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Sleep Paralysis - A Night of Misery
"I sleep—for a while—two or three hours—then a dream—no—a nightmare seizes me in its grip . . . I sense it and I know it . . . and I am also aware that somebody is coming up to me, looking at me, running his fingers over me, climbing onto my bed, kneeling on my chest, taking me by the throat and squeezing . . . squeezing . . . with all its might, trying to strangle me. I struggle, but I am tied down by that dreadful feeling of helplessness that paralyzes us in our dreams. I want to cry out—but I can't. I want to move——I can't do it. I try, making terrible, strenuous efforts, gasping for breath, to turn on my side, to throw off this creature who is crushing me and choking me—but I can't! Then, suddenly, I wake up, panic-stricken, covered in sweat. I light a candle. I am alone." - Guy de Maupassant (Cheyne 2013, 7). Recent experiments have shown that activation of the neurotransmitters GABA and glycerine in REM sleep initiates motor atonia, which may still be intact while one is awake. This experience, known as sleep paralysis, can be horrifying. This essay will preview a brief background of sleep paralysis, causes of paralysis, formation of hallucinations, and possible treatments for sleep paralysis. Supernatural beliefs and the general definition of sleep paralysis will be described as well.
Sleep Paralysis is a temporary skeletal muscle paralysis that normally occurs when one is waking up, but may also occur as one is falling asleep (Cheyne and Pennycook 2013, 1, Anonymous 2012, 8). Muscle paralysis, or motor atonia, usually lasts a few minutes or even seconds, but one may feel as though they are paralyzed for hours as they are aware of their inability to speak or move. The only muscles able to move are those in the eyes, diaphragm, and any non-voluntary muscles (DeGuzman et al. 2010, 5, Sharpless et al. 2011, 2).
Since one's eyes are fully functional (as they are controlled by the cranial nerves), one is aware of their physical surroundings and can often project their dreams into their rooms. Those experiences are called hypnagogic or hypnopompic hallucinations, and occur in an estimated 20 percent of sleep paralysis episodes (Morton 2010, 6, 7). Hypnagogic hallucinations are those that occur as one falls asleep. In contrast, hypnopompic hallucination refer to those that take place as one wakes up (Cheyne 2013, 8). Considering that one feels vulnerable and sees paralysis as abnormal, hallucinations are often realistic and horrific (Anonymous 2012, 9). The hallucinations can be split into 3 categories: intruder, incubus, and vestibular-motor experiences.
Hallucinations in which visual, auditory, and tactile sensations contribute to strong feelings of the presence of another being in the room, such as the experience described in the quote above, are known as intruder experiences (Cheyne and Pennycook 2013, 4). The victim may see a shadowy figure dash across the corner of their eye or may hear faint whispers along with nearing footsteps, but no creature truly invades their privacy. "I suddenly could not move.... I heard two distinct voices: One was a demonic woman that said "we should have never let you get away from us"... I struggled and struggled and felt my mouth moving and calling my sister Rose... After what seemed like an eternity, the pressure suddenly left and I got up. I ran downstairs and asked Rose if she could hear me calling her name, she said No" (Anonymous 2007, 1).
Though the diaphragm is functioning properly, breathing is automatic and cannot be controlled by a victim of sleep paralysis. This may trick the victim into believing that they are suffocating (Cheyne 2013, 16). Incubus hallucinations, shown in the image above, involve feelings of intense chest pressure, suffocation, and near death experiences (Cheyne and Pennycook 2013, 5). These experiences are often called "old hag attacks" because one may often see a demonic figure, such as a witch, sitting on one's chest, as described in the quote by Guy de Maussipant above (MacKinnon 2013, 2).
Vestbular-motor experiences are much less frightening than intruder and incubus because they focus on one's body instead of the sensed presence of a devilish creature (Cheyne and Girard 2008, 4). Vestibular-motor hallucinations consist of illusory movement experiences (IMEs) and out of body experiences (OBEs). IMEs include feelings of floating, flying, falling and motor hallucinations. Motor hallucinations are those in which one believes they moved a limb or even their whole body until they realize that they were paralyzed (Cheyne and Girard 2008, 13). According to an experiment in 2008, IMEs are more common than OBEs which involve seeing one's body from up above and result in alienation from one's body (Cheyne and Girard 2008, 3, 8). The photo displayed above is an example of an OBE.
