REM Sleep Behavior Disorder 

  • Author: Syed M S Ahmed, MD; Chief Editor: Selim R Benbadis, MD   more...
 
Updated: Feb 23, 2012
 

Background

Rapid eye movement (REM) sleep behavior disorder (RBD) is a sleep disorder characterized by the loss of normal voluntary muscle atonia during REM sleep, in association with complex motor behavior while dreaming. (See Etiology.)[1, 2, 3, 4]

The International Classification of Sleep Disorders requires the following criteria for the clinical diagnosis of RBD (see Presentation and Workup)[5] :

  • Presence of REM sleep without atonia (RSWA) on polysomnography (PSG)
  • The presence of at least 1 of the following conditions - (1) Sleep-related behaviors, by history, that have been injurious, potentially injurious, or disruptive (eg, dream enactment behavior); (2) abnormal REM sleep behavior documented during PSG monitoring
  • Absence of epileptiform activity on electroencephalogram (EEG) during REM sleep (unless RBD can be clearly distinguished from any concurrent REM sleep-related seizure disorder)
  • Sleep disorder not better explained by another sleep disorder, a medical or neurologic disorder, a mental disorder, medication use, or a substance use disorder

Patient education

Educate the patient and his or her bed partner for environmental safety. Potentially dangerous objects should be removed from the bedroom, and the mattress should be placed on the floor or a cushion placed around the bed. (See Treatment.)

For patient education information, see the Sleep Disorders Center, as well as REM Sleep Behavior Disorder, Disorders That Disrupt Sleep (Parasomnias), and Sleep Disorders and Aging.

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Etiology

The precise etiology and neural structures involved in RBD are unknown. Based on animal (cats, rats), lesional, and neuropathologic studies, sleep-regulating nuclei, particularly the pontine tegmentum, are thought to be involved in the pathogenesis of RBD. Also, a complex interplay of various neurochemical systems, such as the noradrenergic, cholinergic, and serotonergic systems, seems to exist in the pathogenesis of the condition.[1, 6]

Normally, generalized atonia of skeletal muscles occurs during REM sleep. This atonia results from active inhibition of the final common pathway of spinal motor neurons by way of the medullary magnocellular reticular formation (MCRF); this suppresses anterior horn cell activity via projections of the ventral lateral reticulospinal tract.

Various pontine nuclei are known to influence the REM and non-REM sleep circuits, including the locus coeruleus(LC), pedunculopontine nucleus (PPN), and laterodorsal tegmental nucleus (LDTN).[7] In addition, forebrain cortical and subcortical structures and the substantia nigra, thalamus, hypothalamus, basal forebrain, and frontal cortex are also involved. However, their precise roles are unknown.

Idiopathic RBD

RBD may be idiopathic. However, several studies have suggested that idiopathic RBD is a potential marker for the later development of neurodegenerative disorders characterized by alpha-synuclein deposition. These include Parkinson disease, multiple system atrophy, dementia with Lewy bodies, and pure autonomic failure, with the risk varying among different studies. (RBD is less frequently associated with nonsynucleinopathies.)[1, 2, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17]

In fact, studies have suggested that RBD may be associated with alpha-synuclein–mediated degeneration of sleep-regulating nuclei in the brainstem, particularly the pontine tegmentum.

In essence, RBD may be the prodrome of neurodegenerative disease, such as diffuse Lew body (DLB) disease or Parkinson disease.[1, 18] In experimental studies in cats, bilateral pontine lesions resulted in a persistent absence of REM atonia associated with prominent motor activity during REM sleep similar to that observed in RBD in humans.

Studies by Eisensehr et al using iodine 123 (123 I) immunoperoxidase technique (IPT) single photon-emission computed tomography (SPECT) scanning demonstrated that striatal presynaptic dopamine transporters are reduced in idiopathic RBD.[19]

Studies by Fantini et al demonstrated impairment of cortical activity in idiopathic RBD, particularly in the occipital region during both wakefulness and REM sleep, compared with controls.[20] Results were similar to those of functional studies, such as of the perfusion and metabolic impairment pattern, observed in DLB disease and in Parkinson disease. Similar cortical activity in the frontal and temporal regions was impaired only during wakefulness.

Research evidence suggests, therefore, that many cases of idiopathic RBD may not be truly idiopathic, leading some to suggest the term cryptogenic rather than idiopathic.[21]

Secondary RBD

In addition, RBD may occur in association with various neurologic conditions (ie, secondary RBD), including vascular lesions, brainstem neoplasms, demyelinating disease, autoimmune/inflammatory disorders, and neurodegenerative disorders.

Genetics

Nightingale et al suggested in a study that 36% of persons with narcolepsy experience symptoms of RBD.[22] This link led to the identification of a strong association of RBD with HLA class II genes.[23, 24, 25]

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Epidemiology

The exact incidence and prevalence of RBD are unknown because of inadequate reporting and misdiagnosis. However, in the United States, a telephone survey indicated a 2% overall prevalence of violent behaviors during sleep, 25% of which were likely to be due to RBD. This gives a prevalence of 0.5% of RBD in the general population.

RBD occurs predominantly in males.[26] In a report by Olson et al involving 93 patients with RBD, only 12 patients (13%) were female.[4]

Typically, RBD is a disease of elderly persons.[8] The risk increases after the sixth decade, although the disease may occur at any age, including in childhood.[26]

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Prognosis

The prognosis of RBD depends on its etiology. In idiopathic cases, the symptoms are controlled with medications. In secondary cases, the prognosis depends on the underlying primary disease.

No deaths have been reported in idiopathic cases of RBD; however, patients and bed partners may experience serious injury.[27] In the reported cases, 32% of patients had injured themselves and 64% had assaulted their spouse.[4] Subdural hematomas occurred in 2 patients.[4] In secondary cases, the morbidity and mortality rates depend on the underlying disease itself.

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Contributor Information and Disclosures
Author

Syed M S Ahmed, MD  Neurologist and Sleep Specialist, The Sleep Disorder Clinic of Washington, The Neurology Clinic of Washington; Staff Attending in Neurology and Sleep Medicine, Montgomery General Hospital; Staff Attending in Neurology and Sleep Medicine, Suburban Hospital

Syed M S Ahmed, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, and Maryland State Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

ABM Salah Uddin, MD  Private Practice, Norwood Neurology; Consulting Staff, Department of Neurology, St Vincent's Hospital

ABM Salah Uddin, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, and American Medical Association

Disclosure: Nothing to disclose.

Tambi Jarmi, MD  Resident Physician, Department of Internal Medicine, Carraway Methodist Medical Center

Tambi Jarmi, MD is a member of the following medical societies: American College of Physicians and American Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Additional Contributors

Erasmo A Passaro, MD Director, Comprehensive Epilepsy Program/Clinical Neurophysiology Lab, Bayfront Medical Center Florida Center for Neurology

Erasmo A Passaro, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Association, and American Society of Neuroimaging

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Takeda Honoraria Speaking and teaching

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

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