Cerebrospinal hypocretin, daytime sleepiness and sleep architecture in Parkinson's disease dementia
Identifieur interne : 000036 ( Main/Corpus ); précédent : 000035; suivant : 000037Cerebrospinal hypocretin, daytime sleepiness and sleep architecture in Parkinson's disease dementia
Auteurs : Yaroslau Compta ; Joan Santamaria ; Luca Ratti ; Eduardo Tolosa ; Alex Iranzo ; Esteban Muoz ; Francesc Valldeoriola ; Roser Casamitjana ; Jose Ros ; Maria J. MartiSource :
- Brain [ 0006-8950 ] ; 2009-12.
Abstract
Excessive daytime sleepiness is common in Parkinson's disease and has been associated with Parkinson's disease-related dementia. Narcoleptic features have been observed in Parkinson's disease patients with excessive daytime sleepiness and hypocretin cell loss has been found in the hypothalamus of Parkinson's disease patients, in association with advanced disease. However, studies on cerebrospinal fluid levels of hypocretin-1 (orexin A) in Parkinson's disease have been inconclusive. Reports of sleep studies in Parkinson's disease patients with and without excessive daytime sleepiness have also been disparate, pointing towards a variety of causes underlying excessive daytime sleepiness. In this study, we aimed to measure cerebrospinal fluid hypocretin-1 levels in Parkinson's disease patients with and without dementia and to study their relationship to dementia and clinical excessive daytime sleepiness, as well as to describe potentially related sleep architecture changes. Twenty-one Parkinson's disease patients without dementia and 20 Parkinson's disease patients with dementia, along with 22 control subjects without sleep complaints, were included. Both Epworth sleepiness scale, obtained with the help of the caregivers, and mini-mental state examination were recorded. Lumbar cerebrospinal fluid hypocretin-1 levels were measured in all individuals using a radio-immunoassay technique. Additionally, eight Parkinson's disease patients without dementia and seven Parkinson's disease patients with dementia underwent video-polysomnogram and multiple sleep latencies test. Epworth sleepiness scale scores were higher in Parkinson's disease patients without dementia and Parkinson's disease patients with dementia than controls (P < 0.01) and scores >10 were more frequent in Parkinson's disease patients with dementia than in Parkinson's disease patients without dementia (P 0.04). Cerebrospinal fluid hypocretin-1 levels were similar among groups (controls 321.15 47.15 pg/ml; without dementia 300.99 58.68 pg/ml; with dementia 309.94 65.95 pg/ml; P 0.67), and unrelated to either epworth sleepiness scale or mini-mental state examination. Dominant occipital frequency awake was slower in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia (P 0.05). Presence of slow dominant occipital frequency and/or loss of normal non-rapid eye movement sleep architecture was more frequent among Parkinson's disease patients with dementia (P 0.029). Thus, excessive daytime sleepiness is more frequent in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia, but lumbar cerebrospinal fluid hypocretin-1 levels are normal and unrelated to severity of sleepiness or the cognitive status. Lumbar cerebrospinal fluid does not accurately reflect the hypocretin cell loss known to occur in the hypothalamus of advanced Parkinson's disease. Alternatively, mechanisms other than hypocretin cells dysfunction may be responsible for excessive daytime sleepiness and the sleep architecture alterations seen in these patients.
