Logan Steele
Muscle atonia is a state of reduced muscle tone or paralysis that occurs during REM sleep. It is considered a normal function of REM sleep, during which the brain is highly active. The absence of muscle atonia during sleep can result in REM sleep behaviour disorder, where individuals act out their dreams, sometimes violently or injuriously. The mechanisms causing muscle atonia are complex and involve specific neuronal circuitry.
| Characteristics | Values |
|---|---|
| Definition | Sustained (tonic) loss of normal muscle atonia during REM sleep, and/or by intermittent (phasic) excessive electromyographic activity during REM sleep |
| Occurrence | During REM sleep |
| Cause | Motoneurons not generating action potentials |
| Brain circuitry location | Pontine and medullary brainstem |
| Neurons involved | Glutamatergic neurons, glycinergic pre-motor neurons, spinal motoneurons |
| Related disorder | REM behavior disorder |
| REM behavior disorder characteristics | Abnormal behaviours during REM sleep, sleep disruption, injury to self or bed partner |
| REM behavior disorder diagnosis | Careful evaluation, sleep study |
| Related disorder 2 | Narcolepsy |
| Related disorder 3 | Restless leg syndrome |
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What You'll Learn
Muscle atonia is a fundamental characteristic of REM sleep
Muscle atonia is a state of reduced muscle tone during sleep. It is a fundamental characteristic of rapid eye movement (REM) sleep, which is associated with dreaming. During REM sleep, the body experiences reduced muscle tone in many of its muscles, which may be referred to as REM sleep muscle paralysis or muscle atonia. This is considered a normal and necessary function of REM sleep.
The mechanisms causing muscle atonia during REM sleep are complex and involve specific neuronal circuitry. The supraspinal mechanisms responsible for REM atonia originate in the perilocus coeruleus (LC)-alpha nucleus in the pons, which sends excitatory projections to the nucleus reticularis magnocellularis in the medulla. This results in descending inhibitory projections to the spinal alpha motoneurons, leading to hyperpolarization and muscle atonia. Thus, REM atonia is the result of an active process rather than passive cessation of muscle tone.
During REM sleep, certain areas of the brain are highly active, and the brain demonstrates increased cerebral blood flow. This challenges the traditional notion of sleep as a passive process and indicates that the brain is not inactive during sleep. In fact, specific areas of the brain may be even more active during REM sleep than during wakefulness.
The occurrence of muscle atonia during REM sleep is crucial for preventing the physical acting out of dreams, which could lead to violent or injurious behaviour. When muscle atonia is absent during REM sleep, individuals may experience REM behaviour disorder, characterised by abnormal behaviours such as twitching, utterances, flailing, kicking, and even leaving the bed. These behaviours can cause sleep disruption and pose risks of injury to both the individual and their bed partner.
While muscle atonia is typically associated with REM sleep, it can also occur during non-REM sleep. Studies have reported extended epochs of muscle atonia in non-REM sleep, suggesting that muscle atonia may be a marker of homeostatic and circadian REM sleep regulation. Furthermore, muscle atonia is not always synchronous with other REM sleep components, and its presence or absence can be influenced by various factors, including pharmacological treatments and state-dependent drives.
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Motoneurons and action potentials
Muscle atonia refers to the sustained (tonic) loss of normal muscle function during REM sleep, resulting in reduced muscle tone or temporary paralysis. This condition is considered a normal and fundamental characteristic of REM sleep, mediated by a highly specialised neuronal system.
Now, let's delve into the role of motoneurons and action potentials in relation to muscle atonia:
Motoneurons, or motor neurons, play a crucial role in muscle function, including the state of atonia during REM sleep. Motoneurons are a type of neuron that specifically connects to muscle fibres and stimulates their contraction. During REM sleep, these motoneurons typically do not generate action potentials, leading to the state of muscle atonia.
Action potentials are rapid electrical impulses that serve as the fundamental units of communication between neurons. They occur when the combined effect of excitatory and inhibitory inputs causes a change in the neuron's membrane potential, resulting in a rapid upward (positive) spike followed by a rapid fall, known as an up-and-down cycle. This cycle is key to the generation of action potentials, which are essential for cell-to-cell communication and the transmission of signals along a neuron's axon.
The generation of action potentials in motoneurons specifically arises at the initial segment of the cell's axon, near its soma. This generation results from a summation of currents produced at synapses on the soma and dendrites. If these currents surpass a certain threshold voltage, typically around 50 mV, an action potential is triggered. This threshold voltage is known as the action potential threshold.
During REM sleep, the absence of action potentials in motoneurons leads to muscle atonia, preventing the individual from acting out their dreams physically. This protective mechanism ensures that the body remains relaxed and immobile during the dream state, safeguarding the individual from potential self-harm or injury.
Several processes are believed to contribute to the decreased discharge of motoneurons during REM sleep, including postsynaptic inhibition, disfacilitation (withdrawal of excitatory input), and presynaptic inhibition of muscle afferents. These processes help maintain the state of muscle atonia, which is crucial for undisturbed sleep and safety.
