Longitudinal assessment of excessive daytime sleepiness in early Parkinson’s disease
BackgroundExcessive daytime sleepiness (EDS) is common and disabling in Parkinson’s disease (PD). Predictors of EDS are unclear, and data on biological correlates of EDS in PD are limited. We investigated clinical, imaging and biological variables associated with longitudinal changes in sleepiness i...
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| Vydáno v: | Journal of neurology, neurosurgery and psychiatry Ročník 88; číslo 8; s. 653 - 662 |
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| Hlavní autoři: | , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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England
BMJ Publishing Group LTD
01.08.2017
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| ISSN: | 0022-3050, 1468-330X, 1468-330X |
| On-line přístup: | Získat plný text |
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| Abstract | BackgroundExcessive daytime sleepiness (EDS) is common and disabling in Parkinson’s disease (PD). Predictors of EDS are unclear, and data on biological correlates of EDS in PD are limited. We investigated clinical, imaging and biological variables associated with longitudinal changes in sleepiness in early PD.MethodsThe Parkinson’s Progression Markers Initiative is a prospective cohort study evaluating progression markers in participants with PD who are unmedicated at baseline (n=423) and healthy controls (HC; n=196). EDS was measured with the Epworth Sleepiness Scale (ESS). Clinical, biological and imaging variables were assessed for associations with EDS for up to 3 years. A machine learning approach (random survival forests) was used to investigate baseline predictors of incident EDS.ResultsESS increased in PD from baseline to year 3 (mean±SD 5.8±3.5 to 7.55±4.6, p<0.0001), with no change in HC. Longitudinally, EDS in PD was associated with non-tremor dominant phenotype, autonomic dysfunction, depression, anxiety and probable behaviour disorder, but not cognitive dysfunction or motor severity. Dopaminergic therapy was associated with EDS at years 2 and 3, as dose increased. EDS was also associated with presynaptic dopaminergic dysfunction, whereas biofluid markers at year 1 showed no significant associations with EDS. A predictive index for EDS was generated, which included seven baseline characteristics, including non-motor symptoms and cerebrospinal fluid phosphorylated-tau/total-tau ratio.ConclusionsIn early PD, EDS increases significantly over time and is associated with several clinical variables. The influence of dopaminergic therapy on EDS is dose dependent. Further longitudinal analyses will better characterise associations with imaging and biomarkers. |
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| AbstractList | Excessive daytime sleepiness (EDS) is common and disabling in Parkinson's disease (PD). Predictors of EDS are unclear, and data on biological correlates of EDS in PD are limited. We investigated clinical, imaging and biological variables associated with longitudinal changes in sleepiness in early PD.
The Parkinson's Progression Markers Initiative is a prospective cohort study evaluating progression markers in participants with PD who are unmedicated at baseline (n=423) and healthy controls (HC; n=196). EDS was measured with the Epworth Sleepiness Scale (ESS). Clinical, biological and imaging variables were assessed for associations with EDS for up to 3 years. A machine learning approach (random survival forests) was used to investigate baseline predictors of incident EDS.
ESS increased in PD from baseline to year 3 (mean±SD 5.8±3.5 to 7.55±4.6, p<0.0001), with no change in HC. Longitudinally, EDS in PD was associated with non-tremor dominant phenotype, autonomic dysfunction, depression, anxiety and probable behaviour disorder, but not cognitive dysfunction or motor severity. Dopaminergic therapy was associated with EDS at years 2 and 3, as dose increased. EDS was also associated with presynaptic dopaminergic dysfunction, whereas biofluid markers at year 1 showed no significant associations with EDS. A predictive index for EDS was generated, which included seven baseline characteristics, including non-motor symptoms and cerebrospinal fluid phosphorylated-tau/total-tau ratio.
