Sleep Paralysis: Reality and Terrible Fantasy Become One

Jim Wiltsee
April 14th, 2009
Professor Grobstein
Neuro Paper II

                               Sleep Paralysis: Reality and Terrible Fantasy Become One
      In high school one of my friends was freaked out because of her experience the previous night while sleeping; an experience she explained as being consciously awake, but unable to move.  The rest of us thought it was interesting, but that it must be just some random occurrence. Roughly, a month after that conversation, the same thing she described happened to me.  This prompted me to look up the basics of it and I realized it was called sleep paralysis (SP).  Then more recently, during my sophomore and junior years it happened again.  Now learning about inputs during sleep and the regulation of neurons throughout the nervous system and brain, I’ll address the scientific aspects but focus more specifically on the cultural/personal aspects of this phenomenon.
      Until my friend brought up her experience, I had never suffered from an episode of sleep paralysis.  Did learning about sleep paralysis frame my mind, so that it could happen to me?  I’m not sure, but doing more research, studies have shown that 5-40% of the population have had an episode of SP once in their lives (Davies).  This percentage varies depending upon differences in the definition, age of subjects, and sociocultural factors (Solomonova).   For instance, the percentage varies among ethnic groups, with one ethnicity having a 62% occurrence of SP.  The common definition of SP is a brief episode of the inability to move or speak combined with waking consciousness.  During these episodes, there are often intrusions of frightening, dreamlike hallucinations (Solomonova).  Episodes frequently occur at sleep onset, termed hypnagogic, or while waking up from sleep, termed hypnopompic (Solomonova).
      The human sleep cycle is made up of cycles of rapid eye movement (REM) and non-REM (NREM) sleep phases.  Sleep progresses through four NREM stages, which take nearly 70 to 90 minutes.  Stage 1 sleep represents the transition from drowsy wakefulness to deep sleep stages, stage 2 is characterized by the appearance of K-complexes and sleep spindles, and stage 3 and stage 4 are deep stages of sleep. Thereafter, the individual enters into a REM sleep episode followed by reentry into NREM. Periods of NREM sleep constitute nearly 80% of the total sleep time while REM sleep accounts for 20% of the sleep time. During each night, individuals experience approximately five cycles of NREM sleep and REM sleep (Srinivasan).
      Much of the brain circuitry that regulates sleep and produces wakefulness includes cell groups in the brainstem, hypothalamus, and basal forebrain, which are important for arousing the cerebral cortex and the thalamus.  Neuron firing is inhibited during sleep by a system of GABA containing neurons and the active state of ventrolateral preoptic nucleus.  This switch between wake and sleep states seems to be stabilized by orexin neurons in the lateral hypothalamus (Saper).  During REM sleep the body is in a paralyzed state due to neuron firing from the pedunculopontine and laterodorsal tagmental nuclei, which causes cortical activation, vivid dreams, and total loss of muscle tone in the body (Saper).
      The exact physiological reasons for sleep paralysis are not known.  It has been hypothesized that there may be a genetic factor involved.  Scientists theorize that sleep paralysis is probably due to an inappropriate timing of the switch from REM sleep to wakefulness, which has to do with environmental factors. (Dahlitz)  This transitional state between REM sleep and wakefulness causes the individual to have total muscle atonia and consciousness, and commonly the individual hears vibrating, humming, or buzzing noises (as noted by some of the responses) (Parker).  
      Although there are common features between SP and REM sleep, such as they both occur during changes in the degree of wakefulness and both involve the loss of muscle tone, SP usually occurs before periods of NREM.  A Study by Takeuchi et al. showed that SP is physiologically different from lucid dreams and sleep disorders during REM sleep because SP involves alpha trains, which intrude REM sleep, leading to an arousal state and muscle atonia (Parker).  The Electroencephalography (EEG) pattern is similar to that of a waking state.  On the other hand, in a more recent study by Fukuda, electrical responses typical of REM sleep were displayed, even when the brain was awake during SP.  He concluded as a result that there is a biological connection between SP as hallucinations and dreaming (Bower).
      There seems to be three common occurrences during episodes of SP:  Intruder, Incubus, and Vestibular-Motor (V-M) Hallucinations.  These were many of the characteristics that people described in their personal experiences as they responded to the last web paper Sleep Paralysis: Awake But Still Asleep (/exchange/node/1740).  The intruder experience is described as having the feeling of a presence (without hearing or seeing something) or sensing something with visual, auditory, or touching senses (e.g. something is pulling at your covers).  The intruder experience is frightening because of the waking consciousness while paralyzed, helpless, and often laying on your back.  The incubus experience includes difficulty breathing, choking, smothering, sensations of pressure, or of imminent death.  Sometimes people also feel like they are being physically or sexually (especially for the female populations) assaulted (Cheyne). 
      One researcher believes that the inner brain structure is accountable for these two sensations.  This part of the brain monitors one’s surrounding for threats and launches a response to the false positive.  The reaction to the threat may be more intense because of the inhibition of the dampening effects of the feedback loops of the motor programs associated with the fight or flight response and the inability to breathe deeply (Cheyne). When this system is activated during REM sleep in the absence of any real threat, a sense of an ominous entity is activated.  This entity seems to take inputs from other neural areas and the spatial nature, which may be why different individuals have different hallucinations across cultures, genders, environments and personalities (Nielsen).  This may be why in history SP was seen as curses by a witch (during the witch hunts) and different cultures had different tales relating to SP (Davies).  Also, this may be why African Americans have higher rates of SP because they are seen to have more stressors and anxiety in their lives (Bower).  Lastly, there seems to be a link between anxiety and SP sensed presence hallucinations, such as a heritable factor and it first appears during early childhood (as many respondents pointed out) (Solomonova).
      The third occurrence is the V-M hallucination where a person feels the sensation of floating, linear or angular acceleration, falling and spinning, and also out-of-body experiences (seeing oneself from an external point-of-view) (Cheyne).  To some individuals, these experiences may even be enjoyable.  The hypothesis behind this occurrence is the changes in the functioning of the pontine and cortical vestibular centers and motor programs, and the corollary discharges they give off.  Since this system is responsible for distinguishing one’s own body and self from the surrounding atmosphere, changes to this system may account for the V-M hallucinations (Bower). 
      Some previous history, proposed evolution, and proposed reasons can be theorized.  In the far past this SP was seen as a curse on a person or an evil spirit affecting a person.  Another theory was that gastric disturbances led to undigested vapors rising and irritating the brain and nervous system.  Another gastric theory was that distension in the stomach impeded circulation and led to a stagnation of the blood.  Others saw it as a pathological neurosis from a repressed sexuality (Davies).  A theory of the proposed evolution of SP is for predator detection and risk assessment mechanisms.  This would allow a human to have increased sensitivity while staying aversive (Cheyne).  As noted with anxiety and genetics, other factors that seem to increase episodes of SP are panic attacks, post traumatic stress disorder strenuous physical activity, mental disorders, jet lag, shift work, or other factors that disturb sleep.  Gender does not seem to play a part in determining SP, except when it comes to pregnant women (Parker).
      Personally, I never knew what the reason behind sleep paralysis and for the most part the scientific community does not either.  I have learned that not only science, but also culture and environment play into SP and the hallucinations that accompany it.  This seems possible because emotion in itself is internally generated and can powerfully influence the conscious mind (Hobson).  Since many of your sensory neurons are paralyzed during an episode of SP, it makes sense that your occurrence reflects an internally developed input.  All three of my personal experiences have involved the intruder and incubus experiences, which have not been pleasant because they did involve a hallucination from something currently affecting my life.        

