Biology 202
2000 Third Web Report
On Serendip

Another Explanation for Hallucination during Sleep Paralysis: Mismatch between Brainís Expectation and Sensory Input

Hiro Takahashi

In this web research, I have pursued the second hypothesis of my previous web paper that the corollary discharge signals may trigger hallucination during sleep paralysis (1). This time, I have hypothesized that mismatch between internal expectation and sensory input causes increased level of serotonin and thus, higher blood pressure in the brain, which then induces hallucination. For evidences to support my guess, I have made a connection between hallucination and motion sickness because the current science supports that motion sickness results from mistracking of the sensory information in the brain. These two situations seem very unrelated, for one centers around perception of unreal existence, and the other involves nausea and vomiting. Nevertheless, I have found a similarity that both brain confusion requires a high level of serotonin. As a consequence of the comparison, I have concluded that the conflict in the brain can stimulate hallucination during sleep paralysis.

In my second web paper, I have suggested a possibility that corollary discharge signals trigger hallucination during sleep paralysis (1). As a victim finds himself under total paralysis, he struggles to escape the uncomfortable, fearful condition. His I-function in the brain sends the activator signals to the skeletal muscles in the limbs. At the same time, the I-function issues corollary discharge signals to other parts of the brain, telling them about the command sent to the muscles. Because of the corollary discharge signal, the brain expects a certain motor symphony produced by the muscles. In a usual circumstances, the internal expectation matches the sensory input from the muscles, informing of its position and movement. However in an episode of sleep paralysis, the skeletal muscles cannot move, and the brain receives a different sensory input from what it has expected. For one of my hypothesis in the last paper, I have proposed that this mismatch in the brain somehow causes hallucination during sleep paralysis (1). The neurological aspects of motion sickness provide some supports for my hypothesis because in the present scientific view, nausea and vomiting in a moving vehicle result from the mismatch in the brain. Motion sickness, commonly associated with symptoms like headache, nausea, and vomiting, takes place in a moving vehicle, including a space ship. According to NASA, about 2/3 of the astronauts experience it shortly after entry to the orbit because of the loss of gravitational field (2). Within the Earth's gravitational field, vestibular system in the inner ear senses the direction of the force and uses the information, along with the visual and other inputs, to interpret the head and body position (2), (3). However in a zero-gravitational field, vestibular system cannot feel the gravity and sends the brain different signals from visual and other sensory inputs (2), (3). This set of different sensory inputs does not match with any of the previously stored neural patterns, and the brain interprets this mistracking as the effects of neurotoxins (2), (4). Consequently, the brain triggers vomiting as a defense mechanism to expel the poisons from the stomach, into which the toxins have possibly entered with food (4), (6).

Hallucination and motion sickness seem very different, but a neurotransmitter serotonin links them together. Serotonin affects various conditions in one's body, such as emotions, sleep cycles, pituitary hormone secretion, appetite control, and pain perception (6), (7), (8), (9). The most important function for motion sickness is appetite control. After each meal, individual's glucose concentration in blood increases, and high blood sugar level stimulates the release of insulin, which then increases the brain level of the amino acid tryptophan, a serotonin precursor (6), (7). High serotonin concentration decreases one's desire to eat because sugar consumption is unnecessary when the glucose level is high (6), (7). Nausea and vomiting usually occurs when one overeats, hence when the blood sugar and serotonin concentrations are extremely high. Similarly, even without overeating, nausea and vomiting in motion sickness may result from abnormally high serotonin level. When the mismatch happens in the brain, the alarmed brain misunderstands that some poisonous agents have entered the stomach, and it probably signals to release more serotonin to induce vomiting so that the toxin will exit the body. As well as in vomiting, the release of serotonin is necessary in inducing hallucination during sleep paralysis. In addition to the functions described the previous paragraph, serotonin causes the smooth muscles of blood vessels to constrict and raises the blood pressure (8), (10). When the blood pressure increases in the brain, the membrane potential in the optic/auditory cortex change, and triggers hallucination. In the last paper, my main hypothesis has focused on fear as the major hallucination-stimulating factor, for it stimulates fight-or-flight response and release of serotonin (1). And yet, because the brain's confused state in motion sickness establishes high serotonin level in the body, the increased serotonin concentration in hallucination during sleep paralysis may also follow the mismatch between internal expectation and sensory input.