In early PD, EDS increases significantly over time and is associated with several clinical variables. The influence of dopaminergic therapy on EDS is dose dependent. Further longitudinal analyses will better characterise associations with imaging and biomarkers. Excessive daytime sleepiness (EDS) is common and disabling in Parkinson's disease (PD). Predictors of EDS are unclear, and data on biological correlates of EDS in PD are limited. We investigated clinical, imaging and biological variables associated with longitudinal changes in sleepiness in early PD.BACKGROUNDExcessive daytime sleepiness (EDS) is common and disabling in Parkinson's disease (PD). Predictors of EDS are unclear, and data on biological correlates of EDS in PD are limited. We investigated clinical, imaging and biological variables associated with longitudinal changes in sleepiness in early PD.The Parkinson's Progression Markers Initiative is a prospective cohort study evaluating progression markers in participants with PD who are unmedicated at baseline (n=423) and healthy controls (HC; n=196). EDS was measured with the Epworth Sleepiness Scale (ESS). Clinical, biological and imaging variables were assessed for associations with EDS for up to 3 years. A machine learning approach (random survival forests) was used to investigate baseline predictors of incident EDS.METHODSThe Parkinson's Progression Markers Initiative is a prospective cohort study evaluating progression markers in participants with PD who are unmedicated at baseline (n=423) and healthy controls (HC; n=196). EDS was measured with the Epworth Sleepiness Scale (ESS). Clinical, biological and imaging variables were assessed for associations with EDS for up to 3 years. A machine learning approach (random survival forests) was used to investigate baseline predictors of incident EDS.ESS increased in PD from baseline to year 3 (mean±SD 5.8±3.5 to 7.55±4.6, p<0.0001), with no change in HC. Longitudinally, EDS in PD was associated with non-tremor dominant phenotype, autonomic dysfunction, depression, anxiety and probable behaviour disorder, but not cognitive dysfunction or motor severity. Dopaminergic therapy was associated with EDS at years 2 and 3, as dose increased. EDS was also associated with presynaptic dopaminergic dysfunction, whereas biofluid markers at year 1 showed no significant associations with EDS. A predictive index for EDS was generated, which included seven baseline characteristics, including non-motor symptoms and cerebrospinal fluid phosphorylated-tau/total-tau ratio.RESULTSESS increased in PD from baseline to year 3 (mean±SD 5.8±3.5 to 7.55±4.6, p<0.0001), with no change in HC. Longitudinally, EDS in PD was associated with non-tremor dominant phenotype, autonomic dysfunction, depression, anxiety and probable behaviour disorder, but not cognitive dysfunction or motor severity. Dopaminergic therapy was associated with EDS at years 2 and 3, as dose increased. EDS was also associated with presynaptic dopaminergic dysfunction, whereas biofluid markers at year 1 showed no significant associations with EDS. A predictive index for EDS was generated, which included seven baseline characteristics, including non-motor symptoms and cerebrospinal fluid phosphorylated-tau/total-tau ratio.In early PD, EDS increases significantly over time and is associated with several clinical variables. The influence of dopaminergic therapy on EDS is dose dependent. Further longitudinal analyses will better characterise associations with imaging and biomarkers.CONCLUSIONSIn early PD, EDS increases significantly over time and is associated with several clinical variables. The influence of dopaminergic therapy on EDS is dose dependent. Further longitudinal analyses will better characterise associations with imaging and biomarkers. BackgroundExcessive daytime sleepiness (EDS) is common and disabling in Parkinson’s disease (PD). Predictors of EDS are unclear, and data on biological correlates of EDS in PD are limited. We investigated clinical, imaging and biological variables associated with longitudinal changes in sleepiness in early PD.MethodsThe Parkinson’s Progression Markers Initiative is a prospective cohort study evaluating progression