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MacKinnon 2013

Created By: Jessica De anda

The phenomenon of sleep paralysis can be recognised in reports across different cultures and throughout history. [1Perhaps the most famous historic example of sleep paralysis in art is Henry Fuseli’s 1781 painting “The Nightmare”. This painting features many of the classic symptoms of sleep paralysis. The central figure is portrayed lying on her back with a demon sitting on her chest, and strange looking creatures in the background. Many consider it Fuseli’s greatest work and it is believed to be one of the first artistic impressions of sleep paralysis (French & Santomauro, 2007).

Historical Accounts of Sleep Paralysis in Medicine

In the history of Western medicine, sleep paralysis has been documented for at least 300 years. Writing in 2008 Kompanje describes a 1664 case report from Dutch physician Isbrand Van Diemerbroeck titled ‘Of the Night-mare’. It describes a patient’s symptoms:

“…in the night time, when she was composing herself to sleep, sometimes she believed the devil lay upon her and held her down, sometimes that she was choked by a great dog or thief lying upon her breast, so that she could hardly speak or breath and when she endeavoured to throw off the burthen, she was not able to stir her members.”

- Citation literal from Van Diemerbroeck, 1689

Van Diemerbroeck diagnosed the case as follows:

“This affection is called Incubus or the Night-Mare, which is an Intercepting of the Motion of the Voice and Respiration, with a false dream of something lying ponderous upon the Breast… the Motion of the Muscles fail… Now, because the motion of the Muscles, for the most part ceases in time of sleep, except the Respiratory Muscles, therefore the failing of their Motion is first perceived, by reason of the extraordinary trouble that arises for want of Respiration. Now the patient…not understanding the cause in that Condition, believes herself to be overlayed by some Demon, Thief, or other ponderous Body being neither able to move… nor to Breath”

- Citation literal from Van Diemerbroeck, 1689

Van Diemerbroeck’s report accurately represents a case of sleep paralysis, suggesting that this condition has been known by medical professionals for hundreds of years. There is evidence that Persian doctors also knew of sleep paralysis. A 10th century Persian medical text by renowned physician Rhazes (865-925 CE) describes the following condition:

“…when the night-mare (kabus) happens, the person senses a heavy thing upon him and finds he unable to scream…”

- in Golzari et al, 2012

Rhazes’ student Akhawayni went further, detailing his ideas for cause and treatment for this condition:

“The nightmare… is caused by rising of vapours from the stomach to the brain… The therapy includes bloodletting from the superficial vein of the arm and from the leg vein and thinning the diet, especially in patients with red eyes and face”.

Greek doctors were also aware of sleep paralysis, with Galen discussing the condition in the second century CE. The earliest written account of sleep paralysis can be found in a Chinese book on dreaming, dating back to 400 BCE. It is interesting to note that a lot of these early examples refer to sleep paralysis attacks as a night-mare. In fact the symptoms of sleep paralysis implied in the original meaning of the word ‘nightmare’, as opposed to what we think of as a nightmare today (merely a bad dream). Despite the fact that the medical professions have long known about sleep paralysis and known it to be a natural phenomenon, throughout history sleep paralysis has often been interpreted as supernatural connotations, and this interpretation has sometimes had deadly consequences.

Sleep Paralysis and Witch Trials

The ‘mare’ of the word ‘nightmare’ is derived from the Norse word ‘mara’. This refers to a supernatural – usually female – being that lies on people’s chests at night suffocating them. Whilst examples of this depiction of the nightmare can be found across Europe, by the early modern era (1500-1800) this explanation of sleep paralysis experiences had been largely forgotten, and [4in many parts of Europe including Britain and France, sleep paralysis was frequently interpreted as witch attacks. Writing in 2003, Davies quotes examples of sleep paralysis found in evidence used at the Salem Witch Trials of 1692. Accused witch Susan Martin had reportedly told Robert Downer that “some She-Devil would shortly fetch him away”. That night, Downer claimed “as he lay in his bed, there came in at the window, the likeness of a cat, which flew upon him, took fast hold of his throat, lay on him a considerable while, and almost killed him.” Another accuser, Bernard Peach, gave ‘evidence’, testifying that “he heard a scrabbling at the window, whereat he then saw Susanna Martin come in, and jump down upon the floor. She took hold of this deponent’s feet, and drawing his body up into an heap, she lay upon him near two hours; in all which time he could neither speak nor stir.” When the paralysis began to wear off he bit Martin’s fingers and she “went from the chamber, down the stairs, out at the door.”

