Sleep Paralysis
During rapid eye movement (REM), we encounter vivid dreams. However, to prevent any potential harm that could arise from physically acting out these dreams, the brain has devised a clever solution: it induces a temporary paralysis of the body. The suppression of muscle activity during this paralysis is initiated by specific areas of the brain. Nonetheless, there are instances when the sensory and motor components of REM sleep become disconnected, causing individuals to wake up before the paralysis dissipates. This leads to a condition called sleep paralysis, in which individuals experience a temporary inability to move while maintaining awareness of their surroundings. People with sleep paralysis frequently describe having hallucinations, such as perceiving aliens or shadowy figures in their room.
Although our comprehension of the mechanism responsible for inducing muscle paralysis during sleep paralysis is quite substantial, our understanding of the origins of the hallucinations that accompany it remains limited. In the state of sleep paralysis, there is a dissociation between the brain's signals for movement and the sensory input received from the body, resulting in an absence of sensory feedback. This disruption in neural signals may cause distortions in the perception of one's body and self. The functioning of specific brain regions responsible for processing sensory information and body representation, such as the temporoparietal junction and the right superior parietal lobule, could be influenced. Research has demonstrated that stimulating the temporoparietal junction can create the illusion of someone else mimicking one's body, while individuals with schizophrenia, who attribute their actions to others, exhibit heightened activity in this brain region. The involvement of the mirror neuron system and the interplay between various brain regions and sensory feedback have also been suggested as potential factors contributing to these hallucinations.
However, the underlying neuropharmacological mechanisms responsible for these hallucinations during sleep paralysis, especially the "ghostly" experiences, have not been fully explained. Activation of serotonin 2A receptors (5-HT2AR) may significantly induce these hallucinations, although further research is needed to understand this relationship.
Sleep paralyses: paranoia and panic-like fear reactions
Much like the impact of hallucinogenic substances such as LSD and psilocybin, sleep paralysis frequently induces intense fear and unsettling hallucinations, along with paranoid thoughts and panic-like responses. Fear is a prominent feature of sleep paralysis and is reported by individuals, regardless of whether they experience hallucinations or not. Interestingly, it seems that the fear felt during sleep paralysis is unaffected by prior knowledge or repeated occurrences. The fear response appears to entail the activation of the amygdala, a crucial brain region linked to fear. Therefore, the fear experienced during sleep paralysis is not solely a result of realizing one's paralysis or catastrophic thoughts about the event (e.g., "I am dying"), although these factors contribute to the overall fear and can create a feedback loop.
The increased levels of fear observed during sleep paralysis coincide with the known association between the activation of serotonin 2A receptors (5-HT2AR) and fear responses. This could elucidate why sleep paralysis is universally described as a terrifying experience and seldom reported as being neutral or benign. The fear and paranoia induced by hallucinogenic drugs depend on the individual's environment and emotional state during drug use. These elements could also have an impact on sleep paralysis. However, considering the inherently distressing characteristics of sleep paralysis, including paralysis, chest pain, and difficulty breathing, which can evoke sensations of helplessness, fear is expected to be the predominant reaction. Cultural beliefs can further amplify the underlying fear during sleep paralysis. When an individual's culture attributes sleep paralysis to malevolent supernatural forces, such as a "demonic attack," the fear they experience may intensify as a result of elevated serotonin release in the amygdala. Research has indicated that individuals experiencing sleep paralysis in Egypt, perceiving their encounters as supernatural assaults, express heightened levels of fear during the episodes compared to Danish individuals who primarily regard sleep paralysis as a physiological anomaly.
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The relation between the HTR2A gene and hallucinations
Individuals with elevated levels of 5-HT2A receptors, particularly in specific brain regions, may have a greater predisposition to experiencing hallucinations during sleep paralysis. These hallucinations could potentially be associated with the function of the HTR2A gene located on chromosome 13, which contributes to the production of a higher density of these receptors. Furthermore, variations or modifications in the HTR2A gene and its expression may serve as vulnerability factors that increase the likelihood of developing mood disorders, including anxiety and depression.
Conclusion
It is crucial to emphasize that although sleep paralysis can be unsettling and lead to feelings of fear and anxiety, most episodes are benign and not linked to serious medical conditions. Therefore, treatment is typically unnecessary except in cases where the episodes are repetitive and cause significant distress. Although there is a lack of clinical trials, selective serotonin reuptake inhibitors (SSRIs) are commonly used in clinical practice to alleviate distressing symptoms of sleep paralysis. This is because SSRIs modulate serotonin, which plays a crucial role in the sleep/wake cycle and has anxiolytic (anti-anxiety) effects.
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