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DOI: 10.1093/brain/awp263
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Marti</name><affiliation><mods:affiliation>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: mjmarti@clinic.ub.es</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2009-12">2009-12</date><biblScope unit="volume">132</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="3308">3308</biblScope><biblScope unit="page" to="3317">3317</biblScope></imprint><idno type="ISSN">0006-8950</idno></series><idno type="istex">6A9494669245A5370D71D959BFCD659160A5BDA1</idno><idno type="DOI">10.1093/brain/awp263</idno><idno type="ArticleID">awp263</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Excessive daytime sleepiness is common in Parkinson's disease and has been associated with Parkinson's disease-related dementia. Narcoleptic features have been observed in Parkinson's disease patients with excessive daytime sleepiness and hypocretin cell loss has been found in the hypothalamus of Parkinson's disease patients, in association with advanced disease. However, studies on cerebrospinal fluid levels of hypocretin-1 (orexin A) in Parkinson's disease have been inconclusive. Reports of sleep studies in Parkinson's disease patients with and without excessive daytime sleepiness have also been disparate, pointing towards a variety of causes underlying excessive daytime sleepiness. In this study, we aimed to measure cerebrospinal fluid hypocretin-1 levels in Parkinson's disease patients with and without dementia and to study their relationship to dementia and clinical excessive daytime sleepiness, as well as to describe potentially related sleep architecture changes. Twenty-one Parkinson's disease patients without dementia and 20 Parkinson's disease patients with dementia, along with 22 control subjects without sleep complaints, were included. Both Epworth sleepiness scale, obtained with the help of the caregivers, and mini-mental state examination were recorded. Lumbar cerebrospinal fluid hypocretin-1 levels were measured in all individuals using a radio-immunoassay technique. Additionally, eight Parkinson's disease patients without dementia and seven Parkinson's disease patients with dementia underwent video-polysomnogram and multiple sleep latencies test. Epworth sleepiness scale scores were higher in Parkinson's disease patients without dementia and Parkinson's disease patients with dementia than controls (P < 0.01) and scores >10 were more frequent in Parkinson's disease patients with dementia than in Parkinson's disease patients without dementia (P 0.04). Cerebrospinal fluid hypocretin-1 levels were similar among groups (controls 321.15 47.15 pg/ml; without dementia 300.99 58.68 pg/ml; with dementia 309.94 65.95 pg/ml; P 0.67), and unrelated to either epworth sleepiness scale or mini-mental state examination. Dominant occipital frequency awake was slower in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia (P 0.05). Presence of slow dominant occipital frequency and/or loss of normal non-rapid eye movement sleep architecture was more frequent among Parkinson's disease patients with dementia (P 0.029). Thus, excessive daytime sleepiness is more frequent in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia, but lumbar cerebrospinal fluid hypocretin-1 levels are normal and unrelated to severity of sleepiness or the cognitive status. Lumbar cerebrospinal fluid does not accurately reflect the hypocretin cell loss known to occur in the hypothalamus of advanced Parkinson's disease. Alternatively, mechanisms other than hypocretin cells dysfunction may be responsible for excessive daytime sleepiness and the sleep architecture alterations seen in these patients.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Yaroslau Compta</name><affiliations><json:string>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Joan Santamaria</name><affiliations><json:string>2 Multidisciplinary Sleep Disorders Unit and Neurology Service, ICN, IDIBAPS, CIBERNED, Hospital Clnic, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Luca Ratti</name><affiliations><json:string>2 Multidisciplinary Sleep Disorders Unit and Neurology Service, ICN, IDIBAPS, CIBERNED, Hospital Clnic, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Eduardo Tolosa</name><affiliations><json:string>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Alex Iranzo</name><affiliations><json:string>2 Multidisciplinary Sleep Disorders Unit and Neurology Service, ICN, IDIBAPS, CIBERNED, Hospital Clnic, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Esteban Muoz</name><affiliations><json:string>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Francesc Valldeoriola</name><affiliations><json:string>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Roser Casamitjana</name><affiliations><json:string>3 Biochemistry and Molecular Genetics Laboratory, Centre de Diagnstic Biomdic (CDB), IDIBAPS, Hospital Clnic, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Jose Ros</name><affiliations><json:string>4 Statistics and Methodologic Support Unit, Unitat dAvaluaci, Suport i Prevenci (UASP), Hospital Clnic, IDIBAPS, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Maria J. Marti</name><affiliations><json:string>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</json:string><json:string>E-mail: mjmarti@clinic.ub.es</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Original