Movement Disorders (revue)

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Restless legs syndrome: Evidence for nocturnal hypothalamic‐pituitary‐adrenal system activation

Identifieur interne : 001F32 ( Istex/Corpus ); précédent : 001F31; suivant : 001F33

Restless legs syndrome: Evidence for nocturnal hypothalamic‐pituitary‐adrenal system activation

Auteurs : Claudia Schilling ; Michael Schredl ; Philipp Strobl ; Michael Deuschle

Source :

RBID : ISTEX:78AB4FF1FF63AB03381DC1BE8469D7C8C7F2C9E1

English descriptors

Abstract

Epidemiological studies consistently point to a relationship between restless legs syndrome (RLS) and cardiovascular disease. The mechanism underlying this association is unclear. Activation of the hypothalamic‐pituitary‐adrenal (HPA) system has been shown to contribute to the metabolic syndrome and an enhanced cardiovascular risk. We investigated cortisol levels as an indicator of HPA system activity in RLS during the nighttime, when RLS symptoms are at their maximum. We assessed nocturnal urinary cortisol excretion in 73 patients with RLS and 34 healthy controls, controlling for age and gender. Urine sampling was paralleled by polysomnographic recordings. We found significantly enhanced nocturnal cortisol excretion in RLS, demonstrating nocturnal HPA system overactivity in RLS. HPA system overactivity is a possible mechanism contributing to the enhanced load of cardiovascular disease in RLS patients. Nocturnal cortisol release showed weak correlations with some polysomnographic parameters of disturbed sleep, making a potential contribution of RLS‐induced sleep disruption to HPA system activation conceivable. © 2010 Movement Disorder Society

Url:
DOI: 10.1002/mds.23026

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ISTEX:78AB4FF1FF63AB03381DC1BE8469D7C8C7F2C9E1

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<namePart type="family">Schredl</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Sleep Laboratory, Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Mannheim, Germany</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
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</name>
<name type="personal">
<namePart type="given">Philipp</namePart>
<namePart type="family">Strobl</namePart>
<affiliation>Sleep Laboratory, Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Mannheim, Germany</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Michael</namePart>
<namePart type="family">Deuschle</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Sleep Laboratory, Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Mannheim, Germany</affiliation>
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<dateIssued encoding="w3cdtf">2010-06-15</dateIssued>
<dateCaptured encoding="w3cdtf">2009-11-04</dateCaptured>
<dateValid encoding="w3cdtf">2009-12-21</dateValid>
<copyrightDate encoding="w3cdtf">2010</copyrightDate>
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<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<extent unit="words">4229</extent>
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<abstract lang="en">Epidemiological studies consistently point to a relationship between restless legs syndrome (RLS) and cardiovascular disease. The mechanism underlying this association is unclear. Activation of the hypothalamic‐pituitary‐adrenal (HPA) system has been shown to contribute to the metabolic syndrome and an enhanced cardiovascular risk. We investigated cortisol levels as an indicator of HPA system activity in RLS during the nighttime, when RLS symptoms are at their maximum. We assessed nocturnal urinary cortisol excretion in 73 patients with RLS and 34 healthy controls, controlling for age and gender. Urine sampling was paralleled by polysomnographic recordings. We found significantly enhanced nocturnal cortisol excretion in RLS, demonstrating nocturnal HPA system overactivity in RLS. HPA system overactivity is a possible mechanism contributing to the enhanced load of cardiovascular disease in RLS patients. Nocturnal cortisol release showed weak correlations with some polysomnographic parameters of disturbed sleep, making a potential contribution of RLS‐induced sleep disruption to HPA system activation conceivable. © 2010 Movement Disorder Society</abstract>
<note type="content">*Potential conflict of interest: Nothing to report.</note>
<subject lang="en">
<genre>Keywords</genre>
<topic>cortisol</topic>
<topic>restless legs syndrome</topic>
<topic>HPA system</topic>
<topic>cardiovascular</topic>
<topic>polysomnography</topic>
</subject>
<relatedItem type="host">
<titleInfo>
<title>Movement Disorders</title>
</titleInfo>
<titleInfo type="abbreviated">
<title>Mov. Disord.</title>
</titleInfo>
<subject>
<genre>article category</genre>
<topic>Research Article</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>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>25</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>1047</start>
<end>1052</end>
<total>6</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">78AB4FF1FF63AB03381DC1BE8469D7C8C7F2C9E1</identifier>
<identifier type="DOI">10.1002/mds.23026</identifier>
<identifier type="ArticleID">MDS23026</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition>
<recordInfo>
<recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
<recordContentSource>WILEY</recordContentSource>
</recordInfo>
</mods>
</metadata>
<serie></serie>
</istex>
</record>

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