Levodopa use and sleep in patients with dementia with Lewy bodies
Identifieur interne : 000C75 ( Main/Corpus ); précédent : 000C74; suivant : 000C76Levodopa use and sleep in patients with dementia with Lewy bodies
Auteurs : Sophie Molloy ; Thais Minett ; John T. O'Brien ; Ian G. Mckeith ; David J. BurnSource :
- Movement Disorders [ 0885-3185 ] ; 2009-03-15.
English descriptors
- KwdEn :
Abstract
Sleep disturbance and excessive daytime somnolence (EDS) are features of Parkinson's disease (PD) and dementia with Lewy bodies (DLB) that may be influenced by dopamine replacement therapy. The effect of levodopa on sleep and EDS in DLB is unknown and unclear in PD. The aim of this study is to determine if levodopa treatment alters sleep symptoms and EDS in DLB. Dopamine naïve patients with DLB (n = 15; mean mini mental state examination (MMSE) score 17.7(4.6)) and PD (n = 9; mean MMSE 25.5(2.2)) were assessed using the Epworth sleep scale, Parkinson's disease sleep scale, and the neuropsychiatric inventory prior to initiating treatment with levodopa. All measures were repeated after 3 and 6 months of levodopa therapy. The median final daily levodopa dose was 300 mg in both groups. Baseline sleep measures were comparable between groups. Levodopa treatment did not affect sleep or lead to increased EDS in DLB patients. The use of levodopa does not appear to adversely affect subjective sleep measures or increase EDS in DLB patients. © 2009 Movement Disorder Society
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DOI: 10.1002/mds.22411
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ISTEX:000A8BBED6A1B41EBB64C282DD7B9042F8C2F9B1Le document en format XML
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The effect of levodopa on sleep and EDS in DLB is unknown and unclear in PD. The aim of this study is to determine if levodopa treatment alters sleep symptoms and EDS in DLB. Dopamine naïve patients with DLB (n = 15; mean mini mental state examination (MMSE) score 17.7(4.6)) and PD (n = 9; mean MMSE 25.5(2.2)) were assessed using the Epworth sleep scale, Parkinson's disease sleep scale, and the neuropsychiatric inventory prior to initiating treatment with levodopa. All measures were repeated after 3 and 6 months of levodopa therapy. The median final daily levodopa dose was 300 mg in both groups. Baseline sleep measures were comparable between groups. Levodopa treatment did not affect sleep or lead to increased EDS in DLB patients. 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The effect of levodopa on sleep and EDS in DLB is unknown and unclear in PD. The aim of this study is to determine if levodopa treatment alters sleep symptoms and EDS in DLB. Dopamine naïve patients with DLB (n = 15; mean mini mental state examination (MMSE) score 17.7(4.6)) and PD (n = 9; mean MMSE 25.5(2.2)) were assessed using the Epworth sleep scale, Parkinson's disease sleep scale, and the neuropsychiatric inventory prior to initiating treatment with levodopa. All measures were repeated after 3 and 6 months of levodopa therapy. The median final daily levodopa dose was 300 mg in both groups. Baseline sleep measures were comparable between groups. Levodopa treatment did not affect sleep or lead to increased EDS in DLB patients. The use of levodopa does not appear to adversely affect subjective sleep measures or increase EDS in DLB patients. © 2009 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn3"><p>Potential conflict of interest: SM's research was funded by PPP healthcare from August 2001‐03.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Levodopa use and sleep in patients with dementia with Lewy bodies</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Levodopa Use and Sleep in Patients with DLB</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Levodopa use and sleep in patients with dementia with Lewy bodies</title></titleInfo><name type="personal"><namePart type="given">Sophie</namePart><namePart type="family">Molloy</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Wolfson Research Centre, Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, United Kingdom</affiliation><description>Correspondence: Department of Neurology, Imperial Hospitals Trust, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, United Kingdom</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thais</namePart><namePart type="family">Minett</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Preventative Medicine, Federal University of São Paulo, Rua Borges Lagoa, São Paulo, Brazil</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John T.</namePart><namePart type="family">O'Brien</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Wolfson Research Centre, Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ian G.</namePart><namePart type="family">McKeith</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Wolfson Research Centre, Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David J.</namePart><namePart type="family">Burn</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Wolfson Research Centre, Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-03-15</dateIssued><dateCaptured encoding="w3cdtf">2008-07-28</dateCaptured><dateValid encoding="w3cdtf">2008-11-05</dateValid><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">1</extent><extent unit="references">27</extent><extent unit="words">2902</extent></physicalDescription><abstract lang="en">Sleep disturbance and excessive daytime somnolence (EDS) are features of Parkinson's disease (PD) and dementia with Lewy bodies (DLB) that may be influenced by dopamine replacement therapy. The effect of levodopa on sleep and EDS in DLB is unknown and unclear in PD. The aim of this study is to determine if levodopa treatment alters sleep symptoms and EDS in DLB. Dopamine naïve patients with DLB (n = 15; mean mini mental state examination (MMSE) score 17.7(4.6)) and PD (n = 9; mean MMSE 25.5(2.2)) were assessed using the Epworth sleep scale, Parkinson's disease sleep scale, and the neuropsychiatric inventory prior to initiating treatment with levodopa. All measures were repeated after 3 and 6 months of levodopa therapy. The median final daily levodopa dose was 300 mg in both groups. Baseline sleep measures were comparable between groups. Levodopa treatment did not affect sleep or lead to increased EDS in DLB patients. The use of levodopa does not appear to adversely affect subjective sleep measures or increase EDS in DLB patients. © 2009 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: SM's research was funded by PPP healthcare from August 2001‐03.</note><subject lang="en"><genre>Keywords</genre><topic>levodopa</topic><topic>sleep</topic><topic>dementia with Lewy bodies</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><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>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>609</start><end>612</end><total>4</total></extent></part></relatedItem><identifier type="istex">000A8BBED6A1B41EBB64C282DD7B9042F8C2F9B1</identifier><identifier type="DOI">10.1002/mds.22411</identifier><identifier type="ArticleID">MDS22411</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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