Articles</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dementia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>excessive daytime sleepiness</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hypocretin-1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>sleep architecture</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Excessive daytime sleepiness is common in Parkinson's disease and has been associated with Parkinson's disease-related dementia. Narcoleptic features have been observed in Parkinson's disease patients with excessive daytime sleepiness and hypocretin cell loss has been found in the hypothalamus of Parkinson's disease patients, in association with advanced disease. However, studies on cerebrospinal fluid levels of hypocretin-1 (orexin A) in Parkinson's disease have been inconclusive. Reports of sleep studies in Parkinson's disease patients with and without excessive daytime sleepiness have also been disparate, pointing towards a variety of causes underlying excessive daytime sleepiness. In this study, we aimed to measure cerebrospinal fluid hypocretin-1 levels in Parkinson's disease patients with and without dementia and to study their relationship to dementia and clinical excessive daytime sleepiness, as well as to describe potentially related sleep architecture changes. Twenty-one Parkinson's disease patients without dementia and 20 Parkinson's disease patients with dementia, along with 22 control subjects without sleep complaints, were included. Both Epworth sleepiness scale, obtained with the help of the caregivers, and mini-mental state examination were recorded. Lumbar cerebrospinal fluid hypocretin-1 levels were measured in all individuals using a radio-immunoassay technique. Additionally, eight Parkinson's disease patients without dementia and seven Parkinson's disease patients with dementia underwent video-polysomnogram and multiple sleep latencies test. Epworth sleepiness scale scores were higher in Parkinson's disease patients without dementia and Parkinson's disease patients with dementia than controls (P > 0.01) and scores >10 were more frequent in Parkinson's disease patients with dementia than in Parkinson's disease patients without dementia (P 0.04). Cerebrospinal fluid hypocretin-1 levels were similar among groups (controls 321.15 47.15 pg/ml; without dementia 300.99 58.68 pg/ml; with dementia 309.94 65.95 pg/ml; P 0.67), and unrelated to either epworth sleepiness scale or mini-mental state examination. Dominant occipital frequency awake was slower in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia (P 0.05). Presence of slow dominant occipital frequency and/or loss of normal non-rapid eye movement sleep architecture was more frequent among Parkinson's disease patients with dementia (P 0.029). Thus, excessive daytime sleepiness is more frequent in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia, but lumbar cerebrospinal fluid hypocretin-1 levels are normal and unrelated to severity of sleepiness or the cognitive status. Lumbar cerebrospinal fluid does not accurately reflect the hypocretin cell loss known to occur in the hypothalamus of advanced Parkinson's disease. Alternatively, mechanisms other than hypocretin cells dysfunction may be responsible for excessive daytime sleepiness and the sleep architecture alterations seen in these patients.</abstract><qualityIndicators><score>8.5</score><pdfVersion>1.4</pdfVersion><pdfPageSize>612.68 x 790.866 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>3102</abstractCharCount><pdfWordCount>7006</pdfWordCount><pdfCharCount>45249</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>414</abstractWordCount></qualityIndicators><title>Cerebrospinal hypocretin, daytime sleepiness and sleep architecture in Parkinson's disease 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dementia</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>OUP</p></availability><date>2009-10-24</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Cerebrospinal hypocretin, daytime sleepiness and sleep architecture in Parkinson's disease dementia</title><author><persName><forename type="first">Yaroslau</forename><surname>Compta</surname></persName><affiliation>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Joan</forename><surname>Santamaria</surname></persName><affiliation>2 Multidisciplinary Sleep Disorders Unit and Neurology Service, ICN, IDIBAPS, CIBERNED, Hospital Clnic, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Luca</forename><surname>Ratti</surname></persName><affiliation>2 Multidisciplinary Sleep Disorders Unit and Neurology Service, ICN, IDIBAPS, CIBERNED, Hospital Clnic, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Eduardo</forename><surname>Tolosa</surname></persName><affiliation>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Alex</forename><surname>Iranzo</surname></persName><affiliation>2 Multidisciplinary Sleep Disorders Unit and Neurology Service, ICN, IDIBAPS, CIBERNED, Hospital Clnic, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Esteban</forename><surname>Muoz</surname></persName><affiliation>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Francesc</forename><surname>Valldeoriola</surname></persName><affiliation>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Roser</forename><surname>Casamitjana</surname></persName><affiliation>3 Biochemistry and Molecular Genetics Laboratory, Centre de Diagnstic Biomdic (CDB), IDIBAPS, Hospital Clnic, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Jose</forename><surname>Ros</surname></persName><affiliation>4 Statistics and Methodologic Support Unit, Unitat dAvaluaci, Suport i Prevenci (UASP), Hospital Clnic, IDIBAPS, Barcelona, Catalonia, Spain</affiliation></author><author corresp="yes"><persName><forename type="first">Maria J.