markers in participants with PD who are unmedicated at baseline (n=423) and healthy controls (HC; n=196). EDS was measured with the Epworth Sleepiness Scale (ESS). Clinical, biological and imaging variables were assessed for associations with EDS for up to 3 years. A machine learning approach (random survival forests) was used to investigate baseline predictors of incident EDS.ResultsESS increased in PD from baseline to year 3 (mean±SD 5.8±3.5 to 7.55±4.6, p<0.0001), with no change in HC. Longitudinally, EDS in PD was associated with non-tremor dominant phenotype, autonomic dysfunction, depression, anxiety and probable behaviour disorder, but not cognitive dysfunction or motor severity. Dopaminergic therapy was associated with EDS at years 2 and 3, as dose increased. EDS was also associated with presynaptic dopaminergic dysfunction, whereas biofluid markers at year 1 showed no significant associations with EDS. A predictive index for EDS was generated, which included seven baseline characteristics, including non-motor symptoms and cerebrospinal fluid phosphorylated-tau/total-tau ratio.ConclusionsIn early PD, EDS increases significantly over time and is associated with several clinical variables. The influence of dopaminergic therapy on EDS is dose dependent. Further longitudinal analyses will better characterise associations with imaging and biomarkers. Background Excessive daytime sleepiness (EDS) is common and disabling in Parkinson's disease (PD). Predictors of EDS are unclear, and data on biological correlates of EDS in PD are limited. We investigated clinical, imaging and biological variables associated with longitudinal changes in sleepiness in early PD. Methods The Parkinson's Progression Markers Initiative is a prospective cohort study evaluating progression markers in participants with PD who are unmedicated at baseline (n=423) and healthy controls (HC; n=196). EDS was measured with the Epworth Sleepiness Scale (ESS). Clinical, biological and imaging variables were assessed for associations with EDS for up to 3 years. A machine learning approach (random survival forests) was used to investigate baseline predictors of incident EDS. Results ESS increased in PD from baseline to year 3 (mean±SD 5.8±3.5 to 7.55±4.6, p<0.0001), with no change in HC. Longitudinally, EDS in PD was associated with non-tremor dominant phenotype, autonomic dysfunction, depression, anxiety and probable behaviour disorder, but not cognitive dysfunction or motor severity. Dopaminergic therapy was associated with EDS at years 2 and 3, as dose increased. EDS was also associated with presynaptic dopaminergic dysfunction, whereas biofluid markers at year 1 showed no significant associations with EDS. A predictive index for EDS was generated, which included seven baseline characteristics, including non-motor symptoms and cerebrospinal fluid phosphorylated-tau/total-tau ratio. Conclusions In early PD, EDS increases significantly over time and is associated with several clinical variables. The influence of dopaminergic therapy on EDS is dose dependent. Further longitudinal analyses will better characterise associations with imaging and biomarkers. |
| Author | Amara, Amy W Iranzo, Alex Videnovic, Aleksandar Postuma, Ron Foldvary-Schaefer, Nancy Marek, Ken Long, Jeffrey D Oertel, Wolfgang Högl, Birgit Mayer, Geert Chahine, Lama M Caspell-Garcia, Chelsea Coffey, Christopher Simuni, Tanya Lasch, Shirley |
| AuthorAffiliation | 10 Department of Neurology, Philipps University, Marburg, Germany 6 Neurology Service, Hospital Clinic de Barcelona, IDIBAPS, CIBERNED, Barcelona, Spain 4 Department of Neurology, Innsbruck Medical University, Innsbruck, Austria 1 Department of Neurology, The University of Alabama at Birmingham, Birmingham, Alabama, USA 3 Department of Biostatistics, The University of Iowa, Iowa City, Iowa, USA 11 Charitable Hertie Foundation, Frankfurt, Germany 8 Cleveland Clinic Neurological Institute, Cleveland, Ohio, USA 5 Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA 12 Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA 9 Division of Neurology, McGill University, Montreal, Québec, Canada 2 Department of Neurology, The University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA 7 Department of Neurology, Hephata-Klinik,Hephata Hessisches Diakoniezentrum, e.V., Schwalmstadt-Treysa, Germany 13 Department of Neurology, Northwest |
