Ashwin Lewis
REM sleep behaviour disorder (RBD) is a parasomnia characterised by abnormal behaviour during sleep, such as dream enactment. RBD is strongly associated with neurodegenerative diseases, including Parkinson's disease, Lewy body dementia, and multiple system atrophy. A core diagnostic criterion of RBD is REM sleep without atonia (RSWA), which is defined as increased tonic or phasic muscle activity during REM sleep. RSWA can be detected through polysomnographic (PSG) recordings, which capture abnormal muscle activity in the chin, leg, and arm. RSWA is also associated with certain antidepressants, such as selective serotonin reuptake inhibitors (SSRIs) and selective norepinephrine reuptake inhibitors (SNRIs), which are linked to a higher prevalence of RSWA.
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What You'll Learn
RSWA is a requisite diagnostic feature of RBD
REM sleep behaviour disorder (RBD) is characterised by abnormal behaviour during rapid eye movement (REM) sleep, corresponding to the current dream content. This abnormal behaviour is known as dream enactment behaviour (DEB) or dream-enacting behaviour (DEB).
RBD is a parasomnia, which is a sleep disorder characterised by abnormal behaviour during sleep. It is considered an early stage of neurodegeneration, leading to alpha-synucleinopathies, which include Parkinson's disease, Lewy body dementia, and multiple system atrophy.
REM sleep without atonia (RSWA) is a polysomnographic finding of persistent muscle tone during REM sleep, resulting in paroxysmal phasic or tonic EMG activity. RSWA is characterised by increased phasic or tonic muscle activity seen on polysomnographic electromyogram channels. RSWA can occur without DEB, but the two often occur together. RSWA is a requisite diagnostic feature of RBD, but it may also be seen in patients without clinical symptoms or signs of DEB. RSWA without clinical symptoms, as well as clinically overt RBD, is often associated with neurodegenerative disorders.
RSWA is diagnosed with a video-PSG and is characterised by a loss of normal atonia during REM sleep, leading to an increase in phasic or tonic muscle activity in surface EMG recordings. The surface electrodes are placed at the mentalis or submentalis muscle (for detection of tonic or phasic RSWA) and bilateral tibialis anterior muscles (for detection of phasic RSWA).
The American Academy of Sleep Medicine (AASM) has established formal suggested diagnostic standards for the scoring of RSWA during PSG. The AASM standard requires that at least five mini-epochs of 3-second duration contain abnormally excessive phasic muscle activity within a single 30-second epoch of REM sleep, and that abnormally excessive tonic muscle activity in the chin EMG channel lasts over 15 seconds in duration.
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RSWA is linked to antidepressant therapy
REM sleep without atonia (RSWA) is characterised by increased phasic or tonic muscle activity during sleep. RSWA is a necessary diagnostic criterion for REM sleep behaviour disorder (RBD), which is characterised by dream-enacting behaviour. RSWA can occur without dream-enacting behaviour and has been observed in neurologically normal individuals, especially those receiving antidepressant therapy.
Selective serotonin reuptake inhibitors (SSRIs) and selective norepinephrine reuptake inhibitors (SNRIs) have been associated with a higher prevalence of RSWA. A study of patients taking SSRIs and SNRIs found that 12.2% had RSWA, compared to 2.1% in the general sleep lab population. This suggests that SSRIs and SNRIs are associated with a higher risk of RSWA.
SSRIs, by increasing serotonergic activity, may prevent the passive mechanism that normally results in decreased neuronal activity in the descending pathways during REM sleep. Tricyclic antidepressants (TCAs), which have anticholinergic properties, may block the active mechanism that normally inhibits lower motor neurons during REM sleep.
Dopaminergic dysfunction also contributes to the development of RSWA. Bupropion, which acts on dopamine reuptake rather than serotonergic or acetylcholinergic neurotransmission, has been associated with lower levels of RSWA compared to other antidepressants.
In summary, RSWA is linked to antidepressant therapy, particularly the use of SSRIs and SNRIs, which are associated with a higher prevalence of RSWA. The type of antidepressant treatment appears to impact the levels of RSWA, with some evidence suggesting that certain antidepressants may unmask RBD rather than cause it.
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RSWA is a predictor of phenoconversion to overt parkinsonism or dementia
Rapid eye movement (REM) sleep behaviour disorder (RBD) is a parasomnia characterised by repeated episodes of dream enactment behaviour and REM sleep without atonia (RSWA) during polysomnography recording. RSWA is characterised by increased phasic or tonic muscle activity seen on polysomnographic electromyogram channels. RSWA is a requisite diagnostic feature of RBD, but may also be seen in patients without clinical symptoms or signs of dream enactment.
