Muscles Paralyzed During Rem Sleep: Why And What Happens?

During the REM stage of sleep, the body's muscles are temporarily paralysed, known as muscle atonia. This prevents us from acting out our dreams and causing potential harm to ourselves or our bed partners. This muscle paralysis is caused by two powerful brain chemical systems that work together to paralyse the body's muscles. These brain chemicals are gamma-aminobutyric acid (GABA) and glycine, which are neurotransmitters that switch off the cells in the brain that allow muscles to be active.

REM sleep is characterised by rapid eye movement, cortical activation, vivid dreaming, skeletal muscle paralysis and muscle twitches

REM sleep is characterised by rapid eye movement, cortical activation, vivid dreaming, skeletal muscle paralysis, and muscle twitches. During REM sleep, the brain is intensely active, but the skeletal motor system is forced into a state of muscle paralysis. This is to prevent the body from acting out what is going on in the brain and causing potential injury.

Two powerful brain chemical systems work together to paralyse skeletal muscles during REM sleep. These are the neurotransmitters gamma-aminobutyric acid (GABA) and glycine, which cause paralysis by "switching off" the specialised cells in the brain that allow muscles to be active.

REM sleep is the most dream-filled phase of sleep, and it usually begins about 90 minutes into a night's rest. The brain is very active during this time, and dreams are at their most intense. The voluntary muscles of the body—arms, legs, fingers, and anything under conscious control—are paralysed. This paralysis keeps people still even as their brains act out fantastical scenarios.

REM sleep is also characterised by cortical activation and muscle twitches. A distributed network of micro-circuits within the brainstem, forebrain, and hypothalamus is required for generating and sculpting REM sleep. Disturbances in the normal control of REM sleep underlie sleep disorders such as narcolepsy and REM sleep behaviour disorder.

During REM sleep, the brain is very active, but the body's muscles are paralysed

Two powerful brain chemical systems work together to paralyse the body's muscles during REM sleep. The neurotransmitters gamma-aminobutyric acid (GABA) and glycine cause paralysis by "switching off" the cells in the brain that allow muscles to be active.

REM sleep is the most dream-filled phase of sleep, usually beginning about 90 minutes into a night's rest. During this phase, the brain is intensely active, dreams are at their most intense, and the body's muscles are paralysed.

REM sleep paralysis is only reversed when the motor cells are cut off from all sources of GABA and glycine. Neither metabotropic nor ionotropic receptor mechanisms alone are sufficient for generating REM paralysis. These results demonstrate that multiple receptor mechanisms trigger REM sleep paralysis.

REM sleep behaviour disorder (RBD) is a condition in which people don't become paralysed during REM sleep. They act out their dreams, talking, thrashing, punching, or hitting in their sleep. This can result in injury to themselves or their bed partners. RBD is often linked to other neurological conditions, such as Parkinson's disease and Lewy body dementia.

Understanding the precise mechanisms behind these chemicals' role in REM sleep is important for developing treatments for sleep disorders.

Two brain chemical systems work together to paralyse skeletal muscles during REM sleep

During REM sleep, the brain is highly active and dreams are at their most intense. However, the body's voluntary muscles are paralysed, which prevents people from acting out their dreams. This paralysis is caused by two brain chemical systems working together to "switch off" the specialised cells in the brain that allow muscles to be active. These chemicals are gamma-aminobutyric acid (GABA) and glycine.

GABA and glycine are neurotransmitters that work together to maintain motor control during sleep. They do this by binding to three different types of receptors on motor neurons, "switching them off" and causing muscle paralysis.

The discovery of the role of these two neurotransmitters in REM sleep paralysis has important implications for the treatment of sleep disorders such as narcolepsy, REM sleep behaviour disorder, and tooth grinding. It is hoped that this knowledge will lead to the development of new treatments for these conditions.

REM sleep paralysis is caused by the activation of both metabotropic GABAB and ionotropic GABAA/glycine receptors

During REM sleep, the central nervous system is highly active, but the body's skeletal muscles are paralysed. This paralysis is caused by the activation of both metabotropic GABAB and ionotropic GABAA/glycine receptors, which inhibit motoneurons by switching them off.

REM sleep paralysis is a defining feature of normal REM sleep, and it may serve to prevent the body from acting out dreams, which could be dangerous.

REM sleep is initiated and maintained by the interaction of various neurotransmitter systems in the brainstem, forebrain, and hypothalamus. Brainstem circuits that control REM sleep contain GABA and glycine neurons that project to and synapse on motoneurons. Motoneurons themselves express GABAB, GABAA, and glycine receptors, which trigger hyperpolarisation when activated.

Two theories have been proposed to explain the cause of REM sleep paralysis: active inhibition or reduced excitation of somatic motoneuron activity. The activation of both metabotropic GABAB and ionotropic GABAA/glycine receptors supports the former theory.

The simultaneous activation of both types of receptors is required to trigger REM sleep paralysis. Neither metabotropic nor ionotropic receptor mechanisms alone are sufficient to induce REM paralysis.

The findings on the mechanisms of REM sleep paralysis could help in the development of treatments for sleep disorders such as REM sleep behaviour disorder, narcolepsy, and tooth grinding.

REM sleep behaviour disorder is caused by the absence of muscle paralysis during REM sleep

During the REM stage of sleep, the body's muscles are usually paralysed, a state known as muscle atonia. This prevents the body from acting out dreams and is thought to be caused by the neurotransmitters gamma-aminobutyric acid (GABA) and glycine, which "switch off" the cells that allow muscles to be active.

However, in people with REM sleep behaviour disorder, this paralysis does not occur, meaning that they physically act out their dreams. This can include anything from mild muscle twitches to violent movements such as punching or kicking. The person is often unaware of their behaviour and may only find out if their bed partner or roommate tells them, or if they wake up with an injury.

The cause of REM sleep behaviour disorder is not fully understood but is thought to be related to certain neural pathways in the brain. It is also associated with other neurological conditions, including Parkinson's disease, Lewy body dementia, and multiple system atrophy. In fact, around 80-97% of people with isolated (idiopathic) REM sleep behaviour disorder will develop one of these conditions within 14-16 years of their diagnosis.

Due to the risk of injury to the person or their bed partner, it is important to seek treatment for REM sleep behaviour disorder. This can involve creating a safe sleeping environment, such as removing sharp objects from the bedroom or sleeping in a different room. Medication such as melatonin or clonazepam may also be prescribed to reduce symptoms.

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