Hallucinations During Sleep Paralysis

Sleep paralysis (SP) is a physiological phenomenon that occurs during REM sleep[1]. Researchers claim that sleep paralysis has physiological importance, as during SP, muscle atonia causes the skeletal muscles to paralyse the body, only allowing the eyes to move during REM sleep[1],[2],[3]. This muscle atonia prevents the sleeper from enacting their dreams and harming themselves during REM sleep states[1]. Studies of sleep paralysis and its hallucinations can help researchers to further understand the workings of the human brain. Sleeping individuals experience SP as they transition from REM sleep state to wakefulness[4]. As they transition, most individuals experiencing SP will experience vivid hallucinations. These perceptual experiences can occur at sleep onset and during awakening; these situations are labelled hypnogagic and hypnopompic hallucinations, respectively[4]. The hallucinations are categorized in three ways: Intruder, Incubus and Vestibular- Motor (V- M), which activate the limbic system, parietal operculum , the parietal lobe, and other neurophysiological structures. Recent studies show that trauma, anxiety disorders, sleep disturbances, supine position[2], [4], [5], [7] and the fear emotion [5] play a role in triggering sleep paralysis, while other studies show that the blockage of the GABA and glycine receptors, simultaneously, inhibit muscle atonia during sleep paralysis[1].

Documentary: The Entity
Scientists explanation of sleep paralysis.
ZeEthiopia. (2012, September). Sleep Paralysis. Retrieved from
http://www.youtube.com/watch?v=E0B4kXnrlBQ

1. Categories of Hallucinoid Experiences

Hallucinoid experiences can occur during sleep onset and during awakening[9]. These experiences can have one of three factors, or a mixture of all three.

National Geographic: Sleep Paralysis
Scientists explanation of sleep paralysis.
NationalGeographic. (2012, August).
Sleep Paralysis. Retrieved from
http://www.youtube.com/watch?feature=player_embedded&v=PCZSAwSasdQ

1.1 Intruder

Intruder hallucinations are composed of threatening and fearful experiences[5], [10]. Individuals experiencing such hallucinations report noises, apparitions, sensations of touching, and a vague sense of presence[5], [10]. These are more common among novice SP experiencing individuals[10].

1.2 Incubus

Incubus hallucinations are assaultive, as they are characterized with breathing difficulties, suffocation, bodily pressure, pain, and thoughts of death caused by an exogenous threat[10]. This external threat can appear as supernatural beings from our worst nightmares[6], [10]. Individuals experiences SP describe demons (incubus and secubus), witches, ghosts, and even aliens[6]. In a study conducted by McNally and Clancy, participants experiencing sleep paralysis report abductions by space aliens[4], [10]. 7 participants recall having unusual encounters, such as sexual intercourse and meeting their hybrid offspring[4], [6].

1.3 V- M

Vestibular- motor hallucinations (V-M), on the contrary, are associated with positive feelings of bliss as they are characterized by sensations of linear and angular accelerations (floating, flying, and falling), out of body experiences (OBE's), autoscopy (being able to see oneself from an external view), and fictitious motor movements (such as arm movements or walking around one's environment)[10]. These hallucinations are more common among experienced SP individuals, as they begin to experience less fear[10].

1.4 Mixed

A combined hallucination of two to all three of the hallucination factors can occur during sleep paralysis[10]. In an article published in 2005, Chayne finds that novice experients of SP hallucinations are able to distinguish between the V-M hallucinations from the Incubus and Intruder hallucinations more than more experienced individuals[10]. Experienced SP individuals experience a blending of the hallucinatory factors of V-M, Incubus, and Intruder[10]. For example, McNally and Clancy describe the content of the alien abduction hallucinations as electrical sensations (which are sometimes painful), seeing aliens in the room, visualizations of flashing illuminated objects, and levitation[6]. Participants experiencing these abduction hallucinations report having multiple episodes with these characteristics[6], which are composed of factors of all three types of SP hallucinations. Chayne attributes this combination to the possibility of the co-occurrence of hallucinatory factors within the episodes[10].

