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Results for “REM Sleep Behavior Disorder”

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PubMedDate not supplied

Activation by selegiline (Eldepryle) of REM sleep behavior disorder in parkinsonism.

Abnormal sleep-wake organization is frequently seen in idiopathic parkinsonism (PD) and other parkinsonism syndromes. A 1993 article in The Annals of Neurology first described the high rate of REM behavior disorder (RBD) in non-demented PD patients (1). In this article, we present the case reports of three non-demented PD patients who manifested RBD while on recommended doses of selegiline (Eldepryle). None of them had problems severe enough to suggest RBD while they were being treated with varying doses of other dopaminergic agents (carbidopa/L-dopa, pergolide) unaccompanied by selegiline.

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PubMed1997

Probable diffuse Lewy body disease presenting as REM sleep behavior disorder.

Rapid eye movement sleep behavior disorder may herald several neurodegenerative disorders associated with parkinsonism, including Parkinson's disease. A 72-year-old man with a 17-year history of rapid eye movement sleep behavior disorder confirmed by polysomnography developed a progressive dementia that met operational clinical criteria for diffuse Lewy body disease. The differential diagnosis of progressive neurodegenerative disorders heralding as rapid eye movement sleep behavior disorder should now include diffuse Lewy body disease.

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PubMed2001

[Treatment of parasomnias].

In this article the most frequent and interesting treatments for parasomnias are reviewed. Arousal disorders, REM sleep behavior disorders and nightmares, bruxism (which can occur in any sleep state) are considered. The pathophysiological mechanisms of parasomnias are unknown, explaining why there is rarely a specific treatment precipitating. Management depends on the patient's age, the frequency and intensity of the episodes, the familial structure, the presence of precipitating and risk factors, psychological disorders and the parasomnia itself. Different therapeutic approaches are described including (1), explanation and reassurance, (2) counselling to avoid precipitating factors such as irregular sleep patterns, alcohol or drug intake (3) strategies to avoid injury (4) psychological approaches such as behavioral therapies in some parasomnias such as nightmares or arousal disorders. However, very few controlled studies have been done making it difficult to provide recommendations based on controlled clinical trials. Pharmacologic treatments are rarely necessary except in REM sleep behavior disorders; they are most often needed for short term.

Humans↗
PubMed2005

Slow-wave sleep and delta power in rapid eye movement sleep behavior disorder.

Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by the loss of normal muscle atonia during REM sleep, leading to an increase of phasic muscle activity and complex motor behaviors during the night. There is some evidence that RBD patients have more of slow-wave sleep (SWS) than healthy elderly subjects. No study has looked at quantitative electroencephalogram analysis during non-REM sleep in either primary or secondary RBD. The aim of this study was to assess the increase of SWS and to analyze different electroencephalographic frequency ranges during non-REM sleep in 28 idiopathic RBD patients compared with 28 age- and sex-matched healthy volunteers. Idiopathic RBD patients spent more time in SWS (men: 1.4%; women: 5.9%) than control subjects (men: 0.4%; women: 0.6%; p = 0.004). Spectral analyses demonstrated that idiopathic RBD patients had increased all-night delta power in comparison with control subjects (p = 002). This study shows an increase of SWS and power in the delta band during non-REM sleep in idiopathic RBD patients compared with control subjects. Results are discussed about the possible nigrostriatal dopaminergic impairment in RBD patients and the association between RBD and neurodegenerative disorders.

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PubMed2003

Slowing of electroencephalogram in rapid eye movement sleep behavior disorder.

Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by a loss of atonia and an increase in phasic muscle activity during REM sleep, leading to complex nocturnal motor behaviors. Brainstem structures responsible for the pathogenesis of RBD are also implicated in cortical activation. To verify the hypothesis that electroencephalogram (EEG) activation will be impaired in RBD, we performed quantitative analyses of waking and REM sleep EEG in 15 idiopathic RBD patients and 15 age- and gender-matched healthy subjects. During wakefulness, RBD patients showed a considerably higher theta power in frontal, temporal, and occipital regions with a lower beta power in the occipital region. The dominant occipital frequency was significantly lower in RBD. During REM sleep, beta power in the occipital region was lower in RBD. This study shows for the first time an impaired cortical activation during both wakefulness and REM sleep in idiopathic RBD, despite an absence of changes on sleep architecture compared with controls. EEG slowing in these patients may represent an early sign of central nervous system dysfunction, perhaps paralleled by subclinical cognitive deficits. The topographical distribution of EEG slowing and possible pathophysiological mechanisms are discussed in light of the known association between RBD and neurodegenerative disorders.

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