</forename><surname>Marti</surname></persName><email>mjmarti@clinic.ub.es</email><affiliation>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</affiliation></author></analytic><monogr><title level="j">Brain</title><idno type="pISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2009-12"></date><biblScope unit="volume">132</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="3308">3308</biblScope><biblScope unit="page" to="3317">3317</biblScope></imprint></monogr><idno type="istex">6A9494669245A5370D71D959BFCD659160A5BDA1</idno><idno type="DOI">10.1093/brain/awp263</idno><idno type="ArticleID">awp263</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2009-10-24</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Excessive daytime sleepiness is common in Parkinson's disease and has been associated with Parkinson's disease-related dementia. Narcoleptic features have been observed in Parkinson's disease patients with excessive daytime sleepiness and hypocretin cell loss has been found in the hypothalamus of Parkinson's disease patients, in association with advanced disease. However, studies on cerebrospinal fluid levels of hypocretin-1 (orexin A) in Parkinson's disease have been inconclusive. Reports of sleep studies in Parkinson's disease patients with and without excessive daytime sleepiness have also been disparate, pointing towards a variety of causes underlying excessive daytime sleepiness. In this study, we aimed to measure cerebrospinal fluid hypocretin-1 levels in Parkinson's disease patients with and without dementia and to study their relationship to dementia and clinical excessive daytime sleepiness, as well as to describe potentially related sleep architecture changes. Twenty-one Parkinson's disease patients without dementia and 20 Parkinson's disease patients with dementia, along with 22 control subjects without sleep complaints, were included. Both Epworth sleepiness scale, obtained with the help of the caregivers, and mini-mental state examination were recorded. Lumbar cerebrospinal fluid hypocretin-1 levels were measured in all individuals using a radio-immunoassay technique. Additionally, eight Parkinson's disease patients without dementia and seven Parkinson's disease patients with dementia underwent video-polysomnogram and multiple sleep latencies test. Epworth sleepiness scale scores were higher in Parkinson's disease patients without dementia and Parkinson's disease patients with dementia than controls (P < 0.01) and scores >10 were more frequent in Parkinson's disease patients with dementia than in Parkinson's disease patients without dementia (P 0.04). Cerebrospinal fluid hypocretin-1 levels were similar among groups (controls 321.15 47.15 pg/ml; without dementia 300.99 58.68 pg/ml; with dementia 309.94 65.95 pg/ml; P 0.67), and unrelated to either epworth sleepiness scale or mini-mental state examination. Dominant occipital frequency awake was slower in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia (P 0.05). Presence of slow dominant occipital frequency and/or loss of normal non-rapid eye movement sleep architecture was more frequent among Parkinson's disease patients with dementia (P 0.029). Thus, excessive daytime sleepiness is more frequent in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia, but lumbar cerebrospinal fluid hypocretin-1 levels are normal and unrelated to severity of sleepiness or the cognitive status. Lumbar cerebrospinal fluid does not accurately reflect the hypocretin cell loss known to occur in the hypothalamus of advanced Parkinson's disease. Alternatively, mechanisms other than hypocretin cells dysfunction may be responsible for excessive daytime sleepiness and the sleep architecture alterations seen in these patients.</p></abstract><textClass><keywords scheme="keyword"><list><item><term>Original Articles</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>dementia</term></item><item><term>excessive daytime sleepiness</term></item><item><term>hypocretin-1</term></item><item><term>sleep architecture</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2009-10-24">Created</change><change when="2009-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6A9494669245A5370D71D959BFCD659160A5BDA1/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">brain</journal-id><journal-id journal-id-type="publisher-id">brainj</journal-id><journal-title>Brain</journal-title><issn pub-type="ppub">0006-8950</issn><issn pub-type="epub">1460-2156</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1093/brain/awp263</article-id><article-id pub-id-type="publisher-id">awp263</article-id><article-categories><subj-group><subject>Original Articles</subject></subj-group></article-categories><title-group><article-title>Cerebrospinal hypocretin, daytime sleepiness and sleep architecture in Parkinson's disease dementia</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Compta</surname><given-names>Yaroslau</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Santamaria</surname><given-names>Joan</given-names></name><xref ref-type="aff" rid="AFF2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ratti</surname><given-names>Luca</given-names></name><xref ref-type="aff" rid="AFF2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Tolosa</surname><given-names>Eduardo</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Iranzo</surname><given-names>Alex</given-names></name><xref ref-type="aff" rid="AFF2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Muñoz</surname><given-names>Esteban</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Valldeoriola</surname><given-names>Francesc</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Casamitjana</surname><given-names>Roser</given-names></name><xref ref-type="aff" rid="AFF3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ríos</surname><given-names>Jose</given-names></name><xref ref-type="aff" rid="AFF4"><sup>4</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Marti</surname><given-names>Maria J.