Medical Comorbidity of Sleep Disorders

Dimitris Dikeos; Georgios Georgantopoulos

Disclosures

Curr Opin Psychiatry. 2011;24(4):346-354. 

In This Article

Rapid Eye Movement Behaviour Disorder

RBD is a condition characterized by loss of muscular atonia and the appearance of motor behaviours (usually violent) during REM sleep (i.e. when dreaming).[3] The abnormal motor and vocal behaviours during REM sleep have different degrees of severity across different nights and through a single night, ranging from mild limb jerking to jumping out of bed. Typical behaviours include punching, kicking, beating, biting, sitting on the bed, jumping out of bed, whispering, talking, shouting, swearing, crying, laughing and singing. Patients and their bed partners may suffer lacerations, contusions and fractures. Nonviolent behaviours (e.g. gesturing, elaborated pseudo-purposeful behaviours, whistling) may occasionally coexist with the typical violent behaviour.[65–68] Recalled dreams commonly have a negative emotional content and include being attacked, robbed or chased by people, frightened or attacked by animals and falling off a cliff.[3,68]

RBD usually develops after the age of 50 and its prevalence is estimated to be less than 1% of the general population.[65,67] For the diagnosis, the clinical description is needed, corroborated usually by the bed partner; all-night polysomnography with infrared video monitoring is performed, mainly for differential diagnosis.[3] RBD is considered to be either idiopathic or secondary to neurological conditions such as Parkinson's disease, dementia with Lewy bodies (DLB), multiple system atrophy (MSA), narcolepsy, and so on.[68,69]

Rapid Eye Movement Sleep Behaviour Disorder in Neurological Disorders

Compared with the population prevalence of 1%, RBD is found in 15–60% of Parkinson's disease patients (particularly those having the akinetic/rigid manifestation of the disease[70]), in 50–83% of patients with DLB and in 90–100% of patients with MSA.[59] As all three of the above are synucleinopathies, it is considered that alpha synuclein pathology is a causative factor of RBD, at least in the majority of cases. On the other hand, RBD prevalence is also found to be high in narcolepsy and elevated (though to a lesser degree) in other neurological disorders such as spinocerebellar ataxias, Huntington's disease, ALS, Guillain-Barré, multiple sclerosis, epilepsy, autism, Tourette syndrome, Alzheimer's disease, inflammatory encephalitis, stroke, TBI, brain stem tumours and so on, which are unrelated to synuclein disturbance.[68–72] RBD can also be triggered by the administration of certain drugs, especially antidepressants belonging to the serotonin-uptake inhibitors.[68,73]

Rapid Eye Movement Sleep Behaviour Disorder as a Precursor of Neurodegenerative Disorders

Clinically, the most important aspect is that the appearance of RBD, in the absence of an apparent neurological condition or administration of drugs that may account for its presence, seems to be a preclinical marker for the development of a neurodegenerative disease, usually Parkinson's disease or DLB.[68,69] In a recent follow-up study of 93 patients who had been diagnosed with idiopathic RBD and were examined for a period up to 12 years (mean 5.2 years), it was estimated that the risk for the development of a neurodegenerative disease (Parkinson's disease, DLB, Alzheimer's disease and MSA) was 17.7% in 5 years, 40.6% in 10 years and 52.4% in 12 years.[74] Cumulative incidence of neurodegenerative disorders in various longitudinal studies following patients with RBD was 16–65% for Parkinson's disease, 8–15% for DLB, 4% for Alzheimer's disease and 1–2% for MSA.[31••]

In recent years, several studies have been conducted in the attempt to identify indices of the probability of transition of RBD to a neurodegenerative disorder; autonomic dysfunction due to adrenergic neuron dysfunction is assessed by iodine-131-meta-iodobenzylguanidine (I-MIBG) cardiac scintigraphy[75] or R-R variability,[76] and midbrain structures are assessed by sonography,[77,78] MRI,[79,80] diffusion tensor imaging (DTI)[79] and regional blood flow.[81] The conclusions of these studies as well as of older similar ones (reviewed in [68]) are still inconclusive, and, as there are not many publications that have followed those patients with RBD who did not develop a neurodegenerative disorder, the matter is still unresolved.[82]

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