that REM sleep propensity is similar during light phase in Orex-KO and WT mice. However, during the dark phase, REM sleep propensity was not suppressed in Orex-KO mice when hypocretin/orexin neuropeptides are normally released. Altogether our data suggest that in addition to the well-known wake-promoting role of hypocretin/orexin, these neuropeptides would also suppress REM sleep. Therefore, hypocretin/orexin deficiency would facilitate the occurrence of REM sleep at any time of day in an opportunistic manner as seen in human narcolepsy.

Abstract Study Objectives Recurrent isolated sleep paralysis (RISP) is a rapid eye movement (REM) parasomnia characterized by a dissociative state with characteristics of REM sleep and wakefulness. Pathophysiology has not yet been clarified and very little research has been performed using objective polysomnographic measures with inconsistent results. The main aim of our study was to find whether higher REM sleep fragmentation is consistent with the theory of state dissociation or whether signs of dissociation can be detected by spectral analysis. Methods A total of 19 participants in the RISP group and 19 age- and gender-matched participants in the control group underwent two consecutive full-night video-polysomnography recordings with 19-channel electroencephalography. Apart from sleep macrostructure, other REM sleep characteristics such as REM sleep arousal index, percentage of wakefulness and stage shifts within REM sleep period were analyzed, as well as power spectral analysis during REM sleep. Results No difference was found in the macrostructural parameters of REM sleep (percentage of REM sleep and REM latency). Similarly, no significant difference was detected in REM sleep fragmentation (assessed by REM sleep arousal index, percentage of wakefulness and stage shifts within REM sleep). Power spectral analysis showed higher bifrontal beta activity in the RISP group during REM sleep. Conclusions The results showed an underlying persistent trait of higher cortical activity that may predispose patients with sleep paralysis to be more likely to experience recurrent episodes, without any apparent macrostructural features including higher REM sleep fragmentation.

Background and Objectives: While sleep paralysis (SP) is a well-defined disorder, its pathophysiology and causes remain elusive. We aimed to assess the prevalence of sleep paralysis among higher education students and determine factors associated with SP with a focus on psychoactive substance and medication use. Materials and Methods: We conducted a cross-sectional online survey across higher education institutions in Lithuania, asking students to report the occurrence and frequency of SP as well as its characteristics and self-rated sleep quality alongside demographic data and history of medication and psychoactive substance use. Subgroup comparisons and correlation analyses were performed in search of factors associated with reported SP. Results: The study sample consisted of 275 respondents aged 22.9 ± 4.7 years (240, 87.3% female), 119 (43.3%) of whom reported having experienced SP (average age at first episode 16.4 ± 4.2 years), with 87 (73.1%) more than once. The phenomenology of SP episodes included mostly visual, auditory, sensory, or olfactory hallucinations (73, 61.3%), feelings of fear or anxiety (56, 47.1%), incubus-like phenomena (17, 14.3%), and autonomic symptoms (6, 5.0%). Having experienced SP was associated with the use of antidepressants or recreational stimulant use (χ2 = 5.258, p = 0.022) as well as higher alcohol intake (Z = −3.568, p < 0.001) and lower self-rated sleep quality (Z = −2.413, p = 0.016). Earlier age of onset, hallucinations during paralysis, specific time of manifestation during the night, and overall nightmare frequency were related to the recurrence of SP. Respondents tied SP episodes mostly to stress or anxiety (55, 46.2%), the supine sleeping position (31, 26.1%), disturbed sleep cycles (28, 23.5%), and emotional or traumatic experiences (28, 23.5%). Conclusions: Our study suggests that SP is prevalent among students with a tendency to recur. We report a correlational association between SP and the use of antidepressants or stimulant drugs, suggesting the need to further explore the possible role of psychoactive agents in this disorder.