Even after the brief period of extended motor atonia (paralysis) has worn off, one may suffer from post-episode distress (a lingering feeling of depression or anxiety) (Anonymous 2012, 11). Scientists have uncovered a strong connection between fear and the intensity of the hallucinations to post-episode distress (Cheyne and Pennycook 2013, 13). For instance, those who experience incubus or intruder hallucinations are more susceptible to post-episode distress than those who experience vestibular-motor hallucinations as incubus and intruder experiences are more vivid and horrific.
Sleep paralysis is quite common seeing that over 50 percent of the world population will undergo 1 or more episodes of sleep paralysis (Morton 2010, 1). Even then the experience is seemingly foreign and abnormal. For that reason, people often seek supernatural explanations and describe their hallucinatory incident as encounters with the devil, demons, and even aliens. Different cultures have different explanations for hallucinations. For example, Africans interpreted the episodes as acts of voodoo magic from zombies while Europeans often believed the evil creatures were witches (MacKinnon 2013, 3, 4). Supernatural beliefs about sleep paralysis date back to 1781 and further. In 1781, Henry Fuseli painted "the Nightmare" which represents sleep paralysis itself. "The Nightmare" (shown below) portrays incubus hallucinations as the portrait has a woman lying immobilized and a demon sitting on her chest as though trying to suffocate her (MacKinnon 2013, 1). Though not fully proven, some scientists believe that the vividness of an episode, among other factors, may push forth supernatural beliefs (Cheyne and Pennycook 2013, 15).
Sleep paralysis and its effects are widely known, but the causes of the episodes have only recently been studied. Sleep remains the primary cause of sleep paralysis. The sleep cycle is divided into 5 stages: 4 of non-rapid eye movement (NREM) and 1 of rapid eye movement (REM). NREM is the period of sleep in which brain waves are slowed as the body regenerates and repairs itself; each of the 4 stages lasts for 5 to 15 minutes for a total of 90 minutes (Johnson 2012, 2, 6). As one drifts into stage 1 of NREM sleep, one experiences a falling sensation which may be followed by an abrupt muscle contraction (Johnson 2012, 3). While in stage 2 (light sleep), the body slowly adjusts to stages 3 and 4 of deep sleep (Johnson 2012, 4). The final stage is a 10 minute period of REM. As the cycle repeats itself, REM periods grow longer. REM is the stage of sleep in which dreams occur and, according to EEG recordings, brain waves are similar in speed to those during wakefulness ( Johnson 2012, 7).
The REM portion of one's sleep is where motor atonia occurs as a result of dreams. Within a dream, one is constantly moving, therefore one's central nervous system (CNS) is sending frequent motor instruction to the body (DeGuzman et al. 2010, 4). In order to prevent a person from reenacting their dream, signals sent from neurons to cells called nerve impulses must be blocked, thus paralyzing the person (Anonymous 2012, 2).
Nerve impulses are transported between synapses and consist of 5 stages: resting potential, action potential, repolarization, hyperpolarization, and the refractory period. A neuron is in resting potential when it is polarized. During polarization, the neuron is not stimulated (Wiley 2013, 2). Polarized nerve cells contain potassium with a negative charge on the inside of the cell membrane and sodium with a positive charge on the outside (Wiley 2013, 3). When a stimulus is presented, the neuron's gated channels (channels in the membrane of a neuron that open and close) permits positive sodium ions to enter the cell turning the inside positive. This is called action potential (Wiley 2013, 4). Repolarization comes after the action potential as the cell membrane allows negative potassium ions to exit the cell (Wiley 2013, 5). Hyperpolarization then takes place as there are more potassium ions outside than there are sodium ions inside (Wiley 2013, 6). After the impulse passes through the neuron, potassium ions return inside and sodium ions return outside the cell in the final step called the refractory period (Wiley 2013, 7, 8).
