The pathophysiology of<unk>  has not been concretely identified, although there are several theories about its cause. The first of these stems from the understanding that<unk>  is a parasomnia resulting from dysfunctional overlap of the REM and waking stages of sleep. Polysomnographic studies found that individuals who experience<unk>  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 precipitate an episode of<unk> , because fragmentation of REM sleep commonly occurs when sleep patterns are disrupted and has now been seen in combination with<unk> . 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. In this case, cholinergic sleep “on” neural populations are hyperactivated 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. During normal REM sleep, the threshold for a stimulus to cause arousal is greatly elevated. Under normal conditions, medial and vestibular nuclei, cortical, thalamic, and cerebellar centers coordinate things such as head and eye movement, and orientation in<unk> ace. In individuals reporting<unk> , there is almost no blocking of exogenous stimuli, which means it is much easier for a stimulus to arouse the individual. The vestibular nuclei in particular has been identified as being closely related to dreaming during the REM stage of sleep. According to this hypothesis, vestibular-motor disorientation, unlike hallucinations, arise from completely endogenous sources of stimuli. If the effects of sleep “on” neural populations cannot be counteracted, characteristics of REM sleep are retained upon awakening. Common consequences of<unk>  include headaches, muscle pains or weakness or paranoia. As the correlation with REM sleep suggests, the<unk>  is not complete: use of EOG traces shows that eye movement is still possible during such episodes; however, the individual experiencing<unk>  is unable to<unk> eak. Research has found a genetic component in<unk> . The characteristic fragmentation of REM sleep, hypnopompic, and hypnagogic hallucinations have a heritable component in other parasomnias, which lends credence to the idea that<unk>  is also genetic. Twin studies have shown that if one twin of a monozygotic pair (identical twins) experiences<unk>  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 a 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. Hallucinations A picture of a succubus-like vision, in contrast to the incubus. My Dream, My Bad Dream, 1915, by Fritz Schwimbeck Several types of hallucinations have been linked to<unk> : the belief that there is an intruder in the room, the presence of an incubus, and the sensation of floating. A neurological hypothesis is that in<unk>  the mechanisms which usually coordinate body movement and provide information on body position become activated and, because there is no actual movement, induce a floating sensation. The intruder and incubus hallucinations highly correlate with one another, and moderately correlated with the third hallucination, vestibular-motor disorientation, also known as out-of-body experiences, which differ from the other two in not involving the threat-activated vigilance system. Threat hyper-vigilance A hyper-vigilant state created in the midbrain may further contribute to hallucinations. More<unk> ecifically, the emergency response is activated in the brain when individuals wake up paralyzed and feel vulnerable to attack. This helplessness can intensify the effects of the threat response well above the level typical of normal dreams, which could explain why such visions during<unk>  are so vivid. The threat-activated vigilance system is a protective mechanism that differentiates between dangerous situations and determines whether the fear response is appropriate. The hyper-vigilance response can lead to the creation of endogenous stimuli that contribute to the perceived threat. A similar process may explain hallucinations, with slight variations, in which an evil presence is perceived by the subject to be attempting to suffocate them, either by pressing heavily on the chest or by strangulation. A neurological explanation holds that this results from a combination of the threat vigilance activation system and the muscle<unk>  associated with<unk>  that removes voluntary control of breathing. Several features of REM breathing patterns exacerbate the feeling of suffocation. These include shallow rapid breathing, hypercapnia, and slight blockage of the airway, which is a symptom prevalent in sleep apnea patients. According to this account, the subjects attempt to breathe deeply and find themselves unable to do so, creating a sensation of resistance, which the threat-activated vigilance system interprets as an unearthly being sitting on their chest, threatening suffocation. The sensation of entrapment causes a feedback loop when the fear of suffocation increases as a result of continued helplessness, causing the subjects to struggle to end the<unk>  episode.
Sleep paralysis
Narcolepsy
Sedation
Night terror
Sleep disorder
Hypokalemic periodic paralysis
Syncope 
Atonic seizure