| AuthorAffiliation_xml | – name: 9 Division of Neurology, McGill University, Montreal, Québec, Canada – name: 4 Department of Neurology, Innsbruck Medical University, Innsbruck, Austria – name: 11 Charitable Hertie Foundation, Frankfurt, Germany – name: 3 Department of Biostatistics, The University of Iowa, Iowa City, Iowa, USA – name: 7 Department of Neurology, Hephata-Klinik,Hephata Hessisches Diakoniezentrum, e.V., Schwalmstadt-Treysa, Germany – name: 5 Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA – name: 6 Neurology Service, Hospital Clinic de Barcelona, IDIBAPS, CIBERNED, Barcelona, Spain – name: 13 Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA – name: 1 Department of Neurology, The University of Alabama at Birmingham, Birmingham, Alabama, USA – name: 2 Department of Neurology, The University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA – name: 8 Cleveland Clinic Neurological Institute, Cleveland, Ohio, USA – name: 10 Department of Neurology, Philipps University, Marburg, Germany – name: 12 Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA |
| Author_xml | – sequence: 1 givenname: Amy W surname: Amara fullname: Amara, Amy W email: amyamara@uab.edu organization: Department of Neurology, The University of Alabama at Birmingham, Birmingham, Alabama, USA – sequence: 2 givenname: Lama M surname: Chahine fullname: Chahine, Lama M email: amyamara@uab.edu organization: Department of Neurology, The University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA – sequence: 3 givenname: Chelsea surname: Caspell-Garcia fullname: Caspell-Garcia, Chelsea email: amyamara@uab.edu organization: Department of Biostatistics, The University of Iowa, Iowa City, Iowa, USA – sequence: 4 givenname: Jeffrey D surname: Long fullname: Long, Jeffrey D email: amyamara@uab.edu organization: Department of Biostatistics, The University of Iowa, Iowa City, Iowa, USA – sequence: 5 givenname: Christopher surname: Coffey fullname: Coffey, Christopher email: amyamara@uab.edu organization: Department of Biostatistics, The University of Iowa, Iowa City, Iowa, USA – sequence: 6 givenname: Birgit surname: Högl fullname: Högl, Birgit email: amyamara@uab.edu organization: Department of Neurology, Innsbruck Medical University, Innsbruck, Austria – sequence: 7 givenname: Aleksandar surname: Videnovic fullname: Videnovic, Aleksandar email: amyamara@uab.edu organization: Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA – sequence: 8 givenname: Alex surname: Iranzo fullname: Iranzo, Alex email: amyamara@uab.edu organization: Neurology Service, Hospital Clinic de Barcelona, IDIBAPS, CIBERNED, Barcelona, Spain – sequence: 9 givenname: Geert surname: Mayer fullname: Mayer, Geert email: amyamara@uab.edu organization: Department of Neurology, Hephata-Klinik, Hephata Hessisches Diakoniezentrum, e.V., Schwalmstadt-Treysa, Germany – sequence: 10 givenname: Nancy surname: Foldvary-Schaefer fullname: Foldvary-Schaefer, Nancy email: amyamara@uab.edu organization: Cleveland Clinic Neurological Institute, Cleveland, Ohio, USA – sequence: 11 givenname: Ron surname: Postuma fullname: Postuma, Ron email: amyamara@uab.edu organization: Division of Neurology, McGill University, Montreal, Québec, Canada – sequence: 12 givenname: Wolfgang surname: Oertel fullname: Oertel, Wolfgang email: amyamara@uab.edu organization: Charitable Hertie Foundation, Frankfurt, Germany – sequence: 13 givenname: Shirley surname: Lasch fullname: Lasch, Shirley email: amyamara@uab.edu organization: Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA – sequence: 14 givenname: Ken surname: Marek fullname: Marek, Ken email: amyamara@uab.edu organization: Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA – sequence: 15 givenname: Tanya surname: Simuni fullname: Simuni, Tanya email: amyamara@uab.edu organization: Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28554959$$D View this record in MEDLINE/PubMed |
