Sleep Paralysis: A Brief Overview of the Intersections of Neurophysiology and Culture

One of the largest epidemiological reviews on the subject, comprising data from 35 studies, found that the lifetime prevalence of sleep paralysis was nearly 8% in the general population (5). Rates of sleep paralysis appear to be higher in non-White populations. Two minority groups found to have especially high rates of sleep paralysis, near 40%, were college students of Asian descent and psychiatric patients of African descent. Psychiatric patients overall were estimated to have lifetime prevalence rates of sleep paralysis over 30%, with particularly high rates among individuals with panic disorder.

During normal REM sleep, neurons containing gamma-aminobutyric acid and glycine that originate in the ventral medial medulla directly inhibit motor neurons in the spinal cord to produce a state of atonia (6). This feature of REM sleep prevents an individual from acting out dreams and reduces the potential for injury during this stage of sleep. Conversely, wakefulness is regulated by the neuropeptide orexin, which stimulates noradrenergic, histaminergic, cholinergic, and serotonergic neurons that in turn promote cortical arousal. Sleep paralysis occurs when these two processes pathologically overlap and the atonia of REM sleep persists into wakefulness.

The involvement of serotonergic transmission in the sleep-wake cycle could partially explain why psychiatric patients, especially those with panic disorder, experience sleep paralysis at greater rates. In wakefulness, orexinergic neurons directly stimulate serotonergic neurons in the dorsal raphe nucleus leading to enhanced alertness. During REM sleep, these serotonergic neurons stop firing, suggesting that the dorsal raphe nucleus plays a specific role in inhibiting REM sleep (7). Altered signaling at serotonin-2A receptors has been implicated in the hallucinatory experiences associated with sleep paralysis. Increased serotonin-2A receptor densities in areas responsible for visual processing, such as the inferolateral temporal cortex, have been associated with the development of visual hallucinations among individuals with schizophrenia or Parkinson’s disease (8). There are also similarities between the hallucinatory experiences of sleep paralysis and those induced by the serotonin-2A agonists LSD and psilocybin. Dopaminergic hallucinations tend to be experienced as lifelike, with little or no insight that the hallucinations are not real. In contrast, serotonergic hallucinations tend to feature the maintenance of some level of insight, have a “dreamlike,” “mystical,” or dissociative quality, and include greater attribution of personal relevance to meaningless stimuli (7). As exemplified in the following sections, experiences of sleep paralysis often share characteristics with these serotonergic hallucinations.

Despite the universal neurophysiological abnormalities known to induce episodes of sleep paralysis, there is great variability in subjective experiences across cultures. In a phenomenon known as cultural priming, shared cultural narratives of sleep paralysis, such as attacks from sinister figures, can predispose individuals to experience a greater fear reaction, a more intense effort to escape paralysis, and culture-dependent hallucinations. The clinical significance of cultural priming is apparent in sleep paralysis, such that cultures with elaborate narratives surrounding sleep paralysis are associated with a higher number of lifetime episodes, greater distress, and longer durations of immobility (9).

One example of a culturally primed sleep paralysis experience is that of the Inuit, who highlight dissociative characteristics and refer to episodes as uqumangirniq. After episodes of sleep paralysis, many Inuit describe a distinct out-of-body sensation closely tied to a traditional belief in three souls—the breath, the name, and the tarniq, a life force that floats within the body but can also exist outside the body. Separation of the tarniq from the body for an extended period is believed to result in death. Traditionally, shamans were respected members of the community. However, narratives of malevolent shamans also existed, and sleep paralysis was commonly attributed to spiritual attacks from such figures. Fear of these shamans during hallucinations and death by separation from the tarniq exacerbated somatic symptoms, such as dyspnea, during sleep paralysis episodes. After exposure to Christianity, the Inuit more commonly described their experience as “the devil pulling them from their bodies” (10). Over time, younger Inuit also became more likely to view sleep paralysis as not significant or “just part of dreams,” and others developed dualistic causal views of sleep paralysis that incorporate contemporary scientific explanations with traditional accounts (9, 10).

Various cultures attribute chest pressure and dyspnea during sleep paralysis to hallucinatory figures. In Brazil, folklore influences the experience in the form of the pisadeira, a long-fingernailed creature who stalks homes at night to disturb sleepers by crushing their chests (11). In contrast, throughout Asia, hallucinated intruders who are said to cause chest pressure are more often ghostly in nature—the kanashibari in Japan, the kwishin in Korea, and khmaoch sângkât in Cambodia are several examples (12, 13). Khmaoch sângkât, “the ghost that pushes you down,” was the focus of a major study involving Cambodian refugees who witnessed genocide under the Khmer Rouge regime. This population was found to have extremely high rates of both sleep paralysis and posttraumatic stress disorder (PTSD), and sleep paralysis symptoms were frequently associated with past trauma (14). Many patients reported seeing a canine-toothed figure in Khmer Rouge garb. Others experienced hallucinations and dyspnea as near-drowning events during monsoons or as executions in which victims wore bags over their heads, similar to executions they had witnessed. It is thought that the relationship between sleep paralysis and PTSD is bidirectional, with frequent awakenings and activation of brain fear systems from PTSD increasing the likelihood of sleep paralysis, and sleep paralysis itself acting as a trauma cue that intensifies fear network formation (14).

