Sleep Paralysis - Pathophysiology

Pathophysiology

The pathophysiology of sleep paralysis has not been concretely identified, although there are several theories about what causes an individual to develop sleep paralysis. The first of these stems from the understanding that sleep paralysis is a parasomnia resulting from inappropriate overlap of the REM and waking stages of sleep. Polysomnographic studies found that individuals with sleep paralysis had 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 bodies that regulate sleep are out of balance in such a way that allows for the different sleep states to overlap. In this case, cholinergic sleep on neural populations are hyper activated and the serotonergic sleep off neural populations are under-activated. 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. Normally during REM sleep the threshold for a stimulus capable of causing arousal is greatly elevated; however, in individuals with SP there is almost no blocking of exogenous stimuli, which means it is much easier for the individual to be aroused by a stimulus. There may also be a problem with the regulation of melatonin, which under normal circumstances regulates the serotonergic neural populations. 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. 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 the sleep on neural populations cannot be counteracted, we retain characteristics of the REM stage of sleep once we have awoken.

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.