Fear-Induced Hallucination: How Sleep Paralysis Triggers Hallucination

Biology 202
2000 Second Web Report
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Fear-Induced Hallucination: How Sleep Paralysis Triggers Hallucination

Hiro Takahashi

I researched the web to find out how hallucination starts during an episode of Sleep Paralysis. As I have written in my previous paper, a Sleep Paralysis, although often believed as an evil's work, results from some errors of the neural transmission in the brain during REM sleep (1). During a frightening state of Sleep Paralysis, one experiences total body immobility and cannot speak or move besides little eye movements and respiration (2, 3). Often, the paralysis is accompanied with visual and/or auditory hallucination (2, 3). How does Sleep Paralysis trigger hallucination? In order to answer this question, I have referred to my personal experience of seeing stars after doing handstand. According to Dr. Grobstein, as I stand on my hands, the blood rushes into my brain and causes the membrane potential of the neurons to change (4). The change triggers firing of the neurons in the brain, most likely in the visual cortex in this case, without any external stimuli, and I see the stars that do not really exist as a result (4). From this observation, I have predicted that hallucination during Sleep Paralysis also occurs due to the sudden high blood pressure in the brain and the change in the membrane potential of the neurons in the visual and/or auditory cortex. For one feels mortal fear under the state of paralysis, I also expect that the terror or panic somehow increase the blood pressure in the brain. I have built an explanation for the phenomenon based on an assumption that the extreme fright causes the change in membrane potential.

The emotion of fear is perceived in a structure called amygdala in the brain (5, 6, 7). It is a small, almond looking structure deep inside the brain and has several distinct nuclei, including, medial, lateral, basal, and central (5, 6). The lateral nucleus seems to receive input from thalamus and cortical sensory and association areas (5). Then the basolateral nucleus integrate the input as fear and send the information to the central nucleus, from which a major output transmits through projections to the hypothalamus and brainstem autonomic areas (5).

The study of brain in schizophrenia patients suggests that hallucination and amygdala have some connections. Schizophrenia is a neurobiological disorder diagnosed by a patient's inability to interpret a stimuli and select an appropriate response (i.e.: saying "good bye" instead of "thank you" when receiving a gift) (8). Other characteristics of this disorder include alterations of the senses, changes in emotions, movements and behavior, and most importantly, delusions and hallucinations (8). In one study, researchers have tested six hallucinating schizophrenics and have discovered the parts of brain activated when hallucination occurs (9). The active parts include bilateral thalamus, left hippocampus/parahippocampal gyrus, right anterior cingulate, and left orbitofrontal cortex, and they are responsible for generating mental activity and for integrating current and past cognitive/emotional experiences (9). The location of all these structures, deep inside the brain and very close to amygdala and hypothalamus (6), suggests that the active parts may have some interactions with amygdala during a hallucination state. Also, for amygdala plays important roles in emotions, especially fear, hallucination seems closely related to amygdala and terror.

The perception of fear integrated by amygdala activates "fight-or-flight" response, in which an animal respond quickly to a danger due to the function of hormone epinephrine and neurotransmitter norepinephrine (6, 10, 11, 12). Epinephrine, also called adrenaline, is primarily produced in the adrenal glands while norepinephrine, also called noradrenaline, is made in the brain and limbic system (10, 11). When the amygdala interprets fear, it stimulates the release of both epinephrine and norepinephrine into the body's system (7). The high concentration of epinephrine in the blood stream increases the heart and respiratory rates for more oxygen intake and constricts peripheral blood vessels for more blood flow into the large muscles, thereby preparing the body for fight or flight (7, 10, 11, 12). Norepinephrine, when released, mainly tenses the smooth muscles around the blood vessels, increasing the blood pressure (10, 11). The blood pressure in the brain probably increases tremendously in response to fear, too. The sudden increase in the blood pressure, then, may cause the membrane potential to change in the visual and/or auditory cortex, triggering hallucination to happen. Moreover, in the fear reaction, the pupils dilate to let more light and increase peripheral vision to observe threat (10, 12). This response may increase the chance of hallucination to happen, for a large amount of light enters the eye at one time.

