Neurobiology

In a 1999 paper Cheyne, Rueffler and Newby-Clark define the three main clusters of sleep paralysis hallucinations as ‘Intruder’, ‘Incubus’ and ‘Unusual Bodily Experiences’.

They also suggest neurological correlates of each cluster.

Intruder – The feeling/sight of a presence in the room with you.

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These hallucinations may be caused by a hypervigilant brain state, in which detection thresholds are lowered and become biased towards cues of threat and danger. The amygdala is the emotion and threat recognition centre of the brain. During REM, the sleep state immediately adjacent to an episode of sleep paralysis, the amygdala is very active. Bursts of activity from the brainstem pass through the thalamus, which passes activity onto the amygdala. In waking life, the role of the pathway connecting these two structures is to analyse stimuli so that in the case of a dangerous or threatening situation quick emergency reactions can be taken without time-consuming processing by the relevant sensory cortices. Normally during a fear response, the immediate sensing of danger is quickly confirmed or dis-confirmed. In sleep paralysis, the sleeper becomes conscious but the amygdala remains very active, as in REM sleep. Deprived of external cues that would normally allow a sense of fear to be disconfirmed, attempts to analyse the source of the fear will fail. This may lead to a sense of apprehension that may last minutes, rather than milliseconds.


Incubus – Feelings of pressure, choking or suffocation.

The cluster of symptoms associated with ‘incubus’ may reflect the nature of respiration during REM sleep. Just as we don’t notice our heartbeat when we aren’t paying attention to it, our breathing during REM sleep is a natural reflex. It is rapid and shallow and there is a deprivation of oxygen (hypoxia), high amounts of blood CO2 (hypercapnia) and an occlusion of airways. Due to the paralysis that naturally occurs during REM sleep the contribution of throat muscles to breathing are reduced. As a result of all this, it is impossible for a person to voluntarily control their breathing during REM.

Usually this is unnoticeable when asleep, but a sleep paralysis sufferer becomes consciously aware whilst remaining in a state of REM-induced paralysis. Efforts to take voluntary control of breathing are unsuccessful, and the struggle for breath may manifest in a feeling of breathlessness and lead to panic. In addition to this, paralysis in the muscles of our upper airways may contribute to feelings of choking and suffocation.

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Unusual Bodily Experiences – Feelings of being moved, drifting, rolling, floating, cold or heat, as well as out-of-body experiences.

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These symptoms are associated with activity of sub-cortical brain structures (see fig 2.). When we’re awake, co-ordination of bodily movements is controlled by a number of brain areas, including the medial and superior vestibular nuclei. These vestibular nuclei are also associated with control of the sleep/wake cycle. These areas are active during REM sleep, with their activity very similar to what would be taking place if they were co-ordinating body movements. They remain active during a sleep paralysis attack. However during sleep paralysis the body cannot move, and the sufferer is aware of this. This dual awareness of movement and paralysis leads to a mismatch in the brain, which struggles to interpret conflicting information. A sense of body movement can be the result of the brain trying to correct and satisfy the mismatch between neural activation and sensory experience.

This may also be a common cause or contributing factor to out-of-body experiences. A feeling of floating is consistent with the sense of acceleration that can be produced by the vestibular nuclei. In this case the mismatch between brain activity and physical experience is resolved by splitting the ‘phenomenal self’ from the ‘physical self’, thus creating an out-of-body experience.

In the first neurophysiological study of Isolated Sleep Paralysis, Takeuchi et al used EEG to record participants’ brain activity during various stages of sleep, and during episodes of sleep paralysis. They found sleep paralysis to be characterised by large amounts of ‘alpha-wave’ brain activity and muscle paralysis. This suggests a state of dissociation between different stages of consciousness, with alpha-wave activity associated with waking activity, but muscle paralysis associated with REM sleep. They conclude that sleep paralysis is a state of REM sleep with a high level of arousal.

As well as the intrusion of waking brain activity in REM sleep, muscle paralysis (seen only in REM sleep) intrudes into wakefulness. The EEG experiment initially showed alpha-waves intruding into REM sleep, indicating an arousal into waking consciousness. This led to a waking state with a continuation of REM-state muscle paralysis.

In waking life, alpha-wave activity is most common when someone is at rest and not attending to anything. When something that requires attention occurs, such as looking at a picture, this alpha wave activity gets interrupted by beta-wave activity – which is associated with attention. Takeuchi et al observed that during sleep paralysis, alpha-wave brain patterns are frequently interrupted by beta waves, particularly in participants reporting visual hallucinations. This suggests that something has grabbed the attention of the sleep paralysis suffer – very likely a hallucination.

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