                                                Works Cited

Bower. "Night of the Crusher." Science News 168 (2005): 27-30. ProQuest.

Cheyne, and Girard. "Paranoid delusions and threatening hallucinations: A Prospective study of sleep paralysis experiences." Consciousness and Cognition 16 (2007): 959-74. Science Direct.

Dahlitz, and Parkes. "Sleep Paralysis." The Lancet 341 (1993): 406-07.

Davies. "The Nightmare Experience, Sleep Paralysis, and Witchcraft Accusations." Folklore 114 (2003): 181-200.

Hobson. "A model for madness?" Nature 430 (2004): 21.

Nielsen. "Felt Presence: Paranoid delusion or hallucinatory social imagery?" Consciousness and Cognition 16 (2007): 975-83. Science Direct.

Parker, and Blackmore. "Comparing the Content of Sleep Paralysis and Dream Reports." Dreaming 12 (2002): 45-58.

Saper, Scammell, and Lu. "Hypothalamic regulation of sleep and circadian rhythms." Nature 437 (2005): 1257-262.

Solomonova, Nielsen, Stentstrom, Simard, Frantova, and Donderi. "Sensed presence as a correlate of sleep paralysis sitress, social anxiety and waking state social imagery." Consciousness and Cognition 17 (2008): 49-63. Science Direct.