aleczb
Sleep Paralysis
What is Sleep Paralysis Like? A Subjective Standpoint
At some point during the night, something causes you to partially awaken our of a dream causing you to become aware of your body. You feel the soft surface of your bed (or whatever you happen to be sleeping in) pushing up against the parts of your body making contact with it. You feel the covers that are resting on top of you and what parts of your body they are covering. You notice that the parts of your body not covered are cooler and exposed to the air. You feel yourself inhale and exhale. You become proprioceptively aware of the position you are lying in. Everything about this experience suggests having just woken up from sleep, all but the complete inability to move the body parts that you have just regained awareness of. This is you experiencing sleep paralysis.
Typically, upon the realization that you’re paralyzed, anxiety sets in as you begin to move any and all of your body parts to no avail. And your anxiety only grows as you become more desperate to wriggle a foot or jerk your head and find that you are still paralyzed. You’re still confused about what exactly is happening to you, you want to move and to stop being afraid. Though an initial anxious state is common for sleep paralysis, there is the possibility that the paralysed person will remain calm and not experience any negative feelings (read my experience titled “Breathe” for a narrative account of this).
Only a few seconds have passed since you woke up and began to try to move around. Still you are unsuccessful, so you’ve decided to refocus your attention on your surroundings. Your eyes are probably open, so you begin to look around that environment that you were sleeping in, whether it be your bedroom or the living room a friend whose house you were sleeping in. Everything seems to be in order, it’s probably dark and you probably don’t hear much save the blowing or a fan or the ticking of a clock. But as you gather information about your environment, the already present sense of fear inexplicably morphs into something more sinister, a sense of terror. You feel something in the room with you, some abstract evil entity that you know has come to terrorize you. You feel helpless and vulnerable as you begin to rapidly scan your environment for any possible threats, because now you feel. Not all instances of sleep paralysis follow this pattern, some may not be able to open their eyes to get their physical bearings. Some may still be in a partial dream state and believe they are someplace else (read my experience titled “Mom?” for such an example).
At this point, the thought of this demonic entity instills within you a sense of sheer terror that you never thought possible. And it’s about to get worse. What felt like only a general evil energy begins to manifest into your physical world. You see a shadow in the corner of your room, it’s the devil, the entity that you sense is the devil and he’s standing in your room. And he brought friends along too. Shadowy figures begin to fly around your room in a circle as you hear them scratching the walls. Their circular formation begins to close in around your head as you hear them whispering your name in your ear. You sense of terror is now sheer horror. You close your eyes and try with all the energy your body is capable of mustering to move or to scream, but you still can’t. Until you can. Finally, after what has probably been only a minute but feels like an eternity, something gives. Your big toe on your left foot wiggles or you’re able to retract your right elbow. After the initial movement, the paralysis subsides all at once. You sit up quickly yanked on the chain to the lamp on your nightstand. As the entire room fills with light, you find that the flying shadow people are gone, there are no scratches on your wall, nobody is here. And in the spot where the devil had been standing, you see nothing more than a pile of laundry. A pile of laundry which, you would argue, could easily be mistaken for the devil in the right lighting. Your sense of horror is gone, and you are only slightly shaken up from your experience. For a classic account of sleep paralysis such as this, read my experience titled “The Sinister Sound of a Printer”.
My subjective interpretation of sleep paralysis: An experience in which someone wakes up out of dream and realizes that they are paralyzed, the experience is often frightful ad disorienting and can involve terrifying beings or sounds that disappear once the entire dream state has subsided.
What is Sleep Paralysis? An Objective Standpoint
To analyze the phenomenon of sleep paralysis from an objective standpoint we need to consider the role sleep paralysis has played in history and society, the statistics of sleep paralysis occurrences, and of course, the neuroscience behind it.
The historical perspective seems like the best jumping off point, so let’s briefly go over the impact of sleep paralysis has had on society throughout human history. From what we can tell, sleep paralysis has existed in almost every culture across the world for as far back as historical records go. For almost all of human history, people have understood sleep paralysis as something paranormal. Societies in the past lacked the scientific knowledge that we have at our disposal today, so paranormal explanations made sense because it was all they had.