In addition to epinephrine and norepinephrine, another neurotransmitter serotonin seems to play an important role in inducing the fight-or-flight response and hallucination. Like norepinephrine, serotonin affects broad range of conditions, such as depression, aggression, sleep regulation, anxiety, appetite control, temperature regulation, pituitary hormone secretion, pain reception, and blood vessel tone (13). It exists throughout the brain, but its most concentrated region lies in hypothalamus and the pineal gland (11). Hence, when the active potential carrying the information of fear reaches hypothalamus from amygdala, hypothalamus releases serotonin into the system, providing assists to epinephrine and norepinephrine to prepare the body for fight or flight. As a part of the process, serotonin causes the smooth muscles of the blood vessels to constrict. Consequently, the blood pressure rises in the brain, and the membrane potential in the optic/auditory cortex change, triggering hallucination.

The additional evidence for the "fight-or-flight" reaction's responsibility on hallucination comes from the hallucinogenic drugs. Hallucinogens, so called for their ability to induce visual/auditory hallucination, affect the hypothalamus and its regulation of hormones (14). Just like epinephrine, norepinephrine, and serotonin, they cause pupils to dilate, heart rate and breathing rate to increase, the body temperature to change, and/or the blood pressure to rise (14). Moreover, some common hallucinogens have similar structures to norepinephrine or serotonin and bind to the same receptors (14). For example, LSD looks very much like serotonin, and mescaline looks similar to norepinephrine (14). Thus, if the drugs that have very similar properties as epinephrine, norepinephrine, or serotonin can induce hallucination, the hormone or the neurotransmitters should be able to have the same effects. For the hallucinogens also stimulate the conditions produced by fight-or-flight response, the natural reaction to the fear enhanced by epinephrine, norepinephrine, and serotonin seems possible to cause hallucination under favorable conditions.

For a summary, a victim of a Sleep Paralysis feels extreme fear for he discovers he cannot move his body although he has consciousness. Integrating the fright, amygdala triggers the fight-or-flight response by stimulating the release of epinephrine, norepinephrine, and serotonin. These substances constrict the smooth muscles around the blood vessels, causing the blood pressure to rise in the brain. Consequently, the membrane potential in the visual/auditory cortex changes, triggering the firing of the neurons and hallucination to occur. The explanation above is only a hypothesis. There are more possibilities, too.

For another hypothesis, corollary discharge may trigger hallucination during sleep paralysis, as in the situation of phantom pain. In a phenomenon called phantom limb, a person who has lost an arm or leg perceives the position of the missing limb, often with a report of pain in specific parts of the limb (15). This abnormal observation can be explained in the terms of corollary discharge, or reafference. In order for a healthy person or an amputee to move a limb intentionally, a self-conscious part of brain, called I-function, sends a signal to another part of the brain that controls the movement of the limb (4). Then, the region that has just received a signal from I-function triggers the firing of neurons for the action potential to reach particular motor neurons, which then generate a movement (4). Simultaneously, the same region of the brain also sends corollary discharge signal; it transmits the information received from the I-function to many different brain parts (4, 15). As a result, the brain, or "neuromatrix" (15), knows what the limb has been ordered to do (4, 15). (The perception of the phantom limb may emerge due to the corollary discharge signals, spreading the information on the movement that limb is expected to produce (4).) In a healthy person, the neuromatrix receives a sensory input from the limb, which reports the limb's position and the muscle activity (4, 15). When I-function issues a signal to move a limb, the reafference allows the neuromatrix to expect what kind of sensory inputs it will receive even before the limb makes the required motion (4, 15). In an amputee with a phantom limb, the brain receives sensory message reporting that the limb is NOT moving at all (4, 15). In response, the neuromatrix, expecting a sensory input as the limb's motion, may send more frequent and stronger signals to urge the limb to move, and these output signals may cause the perception of cramping or phantom pain (15).