Sleep paralysis (SP), an REM parasomnia, can be characterized as one of the symptoms of narcolepsy. The SP phenomenon involves regaining meta-consciousness by the dreamer during REM, when the physiological atonia of skeletal muscles is accompanied by visual and auditory hallucinations that are perceived as vivid and distressing nightmares. Sensory impressions include personification of an unknown presence, strong chest pressure sensation, and intense fear resulting from subjective interaction with the unfolding nightmare. While the mechanism underlying skeletal muscle atonia is known, the physiology of hallucinations remains unclear. Their complex etiology involves interactions among various membrane receptor systems and neurotransmitters, which leads to altered neuronal functionality and disruptions in sensory perception. According to current knowledge, serotonergic activation of 5-hydroxytryptamine-receptor-2A (5-HT2A)-associated pathways plays a critical role in promoting hallucinogenesis during SP. Furthermore, they share similarities with psychedelic-substance-induced ones (i.e., LSD, psilocybin, and 2,5-dimethoxy-4-iodoamphetamine). These compounds also target the 5-HT2A receptor; however, their molecular mechanism varies from serotonin-induced ones. The current review discusses the intracellular signaling pathways responsible for promoting hallucinations in SP, highlighting the critical role of β-arrestin-2. We propose that the β-arrestin-2 signaling pathway does not directly induce hallucinations but creates a state of network susceptibility that facilitates their abrupt emergence in sensory areas. Understanding the molecular basis of serotonergic hallucinations and gaining better insight into 5-HT2A-receptor-dependent pathways may prove crucial in the treatment of multifactorial neuropsychiatric disorders associated with the dysfunctional activity of serotonin receptors.

Isolated sleep paralysis (ISP) is a temporary state of immobility that occurs during the transition between wakefulness and sleep. Although described as hallucinations within biomedical discourse, frightening multisensory perceptions can often accompany muscle atonia, giving rise to numerous cultural, spiritual, and supernatural explanatory models. Presently, no studies have investigated the experience within Aotearoa New Zealand. In this qualitative phenomenological study, 12 individuals were recruited using stratified purposive sampling and interviewed regarding their experience(s) of ISP. Utilizing inductive thematic analysis, key themes were organized into three main categories: Phenomenological Characteristics, Interpretations, and Coping Strategies. While phenomenological features were congruent with existing global findings, two major interpretive models were identified: spiritual and biomedical, which influenced how ISP was understood, explained, and responded to by participants. Participants conveyed a reluctance to disclose ISP for fears of being labeled mentally ill, while others felt judgment toward their spiritual worldviews. To ascertain generalizability to the wider Aotearoa New Zealand population, a larger quantitative follow‐up study is recommended.

Sleep paralysis is a period of paralysis at either sleep onset or upon awakening and is often accompanied by terrifying hallucinations. We report a case of a 32-year-old healthy men with a history of mild positional obstructive sleep apnea and sleep paralysis. The positional sleep apnea was successfully treated with the Sleep Position Trainer. Remarkably, he did no longer experience episodes of sleep paralysis since using the Sleep Position Trainer. This case highlights a possible elegant noninvasive long-term solution for the treatment of sleep paralysis. Citation: Cui N, van Looij MA, Kasius KM. Successful treatment of sleep paralysis with the Sleep Position Trainer: A case report. J Clin Sleep Med . 2022;18(9):2317–2319.

Ghost encounters were found to be a key part of the trauma ontology among Cambodian refugees at a psychiatric clinic, a key idiom of distress. Fifty-four percent of patients had been bothered by ghost encounters in the last month. The severity of being bothered by ghosts in the last month was highly correlated to PTSD severity (r = .8), and among patients bothered by ghosts in the last month, 85.2% had PTSD, versus among those not so bothered, 15.4%, odds ratio of 31.8 (95% confidence level 11.3–89.3), Chi square = 55.0, p < .001. Ghost visitations occurred in multiple experiential modalities that could be classified into three states of consciousness: full sleep (viz., in dream), hypnagogia, that is, upon falling asleep or awakening (viz., in sleep paralysis [SP] and in non-SP hallucinations), and full waking (viz., in hallucinations, visual aura, somatic sensations [chills or goosebumps], and leg cramps). These ghost visitations gave rise to multiple concerns—for example, of being frightened to death or of having the soul called away—as part of an elaborate cosmology. Several heuristic models are presented including a biocultural model of the interaction of trauma and ghost visitation. An extended case illustrates the article’s findings.