My hypothesis suggests that hallucination during sleep paralysis and motion sickness both involve in confusion in the brain and consequently, an increase in serotonin level; however the outcome differs in these cases. The lack of vomiting in a sleep paralysis episode may be due to the neural inhibitors, which prevents the major muscle movements from acting out a dream. When one vomits, the windpipe closes, and the muscles on abdominal wall and diaphragm produces a sudden and forceful contraction (11). This muscle tightening constricts the stomach and cause it to empty acid chyme, partially digested food, upwards (11). In a person experiencing sleep paralysis, the brain may issue inhibitors not only to the muscles in the limbs but also to the abdominal and diaphragm muscles, restricting their activities only to breathing. As a result, the sudden contraction cannot happen, and the sleeper does not vomit. During sleep stage, the brain may also inactivate the abdominal muscles in order to directly keep one from vomiting so that a sleeper does not choke on his own vomit and die, like some intoxicated people do. During sleep paralysis, hallucination may occur as an alternative response to the high serotonin concentration in the body because of a limited amount of blood flow allowed in the paralyzed body. For the muscles do not move, they require less oxygen and hence, less blood flow. Also, some parts of the brain that is still in REM sleep stage may restrict the blood flow in the major muscles to prevent them from being activated during a dream. As a result, the high serotonin has an increased effect on the active brain, in which the blood pressure increases greatly and suddenly, inducing hallucination.

I have concluded that the mismatching set of sensory input and internal expectation can trigger hallucination in sleep paralysis. However, there may be more different mechanisms that stimulates serotonin release and/or high blood pressure. Besides, there may be more factors other than high blood pressure in the brain that changes the membrane potential in visual/auditory cortex. Understanding the mechanism of hallucination and/or sleep paralysis will lead to discovery of treatment. If hallucination arises in the same way as motion sickness, artificially induced and repetitive experience of sleep paralysis may reduce hallucinatory episodes, for a person's brain can adapt to the neural confusion, as an astronauts overcome motion sickness after several days. If sleep paralysis is really a hereditary disorder as a web page "Evil's Sleep Paralysis" (12) suggests, finding the responsible genes will provide a major access to the cure of the patients. Although sleep paralysis and the associating hallucination do not bring any harm to the victims, discovery of an effective treatment will free them from the fearful experiences. Moreover, a scientific approach to cure the sleep paralysis patients will change the religious or supernatural components of a society. If people gain a knowledge that sleep paralysis and hallucinations are medically treatable, many will lose belief in the existence of gods and/or ghosts. Thus, discovery of scientific treatment for sleep paralysis and hallucination will save the sufferers, but it may bring destruction of very religious bound societies around the world.

WWW Sources

1)Fear-Induced Hallucination: How Sleep Paralysis Triggers Hallucination, my second web paper

2)Space Neuroscience, by NASA

3)Weightlessness and the Human Body, an article by Ronald J. White in Scientific American

4)Autism Science: Cerebellum and the Tracking Module

5)Is Nausea in Pregnancy Nature's Way of Protecting the Fetus from Toxins?, by Rick Weiss

6)Serotonin and Eating Disorders, from Medical Sciences Bulletin, October 1994

7)About 5-HTP, from the Natural Health Company

8)Background Information about Psychedelic Drugs

9)Unlocking the Secrets of Serotonin, by Thrive On Line

10)The Neurologic System, by J. F. Ripka and F. T. Ripka, BioSyn site

11)Nausea and Vomiting, quick facts on nausea and Vomiting

12)The Evil's of Sleep Paralysis

13)Sleep Paralysis: Awake But Still Asleep, my first web paper on Sleep Paralysis




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