Specific paranormal entities that were attributed to sleep paralysis vary from culture to culture. Entities affecting a given culture tend to match up with the specific ways in which that culture interpreted evil paranormal beings be. European societies commonly describe “night hag”, as an umbrella term for sleep demons in their folklore, typically the “night hag” resembles an old threatening witch-like woman. In the ancient Islamic world, sleep paralysis monsters took the form of “jinn” or malicious genie like creatures.
Before we turn to a more scientific way of explaining sleep paralysis, we should determine its prevalence in The United States today. It is estimated that around 8% of the general population has experienced sleep paralysis at some point in their life. Interestingly, the odds that someone will experience sleep paralysis increase if they are a student to around 28%. What’s most intriguing is the prevalence of sleep paralysis among mental health patients, which increases to around 32%. For those with panic disorder the probability of sleep paralysis being a life-long problem is around 35%. Clearly there has to be a strong link between mental illness and sleep paralysis considering more than a third of people with anxiety disorders have to endure and cope with sleep paralysis for their entire lives. What significance does this have scientifically? First we need to try to explain what causes sleep paralysis using neuroscience.
As variant as it can be, the one fundamental component that distinguishes sleep paralysis from other dreaming experiences is the conscious awareness of REM atonia (being unable to move). Although perceptual hallucinations or delusional thoughts often accompany the awareness of REM atonia, they are not necessary to sleep paralysis and often fall somewhere along a spectrum of intensity. The individual experiencing sleep paralysis may be perceptually aware of their physical location and experience no hallucinations, or they may feel as though they are someplace else (such as a childhood bedroom) and experience a myriad of hallucinations.
Studies of sleep paralysis and hallucinations are difficult to conduct because it is exceedingly difficult to predict when an episode will occur. Very few studies about sleep paralysis hallucinations exist that have collected neural data. Despite this, one aspect of sleep paralysis is well understood; the paralysis component.
During REM sleep, the brainstem (the deepest and oldest collections of structures in the human brain) releases the neurotransmitter GABA as well as the amino acid glycine, which bind to receptors in motor neurons and disinhibit them causing muscular paralysis. Without REM sleep atonia, there would be no mechanism to stop a dreaming oganism from acting out its dreams and potentially causing harm to its self or others in its group.
Sleep paralysis is thought to occur when the conscious aspects of REM sleep end before REM atonia, what actually causes this to happen is unknown. The hallucination aspect of sleep paralysis is even more poorly understood. Theories have been presented to account for what we don’t know about sleep paralysis. I’ve decided to give an overview of one of my favorite psychopharmacological theories.
Baland Jalal’s theory to explain sleep paralysis hallucinations starts by implicating a neurotransmitter called orexin, which is responsible for eliciting the arousal and wakefulness of the nervous system. Jalal theorizes that during REM sleep, orexin is released to cortical regions of the brain accounting for the sudden conscious awakening. Orexin also projects to a region of the brain that serves as the ‘hub’ for serotonin (a neurotransmitter with a multitude of purposes), where it causes a release of serotonin to various regions of the brain. At this point the specific serotonin receptor subtype called the 5HT-2A receptor becomes important for explaining the fear and hallucinations.
The 5HT-2A receptor is located in different concentrations in various brain regions, its function differs across these regions. As the serotonin projects to these regions, the chemical binds to 5HT-2A receptors in cortical regions where it’s known to produce feelings of fear, anxiety and visual hallucinations. To compare, LSD is known to produce its subjective effects by activating 5HT-2A receptors, one major component of these subjective effects being visual hallucinations.
Other regions such as the orbitofrontal cortex, when activated by 5HT-2A receptors, may lead to what’s known as ‘top down processing’. Top down processing refers to a way of processing reality in when expectations and context of a situation affects the way the brain interprets stimuli to produce perceptions. Theoretically, in this case, since 5HT-2A activation has set the context as fearful, a benign stimulus such as a chair may be misinterpreted by the brain of the sleep paralysis sufferer as a man standing in the room looking at them.
Our tendency to rely on top down processing (expectations affecting perceptions) may be the culprit for sleep paralysis and other types of hallucinations. Miscommunication between structures unique to a complex brain and deeper structures responsible for REM sleep itself, when activated in ways that are not supposed to happen at the same time seems to explain the strange perceptual experience.
