Sleep Paralysis: REM and the "I Function"

Biology 202
2000 Second Web Report
On Serendip

Is there a possible neurological answer to the terrifying experiences of sleep paralysis? Is it simply a cascade of hallucinatory sequences brought about by a struggle of the I-function to overcome the strong mechanisms of REM sleep?

Sleep paralysis is the phenomenon where a person about to fall asleep or just awakened realizes that they cannot move or speak. The sleeper is almost always lying on their back, and about 30% of the time will have hallucinations, referred to as hypnagogic and hypnopompic experiences (HHEs).1 These include a "vivid imagery, auditory hallucinations, a buzzing sound and/or feeling of "vibrating" inside, tactile (touch) sensations, olfactory (smell) sensations, and sensations of separating or being separated from the body.2 The sleeper awakes to discover that they cannot move except for their eyes. Sometimes, however, these hallucinations include a presence, usually malevolent, threatening, or evil accompanied by severe sense of dread or terror. The presence is likely to be vaguely felt or sensed just out of sight but thought to be watching or monitoring, often with intense interest, sometimes lurking nearby the bed. If the presence is seen, it usually takes the form of a crusher sitting on the chest, succubis/incubus seeking sex with a male/female, or a tormenting old hag.3 Also included in this list is that of alien abduction have, in recent years, has grown in prominence. Usually the experiencer awakens in the night unable to move or cry out as alien beings approach the bed and float the helpless, paralyzed abductee up to a spaceship for a frightening medical examination.4 A recent web-study by UCLA researchers found that from a sample of 250 people with recurrent sleep paralysis, 90% of respondents experience intense fear during their episodes; about 50% have invoked a paranormal or supernatural explanation.5

One way to divide the different stages of sleep is into REM and NREM sleep. REM is when most of what most people would call dreams occur. It is important to note that REM is not the only stage at which dreams can occur.6 REM sleep is associated with muscle atonia (paralysis of voluntary musculature), gating of sensory input, rapid eye and middle ear movements, as well as heart rate and respiration changes (Carskadon & Dement, 1989; Symons, 1993).7 Muscle atonia is crucial during REM, because otherwise we would act out our dreams.

Therefore, several times a night (that is, if you sleep long enough), our bodies are paralyzed at the level of the pons to keep us from acting out our dreams. Cells there send inhibitory signals to motor neurons in the spinal cord via the magnocellular nucleus in the medulla.8 Disruption of this pathway in cats results in the acting out of the REM sequences (Jouvert, 1972).
In order to be more exact about we are talking about, sleep paralysis with these other sensations should be referred to as Awareness during Sleep Paralysis (ASP), or alternatively, RISP (Recurrent Isolated "sleep paralysis"). The question remains: if we all are paralyzed several times a night, then why doesn't everyone experience ASP?

Sleep paralysis with HHEs differs from usual REM dreams in that during ASP, there is either no loss, or a return to waking consciousness. ASP with HHEs differs from dream experience in that the sensory cortex may be receiving both externally and internally generated information.9 During REM sleep, the great majority of external stimuli are blocked out. As we all know, every once in a while, information that cannot be blocked out (an alarm clock, loud noises), will enter and be incorporated into REM sequences. The peculiarity of the HHEs in ASP might be in part a result of the brain's attempts to integrate and make sense of endogenous cortical arousal associated with REM with normal sensory input. This leaves one, in the dark in bed, eyes open and able to move, but otherwise paralyzed. It is possible, also that many of the regions of the brain that create the (internally produced) visual and auditory information of REM sleep are still active to some extent. In other words, the I-function has turned on at the most inappropriate of times.

A similar peculiarity may exist for motor pattern arousal during ASP. Because of the input of external sensory information, and perhaps conflicting expectation and results from motor information, the person is also aware that they cannot move. McCarley and Hobson argue that, during dream generation by internal stimulation of motor programs, we interpret the activity of the pattern generators and their corollary discharge as movement (Remember that these signals are inhibited at the spinal cord). The consequent lack of peripheral feedback, though not normally necessary for effective control, may contribute to a sense of unreality to the apparent movement and hence to the "bizarreness" of dreams. Pontine activation of motor patterns during ASP appears to be less common in ASP than in dreams, if subjective reports of illusory movement are to be taken as evidence. Attempts at voluntary movement during ASP are common, however, and the absence of feedback is most often, though not always, experienced as paralysis rather than illusory movement. This may be because it is no longer simple motor programs that are being elicited. The person is now awake and "willing" certain movements. The consequent lack of feedback is experienced as paralysis (the eyes can move and search; after all REM stands for Rapid Eye Movement). During ASP, the "I function" finds the absence of response to generated motor signal discomforting, until the person either decides to "go with it" (in which case an altered state experience is likely), or is finally able to create a movement.