In order for this process to take place, neurotransmitters (chemicals produced within neurons) are necessary to transport the impulse across synapses (Cherry 2013, 1, 5). As an inhibitory neurotransmitter, gamma-Aminobutyric acid (GABA) reduces neuron activity by blocking upcoming action potentials therefore stopping impulses (Wiley 2013, 9). The blockade formed by GABA, however, is not enough to paralyze a person. According to Patricia Brooks and John Peever (2012, 8), the inhibitory neurotransmitters glycerin and GABA must both block impulses in order to initiate REM motor atonia.
Sometimes, GABA and glycerin continue to block nerve impulses even though it is no longer necessary. In other words, REM motor atonia extends into wakefulness, therefore creating sleep paralysis episodes (Brooks and Peever 2012, 13).
Neurologists were able to find the cause of sleep paralysis, but what induces hypnagogic and hypnopompic hallucinations? James Cheyne and Todd Girard (2008, 6) suggest sleeping in the supine position (face up) is a general cause of hallucinations, but what happens within the brain to trigger such vivid experiences?
Though not all scientists agree, the amygdala is fundamental to conjure hallucinations during sleep paralysis. As illustrated in the image above, on each hemisphere of the brain there is a small, almond-shaped mass of grey matter called the amygdala. The "threatactive vigallince system" as James Cheyne (2013, 3) calls it, is responsible for one's response to intense emotions (including fear) as well as remembering these emotions. Fear is a necessary part in both animal and human development because it allows the organism to detect danger (Cheyne 2013, 5). During sleep, the amygdala is heightened (Morton 2010, 8). As explained above, one feels as though they are defenseless during paralysis thus creating immense fear within the victim. The amygdala interprets the fear and releases the hormone adrenaline (Takahashi 2008, 4). The abundance of adrenaline activates the fight or flight response, therefore increasing the heart and respiratory rates (Takahashi 2008, 5). Blood pressure in the brain also increases causing the membrane potential (the electrical charge) to change in the visual and/or auditory cortex, creating a hallucination (Takahashi 2008, 6). In other words, a victim's eyes and/or ears respond to an absent stimulus. Also an effect of fear, the victim's pupils dilate, meaning the pupils widen to let more light in, and allow the person perceive threat (Takahashi 2008, 7).
Sleep paralysis has no known cure, but it can be treated. Understanding which groups of people are more susceptible to sleep paralysis helps when treating victims.
Possible factors that increase sleep paralysis susceptibility include depression, anxiety, and stress (Cheyne and Pennycook, 14). Antidepressants used to treat these personality disorders have also been found to control the severity of episodes.
Sleep paralysis is a known side effect of narcolepsy, a disorder in which people fall asleep in any given time. Regular ways of coping with narcolepsy has shown positive effects on managing sleep paralysis among narcoleptic patients. Narcolepsy can be controlled by taking regular naps throughout the day, engaging in regular exercise, and enforcing a healthy sleeping pattern (Anonymous 2012, 15).
Studies that show students are more prone to experience these brief episodes than the general population indicate stress and lack of sleep are potential inducers (Sharpless et al. 2011, 3). People should avoid stressful situations and receive the recommended amount of sleep for their age. Ways to improve sleep include creating a comfortable sleep environment, avoiding caffeine intake, and abandoning smoking habits. Regular exercise and healthy eating habits also contribute to more peaceful sleep (Anonymous 2012, 13).
Nationality plays a major role in susceptibility as well. Considering that people of African or Asian origin are more inclined to paralysis than those of Caucasian lineage, they should ensure that other factors that increase sleep paralysis susceptibility do not apply to them (Sharpless et al. 2011, 6).
In conclusion, sleep paralysis is caused by the inhibition of nerve impulses, hypnagogic and hypnopompic hallucinations are formed by the amygdala, and treatments for sleep paralysis can be found by understanding susceptibility. Prolonged motor atonia created in REM sleep causes sleep paralysis episodes. Fear conjured by the amygdala causes rapid breathing and increased heart rate which forms hallucinations. Regular sleep and a healthy lifestyle are the main treatments for sleep paralysis. Seconds of immobility might not be a reason to plead for death, according to many. However when an old hag sits peacefully on one's chest, wearing a twisted smile, even the toughest of the tough will cry their eyes out. They will scream, and find that they cannot even conjure a raspy whisper. They will feel the urge to run, but find that their legs no longer belong to them. They suddenly become mere spirits trapped in a foreign, unresponsive body. However, there are treatments; there is hope.