Bridget Bishop was also accused of witchcraft in testimonies which seem to describe sleep paralysis experiences. Richard Coleman claimed that Bishop had “oppressed him so, that he could neither stir himself, nor wake anyone else, and that he was the night after, molested again in the like manner”.

It was not only in Salem that probable sleep paralysis attacks were used as evidence against accused witches. For a detailed account of many such cases, see Davies (2003).

Sleep Paralysis and Alien Abduction

There is strong evidence that some claims of alien abduction may actually describe episodes of sleep paralysis. In a 1993 study by Spanos and a 2002 paper by Holden & French it is shown that 60% of intense UFO experiences are associated with sleep. In a 2008 study, French et al found that people who claim to have been abducted by aliens report more incidences of sleep paralysis than a control group. Descriptions of alien abduction often bear strong resemblance to accounts of sleep paralysis.

“A female abductee was lying on her back when she woke up from a sound sleep. Her body was completely paralyzed and she experienced the sensation of levitating above her bed. Her heart was pounding, her breathing was shallow, and she felt tense all over. She was terrified. She was able to open her eyes, and when she did so, she saw three beings standing at the foot of her bed in the glowing light. Another female abductee was lying on her back when she woke up in the middle of the night. She was completely paralysed, and felt electrical vibrations throughout her body. She was sweating, struggling to breathe, and felt her heart pounding in terror. When she opened her eyes, she saw an insect like alien being on top of her bed. A male abductee awoke in the middle of the night seized with panic. He was entirely paralysed, and felt electricity shooting throughout his body. He felt his energy draining away from him. He could see several alien beings standing around his bed.”

- in McNally & Clancy, 2005

Whilst sleep paralysis is very likely linked with some alien abduction experiences, most experts agree that it isn’t the sole explanation. Many alleged abductees have no initial memory of the full abduction, and accounts often materialise after memories are ‘recovered’ by therapists and hypnotists. It has been suggested that these ‘recovered memories’ are likely to be false memories manufactured by the interactions between therapist and abductee (Holden & French, 2002).

Other cultural explanations of sleep paralysis

Sleep paralysis attacks and nocturnal attackers are integral to the folklore of many countries. It is interesting how varied accounts and explanations can be across cultures, whilst the core aspect of the experience remains the same. Two of the best-documented examples of nocturnal attackers are Kanashibari in Japan, and the Old Hag of Newfoundland.

The term Kanashibari, meaning ‘to tie with an iron rope’ is derived from the magic of Fudoh-Myohoh, a Buddhist God. The idea of being tied up comes from the belief that ancient Buddhist monks could use magic to paralyse others as if they were bound in a metal rope. Even today, many Japanese believe Kanashibari to be caused by evil spirits. In a 1987 study of Japanese respondents, Fukuda et al found the symptoms of kanashibari to be identical to those of sleep paralysis.



The Old Hag phenomenon is a traditional interpretation of sleep paralysis found in Newfoundland. [2A visit from the Old Hag reportedly starts with the victim becoming conscious and unable to move or speak and feeling a heavy weight pressing down on their chest. Victims sometimes report seeing an animal or human sitting or lying on their chest. Those who claim to experience the Old Hag also report being fully conscious during a visit. In folklore, visits from the Old Hag may be attributed to several factors. The victim may have been overworked, or may be the subject of the hostile or jealous feelings of another person. (Ness, 1978).


In other parts of the world, diverse explanations can be found for sleep paralysis-like experiences. Across the Caribbean, the local term for sleep paralysis is kokma. [3Kokma is believed to be caused by the souls of unbaptized babies who come to strangle victims in their sleep. In many African cultures, voodoo magic is cited as a cause of sleep paralysis, with attacks being the work of zombies coming to visit in the night (Mdlalani, 2009). These are but a few of the many examples of sleep paralysis in different cultures. Again, interested readers are referred to Davies’ 2003 paper on supernatural interpretations of sleep paralysis, which gives many detailed examples from different parts of the world, and Shelly Adler’s 2012 book.


The Malleability of Sleep Paralysis Interpretation

Even more remarkable than the great diversity of explanation of the same phenomenon is how changes within a culture can bring about changes in the interpretation of sleep paralysis, and even the hallucinatory content.