Paralysis is usually broken by attempting to move a small part of the body - a finger, or a toe, for example. Even novices seem to understanding that, if they can move a finger, even the little finger, the experience will end.10 This suggests to me that in a very important way, ASP boils down to a struggle between the I function and central pattern generators. Fine movement, like moving a single finger, requires the motor cortex to over-power and inhibit the signals of pattern generators.

Discussion of the "Presence"

The sense of presence in sleep paralysis is strongly associated with fear and a very basic dread or terror.11 The authors of the Waterloo Sleep Paralysis Page postulate that the cause of this association is the result of activation of the amygdala by bursts originating in the pontine reticular areas. The amygdala is a region of the brain largely responsible for the fear response and aggression. People or animal subjects with lesions to the amygdala will often lash out at an unseen enemy. In most potential emergencies, the immediate sensing of danger is quickly confirmed or disconfirmed. "Reciprocal projections to the polymodal association cortex directly from the amygdala enhance analysis of critical features of the threatening stimulus corroborate the nature and seriousness of the threat (Ledoux, 1994)." In the case of sleep paralysis and the absence of exogenous origins, attempts to analyze the source of fear will inevitably fail. The state of apprehensive "suspicion" that normally might last only the time span of a few neural firings, is protracted during ASP.

It has also been hypothesized that the paralysis of sleep paralysis may also be in part a fear reaction.12 Animals will often play dead either when absolutely exhausted from flight, or trapped by a predator or conspecific rival. This occurs as a sudden and complete paralysis of the musculature, referred to as tonic immobility (TI). "Aside from the motor paralysis, the association of external monitoring, threatening presence, bodily sensations associated with being attacked, mauled, and transported, as well as fear itself, are common features of SP and tonic immobility." You can actually induce TI in some species by restraining the subject in a supine position. The duration of TI is substantially increased in the presence of an image of a predator or even a pair of disembodied staring eyes (Gallup and Master, 1977). In addition, the reported subjective experiences in ASP of the threatening presence and the crushing pressure on the chest are strongly suggestive of the predator/attacker that seizes and holds down its victim. "At the very least the paralysis in the supine position might predispose one to interpret the context in life threatening terms. These may then lead to a series of internally consistent interpretations concerning the meaning of events" In the presence of an invisible, unbeatable pursuer that means harm, the fight/flight mechanisms of the brain may induce a "last resort" full paralysis to stave off a perceived attack. It can take all of a person's will (i.e., I function) to counteract this basic motor program.

Cases of the hag, or other entity sitting on the chest or actually choking the victim fit especially well in this explanation. Meyer (1990) found that only pressures applied to the midline of the dorsal surface at the nape of the neck significantly potentiated the duration of TI and cling catalepsy. "These physical manipulations would certainly produce sensory experiences of dorsal or ventral pressure around the thorax and neck regions such as are reported in the Old Hag experience."

Well, one may ask "why should someone waking up in the middle of the night fell like they can not breathe to begin with?" If we are dealing with a failure to turn off the mechanisms of REM sleep, then we must take a look at breathing in REM. Characteristics of REM respiration include shallow rapid breathing, hypoxia, hypercapnia, and occlusion of airways (Douglas, 1994).13 Both tidal volume and breathing rate are quite variable during REM, and because of paralysis of the major anti-gravity muscles, thoracic contribution to breathing is lower during REM than during NREM sleep (Douglas, 1994). Moreover, because individuals are conscious during SP they may sometimes attempt to breathe deeply when tidal volume decreases, just as they attempt other voluntary movements. When they find their attempts to control breathing volume and rate are unsuccessful, they will feel a sense of resistance possibly interpreted as pressure, or a feeling of choking as the desired larger volume of air fails to enter the lungs. This is consistent with the finding that the pressure on the chest is positively associated with perceived breathing problems (Cheyne, Newby-Clarke, & Rueffer, 1998). In addition, increased airflow resistance because of hypotonia of the upper airway muscles and constriction of the airways would attenuate feelings of choking and suffocation. This could very easily lead to panic and strenuous efforts to overcome the paralysis; all this in the absence of a visible reason. As we search for a cause unseen, and find none (all the more scared because of it), we start to fabricate the malevolent agent - even if its [this is where we run into the muddling of cause and effect in the nervous system. Does a fear response cause us to breathe harder unsuccessfully, or does the person's sudden inability to not breathe as expected/desired trigger a fear response?]

