Diagnosing Rem Sleep Disorder: Brain Waves And Eye Movements

REM sleep behaviour disorder (RBD) is a sleep disorder characterised by a loss of muscle atonia during the rapid eye movement (REM) stage of sleep. Diagnosis of RBD involves a clinical history of dream enactment, complex motor behaviours during REM sleep, and the loss of normal REM sleep muscle atonia, known as REM sleep without atonia (RSWA). Polysomnographic video recording is the most important diagnostic test for RBD, and is usually conducted in a sleep study centre. During the test, the following parameters are monitored: electrical activity of the brain, heart, and muscles; eye movements; and respiratory movements. In patients with RBD, the polysomnogram shows an increase in muscle tone associated with the EEG pattern of REM sleep.

A clinical history of dream enactment

The clinical history of dream enactment is used to inform treatment, which focuses on creating a safe sleeping environment for the patient and their bed partner. This may involve removing sharp objects from the bedroom, placing pillows around the bed, or sleeping in a sleeping bag. If the symptoms are severe, the patient may need to sleep in a separate room from their bed partner.

Polysomnographic rapid eye movement sleep atonia loss

During polysomnographic testing, RBD is identified by an increase in muscle tone associated with the EEG pattern of REM sleep. In healthy individuals, REM sleep is associated with an absence of muscle tone (atonia).

RBD is strongly associated with neurodegenerative diseases, especially synucleinopathies such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. It may also be associated with antidepressant use, narcolepsy, autoimmunity, or developmental disorders.

The pathophysiology of RBD is not yet fully understood, but insights have been drawn from animal lesion studies and functional models. These studies have shown that REM sleep regulation involves key pontine centres, including the subcoeruleus, locus coeruleus, pedunculopontine and laterodorsal tegmental nuclei, and the medullary magnocellular reticular formation.

In summary, polysomnographic rapid eye movement sleep atonia loss is a key diagnostic feature of RBD, which is often identified through polysomnographic video recording. This sleep disorder is associated with various neurological conditions and antidepressant use.

Neurodegenerative disease association

REM sleep behaviour disorder (RBD) is a parasomnia, a sleep disorder that involves unusual and undesirable physical events or experiences that disrupt sleep. It is characterised by patients physically and/or vocally acting out their dreams during the rapid eye movement (REM) stage of sleep. This can cause injury to the patient or their bed partner, especially if they are acting out a violent nightmare.

RBD is strongly associated with neurodegenerative diseases, especially synucleinopathies such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. In fact, up to 97% of people with isolated (idiopathic) RBD will have one of these conditions within 14 years of their RBD diagnosis.

The diagnosis of RBD requires a clinical history of sleep-related complex motor behaviours or REM sleep complex vocal or motor behaviours recorded during polysomnography, accompanied by REM sleep without atonia (RSWA). RSWA is the loss of normal REM sleep muscle atonia, and is required for diagnosis.

The prognosis of RBD depends on several factors, including the presence of an underlying cause such as narcolepsy or use of an antidepressant, the severity of symptoms, and the presence of a neurodegenerative condition. The most important implication of RBD is its association with neurological conditions, particularly Parkinson's disease, multiple system atrophy and Lewy body dementia.

Brain imaging

Neuroimaging studies have shown that RBD is associated with a prominent loss of volume in the pontomesencephalic tegmentum, where cholinergic, GABAergic and glutamatergic neurons are located and implicated in the promotion of REM sleep and muscle atonia.

RBD is also associated with more widespread atrophy in other subcortical and cortical regions whose loss likely contributes to the altered regulation of sleep-wake states and motor activity underlying RBD. These include the medullary reticular formation, hypothalamus, thalamus, putamen, amygdala and anterior cingulate cortex.

In addition, patients with RBD showed larger volume of grey matter in several regions, including the olfactory trigone, medial prefrontal cortex, superior and inferior frontal gyri.

Medication and lesion-induced RBD

RBD can also be caused by brain lesions, specifically in the neuronal network regulating REM atonia in the dorsal medial pons. Brain lesions in the dorsal pons cause REM sleep atonia loss and may cause clinical RBD.

The two main pharmacological treatments for RBD are melatonin and clonazepam. Melatonin has been shown to increase REM sleep atonia levels, thereby diminishing RSWA. It is particularly desirable in symptomatic RBD treatment for patients with comorbid sleep apnea or memory problems, and the recommended starting dose is 3 mg, increased gradually to the range of 6 to 12 mg at bedtime, with the average effective dose being 6 mg. Clonazepam does not appear to reduce RSWA and may instead modulate dreaming or complex motor behaviours. It should be used with caution in elderly patients, especially those with PD, DLB, or MSA.

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