In 2005, Law & Kilmayer interviewed Inuit elders and youths about their experiences of uqumanirniq (the local term for sleep paralysis). They found that the elders attributed the experiences to the work of shamanistic forces, often a hex placed on the victim by a shaman. They also believed uqumanirniq attacks to signal coming misfortune such as a bad hunt. Young Inuits however had very different interpretations. Whilst their accounts of the symptoms of uqumanirniq were the same as the elders, they evoked typical Christian explanations of attacks as the work of the Devil, probably as a result of increasing presence of Christianity in the region. They too thought it to be a harbinger of misfortune, but related this portent to contemporary challenges facing Inuits such as poverty and unemployment. Some young Inuits also explained uqumanirniq in scientific terms. Another example from Zanzibar shows how interpretations of Popobawa – the local traditional interpretation of sleep paralysis – was originally shaped from various explanations, which were replaced with a single explanation in reaction to increasing political instability in the region (Walsh, 2009). These two examples illustrate the extent to which that explanations and interpretations of sleep paralysis are affected by cultural setting and belief.

Illustrated interpretations © Carla MacKinnon
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Anonymous 2007

Created By: Jessica De anda

Demons and Sleep Paralysis

By missvzla (2 stories) (33 posts) (the author is a middle age adult)
Date: 2007-02-21
Country: United States
State: California
Paranormal Category: Old Hags / Night Attacks / Sleep Paralysis

Back in the 80's, I was a bit of a party girl. Hey nothing wrong with that, I was in my early twenties and liked to dance and live it up on the weekends. At that particular time, I lived with my sister Lucille in Whittier near Washington Blvd & Broadway. I would often come home pretty buzzed and would go right to sleep. That was the time that I would see, hear and feel "unexplainable visitors". My niece who was 5 at the time, says she would hear me talking to people and sometimes she would hear me laughing or crying. She assumed I was on the phone so she never gave it much thought (heck she was just 5 why would she). Crazy thing, is that I would also hear people and do remember talking to someone. Many a time I thought it was just the alcohol and that I was in that deep sleep that most drunk people get in when they hit the pillow and crash. But I know I wasn't dreaming. I heard the voice and I could hear my own voice as well. There were several times I could not get up and had my eyes open seeing someone coming down the hallway towards me. I was terrified and kept trying to move any part of my body or yell but I never could. And these were in the morning already so there was light in my room and all through the house.

One day I woke up to find I was being made love to. I'm not kidding, I could feel the darn thing inside me and felt the whole endorphin rush. I would also like to add that the sleep paralysis and conversations were not only when I would could home after partying. This would happen on normal, everyday work nights. My 5 year old niece told us one time that she saw a figure standing at her doorway looking in at her. She hid under the covers and passed out (fell asleep). In the morning she was full of sweat from being under the covers. It's a miracle she didn't suffocate. She said that she thought it was me coming home from a late night but I was already home and in bed. She is now 24 and she still swears she saw a figure looking in at her that night.

Well, one day I was just staring at the walls in my bedroom thinking and my God, if I didn't see faces of demons. The walls had wood paneling on them and yes, wood paneling is like the clouds where you can see several different things in it. But I could actually see two forms of demons. I told my sister about that and she told me to keep quiet because she didn't want me scaring my niece. I really wonder if that had anything to do with all that... The wood paneling was taken down and they painted instead...

Fast forward now to 2003 and I am now living in Sun Valley (next to Burbank) with my sister Rose and we are in the process of packing up because she bought a house in Whittier near my mom. One Saturday morning, I woke up tired, cranky, irritable and just did not want to work. I did not feel like packing any boxes or cleaning or sweeping, I just didn't. I told my sister I was not feeling well, so she left me alone (I could tell she got pissed). So as I'm laying there on the bed (it was about 10:30am) [1I suddenly could not move. I could not scream and I could not think. One thing I could do was HEAR and I heard two distinct voices: One was a demonic woman that said "we should have never let you get away from us" - then a demonic man's voice that said "this time you will not get away from us"... I struggled and struggled and felt my mouth moving and calling my sister Rose, actually I know I was screaming her name - but she was downstairs in the garage and could in no way hear me. 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. I told her what happened and she said why didn't you pray to God? I said that I couldn't think, I was just too scared and it caught me off guard.

