Effect of dopamine agonists on fatigue and somnolence in Parkinson's disease
Identifieur interne : 000A73 ( Main/Corpus ); précédent : 000A72; suivant : 000A74Effect of dopamine agonists on fatigue and somnolence in Parkinson's disease
Auteurs : Daniel Oved ; Ilan Ziv ; Therese A. Treves ; Diana Paleacu ; Eldad Melamed ; Ruth DjaldettiSource :
- Movement Disorders [ 0885-3185 ] ; 2006-08.
English descriptors
Abstract
Dopamine agonists are becoming increasingly important in the treatment of early and advanced symptoms of Parkinson disease (PD). Although dopamine agonists are known to increase somnolence, their effect on fatigue and the relationship between fatigue and somnolence have not been investigated thoroughly. The objective of this study is to quantitatively measure fatigue in patients with PD treated with dopamine agonists and to correlate fatigue with somnolence. Fifteen patients with PD (mean age, 60.6 ± 9.7 years; mean disease duration, 4.1 ± 1.9 years) underwent a continuous (30‐second) motor task using four muscle groups before and after 3 months of treatment with dopamine agonists. A fatigue index, defined as the decay of maximal force during continuous exercise, was calculated. Findings were compared with 15 healthy, age‐matched control subjects. Patients also completed the Multidimensional Fatigue Inventory (MFI), the Epworth Sleepiness Scale (ESS), and the Hamilton Depression Scale at the same time points. Mean fatigue index (FI) before treatment was significantly higher in PD patients than controls (31.37% ± 3.81% vs. 23.39% ± 3.03%, P < 0.001). There was no significant between‐group difference after 3 months of treatment. There was no difference in FI of the more affected side before and after treatment (33.33% ± 6.18% vs. 34.08% ± 5.43%, P > 0.1). No significant change in MFI scores were noted after treatment, although scores on the ESS increased significantly (6.6 ± 2.63 vs. 11.7 ± 5.16; P < 0.05). Fatigue is prevalent in patients with PD but is not influenced by dopamine agonists. Somnolence cannot be attributed to the increase in fatigability and apparently involves a different mechanism. © 2006 Movement Disorder Society
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DOI: 10.1002/mds.20929
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ISTEX:3D2024886689A4FFEFC2A1653A88BC5959151454Le document en format XML
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Although dopamine agonists are known to increase somnolence, their effect on fatigue and the relationship between fatigue and somnolence have not been investigated thoroughly. The objective of this study is to quantitatively measure fatigue in patients with PD treated with dopamine agonists and to correlate fatigue with somnolence. Fifteen patients with PD (mean age, 60.6 ± 9.7 years; mean disease duration, 4.1 ± 1.9 years) underwent a continuous (30‐second) motor task using four muscle groups before and after 3 months of treatment with dopamine agonists. A fatigue index, defined as the decay of maximal force during continuous exercise, was calculated. Findings were compared with 15 healthy, age‐matched control subjects. Patients also completed the Multidimensional Fatigue Inventory (MFI), the Epworth Sleepiness Scale (ESS), and the Hamilton Depression Scale at the same time points. Mean fatigue index (FI) before treatment was significantly higher in PD patients than controls (31.37% ± 3.81% vs. 23.39% ± 3.03%, P < 0.001). There was no significant between‐group difference after 3 months of treatment. There was no difference in FI of the more affected side before and after treatment (33.33% ± 6.18% vs. 34.08% ± 5.43%, P > 0.1). No significant change in MFI scores were noted after treatment, although scores on the ESS increased significantly (6.6 ± 2.63 vs. 11.7 ± 5.16; P < 0.05). Fatigue is prevalent in patients with PD but is not influenced by dopamine agonists. Somnolence cannot be attributed to the increase in fatigability and apparently involves a different mechanism. © 2006 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Daniel Oved MD</name><affiliations><json:string>Department of Neurology, Rabin Medical Center, Beilinson Campus, Petah Tiqwa, Israel</json:string></affiliations></json:item><json:item><name>Ilan Ziv MD</name><affiliations><json:string>Department of Neurology, Rabin Medical Center, Beilinson Campus, Petah Tiqwa, Israel</json:string></affiliations></json:item><json:item><name>Therese A. 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Mean fatigue index (FI) before treatment was significantly higher in PD patients than controls (31.37% ± 3.81% vs. 23.39% ± 3.03%, P < 0.001). There was no significant between‐group difference after 3 months of treatment. There was no difference in FI of the more affected side before and after treatment (33.33% ± 6.18% vs. 34.08% ± 5.43%, P > 0.1). No significant change in MFI scores were noted after treatment, although scores on the ESS increased significantly (6.6 ± 2.63 vs. 11.7 ± 5.16; P < 0.05). Fatigue is prevalent in patients with PD but is not influenced by dopamine agonists. 