
Rapid Eye Movement (REM) sleep is a distinct behavioural state characterised by activated cortical and hippocampal electroencephalograms (EEGs) and concurrent muscle atonia. During REM sleep, the eyes continue to move, but the rest of the body's muscles are stopped, potentially to prevent injury. Research has shown that two powerful brain chemical systems work together to paralyze skeletal muscles during REM sleep. While the brain region responsible for generating phasic twitches in cranial muscles is not clear, it has been found that the brain cells called trigeminal motor neurons communicate the brain's message to move to the facial muscles responsible for chewing.
| Characteristics | Values |
|---|---|
| REM Sleep | Deep sleep where most recalled dreams occur |
| Muscle Activity During REM Sleep | The rest of the body's muscles are stopped, potentially to prevent injury |
| Brain Activity During REM Sleep | The brain remains active and continues to send messages to the muscles |
| Facial Muscle Contractions (FMC) | Commonly observed during sleep and associated with emotional expression during waking |
| Brain Chemicals Involved in REM Sleep | Gamma-aminobutyric acid (GABA) and glycine |
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What You'll Learn
- Facial muscles contract during REM sleep
- Brain cells communicate the brain's message to move facial muscles
- REM sleep is characterised by muscle atonia
- The brain's cortical and hippocampal regions are activated during REM sleep
- REM sleep behaviour disorder is a sleep disorder that can be better understood by studying REM sleep paralysis

Facial muscles contract during REM sleep
During the REM sleep stage, the human body experiences rapid eye movement, which is associated with emotional dream content. Recent studies have shown that facial muscle contractions (FMC) are more frequent during REM sleep than in non-REM sleep. The frequency and duration of these contractions are also higher during this sleep stage.
FMC is associated with emotional expression during waking hours. The corrugator and zygomatic major muscles, which are typically associated with emotional expression, have been observed to contract more during REM sleep. This is consistent with the theoretical perspective that REM sleep is associated with higher emotional variations during dream content.
A study by De Gennaro L, Ferrara M, and others, published in the journal Sleep in 2000, found a positive correlation between facial muscle contractions and REMs during REM sleep. However, these features were never observed to occur simultaneously. The study suggested that limbic activation during REM sleep may be responsible for increased facial muscle activity, which aligns with the perspective of heightened emotional activity during this sleep stage.
Another study, by Isidoro Camacho Garcia, Carlos Jimenez Rodriguez, and Carlos Camacho Garcia, published in the European Journal of Pharmaceutics and Biopharmaceutics in 2021, found that during REM sleep with FMC, the corrugator, and zygomatic muscles were associated with emotional dream content. The study also found that FMC was differentially associated with emotional modality according to the activated facial muscle. These findings further support the idea that facial muscles contract during REM sleep and that this activity is related to the emotional content of dreams.
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Brain cells communicate the brain's message to move facial muscles
Facial expressions are controlled by a network of structures that include the amygdala and multiple, interconnected cortical and subcortical motor areas. The muscles of the upper and lower face are controlled by anatomically distinct motor areas. Facial expressions require distinct patterns of neural activity distributed across multiple facial motor areas in the ventrolateral frontal cortex, the supplementary motor area, and two areas in the midcingulate cortex.
The facial nerve (CN VII) controls several muscles in the face, such as those that help us smile, frown, wrinkle our noses, and raise our eyebrows. It also has sensory and parasympathetic functions. The facial nerve sends signals from the brain to parts of the face and vice versa. Facial nerves extend from the brainstem throughout the face, starting in the brainstem, travelling through the base of the skull near the vestibulocochlear nerve (eighth cranial nerve), and entering the face through an opening near the base of the ear.
The cerebellum, a small, fist-sized portion of the brain located at the back of the head, coordinates voluntary muscle movements and maintains posture, balance, and equilibrium. The brain itself is about 60% fat, with the remaining 40% being a combination of water, protein, carbohydrates, and salts. It contains blood vessels and nerves, including neurons and glial cells.
The brain's gray and white matter are two different regions of the central nervous system. Gray matter refers to the darker, outer portion of the brain, while white matter is the lighter, inner section underneath. In the brain, gray matter is primarily composed of neuron somas, and white matter is made up of axons that connect neurons, wrapped in a protective coating.
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REM sleep is characterised by muscle atonia
Rapid eye movement (REM) sleep is a distinct behavioural state characterised by muscle atonia. During REM sleep, the eyes continue to move, but the rest of the body's muscles are inactive, possibly to prevent injury.