One version of the gene that decides the number of 5HT-2A receptors might drastically increase one’s susceptibility to depression anxiety and sleep paralysis. This is one of the primary reasons I like Jalal’s theory. The version of the 5HT-2A gene (that increases one’s odds of anxiety and sleep paralysis) accounts for the fact that one third of people with anxiety and panic disorders suffer from sleep paralysis over the course of their lives.
Not much can be concluded about the neurological causes of sleep paralysis due to a lack of research. What does seem obvious is that sleep paralysis involves an incongruence between the conscious brain regions and the regions that regulate the physiological process of REM sleep atonia. More research is needed before we can make claims about the cause of the hallucinations.
My objective interpretation of sleep paralysis: A disruption in the sleep-wake cycle that causes a partial awakening out of REM sleep, the subject becomes cognitively aware that they are experiencing REM atonia and as a result of being caught between REM sleep and wakefulness, REM generated perceptions may overlap with the external environment and manifests as terrifying visual, auditory or tactile hallucinations.
Ancient portrait of Jinn
Before we turn to a more scientific way of explaining sleep paralysis, we should determine its prevalence in The United States today. It is estimated that around 8% of the general population has experienced sleep paralysis at some point in their life. Interestingly, the odds that someone will experience sleep paralysis increase if they are a student to around 28%. What’s most intriguing is the prevalence of sleep paralysis among mental health patients, which increases to around 32%. For those with panic disorder the probability of sleep paralysis being a life-long problem is around 35%. Clearly there has to be a strong link between mental illness and sleep paralysis considering more than a third of people with anxiety disorders have to endure and cope with sleep paralysis for their entire lives. What significance does this have scientifically? First we need to try to explain what causes sleep paralysis using neuroscience.
As variant as it can be, the one fundamental component that distinguishes sleep paralysis from other dreaming experiences is the conscious awareness of REM atonia (being unable to move). Although perceptual hallucinations or delusional thoughts often accompany the awareness of REM atonia, they are not necessary to sleep paralysis and often fall somewhere along a spectrum of intensity. The individual experiencing sleep paralysis may be perceptually aware of their physical location and experience no hallucinations, or they may feel as though they are someplace else (such as a childhood bedroom) and experience a myriad of hallucinations.
Studies of sleep paralysis and hallucinations are difficult to conduct because it is exceedingly difficult to predict when an episode will occur. Very few studies about sleep paralysis hallucinations exist that have collected neural data. Despite this, one aspect of sleep paralysis is well understood; the paralysis component.
During REM sleep, the brainstem (the deepest and oldest collections of structures in the human brain) releases the neurotransmitter GABA as well as the amino acid glycine, which bind to receptors in motor neurons and disinhibit them causing muscular paralysis. Without REM sleep atonia, there would be no mechanism to stop a dreaming organism from acting out its dreams and potentially causing harm to its self or others in its group. Sleep paralysis is thought to occur when the conscious aspects of REM sleep end before REM atonia, what actually causes this to happen is unknown.
The hallucinations associated with sleep paralysis are even less well understood. Theories have been presented to account for what we don’t know about sleep paralysis. I’ve decided to give an overview of one of my favorite psychopharmacological theories.
Baland Jalal’s theory to explain sleep paralysis hallucinations starts by implicating a neurotransmitter called orexin, which is responsible for eliciting the arousal and wakefulness of the nervous system. Jalal theorizes that during REM sleep, orexin is released to cortical regions of the brain accounting for the sudden conscious awakening. Orexin also projects to a region of the brain that serves as the ‘hub’ for serotonin (a neurotransmitter with a multitude of purposes), where it causes a release of serotonin to various regions of the brain. At this point the specific serotonin receptor subtype called the 5HT-2A receptor becomes important for explaining the fear and hallucinations.
The 5HT-2A receptor is located in different concentrations in various brain regions, its function differs across these regions. As the serotonin projects to these regions, the chemical binds to 5HT-2A receptors in cortical regions where it’s known to produce feelings of fear, anxiety and visual hallucinations. To compare, LSD is known to produce its subjective effects by activating 5HT-2A receptors, one major component of these subjective effects being visual hallucinations.
Other regions such as the orbitofrontal cortex, when activated by 5HT-2A receptors, may lead to what’s known as top-down processing. Top down processing refers to a way of processing reality in which expectations and context of a situation affects the way the brain interprets stimuli to produce perceptions. Areas of the brain that are associated with top-down processing are corical areas that are also associated with consciousness. Theoretically, in this case, since 5HT-2A activation has set the context as fearful, a benign stimulus such as a chair may be misinterpreted by the brain of the sleep paralysis sufferer as a man standing in the room looking at them.
