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Rapid Eye Movement Sleep Behavior Disorder and Neurodegenerative Disease

Michael Joseph Howell, MD1; Carlos Hugh Schenck, MD2
[+] Author Affiliations
1Department of Neurology, University of Minnesota, Minneapolis
2Department of Psychiatry, University of Minnesota, Minneapolis
JAMA Neurol. 2015;72(6):707-712. doi:10.1001/jamaneurol.2014.4563.
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Importance  The dream enactment of rapid eye movement sleep behavior disorder (RBD) is often the first indication of an impending α-synuclein disorder, such as Parkinson disease, multiple-system atrophy, or dementia with Lewy bodies.

Objective  To provide an overview of RBD from the onset of dream enactment through the emergence of a parkinsonian disorder.

Evidence Review  Peer-reviewed articles, including case reports, case series, retrospective reviews, prospective randomized trials, and basic science investigations, were identified in a PubMed search of articles on RBD from January 1, 1986, through July 31, 2014.

Findings  Under normal conditions, vivid dream mentation combined with skeletal muscle paralysis characterizes rapid eye movement sleep. In RBD, α-synuclein abnormalities in the brainstem disinhibit rapid eye movement sleep motor activity, leading to dream enactment. The behaviors of RBD are often theatrical, with complexity, aggression, and violence; fighting and fleeing actions can be injurious to patients as well as bed partners. Rapid eye movement sleep behavior disorder is distinguished from other parasomnias by clinical features and the demonstration of rapid eye movement sleep without atonia on polysomnography. Consistent with early neurodegeneration, patients with RBD demonstrate subtle motor, cognitive, and autonomic impairments. Approximately 50% of patients with spontaneous RBD will convert to a parkinsonian disorder within a decade. Ultimately, nearly all (81%-90%) patients with RBD develop a neurodegenerative disorder. Among patients with Parkinson disease, RBD predicts a non–tremor-predominant subtype, gait freezing, and an aggressive clinical course. The most commonly cited RBD treatments include low-dose clonazepam or high-dose melatonin taken orally at bedtime.

Conclusions and Relevance  Treatment of RBD can prevent injury to patients and bed partners. Because RBD is a prodromal syndrome of Parkinson disease (or related disorder), it represents a unique opportunity for developing and testing disease-modifying therapies.

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Figure 1.
Normal Rapid Eye Movement Sleep Atonia

This 60-second polysomnographic recording demonstrates normal rapid eye movement sleep atonia. The sharp rapid eye movements can be recognized in the extraocular leads (left outer canthus–M2 and right outer canthus–M2) along with an absence of motor activity measured by chin electromyography (CHIN1-CHIN2).

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Figure 2.
Rapid Eye Movement Sleep Without Atonia

This 60-second polysomnographic recording demonstrates an elevation of rapid eye movement motor activity as measured by chin electromyography (CHIN1-CHIN2). Notice that the motor activity is often temporally associated with the phasic eye movements of rapid eye movement sleep (left outer canthus–M2 and right outer canthus–M2). In addition, the respiratory leads do not demonstrate evidence of sleep-disordered breathing but instead show normal respiratory effort (CHEST and ABD), airflow (FLOW), and oxygenation saturation (OSAT).

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