To this day I wonder who the heck those demons were and what they meant by "we should have never let you get away from us".... Was it the same forces that were tormenting me back at my sister Lucille's house in 1989? What's weird is that was the first time I actually heard a female demon voice because at Lucille's I always heard male voices.... Here we are in 2007 and every now and then I get the sleep paralysis but I am thoroughly prepared. I have dreams where I actually talk down the demons that are attacking me and act like some sort of super hero. I rebuke them in the name of Jesus Christ and it always works, they are defeated. For all of you who have been having this happen to you, I notice that none of you rebuke the demons but instead try to fight them off or scream. Rebuking them in the name of Jesus Christ will send them fleeing, trust me, they are powerful words. I've always felt that there is some kind of power struggle going on for my soul. I have never done drugs or played with Ouija boards or anything like that, but I have been suffering from depression for a while now and I know that demons head straight for those that suffer from this. We are easy targets but we can defeat them with simply rebuking them in Jesus' name.

One time that sleep paralysis hit me, I could not remember the word "Rebuke" and I could not get those bastards off of me. I instead kept telling them in a sissy way to get off me and leave me alone. As you know, any bully hearing those words will just pound on you more. I notice that after the attacks are over, I am exhausted, both mentally and physically. But it seems that they have left me alone for now and I am somewhat at peace...

A funny thing did happen about 3 or 4 months ago though. I was sleeping on a day bed and one morning I got up a little too early for work, so I got up to turn off the alarm before it went off, because it is loud and always scares the heck out of me, and to put on my fuzzy booties. I then laid back down in bed but I scooted all the way towards the bottom of the bed so I could rest my feet up on the metal frame... I somehow managed to fall deep asleep again and was going to be late for work. I say "going to be late" because of the weird thing that happened next. Remember that I had my feet up on the metal frame so they were resting at the top right?. Well something, or someone, "whacked" my feet hard and it startled me awake. I sat up thinking someone was there like my mom, but I was alone... I know I felt it because it shook my whole body and I woke up. It was like some old mother coming by your bed and smacking you with that "get up you good for nothing lazy son of biscuit eater" attitude... But what amazed me was that I was awaken at the usual time that I get up (6am)... That, right there, proves it was no unusual coincidence because first of all, I felt the hard whack and secondly it hit me at the exact time to get up... I have 3 cats that sleep in my room. At the time this happened I had my black cat laying next to me but she never reacted in any way at all like most animals do when they sense a ghostly presence... However this "thing" that whacked me did not seem evil, how do I know? I could just tell or rather I could just feel it. It seemed like a genuine, caring spirit like a guardian angel that people say we all have.

I live at home with my mom now and back in my old room from high school. Nothing weird has ever happened in that room except for the recent whacking of my feet that woke me up. I am not a church goer but I'm strongly anchored in my faith with God and pray to him all day long. I know that my faith protects me like an armor, but I also know I am weak in many areas, one of them being depression. Demons will look for any chink in the armor to break in and depression is one of their favorites so maybe that's why I always feel like I am in some sort of tug of war and have to constantly be on guard. I'm just glad I know now what I didn't know back in 1989 and I sure hope that those of you reading this will start rebuking the demons when you find yourself being pinned down or menaced...

Remember the words "I rebuke you in the name of Jesus Christ"... Say it over and over and say it loudly even if you can only say it in your head... People, please put on your suit of armor and don't be demon doormats anymore... Best of luck to you all.
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Anonymous 2012

Created By: Jessica De anda


Sleep paralysis is caused when hormones produced by the body to help you sleep do not wear off as you wake up.
This means that you remain temporarily paralysed but conscious.
REM sleep

To understand better what causes sleep paralysis, it is useful to know what usually happens when you are asleep.
Sleep occurs in cycles and each cycle is split into two phases – rapid eye movement (REM) sleep and non-REM sleep.
The brain is very active in REM sleep and most dreams occur at this stage of sleep. [1Also, during REM sleep the body is paralysed, apart from the movement of the eyes and diaphragm (the main muscle used in breathing). [2The paralysis is thought to occur to prevent you acting out the actions in your dreams.
Sleep paralysis occurs when the normal muscular paralysis of REM sleep temporarily continues after you have woken up.
Increased risk

Certain factors make you more likely to get sleep paralysis:
[3] age – it is more common in teenagers and young adults
[4] sleep deprivation – sleep paralysis is more common in people who do not get enough sleep
[5] irregular sleeping patterns – people with irregular schedules or who work shifts are more prone to sleep paralysis
[6] narcolepsy – some people with narcolepsy (a sleep disorder where you suddenly fall asleep at inappropriate times) also experience sleep paralysis
[7] family history – you may be more likely to have sleep paralysis if another member of your family also has it; however, this is an area where further research is needed


