Rapid eye movement behavior disorder

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Rapid eye movement behaviour disorder, or RBD was first described in 1986 as a parasomnia involving dissociation of the characteristic stages of sleep. The major and arguably only abnormal feature of RBD is loss of muscle atonia (paralysis) during otherwise intact REM sleep (the stage of sleep in which most vivid dreaming occurs). This loss of motor inhibition leads to a wide spectrum of behavioural release during sleep. This extends from simple limb twitches to more complex integrated movements where sufferers appear to be unconsciously acting out their dreams. These behaviours are often violent in nature and commonly result in injury to either the patient or their bed partner. Injuries range from bruises and cuts to fractures, subdural hematoma and other serious injuries. In contrast, all other aspects of sleep appear similar to normal.

Epidemiology

The most comprehensive assessment so far has estimated RBD prevalence to be around 0.5% in individuals aged 15-100. It is far more common in males: most studies report that only around a tenth of sufferers are female. This may be due to a referral bias, as violent activity carried out by men is more likely to result in harm and injury and is more likely to be reported than injury to male bed partners by women, or it may reflect a true difference in prevalence as a result of genetic or androgenic factors. The mean age of onset is estimated to be around 60 years of age.

Associated Conditions

Various conditions are very similar to RBD in that sufferers exhibit excessive sleep movement and potentially violent behaviour. Such disorders include sleepwalking and sleep terrors, which are associated with other stages of sleep, nocturnal seizures and obstructive sleep apnea which can induce arousals from REM sleep associated with complex behaviours. Because of the similarities between the conditions, polysomnography plays an important role in confirming RBD diagnosis.

It is now apparent that RBD appears in association with a variety of different conditions. Narcolepsy has been reported as a related disorder. This is unsurprising, as both RBD and narcolepsy involve dissociation of sleep states probably arising from a disruption of sleep control mechanisms. RBD has also been reported following cerebrovascular accident and neurinoma (tumour), indicating that damage to the brain stem area may precipitate RBD. RBD is usually chronic, however may be acute and sudden in onset if associated with drug treatment or withdrawal (particularly with alcohol withdrawal) 60% of RBD is idiopathic. This includes RBD that is found in association with conditions such as Parkinson’s disease and dementia with Lewy bodies, where it is often seen to precede the onset of neurodegenerative disease. Monoamine oxidase inhibitors, tricyclic antidepressants, serotonergic synaptic reuptake inhibitors, and noradrenergic antagonists can induce or aggravate RBD symptoms and should be avoided in patients with RBD.

Treatment

RBD is a treatable condition. The standard therapy is the anti-convulsant drug clonazepam, and this is generally received very well. How this drug works to restore REM atonia is unclear, however it is thought to suppress muscle activity, rather than directly restoring atonia.