2. Brain Areas Involved and Neurophysiology

2.1 GABA and Glycine Receptors Causing Muscle Atonia

Muscle atonia is the paralysis of skeletal muscles during REM sleep, preventing the sleeping individual from performing any sort of motor movement[1]. During this period, brain stem systems, which include the ventromedial medulla (VMM) and sublaterodorsal nucleus (SLD)[11], [12], [13], [14], release GABA and glycine neurotransmitters onto motor neurons, in which they cause hyperpolarization[1]. In REM, GABA is responsible for noradrenaline (NA) and serotonine (5- HT) inhbition to prevent acetylcholine's (ACh) maintenance of muscle tone, arousal and wakefulness[3]. In addition, glycine is involved in motoneuron inhibition[3]. The hyperpolarization of motoneurons is attributed to the actions of metabotropic GABAB and ionotropic GABAA/ glycine receptors in the post synaptic neuron[1]. In a study conducted by Brookes and Peever, in 2012, exogenous drugs were used to block the receptors and their effects on the masseter muscle and its innervating trigeminal motoneuron in rats were observed[1]. Their experiments showed that metabotropic GABAB and ionotropic GABAA/ glycine receptors need to be simultaneously activated in order to initiate and maintain muscle atonia in sleeping individuals[1]. This finding contributes to the understanding of the neurophysiology of the human brain during sleep paralysis and clarifies the roles of GABA and glycine receptors.
Although Brookes and Peever's study clarified the impact of the GABA and glycine receptor mediated mechanism on trigeminal motoneurons, their results might not be universal to other motoneurons affected by REM state muscle atonia. Along with the muscles of mastication, the researchers could have included another skeletal muscle group. For example, the skeletal muscle in the superior tarsal and levator palpebrae superioris, which are involved in the movement of the eyelid[20]. During REM sleep, individuals eyelids are closed, even though their eye balls experience rapid eye movement. If Brookes and Peever included this set of skeletal muscle and were able to explain its activity with their results, GABA and glycine receptor mediated mechanisms could be universal to all motoneurons innervating skeletal muscle groups.
In contrast, the skeletal muscle groups involved in the movement of the eyelid might not be impacted by the receptor mechanism studied by Brookes and Peever. This could be due to the fact that individuals experiencing SP, also experience muscle atonia, but are able to open their eyes and observe their environment[2]. If the simultaneous activation of GABA and glycine receptors causes hyperpolarization in motoneurons innervating skeletal muscles, skeletal muscles in the eyelid would not be impacted.
Brooke and Peever's mechanism does not explain Sleep Bruxism, where sufferers grind their teeth during sleep. Although 60- 80% of episodes occur during Non- REM sleep3, the problem lies in the fact that the masseter muscles are not being hyperpolarized and causing experiments to grind their teeth. Brookes and Peever could extend their study to explain the impact of GABA and glycine receptor mediated mechanism on trigeminal motoneurons during Sleep Bruxism.

Simultaneous activity of the GABA and glycine receptors
EMG and EEG results comparing the lack of muscle atonia with GABAB and GABAA/ glycine antagonism and loss of muscle tone with only GABAA/ glycine blockage in REM sleep.
Brooks P.L. and Peever J.H. (2012)

2.2 Threat Activated Vigilance System and the Amygdala

The threat activated vigilance system (TAVS) is an evolutionary mechanism designed to identify external danger through environmental cues[5]. Structures that are involved in TAVS are the pontine tegmentum, associated entorhinal cortex, lateral hypothalamus, anterior cingulate, and the amygdala[5]. The amygdala has a great influence on this system as it lowers the sensory thresholds and causes the scanning of the environment for cues of threat when an ambiguous cue is sensed[5]. Other studies have shown increased blood flow in visual association areas, the object identification system and the limbic system, suggesting their involvement in aiding the TAVS[5]. TAVS' findings may support or disconfirm the presence of the suggested threat[5].