Like in phantom pain, the mismatch between the internal expectation and the sensory input may trigger hallucination in Sleep Paralysis. Unlike an amputee, a victim of Sleep Paralysis still has his limbs, but he cannot move them because of some errors in neurotransmission (1). When one wakes up and discovers himself under total body paralysis, he struggles to escape from the frightening immobile state. His I-function issues some messages urging the whole body to move, and the neuromatrix expects a certain sensory input, the action of skeletal muscle. However, with the body under the powerful control of inhibitors released during REM sleep, the neuromatrix receives a sensory input that the body is not moving, completely opposite from what it expects. As the I-function continues to send more and more signals trying to receive the expected input, somehow the frequent firing of the neurons may stimulate the release of particular substances, which eventually cause the change in membrane potential of optic and/or auditory nerves. Besides, the discrepancy caused by corollary discharge may strongly involve the stimulation of fear. As the neuromatrix keeps receiving a contradictory sensory input, it may perceive that something has gone wrong in the system. This realization may link to the arousal of fear, which then induce the pathway described earlier.

Also, as I have predicted in my previous paper, hallucinations during Sleep Paralysis may result from another error in neurotransmission, in which the brain continues to release the activators that trigger dreaming (1). During an episode of Sleep Paralysis, the nervous and endocrine systems keep releasing the inhibitors and "paralyzing" one's body even after some parts of his brain wakes up. As a result, his body continues to "sleep" even though his conscious part of brain is awake. Similarly, it may be possible for another part of the brain, which is responsible for dreaming, to stay in the state of REM sleep. Then, a person may continue to "see" the images and "hear" the noises produced in the dream that he has just had before conscious arousal.

The origin of hallucinations during Sleep Paralysis is still not clear, but many neuroscientists supports that it has some connection to anxiety (16). So far, many studies on Sleep Paralysis and hallucinations have been done on neurobiological level, but there are many aspects and questions yet to be discovered, explained, or answered. Why do some people experience hallucination and others do not? Which factors determine the hallucinatory images that each victim sees or hears? Are they really hallucination or evil spirits? The hallucination during Sleep Paralysis remains mysterious.

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WWW Sources

1)Sleep Paralysis: Awake But Still Asleep, my previous paper on Sleep Paralysis

2)The Evil's of Sleep Paralysis

3)The Body During Sleep

4)Dr. Paul Grobstein, Eleanor A. Bliss Professor of Biology, Bryn Mawr College, on-line profile of Dr. Grobstein

5)Introduction to the Amygdala, a literary research

6)The Emotional Brain, by Mary Lynn Hendrix, National Institute of Mental Health

7)LeDoux Outlines His Theory of Emotions and Memory, by Beth Azar, American Psychological Association

8)Schizophrenia Facts, by Treatment Advocacy Center

9)Study Links Hallucinations to Specific Brain Abnormalities, by Tori DeAngelis, American Psychological Association

10)Adrenalin and Amphetamine

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

12)The Anxiety Panic Internet Resource, by tAPir

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

14)Background Information about Psychedelic Drugs, a literary research

15)Phantom Limbs, by Ronald Melzack, Scientific American

16)Recurrent Isolated Sleep Paralysis, by Jean-Christophe Terrillon and Sirley Marques-Bonham

 

 

Continuing conversation (to contribute your own observations/thoughts, post a comment below) 10/05/2005, from a Reader on the Web My sleep paralysis experiece leads me to think: 1) i am in deep REM sleep with a "nightmare" occuring, 2) the nightmare has auditory and/or visual content, 3) the amigdala is reponding to this experience, 4) a "resonance" occurs wherein the REM contents trigger the amydala which in turn increases the nightmare contents by mapping fear content/affect onto the nightmare structures. 5) when the amplitutde of passing information increases beyond some level the whole phenomenon without collapsing awakens the consciousness to take neccesary action; the rest of the brain is REM paralized, 6) since the collaspe has not occured, the consciousness is aware of the nightmare contents and thus the sensation of hallucination. (W/o ordinary consciousness such "hallucinations" woule be called "dream stuff" in sleep); my dextromethorphan experience is in keeping with this. 7) At this stage the consciousness can (through will power) awaken the entire nervous system to retore near normality. 8) Here I find that trying to go back to sleep causes the cataplectic like structure to be paroxysmally restored/manifest. I need to awaken sufficiently(wash my face etc.,) to really destroy this structure enough to continue with normal sleep. Regards, nk

 

I read that paper on sleep paralysis you wrote while researching for myself. It sounds exactly like me, it was almost as if i was reading a journal i had writtin myself. I have experianced this multiple times before, at first i thought it was because i was sleeping on a water bed but it happened again even on a normal bed.