RSWA severity is a predictor of phenoconversion to overt parkinsonism or dementia. RSWA severity in isolated RBD patients is a potential predictor for early conversion to Parkinson's disease (PD) or dementia with Lewy bodies. The amount of tonic RSWA has been shown to be predictive of the development of future PD, but not dementia, in previous studies of patients with iRBD. Higher tonic REM muscle activity of patients with iRBD has been associated with an increased risk of phenoconversion to a defined neurodegenerative disease.
In another study, the same group reported that patients with PD with higher amounts of tonic RSWA predicted the development of dementia, regardless of whether the patient had clinical RBD. Tonic RSWA severity is a predictor of early conversion to PD and DLB in isolated RBD patients, while in PD patients it seems to be associated with the progression to dementia. RSWA may change throughout the disease course of RBD. For example, early in the course of iRBD disease, phasic RSWA may be predominant, resulting in more aggressive brief movements and causing more overt, violent, clinically manifest dream-enactment behaviours despite a relatively limited overall amount of RSWA during REM sleep.
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RSWA is a pathological finding
REM sleep without atonia (RSWA) is a pathological finding that can be indicative of several diseases and medications. RSWA is characterised by increased phasic or tonic muscle activity during REM sleep, which can be observed through polysomnographic (PSG) recordings. This is due to a loss of normal atonia during REM sleep, which is typically characterised by low-amplitude and mixed-frequency electro-encephalographic signals. RSWA is often associated with dream-enacting behaviour, but it can also occur without any clinical symptoms.
RSWA is a necessary diagnostic criterion for REM sleep behaviour disorder (RBD) and can be indicative of neurodegenerative disorders. RBD is characterised by abnormal behaviour during REM sleep and is considered a prodromal feature of Parkinson's disease, Lewy body dementia, and multiple system atrophy. RSWA is also linked to an increased risk of developing these neurodegenerative disorders. The presence of RSWA can be a critical indicator for clinicians to help patients with sleep-related complaints by asking about dream enactment behaviour.
The association between RSWA and the intake of selective serotonin reuptake inhibitors (SSRIs) and selective norepinephrine reuptake inhibitors (SNRIs) is well-established. Studies have shown that patients taking these antidepressants are significantly more likely to exhibit RSWA. This is because SSRIs and SNRIs can interfere with the mechanisms that normally achieve REM sleep atonia, leading to increased serotonergic activity and preventing the passive mechanism that inhibits muscle activity during REM sleep.
In addition to its association with antidepressants, RSWA has also been linked to narcolepsy, obstructive sleep apnea (OSA), and alpha-synucleinopathies. RSWA can be a predictor of phenoconversion to overt parkinsonism or dementia, and it might be a prodromal biomarker of Lewy body disease. The severity of RSWA in Lewy body disease increases over time, and it is also associated with idiopathic Parkinson's disease.
The cerebral and brainstem regions, particularly the pontomedullary brainstem, are implicated in RSWA. Quantitative susceptibility mapping (QSM) has been used to detect microstructural tissue changes in these regions, providing insights into the progression of neurodegenerative disorders. The recognition that REM sleep atonia loss progresses over time in iRBD highlights the importance of RSWA as a reference parameter for understanding the severity of these disorders.
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RSWA is linked to synucleinopathies
REM sleep without atonia (RSWA) is characterised by increased phasic or tonic muscle activity during REM sleep. RSWA is a requisite diagnostic feature of REM sleep behaviour disorder (RBD) and can occur with or without dream-enacting behaviour. RSWA is often found in patients taking antidepressants, such as SSRIs and SNRIs, which are associated with a higher prevalence of RSWA.
The link between RSWA and synucleinopathies is supported by mounting experimental evidence from seeding assays and advanced structural biology. As distinct strains of α-synuclein are increasingly used as biomarkers, diagnostic accuracy will likely improve. The Braak staging hypothesis of PD may also be applicable to the timing of RSWA occurrence and RBD symptom expression in synucleinopathies.
Several studies have found a high frequency of RSWA in patients with synucleinopathies, underscoring the need for longitudinal studies in iRSWA patients to understand the conversion to synucleinopathies. RSWA is now considered a biomarker for synucleinopathies and was recently added as an indicative biomarker in the diagnostic criteria for DLB.
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Frequently asked questions
REM sleep without atonia (RSWA) is the finding of persistent muscle tone during REM sleep, resulting in paroxysmal phasic or tonic EMG activity. It is a required criterion for diagnosing REM sleep behaviour disorder (RBD).
RSWA is caused by neurodegeneration of brainstem structures. It is often found in patients taking antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs) and selective norepinephrine reuptake inhibitors (SNRIs).
RSWA is diagnosed using a video-PSG, which involves placing surface electrodes on the mentalis or submentalis muscle and bilateral tibialis anterior muscles to detect tonic or phasic RSWA.