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Although dopamine agonists are known to increase somnolence, their effect on fatigue and the relationship between fatigue and somnolence have not been investigated thoroughly. The objective of this study is to quantitatively measure fatigue in patients with PD treated with dopamine agonists and to correlate fatigue with somnolence. Fifteen patients with PD (mean age, 60.6 ± 9.7 years; mean disease duration, 4.1 ± 1.9 years) underwent a continuous (30‐second) motor task using four muscle groups before and after 3 months of treatment with dopamine agonists. A fatigue index, defined as the decay of maximal force during continuous exercise, was calculated. Findings were compared with 15 healthy, age‐matched control subjects. Patients also completed the Multidimensional Fatigue Inventory (MFI), the Epworth Sleepiness Scale (ESS), and the Hamilton Depression Scale at the same time points. Mean fatigue index (FI) before treatment was significantly higher in PD patients than controls (31.37% ± 3.81% vs. 23.39% ± 3.03%, <i>P</i> < 0.001). There was no significant between‐group difference after 3 months of treatment. There was no difference in FI of the more affected side before and after treatment (33.33% ± 6.18% vs. 34.08% ± 5.43%, <i>P</i> > 0.1). No significant change in MFI scores were noted after treatment, although scores on the ESS increased significantly (6.6 ± 2.63 vs. 11.7 ± 5.16; <i>P</i> < 0.05). Fatigue is prevalent in patients with PD but is not influenced by dopamine agonists. Somnolence cannot be attributed to the increase in fatigability and apparently involves a different mechanism. © 2006 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Effect of dopamine agonists on fatigue and somnolence in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Dopamine Agonists on Fatigue and Somnolence in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effect of dopamine agonists on fatigue and somnolence in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Daniel</namePart><namePart type="family">Oved</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Rabin Medical Center, Beilinson Campus, Petah Tiqwa, Israel</affiliation><description>Correspondence: Department of Neurology, Rabin Medical Center, Beilinson Campus, 49100 Petah Tiqwa, Israel</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ilan</namePart><namePart type="family">Ziv</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Rabin Medical Center, Beilinson Campus, Petah Tiqwa, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Therese A.</namePart><namePart type="family">Treves</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Rabin Medical Center, Beilinson Campus, Petah Tiqwa, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Diana</namePart><namePart type="family">Paleacu</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurology Service and Memory Clinic, Abarbanel Mental Health Center, Bat Yam, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eldad</namePart><namePart type="family">Melamed</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Rabin Medical Center, Beilinson Campus, Petah Tiqwa, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ruth</namePart><namePart type="family">Djaldetti</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Rabin Medical Center, Beilinson Campus, Petah Tiqwa, Israel</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">2006-08</dateIssued><dateCaptured encoding="w3cdtf">2005-08-14</dateCaptured><dateValid encoding="w3cdtf">2005-12-27</dateValid><copyrightDate encoding="w3cdtf">2006</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">20</extent><extent unit="words">3194</extent></physicalDescription><abstract lang="en">Dopamine agonists are becoming increasingly important in the treatment of early and advanced symptoms of Parkinson disease (PD). Although dopamine agonists are known to increase somnolence, their effect on fatigue and the relationship between fatigue and somnolence have not been investigated thoroughly. The objective of this study is to quantitatively measure fatigue in patients with PD treated with dopamine agonists and to correlate fatigue with somnolence. Fifteen patients with PD (mean age, 60.6 ± 9.7 years; mean disease duration, 4.1 ± 1.9 years) underwent a continuous (30‐second) motor task using four muscle groups before and after 3 months of treatment with dopamine agonists. A fatigue index, defined as the decay of maximal force during continuous exercise, was calculated. Findings were compared with 15 healthy, age‐matched control subjects. Patients also completed the Multidimensional Fatigue Inventory (MFI), the Epworth Sleepiness Scale (ESS), and the Hamilton Depression Scale at the same time points. Mean fatigue index (FI) before treatment was significantly higher in PD patients than controls (31.37% ± 3.81% vs. 23.39% ± 3.03%, P < 0.001). There was no significant between‐group difference after 3 months of treatment. There was no difference in FI of the more affected side before and after treatment (33.33% ± 6.18% vs. 34.08% ± 5.43%, P > 0.1). No significant change in MFI scores were noted after treatment, although scores on the ESS increased significantly (6.6 ± 2.63 vs. 11.7 ± 5.16; P < 0.05). Fatigue is prevalent in patients with PD but is not influenced by dopamine agonists. Somnolence cannot be attributed to the increase in fatigability and apparently involves a different mechanism. © 2006 Movement Disorder Society</abstract><note type="funding">National Parkinson's Foundation, USA</note><note type="funding">Alan and Norma Aufzien Chair for Research in Parkinson's Disease</note><note type="funding">Sackler School of Medicine, Tel Aviv University</note><subject lang="en"><genre>Keywords</genre><topic>dopamine agonists</topic><topic>fatigue</topic><topic>somnolence, Parkinson's disease</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><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>2006</date><detail type="volume"><caption>vol.</caption><number>21</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>1257</start><end>1261</end><total>5</total></extent></part></relatedItem><identifier type="istex">3D2024886689A4FFEFC2A1653A88BC5959151454</identifier><identifier type="DOI">10.1002/mds.20929</identifier><identifier type="ArticleID">MDS20929</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 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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