In summary, muscle atonia during REM sleep is a result of the complex interplay between neuronal circuitry and the suppression of motoneuron activity, specifically the absence of action potentials. This temporary paralysis is a normal and essential feature of healthy sleep, allowing for the safe expression of dreams without physical consequences.
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REM sleep behaviour disorder
Muscle atonia refers to the loss of muscle tone or paralysis that normally occurs during REM sleep. This is considered a normal function of REM sleep, during which the body is typically unable to act out dreams.
RBD can be divided into three categories: idiopathic RBD, drug-induced RBD, and secondary RBD due to a medical condition. The diagnosis of RBD requires confirmation by an in-laboratory sleep study (polysomnography) with video recording, which helps to assert abnormal behaviours during REM sleep and excludes other sleep disorders. The individual with RBD may not be aware of having it. When awakened, people may be able to recall the dream they were having, which will match the actions they were performing.
RBD has been associated with antidepressant use, narcolepsy, and other medical conditions. The strongest correlation exists between RBD and comorbid neurodegenerative alpha-synucleinopathies, such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. Symptoms of RBD may precede neurodegenerative disorders by decades, and it is likely that RBD is an early symptom of synucleinopathy rather than a separate disorder. Brainstem circuits that control atonia during REM sleep may be damaged, and motor deficits like those seen in RBD are known to result from lesions in those circuits.
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Muscle atonia in non-REM sleep
Muscle atonia is a sustained (tonic) loss of normal muscle tone during sleep, and it is a fundamental characteristic of REM sleep. It is mediated by an active and highly specialised neuronal system.
However, muscle atonia is not exclusive to REM sleep. Muscle atonia in non-REM sleep (MAN) has been observed in several studies. One study found that submental muscle atonia occurred during the initial part of a non-REM sleep episode following a REM sleep episode. Another study found that muscle atonia occurred during non-REM sleep after selective REM sleep deprivation.
The extent and time course of MAN was studied in a protocol that included a baseline night, a daytime sleep episode with or without selective REM sleep deprivation, and a recovery night. The distribution of the latency to the first occurrence of MAN was bimodal with a first mode shortly after sleep onset and a second mode 40 minutes later. Within a non-REM sleep episode, MAN showed a U-shaped distribution with the highest values before and after REM sleep.
MAN was found to be at a constant level over consecutive 2-hour intervals of nighttime sleep, but showed high initial values when sleep began in the morning. Selective daytime REM sleep deprivation caused an initial enhancement of MAN during recovery sleep. This suggests that episodes of MAN may represent a REM sleep equivalent and may be a marker of homeostatic and circadian REM sleep regulation.
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The brain circuitry governing REM sleep
The brainstem comprises several neural populations that promote non-REM sleep while suppressing REM sleep. However, the vlPAG GABAergic neurons are an exception, as their inhibition or ablation results in increased REM sleep, indicating their role in gating REM sleep. These neurons are thus considered a key node in the REM sleep circuitry.
The interaction between the core of the REM-generating circuit and other forebrain, hypothalamic, and brainstem structures generates REM sleep and its characteristics, such as muscle atonia or paralysis. This paralysis is initiated when glutamatergic SubC (subcoeruleus nucleus) neurons activate neurons in the ventral medial medulla (VMM), leading to the release of GABA and glycine onto skeletal motoneurons. The timing of REM sleep is controlled by the activity of GABAergic neurons in specific brain regions, such as the ventrolateral periaqueductal gray (vlPAG) and the dorsal paragigantocellular reticular nucleus.
Research has also revealed the role of the cortex in controlling REM sleep. Studies using calcium imaging in mice have shown that elevated activation in the occipital cortical regions, including the retrosplenial cortex and visual areas, is associated with the onset of REM sleep. This pontogeniculooccipital (PGO) wave-like activity promotes the transition from non-REM to REM sleep.
Additionally, the thalamus and cortex interact to regulate sleep and wakefulness. Stimulating the thalamus of an awake animal produced slow-wave sleep, while activating cholinergic neurons near the pons-midbrain junction resulted in a state of wakefulness and arousal. These findings highlight the complex interplay of various brain regions and neural circuits in governing REM sleep and the transitions between different sleep stages.
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Frequently asked questions
Muscle Atonia is the loss of normal muscle tone during sleep, specifically during the REM stage. It is a necessary process that prevents people from acting out their dreams.
Muscle atonia occurs when motoneurons are not generating action potentials. This is caused by a combination of postsynaptic inhibition, disfacilitation, and presynaptic inhibition of muscle afferents.
REM stands for Rapid Eye Movement. It is a recurring stage in the sleep-wake cycle, characterised by fast, desynchronized rhythms in the electroencephalogram (EEG), hippocampal theta activity, rapid eye movements, autonomic activation, and loss of postural muscle tone (atonia).
REM Behaviour Disorder is a condition where the body maintains increased muscle tone during REM sleep, allowing the sleeper to move and act out their dreams. This can cause serious injury to the individual or their bed partner.