The main symptom of sleep paralysis is a temporary inability to move or talk.
[8] The paralysis usually happens as you are waking up, but it can also sometimes happen when you are falling asleep.
[9] Not being able to move or talk can be very frightening, particularly as you will be completely conscious throughout the experience.
During an episode of sleep paralysis, you may also experience a very real sensation that there is someone else in the room with you.
These type of hallucinations are a fairly common feature of sleep paralysis, although they do not occur in every case.
[10] The length of time that you are unable to move for can vary from a few seconds to several minutes. After this, you will be able to move and speak as normal.
[11] Immediately after an episode of sleep paralysis you may feel unsettled and anxious. However, the condition does not pose a risk to your overall health.
Many people only experience sleep paralysis once or twice in their life. If it happens several times a month or more regularly, it is known as isolated sleep paralysis.

Treating sleep paralysis

Ensuring you get enough sleep and improving your sleeping environment will help if you have sleep paralysis. In severe cases, medication may be recommended.
Sleeping habits

[12] Sleep paralysis is more common in people who are sleep deprived, so getting enough sleep may help reduce the number of episodes of sleep paralysis. Most adults need 6-8 hours of sleep each night.
Keeping to a regular sleeping schedule, where you go to bed at roughly the same time each night and get up at the same time each morning, can also help.
Tips for improving your sleeping habits include:
[13] creating a restful sleeping environment that is quiet, dark and not too hot or cold
ensuring your bed is comfortable
exercising regularly (but not too close to bedtime)
cutting down on caffeine
not eating or drinking alcohol before bedtime
giving up smoking (if you smoke) because nicotine is a stimulant


If your sleep paralysis is particularly troublesome, you may be prescribed a short course of antidepressant medication, such as a tricyclic antidepressant (TA), typically clomipramine.
[14] Antidepressants affect mood and are usually used to treat depression, but are also sometimes prescribed to treat severe sleep paralysis.
The medication is thought to work by altering the amount and depth of REM sleep. This should prevent the temporary paralysis when you wake up or fall asleep, and it should also help reduce any hallucinations you may have.
You may be advised to take the medication for a month or two to see whether it improves your symptoms.
Possible side effects of TAs can include:
dry mouth
difficulty urinating
blurred vision
These side effects should ease after 7-10 days as your body starts to get used to the medication. You should visit your GP if the side effects have not eased after this time.
Read more about the side effects of TAs.

Sleep paralysis can sometimes be a symptom of another sleep disorder called narcolepsy, which causes severe daytime sleepiness and an inability to stay alert for more than a few hours.
Although there is no cure for narcolepsy, the condition can usually be managed with medication.
A number of lifestyle adjustments may also help, including:
[15] taking frequent brief naps during the day
sticking to a strict bedtime routine where you go to bed at the same time each night
ensuring you get at least eight hours of sleep every night
avoiding stressful situations, eating a healthy, balanced diet and taking regular exercise (but not too close to bedtime)

Read more treatment advice for narcolepsy.

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Wiley 2013

Created By: Jessica De anda

Understanding the Transmission of Nerve Impulses
Nerve impulses have a domino effect. Each neuron receives an impulse and must pass it on to the next neuron and make sure the correct impulse continues on its path. Through a chain of chemical events, the dendrites (part of a neuron) pick up an impulse that's shuttled through the axon and transmitted to the next neuron. The entire impulse passes through a neuron in about seven milliseconds — faster than a lightning strike. Here's what happens in just six easy steps:

Polarization of the neuron's membrane: Sodium is on the outside, and potassium is on the inside.

[1] Cell membranes surround neurons just as any other cell in the body has a membrane. [2When a neuron is not stimulated — it's just sitting with no impulse to carry or transmit — its membrane is polarized. Not paralyzed. Polarized. Being polarized means that the electrical charge on the outside of the membrane is positive while the electrical charge on the inside of the membrane is negative. [3The outside of the cell contains excess sodium ions (Na+); the inside of the cell contains excess potassium ions (K+). (Ions are atoms of an element with a positive or negative charge.)