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| IngestDate | Tue Nov 04 02:00:19 EST 2025 Thu Sep 04 19:55:16 EDT 2025 Tue Oct 07 07:27:25 EDT 2025 Thu Apr 03 06:58:55 EDT 2025 Tue Nov 18 21:08:30 EST 2025 Sat Nov 29 02:37:13 EST 2025 Thu Apr 24 23:07:14 EDT 2025 |
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| Issue | 8 |
| Keywords | Biomarkers Excessive daytime sleepiness Non-motor symptoms Sleep Parkinson’s disease |
| Language | English |
| License | Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Undefined-3 Contributors AWA: research project: conception and execution; statistical analysis: review and critique; manuscript preparation:writing the first draft, review and critique. LMC: research project:conception; statistical analysis: review and critique; manuscript preparation:drafting/revising manuscript and review and critique. CC-G and JDL: statistical analysis: design, execution and review and critique; manuscript preparation:review and critique. CC: statistical analysis: review and critique; manuscript preparation: review and critique. BH and AV: research project: conception;statistical analysis: review and critique; manuscript preparation: review and critique. AI: research project: organisation; statistical analysis: review and critique; manuscript preparation: review and critique. GM: research project:conception and execution; manuscript preparation: review and critique. NF-S:manuscript preparation: review and critique. RP: statistical analysis: review and critique; manuscript preparation: review and critique. WO: research project: conception and organisation; statistical analysis: review and critique; manuscript preparation: review and critique. SL: research project:conception, organisation and execution; statistical analysis: review and critique; manuscript preparation: review and critique. KM: research project:conception, organisation and execution; statistical analysis: design and review and critique; manuscript preparation: review and critique. TS: research project: conception, organisation and execution; statistical analysis: designand review and critique: manuscript preparation: drafting and review and critique. |
| OpenAccessLink | https://www.ncbi.nlm.nih.gov/pmc/articles/7282477 |
| PMID | 28554959 |
| PQID | 1918791083 |
| PQPubID | 2041879 |
| PageCount | 10 |
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| PublicationDate | 2017-08-01 |
| PublicationDateYYYYMMDD | 2017-08-01 |
| PublicationDate_xml | – month: 08 year: 2017 text: 2017-08-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | England |
| PublicationPlace_xml | – name: England – name: London |
| PublicationTitle | Journal of neurology, neurosurgery and psychiatry |
| PublicationTitleAlternate | J Neurol Neurosurg Psychiatry |
| PublicationYear | 2017 |
| Publisher | BMJ Publishing Group LTD |
| Publisher_xml | – name: BMJ Publishing Group LTD |
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| Snippet | BackgroundExcessive daytime sleepiness (EDS) is common and disabling in Parkinson’s disease (PD). Predictors of EDS are unclear, and data on biological... Excessive daytime sleepiness (EDS) is common and disabling in Parkinson's disease (PD). Predictors of EDS are unclear, and data on biological correlates of EDS... Background Excessive daytime sleepiness (EDS) is common and disabling in Parkinson's disease (PD). Predictors of EDS are unclear, and data on biological... |
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| SubjectTerms | Adult Aged Anxiety Case-Control Studies Cross-Sectional Studies Disorders of Excessive Somnolence - chemically induced Disorders of Excessive Somnolence - diagnosis Disorders of Excessive Somnolence - epidemiology Dopamine Dopamine Agents - adverse effects Dopamine Agents - therapeutic use Dose-Response Relationship, Drug Female Humans Longitudinal Studies Male Medical prognosis Middle Aged Neurodegeneration Neurologic Examination - drug effects Parkinson Disease - diagnosis Parkinson Disease - drug therapy Parkinson Disease - epidemiology Parkinson's disease Prognosis Sleep Wake Disorders - diagnosis Sleep Wake Disorders - drug therapy Sleep Wake Disorders - epidemiology Studies |
| Title | Longitudinal assessment of excessive daytime sleepiness in early Parkinson’s disease |
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