It also seems to me that as long as the person is in the grips of paralysis while the I function is active (i.e., they are awake and aware), and they are in an unexplained and fearful state, the I function will create scenery consistent with a fearful unknown. One of the features of ASP is the difference in cultural associations. The visual hallucinations have been interpreted throughout time and in different cultures as being: indigestion in Hellenic Greece, guilt for the Romans and the Egyptians, witchcraft for the Mexicans and Yoruba people, demons for Medieval Europe, djinn for the Arabs, vampires for Europeans, Hag for the Irish and Scottish and other Europeans, spectral foxes for the Japanese, cats for the Chinese, ancestral ghosts for South-East Asians, etc. Recently in the West, they have been interpreted as complex interactions with space aliens. Yet, Despite the various interpretations, the descriptions of the hallucinations are remarkably similar.13

Perhaps most importantly, no matter what form the manifestation takes, attempts to move a finger or a toe will banish the evil agent and allow the individual to go back to sleep.

In conclusion, these are only pieces of the puzzle. Sleep paralysis as a phenomenon has only been studied extensively in recent years. This was due in part to the silence of many people experiencing ASP afraid that they were simply losing their minds. Also, it was due in art to its association to narcolepsy and the failure to study ASP as a phenomenon in and of itself.
Some of the unanswered questions for neuroscience include - why would someone awake in the midst of REM? What are the cognitive aspects of these experiences? Can these experiences be guided by a third party (spouse, parent)?
There are larger, more basic questions outside of physiology and neuroscience left in regards to ASP. They deal with the nature of reality. Trionica.com poses the following questions:

1. Process/Content Issues: When the consciousness of the experiencer is Aware while the body of the experiencer is in Sleep Paralysis, to what extent is the experiencer perceiving and to what extent is the experiencer hallucinating the objects of awareness (the content of the experience)?

2. The Reality of Other Beings: Are the beings encountered by ASP experiencers real beings?[I'd like to add: a)at what plane/level of reality might they exist, and b)how much does it matter if they are "real" or not? 14

We are a long way from satisfactorily answering either 1) or 2), but we can keep picking away at them.

WWW Sources

1. Sleep Paralysis and Associated Hypnagogic and Hypnopompic Experiences

2. Sleep Paralysis, Lucid Dreams, and OBE's: Glossary

3. Trionica.com

4. Trionica.com: Alien Abduction Experiences

5. Does Recurrent Isolated Recurrent Sleep Paralysis Involve More than the Cognitive Neurosciences?

6. Trionica.com

7. Cheyne: SP as an Anomolous REM

8. Carlson. Physiology and Behavior,6th Ed. Boston: Allyn and Bacon, 1998.

9. SP as an Anomolous REM

10. Trionica.com: Awareness during Sleep Paralysis: Active Responses

11. Cheyne: The Inruder

12. Cheyne: Incubus

13. Nocturnal Assault Research Center: ASP and Hag Phenomenon

14. Trionica.com:Alien Abduction Experiences

 

 

Comments made prior to 2007

I was reading the article on sleep paralysis, and i think i get it too. They first started when i started college and for a year i had them about 3-4 times a week, now 3years on i get them about 4 times a week. There really scary and very vivid and have developed.

 

When i fell asleep i thought i was awake but i was still dreaming.I remember trying to move and scream but i couldnt.then the dreams developed i was able to call out peoples names and even bang on the wall. they carried on developing, soon i was able to walk round my house, even look in mirrors and open door but i still couldnt wake myself up. One time i seen a tall black figure coming towards me and another time i was being thrown about my room but no1 was doing it to me.The only way i could wake myself up was to tell myself to wake up and i would.When ive woken sometimes ive gone straight back into the dream.The only way i would no if i was dreaming was to try and turn on a light, if I couldnt then i knew that i was still dreaming.is this sleep paralysis? ... Sarah, 6 January 2007