One version of the gene that decides the number of 5HT-2A receptors might drastically increase one’s susceptibility to depression anxiety and sleep paralysis. This is one of the primary reasons I like Jalal’s theory. The version of the 5HT-2A gene (that increases one’s odds of anxiety and sleep paralysis) accounts for the fact that one third of people with anxiety and panic disorders suffer from sleep paralysis over the course of their lives.
Not much can be concluded about the neurological causes of sleep paralysis due to a lack of research. What does seem obvious is that sleep paralysis involves an incongruence between the conscious brain regions and the regions that regulate the physiological process of REM sleep atonia. More research is needed before we can make claims about the cause of the hallucinations.
Density of Serotonin 2A Receptors in the Brain
Brain Regions Associated With Top-Down Processing
My objective interpretation of sleep paralysis: A disruption in the sleep-wake cycle that causes a partial awakening out of REM sleep, the subject becomes cognitively aware that they are experiencing REM atonia and as a result of being caught between REM sleep and wakefulness, REM generated perceptions may overlap with the external environment and manifests as terrifying visual, auditory or tactile hallucinations.
Sleep Paralysis: Mind and Matter
In order to draw implications of sleep paralysis to the fundamental questions, I think it’s necessary to reinterpret sleep paralysis as: A state of subjective awareness in which one becomes consciously aware of their physical body and disrupts the construction of an internal perceptual world, this causes a hybrid state of reality in which internally generated subjective perceptual experiences coincide with externally generated subjective experiences.
So in a case of sleep paralysis we see an interesting dance going on between the mind and the physical world. More specifically, we see an interesting dance between the subjective world generated by the mind and the way in which the mind interprets the external world.
Certainly it would be easy to distinguish which perceptions are physical and which and internally generated. Any video that captures one’s sleep paralysis experience would show which perceptions could be attributed to something physical and which were internally generated by the mind. I see no reason to argue between what perceptions are physical and what perceptions are generated by the mind. Science deals solely with what physical matter and what is measurable. So it’s clear that sleep paralysis hallucinations are not physical in that sense.
But what about top down perceptions? Certainly a camera would pick up a stack of blankets that the sleep paralysis sufferer interpretes as, for example, a gremlin. The physical stimuli is still there so the IGSPE was not completely fabricated by the mind. It still proves that it is not a gremlin but a stack of blankets. But cameras are designed to pick up particles of light and process them in such a way that the resulting image will make sense to us humans who have vision.
We constantly rely on top down processing to make sense of our physical world, we do this all day every day. And top down processing is performed by the mind for the purpose of altering its perception of the physical world to make perceptions easier to interpret. So here we have a physical process (neural activity of top down processing) shaping and forming ways in which we view other physical processes.
This all calls into question how much we can trust our top down processing abilities to give us reliable information about the physical world. Surely the person who saw the stack of blankets as a gremlin (because of the top down processing that occured) would later agree on the video that it was not a gremlin but a pile of blankets). But as I stated before, videos are designed to transmit information to us in the ways in which that we typically see it, this includes all the top down perceptions already included in the video that we wouldn't think twice about. We already have neural pathways needed to perform top down processing from previous experiences. By contrast, if a blind individual suddenly gained their ability to see, they would not have the necessary neural architecture in place to make the top down perceptions that you and I do. They would see nothing meaningful in either the video of the environment where the video took place. They would however be able to feel the blanket and identify it as a blanket using their tactile senses.
So it’s not about the physical world, but the way in which the mind interacts with the physical world to produce an external perception.The physical world is not exactly how we perceive it but how our minds interpret incoming stimuli based on past experiences of our same mind interpreting the same stimuli. Depending on what neural pathways are in place to observe a physical stimuli, there could be an infinite number of equally correct ways to interpret the physical world. Ours is only one of those infinite correct ways, it is not the only correct way. Sleep paralysis being to light the importance of top down processing to the mind vs matter question. Not because the hallucinations have and legitimate physical origin, but because to the person having the subjective experience, they are just as real as another top down perception that person would have on any given day.