You're probably wondering: How can the charge inside the cell be negative if the cell contains positive ions? Good question. The answer is that in addition to the K+, negatively charged protein and nucleic acid molecules also inhabit the cell; therefore, the inside is negative as compared to the outside.

Then, if cell membranes allow ions to cross, how does the Na+ stay outside and the K+ stay inside? If this thought crossed your mind, you deserve a huge gold star! The answer is that the Na+ and K+ do, in fact, move back and forth across the membrane. However, Mother Nature thought of everything. There are Na+/K+ pumps on the membrane that pump the Na+ back outside and the K+ back inside. The charge of an ion inhibits membrane permeability (that is, makes it difficult for other things to cross the membrane).

Resting potential gives the neuron a break.

When the neuron is inactive and polarized, it's said to be at its resting potential. It remains this way until a stimulus comes along.

Action potential: Sodium ions move inside the membrane.

[4] When a stimulus reaches a resting neuron, the gated ion channels on the resting neuron's membrane open suddenly and allow the Na+ that was on the outside of the membrane to go rushing into the cell. As this happens, the neuron goes from being polarized to being depolarized.
Remember that when the neuron was polarized, the outside of the membrane was positive, and the inside of the membrane was negative. Well, after more positive ions go charging inside the membrane, the inside becomes positive, as well; polarization is removed and the threshold is reached.

Each neuron has a threshold level — the point at which there's no holding back. After the stimulus goes above the threshold level, more gated ion channels open and allow more Na+ inside the cell. This causes complete depolarization of the neuron and an action potential is created. In this state, the neuron continues to open Na+ channels all along the membrane. When this occurs, it's an all-or-none phenomenon. "All-or-none" means that if a stimulus doesn't exceed the threshold level and cause all the gates to open, no action potential results; however, after the threshold is crossed, there's no turning back: Complete depolarization occurs and the stimulus will be transmitted.

When an impulse travels down an axon covered by a myelin sheath, the impulse must move between the uninsulated gaps called nodes of Ranvier that exist between each Schwann cell.

Repolarization: Potassium ions move outside, and sodium ions stay inside the membrane.

After the inside of the cell becomes flooded with Na+, the gated ion channels on the inside of [5the membrane open to allow the K+ to move to the outside of the membrane. With K+ moving to the outside, the membrane's repolarization restores electrical balance, although it's opposite of the initial polarized membrane that had Na+ on the outside and K+ on the inside. Just after the K+ gates open, the Na+ gates close; otherwise, the membrane couldn't repolarize.

Hyperpolarization: More potassium ions are on the outside than there are sodium ions on the inside.

When the K+ gates finally close, [6the neuron has slightly more K+ on the outside than it has Na+ on the inside. This causes the membrane potential to drop slightly lower than the resting potential, and the membrane is said to be hyperpolarized because it has a greater potential. (Because the membrane's potential is lower, it has more room to "grow."). This period doesn't last long, though (well, none of these steps take long!). [7After the impulse has traveled through the neuron, the action potential is over, and the cell membrane returns to normal (that is, the resting potential).

Refractory period puts everything back to normal: Potassium returns inside, sodium returns outside.

[8] The refractory period is when the Na+ and K+ are returned to their original sides: Na+ on the outside and K+ on the inside. While the neuron is busy returning everything to normal, it doesn't respond to any incoming stimuli. It's kind of like letting your answering machine pick up the phone call that makes your phone ring just as you walk in the door with your hands full. After the Na+/K+ pumps return the ions to their rightful side of the neuron's cell membrane, the neuron is back to its normal polarized state and stays in the resting potential until another impulse comes along.

The following figure shows transmission of an impulse.

Transmission of a nerve impulse: Resting potential and action potential.
Like the gaps between the Schwann cells on an insulated axon, a gap called a synapse or synaptic cleft separates the axon of one neuron and the dendrites of the next neuron. Neurons don't touch. The signal must traverse the synapse to continue on its path through the nervous system. Electrical conduction carries an impulse across synapses in the brain, but in other parts of the body, impulses are carried across synapses as the following chemical changes occur:

Calcium gates open.

At the end of the axon from which the impulse is coming, the membrane depolarizes, gated ion channels open, and calcium ions (Ca2+) are allowed to enter the cell.

Releasing a neurotransmitter.

When the calcium ions rush in, a chemical called a neurotransmitter is released into the synapse.

The neurotransmitter binds with receptors on the neuron.