Well here is the start of it, the most recent attack i had:

I went to bed around 10:00PM and for some reason i was awakened at about 2:00AM. There were no sounds, no music, it was perfectly calm. So i was surprised i was even awake. Never the less it felt like i was totally refreshed so i stayed up watching show tunes for 2 additional hours then i decided i was able to sleep again. This is where everything heads south, I'm laying in bed and just as my eyes are about to close all a sudden i get this weird feeling and my eyes refuse to shut. Then as i was about to adjust myself to a different position i found i could not. My arms felt like they weighed a ton, i could lift them but only half an inch i think it was. It felt like they just moved but i couldn't even move my head to look down at myself, or let alone move my eye balls. I was stuck looking strait ahead. So at this point im totally paralyzed in bed. I feel my heart start to race because i swear to all hells this was real. I felt something under my legs inside my bed pushing the foot side of my bed up. I couldn't see it, i was still stuck looking in one direction but i swear that something was pushing through my bed. I was struck with fear so bad. Then moments later after counting to 10 in my head over and over again i was finally able to move. I rushed and turned the lamp on and jumped out of my bed as if it were possessed. i do not know what happened to me, only it wasn't the first time. It ALWAYS happens the exact same way at the exact same time's, just before i fall asleep all the way. Each time after it happens, I'm unable to return to sleep at all. I was up for the remainder of the morning sitting at my desk with my head on my desk just watching TV that way. if you have ANY suggestions on how i can help myself i would be most greatful. Thank you again for that research paper though, it sure gave me a lot of insight on whats going on with me ... Joshua Valenzuela, 12 September 2006

 

 

i just wanted to say that i read the majority of your paper about sleep paralysis and it has helped me alot in understanding what has been happening to me lately. im currently 21 yrs old and it has been going on every probably the last 6 months. i'd say it has happened during this period maybe 5-6 times or so. what i wanted to throw in there is during the paralysis state, it is quite frightening and i do beleive that there is a release of some of the hormones you mentioned. my experiences include simply waking up unable to move, with barely controllable rolling of my eyes due to tiredness, and a desire to snap out. i usually am hallucinating while im trying to snap out of it and sometimes i hear voices. i beleive my mind is just imaging these though as if i were still in a dream, cause most of the stuff i see or hear is stuff that i've experieneced, seen, or known. Im quite aware of whats happening though cause occassionally i want to not try and snap out of it and see what happens. When i do this, i get a very strong rushing sensation as if im getting lifted up in the air or my body going completely numb. It feels great though but its scary so i always eventually break out and fight back. This portion of feeling numb or being lifted i feel is related to the increased release of feel good hormones like dopamine or epinephrine.. those you stated in your paper. So i do feel like your right on what may be happening. do you think if i don't fight back and it releases too much i could be physically hurt from this? is it dangerous to not fight back and should i experiment on what happens? it is in my own curiousity to know but i don't want to damage myself trying. well, those were questions i couldn't seem to find answers for. so if you wouldn't mind responding back to me, i'd like to have a answer from a specialist ... Ravi, 13 November 2007

 

 

I have suffered from sleep paralysis since I was five years old. I deeply disagree with a few of the theories I have. For years I had the sleep paralysis accompanied by terrifying visions; like someone was in the room with me and beating me severely. I have found that it only happens when I'm overtired. I have to get up and turn on the light when it's over, or it will happen again. I have (details too long for email) ways to cope with this. I still have them but they are no longer accompanied by someone harming me. The reason for my recent research is that my 20 year old daugther is suffering from them, with the vilans present. I would love to find a way to help her so that she does not have to go through what I've been through. FYI For over 30 years I thought this didn't happen to anyone but me ... Maureen Mullins, 19 November 2007