Threat Activated Vigilance System
A simplified schematic of situational context and paralysis affecting the TAVS. Cheyne J. A. and Girard T.A. (2007)

2.3 Vestibular Centres

V-M hallucinations, on the other hand involve vestibular centres and motor programs[5]. The vestibular system is located in the frontal, temporal, and parietal lobes[5]. Parietal- temporal- occipital junction serves as the centre for body schemes and the connection between the body and external world[5]. When the parietal lobe is directly stimulated, rolling, falling and sliding sensations are experienced[5]. As the angular gyrus is central to this system, its stimulation causes out of body experiences (OBEs) and floating sensations[5]. Interestingly, lesion studies of the parietal- occipital cortex show a cessation of dreaming5. V-M hallucinations are caused by the conflicting information that is perceived about position, attitude and motion of the individual's body[2]. Neuroimaging studies show decreases in rCBF, regional cerebral blood flow, in the parietal cortex[2]. Chayne explains that the hypoactivation is due to the failure of vestibular tactile, motor, and visual information integration[2]. This shows that the parietal lobe plays an important role in the vestibular system and in the body's schematics, as its hypoactivation generates V-M hallucinations[2].

2.4 Other Areas

The parietal operculum, a somatic region found to be involved in REM sleep, is another area that receives projections from the amygdala[5]. This region may be involved in the threatening experience of assault, which characterize Intruder and Incubus hallucinations[5].

3. External Causes

3.1 Triggers of SP

Several factors may contribute to triggering SP during sleep. This includes trauma, anxiety disorders and sleep disturbances.
A history of traumatic experiences have been revealed in recent studies of SP. A study conducted by McNally and Clancy, reports that individuals that experience SP often interpret their hallucinations as repressed memories of childhood sexual assaults[6]. These individuals have a higher rate of SP throughout their lifetime than those without any history of childhood sexual assault[6]. This goes to show that traumatized individuals experience SP at a higher rate[6]. This can be backed up by another study that looked at Cambodian refugees who have had traumatic experiences in the Pol Pot regime. 42% of these refugees reported experiencing at least one episode of SP[6], [15]. Again, this shows that traumatic experiences plays a significant role in triggering SP.
Anxiety disorders are another trigger as studies have found that there is a connection between rates of SP and the presence of anxiety disorders. Otto et al. found that outpatients with anxiety disorders, such as panic disorder, generalized anxiety disorder and social anxiety disorder, had a prevalence of approximately 20%[7]. This rate can be higher if the individual is affected by anxiety and other disorders[7], [16]. Despite these findings, Otto et al. attributes sleep disturbances as the cause of SP in anxiety disorders, as sleep disturbances are highly reported in these cases[7].
Poor sleep and insomnia may lead to SP[8]. College students are affected by sleep disturbances and abnormal sleep cycles[7]. According to Spanos et al., college students have a 21% prevalence of SP, with 4% experiencing 5 or more SP episodes throughout their lifetime[7], [17]. This shows that sleep disruptions play a role in causing SP.
In depression studies, Marianna argues that sleep disturbances mediate depression and SP[8]. Her EEG experiment showed that depressed individuals had difficulty initiating and maintaining sleep and reported previous experience of SP[8].

3.2 Sleeping Positions

Although there is no concrete evidence of sleeping positions causing SP, studies have portrayed that individuals often experience SP in the supine position[2], [4], [7]. There is also evidence that OBEs occur at supine positions, where participants experience floating, flying and motor hallucinations[2]. Though this is an interesting observation, its mechanism is still unknown[4], [5]. McCarthy suggests the supine position is a defenceless position that can lead to the feelings of vulnerability and fear[5].

3.3 Fear

Cheyne's 2003 study of SP reveals that the Intruder and Incubus hallucinations are a reaction to fear[5]. Subjects feel fear, leading to the factors of the Intruder hallucination, which then can lead to the Incubus hallucinations[5]. He suggests that there could be a positive feedback loop where Incubus factors causes more fear and intensifies the Incubus hallucinations[5]. Adding to the experience of fear is the feeling of vulnerability, as one is alone, paralyzed in the dark[5]. This increases fear and activates the TAV system[5].

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