Research has shown that two powerful brain chemical systems work together to paralyse skeletal muscles during REM sleep. The neurotransmitters gamma-aminobutyric acid (GABA) and glycine cause REM sleep paralysis by "switching off" the specialised cells in the brain that allow muscles to be active.
In a study, researchers found that blocking only the ionotropic GABAA/glycine receptors in the motor neurons was not enough to prevent REM sleep paralysis. They had to block both the ionotropic receptors and metabotropic GABAB receptors, another receptor system. This suggests that the two neurotransmitters must be present together to maintain motor control during sleep.
The neuronal network responsible for REM sleep and its dysfunctions has been discovered in the pons and medulla. The caudal laterodorsal tegmental nucleus (cLDT) and sublaterodorsal nucleus (SLD) within the dorsolateral pons contain REM-on neurons, while the ventrolateral periaqueductal grey (vlPAG) contains REM-off neurons. The cLDT-SLD neurons project to the basal forebrain via the parabrachial-precoeruleus (PB-PC) complex, which may be critical for the EEG activation seen during REM sleep.
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The brain's cortical and hippocampal regions are activated during REM sleep
During REM sleep, the brain exhibits intense neuronal activity, similar to the levels observed during wakefulness. This includes activation in the cortical and hippocampal regions of the brain.
The cortex is highly active during REM sleep, with global cortical dynamics playing a significant role in controlling sleep states. Calcium imaging studies in mice have revealed distinct sleep stage-dependent patterns of global cortical activity, which are believed to regulate the transition between sleep stages. Specifically, elevated activation in the occipital cortical regions, such as the retrosplenial cortex and visual areas, becomes dominant during REM sleep. This activation is associated with the transition from non-rapid eye movement (NREM) sleep to REM sleep.
The hippocampus also demonstrates increased activity during REM sleep, particularly in the form of rhythmic theta oscillations. This activation provides a window of opportunity for inter-regional coordination between the hippocampus and cortical regions, which is believed to be involved in memory processing.
The prefrontal cortex, specifically the medial prefrontal cortex (mPFC), is another region that is strongly activated during REM sleep. The mPFC interacts with multiple cortical and subcortical areas through its long-range connections, allowing it to coordinate various behaviours and regulate brain-wide activity.
While the exact mechanisms are not yet fully understood, these activations in the cortical and hippocampal regions during REM sleep are believed to be intimately related to the unique neurophysiological state that characterizes this sleep stage.
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REM sleep behaviour disorder is a sleep disorder that can be better understood by studying REM sleep paralysis
REM sleep behaviour disorder (RBD) is a sleep disorder characterised by the physical and vocal enactment of dreams during the rapid eye movement (REM) stage of sleep. This condition is not a mental health issue, but rather a parasomnia, and it can lead to injury and distress for the person affected and their bed partner. Understanding the role of REM sleep paralysis in healthy individuals can help shed light on the nature of RBD.
During typical REM sleep, the body experiences temporary paralysis, known as atonia, affecting most skeletal muscles. This paralysis ensures that individuals can dream safely, preventing them from acting out their dreams. The brain, however, exhibits activity akin to wakefulness, with rapid eye movements, irregular breathing, and heightened blood pressure.
In individuals with RBD, this normal muscle paralysis does not occur, allowing them to physically act out their dreams. Episodes of RBD are confirmed by in-laboratory polysomnograms or clinical histories, and they are not attributed to other factors like sleep or mental health disorders, medication side effects, or substance abuse. The absence of muscle paralysis during REM sleep, or REM sleep without atonia, is a defining feature of RBD.
Research suggests a link between RBD and certain conditions, including Parkinson's disease, Lewy body dementia, and multiple system atrophy (MSA). Lesions in the pons region of the brainstem, which controls muscle paralysis during REM sleep, are associated with these conditions and may contribute to the development of RBD. Understanding the role of REM sleep paralysis and its underlying mechanisms can help improve our understanding of RBD and guide potential treatments or interventions to ensure the safety of individuals with this disorder.
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Frequently asked questions
No, they don't. During REM sleep, the body's muscles are paralysed or inactive. This is caused by two powerful brain chemical systems that work together to paralyse skeletal muscles during REM sleep.
REM stands for rapid eye movement. It is a distinct behavioural state characterised by an activated cortical and hippocampal electroencephalogram (EEG) and concurrent muscle atonia.
According to a study on rats, the neurotransmitters gamma-aminobutyric acid (GABA) and glycine cause REM sleep paralysis by "switching off" the cells in the brain that allow muscles to be active.











