Perceptions involving hallucinatory assaults also exist. For instance, in southwest Nigeria, the Yoruba people have the term ogun oru or “nocturnal warfare.” Among individuals in this population, sleep paralysis is predominantly experienced by females and is influenced by the cultural belief in a contentious rivalry between a spirit husband, oko orun, and an earthly husband (15). In this case, the perceived intruder is often a waterlike spirit husband that perpetrates violent sexual acts.

It is important to note that Western researchers have had the tendency to glamorize non-Western depictions of sleep paralysis while overlooking their own cultural schemas. For instance, some attribute the rise of alien abduction narratives in the United States to a 1975 NBC broadcast about “extraterrestrial abduction accounts” (11). McNally and Clancy (16) challenged ethnocentrism by conducting research with individuals in the United States who reported abduction by extraterrestrials. These researchers found a high prevalence of sleep paralysis within an American population of alien abduction experiencers, suggesting an alternative explanation for their abduction experiences. In addition to perceiving alien beings, many subjects reported similar symptoms, including paralysis, tactile hallucinations with electrical qualities, feelings of levitation, and sexual encounters, such as medical extraction of semen, an event alluded to in the 1975 NBC broadcast. Notably, formal psychiatric interviews of the subjects revealed very little underlying psychopathology (16).

Neurological disorders to consider in a differential diagnosis include narcolepsy, nocturnal seizures, transient compression neuropathies, and certain forms of familial periodic paralysis. Psychiatric conditions, such as psychotic disorders, PTSD, nocturnal panic attacks, sleep terrors, and nightmare disorder, should be distinguished from sleep paralysis by the timing of hallucinations and presence of atonia. Recurrent isolated sleep paralysis has corresponding ICD-10 and ICD-11 codes but does not have a DSM-5 code. However, recurrent episodes leading to clinically significant distress could be classified as an “unspecified sleep-wake disorder” in DSM-5. It is also important for clinicians to keep in mind that patients from ethnic groups with narratives around sleep paralysis may experience a greater symptom burden. For a comprehensive understanding of the way in which cultural factors may be affecting diagnostic and treatment considerations, the DSM-5 Cultural Formulation Interview could be considered.

Regarding treatment, addressing feelings of shame and fear via culturally sensitive reassurance and education alone can have a positive impact (4). Several forms of psychotherapy have been developed, including cognitive-behavioral therapy for isolated sleep paralysis and meditation-relaxation therapy, although empirical evidence is limited (17). Furthermore, basic sleep hygiene should be considered because sleep deprivation commonly exacerbates symptoms. More research is needed for empirically supported pharmacological treatments. Selective serotonin reuptake inhibitors and tricyclic antidepressants, thought to work via their REM-suppressing properties, are the most used medications (4). Sodium oxybate (gamma-hydroxybutyric acid) has been shown to reduce sleep paralysis episodes among individuals with narcolepsy, although its adverse-effect profile and misuse potential make it a less-than-ideal option. Given the hypothesized role of the serotonin-2A receptor in sleep paralysis, the serotonin-2A inverse agonist pimavanserin has been proposed, on a theoretical basis, as a treatment option for sleep paralysis–associated hallucinations (7).

The fact that the same neurophysiological process can manifest differently based on culture, as it does with sleep paralysis, emphasizes the challenge of conceptualizing neuropsychiatric disorders transculturally. Advancements in research continue to suggest that psychiatric conditions are not static, isolated entities but complex, interactive processes. This has led to the questioning of traditional assumptions regarding concepts such as “culture-bound syndromes,” and DSM-5 abandoned the adjective “bound” in favor of the term “cultural concepts of distress,” because the former term “exaggerated the local uniqueness of the categories, contributing to their exoticization” (18).

Sleep paralysis is certainly not the only neuropsychiatric disorder in which culture has been identified to explicitly shape symptoms. For instance, fear of personal embarrassment and negative evaluation by others is considered the hallmark of social anxiety disorder. However, cross-cultural studies have shown that social anxiety disorder in some cultures can instead be characterized by a fear that the individual will offend others. Furthermore, this “other-directed” fear is also an aspect of certain cultural concepts of distress, such as taijin kyofusho in Japan (18). Does this other-directed fear share neurocircuitry across cultures and currently defined neuropsychiatric conditions? If so, are cultural factors modulating other neural processes that create subtle distinctions in the manifestation of these conditions? Such questions speak to the ongoing relevance of cultural neuroscience, the field exploring how sociocultural factors shape the neural mechanisms underlying cognition, emotion, and behavior (19). As it stands, these types of inquiries are often difficult to address, because minority racial, ethnic, and cultural groups are heavily underrepresented in neuroimaging research such as fMRI studies (20). These considerations may enable a more nuanced view of transcultural psychiatric symptoms, a perspective less prone to romanticization and oversimplification, by considering not only the differences but also the similarities in disease processes across cultures. A better understanding of both cultural nuance and neurophysiological universality may not only assist in more accurate nosological classifications and treatments but may also promote cross-cultural understanding in the general population.