The chemical that serves as the neurotransmitter moves across the synapse and binds to proteins on the neuron membrane that's about to receive the impulse. The proteins serve as the receptors, and different proteins serve as receptors for different neurotransmitters — that is, neurotransmitters have specific receptors.

Excitation or inhibition of the membrane occurs.

Whether excitation or inhibition occurs depends on what chemical served as the neurotransmitter and the result that it had. For example, if the neurotransmitter causes the Na+ channels to open, the neuron membrane becomes depolarized, and the impulse is carried through that neuron. [9If the K+ channels open, the neuron membrane becomes hyperpolarized, and inhibition occurs. The impulse is stopped dead if an action potential cannot be generated.

If you're wondering what happens to the neurotransmitter after it binds to the receptor, you're really getting good at this anatomy and physiology stuff. Here's the story: After the neurotransmitter produces its effect, whether it's excitation or inhibition, the receptor releases it and the neurotransmitter goes back into the synapse. In the synapse, the cell "recycles" the degraded neurotransmitter. The chemicals go back into the membrane so that during the next impulse, when the synaptic vesicles bind to the membrane, the complete neurotransmitter can again be released.

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Cherry 2013

Created By: Jessica De anda

What Is a Neurotransmitter?
By Kendra Cherry, About.com Guide

The neurotransmitters cross the synaptic gap to reach the receptor site of the other cell or neuron

Image from the Wikimedia Commons
[1] A neurotransmitter is a chemical messenger that carries, boosts and modulates signals between neurons1 and other cells in the body. In most cases, a neurotransmitter is released from the axon terminal after an action potential2 has reached the synapse. The neurotransmitter then crosses the synaptic gap to reach the receptor site of the other cell or neuron. Then, in a process known as reuptake, the neurotransmitter attaches to the receptor site and is reabsorbed by the neuron.

Neurotransmitters play a major role in everyday life and functioning. Scientists do not yet know exactly how many neurotransmitters exist, but more than 100 chemical messengers have been identified. When neurotransmitters are affected by disease or drugs, there can be a number of different adverse effects on the body. Diseases such as Alzheimer's and Parkinson's are associated with deficits in certain neurotransmitters.

Types of Neurotransmitters

Neurotransmitters can be classified by function:

[2] Excitatory neurotransmitters: These types of neurotransmitters have excitatory effects on the neuron; they increase the likelihood that the neuron will fire an action potential. Some of the major excitatory neurotransmitters include epinephrine and norepinephrine.

[3] Inhibitory neurotransmitters: These types of neurotransmitters have inhibitory effects on the neuron; they decrease the likelihood that the neuron will fire an action potential. Some of the major inhibitory neurotransmitters include serotonin and GABA
Some neurotransmitters, such as acetylcholine and dopamine, can both excitatory and inhibitory effects depending upon the type of receptors that are present.

They can also be categorized as one of six types:

[4] Amino acids: Gamma-aminobutyric acid (GABA) and Glycine Glutamate Aspartate.
Neuropeptides: Oxytocin,endorphins, vasopressin, etc.
Monoamines: Epinephrine, norepinephrine, histamine, dopamine and serotonin.
Purines: Adenosine, ATP.
Lipids and gases: Nitric oxide, cannabinoids.
Identifying Neurotransmitters

The actual identification of neurotransmitters can actually be quite difficult. While scientist can observe the vesicles containing neurotransmitters, actually figuring out what chemicals are stored in the vesicles is not quite so simple. Because of this, neuroscientists have developed a number of guidelines for determining whether or not a chemical should be called a neurotransmitter:

[5] The chemical must be produced inside the neuron
The necessary precursor enzymes must be present in the neuron
There must be enough of the chemical present to actually have an effect on the postsynaptic neuron
The chemical must be released by the presynaptic neuron, and the postsynaptic neuron must contain receptors that the chemical will bind to
There must be a reuptake mechanism or enzyme present that stops the action of the chemical
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Takahashi 2008

Created By: Jessica De anda

Fear-Induced Hallucination: How Sleep Paralysis Triggers Hallucination
Submitted by SerendipUpdate on Wed, 01/09/2008 - 3:43pm Biology 202
Biology 202
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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. [1According 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.
[2] 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). [3]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). [4When the amygdala interprets fear, it stimulates the release of both epinephrine and norepinephrine into the body's system (7). [5]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. [6The 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, [7] 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. [8Consequently, 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.

[9] 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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