Movement Disorders (revue)

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Melatonin as a therapy in rem sleep behavior disorder patients: An open‐labeled pilot study on the possible influence of melatonin on rem‐sleep regulation

Identifieur interne : 001423 ( Istex/Corpus ); précédent : 001422; suivant : 001424

Melatonin as a therapy in rem sleep behavior disorder patients: An open‐labeled pilot study on the possible influence of melatonin on rem‐sleep regulation

Auteurs : Dieter Kunz ; Frederik Bes

Source :

RBID : ISTEX:DA296FBBE60BDE53D24FCDCD727A1C875D9743E0

English descriptors

Abstract

REM sleep behavior disorder (RBD) is clinically impressive by virtue of its vigorous sleep behaviors usually accompanying vivid, striking dreams. The main feature of the disorder, REM sleep without muscle atonia, has been shown in a variety of diseases; therefore, the disorder might possibly be underestimated. In an open‐labeled trial, we treated six consecutive RBD patients over a 6‐week period with 3 mg melatonin given within 30 minutes before bedtime. There was a dramatic clinical improvement in five of the six patients within a week which extended beyond the end of treatment for weeks or months. A second polysomnogram performed 6 weeks after the beginning of treatment showed a significant tendency toward normalization of the percentage of REM sleep, a significant reduction of 30‐second epochs, scored as REM sleep without muscle atonia, a significant reduction of stage‐shifts in REM, and a significant reduction in epochs considered as movement time in REM. All other sleep parameters were not changed consistently. We hypothesize that internal desynchrony might be a part of the underlying pathophysiology in RBD. Our data might give first evidence to the hypothesis that exogenous melatonin, administered to patients with internal desynchrony at the time of the maximal rise of melatonin secretion, might increase the overall amplitude of the circadian pacemaker by reentraining the suprachiasmatic nucleus and thereby restore circadian driven rhythms, one of them being the circadian modulation of REM sleep.

Url:
DOI: 10.1002/1531-8257(199905)14:3<507::AID-MDS1021>3.0.CO;2-8

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ISTEX:DA296FBBE60BDE53D24FCDCD727A1C875D9743E0

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<abstract lang="en">REM sleep behavior disorder (RBD) is clinically impressive by virtue of its vigorous sleep behaviors usually accompanying vivid, striking dreams. The main feature of the disorder, REM sleep without muscle atonia, has been shown in a variety of diseases; therefore, the disorder might possibly be underestimated. In an open‐labeled trial, we treated six consecutive RBD patients over a 6‐week period with 3 mg melatonin given within 30 minutes before bedtime. There was a dramatic clinical improvement in five of the six patients within a week which extended beyond the end of treatment for weeks or months. A second polysomnogram performed 6 weeks after the beginning of treatment showed a significant tendency toward normalization of the percentage of REM sleep, a significant reduction of 30‐second epochs, scored as REM sleep without muscle atonia, a significant reduction of stage‐shifts in REM, and a significant reduction in epochs considered as movement time in REM. All other sleep parameters were not changed consistently. We hypothesize that internal desynchrony might be a part of the underlying pathophysiology in RBD. Our data might give first evidence to the hypothesis that exogenous melatonin, administered to patients with internal desynchrony at the time of the maximal rise of melatonin secretion, might increase the overall amplitude of the circadian pacemaker by reentraining the suprachiasmatic nucleus and thereby restore circadian driven rhythms, one of them being the circadian modulation of REM sleep.</abstract>
<subject lang="en">
<genre>Keywords</genre>
<topic>Circadian rhythms</topic>
<topic>Melatonin</topic>
<topic>Parasomnia</topic>
<topic>Polysomnography</topic>
<topic>REM sleep</topic>
</subject>
<relatedItem type="host">
<titleInfo>
<title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
</titleInfo>
<titleInfo type="abbreviated">
<title>Mov. Disord.</title>
</titleInfo>
<subject>
<genre>article category</genre>
<topic>Brief Report</topic>
</subject>
<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part>
<date>1999</date>
<detail type="volume">
<caption>vol.</caption>
<number>14</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>3</number>
</detail>
<extent unit="pages">
<start>507</start>
<end>511</end>
<total>5</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">DA296FBBE60BDE53D24FCDCD727A1C875D9743E0</identifier>
<identifier type="DOI">10.1002/1531-8257(199905)14:3<507::AID-MDS1021>3.0.CO;2-8</identifier>
<identifier type="ArticleID">MDS1021</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 1999 Movement Disorder Society</accessCondition>
<recordInfo>
<recordOrigin>John Wiley & Sons, Inc.</recordOrigin>
<recordContentSource>WILEY</recordContentSource>
</recordInfo>
</mods>
</metadata>
<serie></serie>
</istex>
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