You can change your cookie settings at any time. 2017 addressing the broad topic physiology of sleep pdf insomnia. Join more than 1,300 other sleep researchers in discovering the professional benefits of Sleep Research Society membership.
Oxford University Press is a department of the University of Oxford. For full access to this pdf, sign in to an existing account, or purchase an annual subscription. John Henry Fuseli – The Nightmare. Episodes generally last less than a couple of minutes.
It may occur as a single episode or be recurrent. Diagnosis is based on a person’s description. Treatment options for sleep paralysis have been poorly studied. People should generally be reassured that the condition is common and not serious.
Males and females are affected equally. Sleep paralysis has been described throughout history. The central symptom of sleep paralysis is being unable to move during awakening. The content and interpretation of these hallucinations are driven by fear, somatic sensations, REM-induced sexual arousal, and REM mentation which are embedded in the sleeper’s cultural narrative. The pathophysiology of sleep paralysis has not been concretely identified, although there are several theories about its cause. REM and waking stages of sleep. Polysomnographic studies found that individuals who experience sleep paralysis have shorter REM sleep latencies than normal along with shortened NREM and REM sleep cycles, and fragmentation of REM sleep.
This study supports the observation that disturbance of regular sleeping patterns can instigate an episode of sleep paralysis, because fragmentation of REM sleep commonly occurs when sleep patterns are disrupted and has now been seen in combination with sleep paralysis. Another major theory is that the neural functions that regulate sleep are out of balance in such a way that causes different sleep states to overlap. As a result, the cells capable of sending the signals that would allow for complete arousal from the sleep state, the serotonergic neural populations, have difficulty in overcoming the signals sent by the cells that keep the brain in the sleep state. During normal REM sleep, the threshold for a stimulus to cause arousal is greatly elevated. However, in individuals with SP, there is almost no blocking of exogenous stimuli, which means it is much easier for a stimulus to arouse the individual.
Melatonin is typically at its lowest point during REM sleep. Inhibition of melatonin at an inappropriate time would make it impossible for the sleep off neural populations to depolarize when presented with a stimulus that would normally lead to complete arousal. According to this hypothesis, vestibular-motor disorientation, unlike hallucinations, arise from completely endogenous sources of stimuli. This could explain why the REM and waking stages of sleep overlap during sleep paralysis, and definitely explains the muscle paralysis experienced on awakening. If the effects of sleep on neural populations cannot be counteracted, characteristics of REM sleep are retained upon awakening. Research has found a genetic component in sleep paralysis. The characteristic fragmentation of REM sleep, hypnopompic, and hypnagogic hallucinations have a heritable component in other parasomnias, which lends credence to the idea that sleep paralysis is also genetic.
Twin studies have shown that if one twin of a monozygotic pair experiences sleep paralysis that other twin is very likely to experience it as well. The identification of a genetic component means that there is some sort of disruption of function at the physiological level. Further studies must be conducted to determine whether there is a mistake in the signaling pathway for arousal as suggested by the first theory presented, or whether the regulation of melatonin or the neural populations themselves have been disrupted. This hypothesis is broadly consistent with the laboratory finding that causing a functional disturbance in the TPJ through electric stimulation can induce an illusory shadow-like person mimicking one’s body postures.