</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib></contrib-group><aff id="AFF1">1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</aff><aff id="AFF2">2 Multidisciplinary Sleep Disorders Unit and Neurology Service, ICN, IDIBAPS, CIBERNED, Hospital Clínic, Barcelona, Catalonia, Spain</aff><aff id="AFF3">3 Biochemistry and Molecular Genetics Laboratory, Centre de Diagnòstic Biomèdic (CDB), IDIBAPS, Hospital Clínic, Barcelona, Catalonia, Spain</aff><aff id="AFF4">4 Statistics and Methodologic Support Unit, Unitat d’Avaluació, Suport i Prevenció (UASP), Hospital Clínic, IDIBAPS, Barcelona, Catalonia, Spain</aff><author-notes><corresp>Correspondence to: Maria J. Marti, MD, PhD, Movement Disorders Unit, ICN, IDIBAPS, CIBERNED, Hospital Clínic, c./Villarroel 170, 08036, Barcelona, Spain E-mail: <email>mjmarti@clinic.ub.es</email></corresp></author-notes><pub-date pub-type="ppub"><month>12</month><year>2009</year></pub-date><pub-date pub-type="epub"><day>24</day><month>10</month><year>2009</year></pub-date><volume>132</volume><issue>12</issue><fpage>3308</fpage><lpage>3317</lpage><history><date date-type="received"><day>13</day><month>5</month><year>2009</year></date><date date-type="rev-recd"><day>25</day><month>8</month><year>2009</year></date><date date-type="accepted"><day>27</day><month>8</month><year>2009</year></date></history><permissions><copyright-statement>© The Author (2009). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</copyright-statement><copyright-year>2009</copyright-year></permissions><abstract><p>Excessive daytime sleepiness is common in Parkinson's disease and has been associated with Parkinson's disease-related dementia. Narcoleptic features have been observed in Parkinson's disease patients with excessive daytime sleepiness and hypocretin cell loss has been found in the hypothalamus of Parkinson's disease patients, in association with advanced disease. However, studies on cerebrospinal fluid levels of hypocretin-1 (orexin A) in Parkinson's disease have been inconclusive. Reports of sleep studies in Parkinson's disease patients with and without excessive daytime sleepiness have also been disparate, pointing towards a variety of causes underlying excessive daytime sleepiness. In this study, we aimed to measure cerebrospinal fluid hypocretin-1 levels in Parkinson's disease patients with and without dementia and to study their relationship to dementia and clinical excessive daytime sleepiness, as well as to describe potentially related sleep architecture changes. Twenty-one Parkinson's disease patients without dementia and 20 Parkinson's disease patients with dementia, along with 22 control subjects without sleep complaints, were included. Both Epworth sleepiness scale, obtained with the help of the caregivers, and mini-mental state examination were recorded. Lumbar cerebrospinal fluid hypocretin-1 levels were measured in all individuals using a radio-immunoassay technique. Additionally, eight Parkinson's disease patients without dementia and seven Parkinson's disease patients with dementia underwent video-polysomnogram and multiple sleep latencies test. Epworth sleepiness scale scores were higher in Parkinson's disease patients without dementia and Parkinson's disease patients with dementia than controls (<italic>P</italic> < 0.01) and scores >10 were more frequent in Parkinson's disease patients with dementia than in Parkinson's disease patients without dementia (<italic>P</italic> = 0.04). Cerebrospinal fluid hypocretin-1 levels were similar among groups (controls = 321.15 ± 47.15 pg/ml; without dementia = 300.99 ± 58.68 pg/ml; with dementia = 309.94 ± 65.95 pg/ml; <italic>P</italic> = 0.67), and unrelated to either epworth sleepiness scale or mini-mental state examination. Dominant occipital frequency awake was slower in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia (<italic>P</italic> = 0.05). Presence of slow dominant occipital frequency and/or loss of normal non-rapid eye movement sleep architecture was more frequent among Parkinson's disease patients with dementia (<italic>P</italic> = 0.029). Thus, excessive daytime sleepiness is more frequent in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia, but lumbar cerebrospinal fluid hypocretin-1 levels are normal and unrelated to severity of sleepiness or the cognitive status. Lumbar cerebrospinal fluid does not accurately reflect the hypocretin cell loss known to occur in the hypothalamus of advanced Parkinson's disease. Alternatively, mechanisms other than hypocretin cells dysfunction may be responsible for excessive daytime sleepiness and the sleep architecture alterations seen in these patients.</p></abstract><kwd-group><kwd>Parkinson's disease</kwd><kwd>dementia</kwd><kwd>excessive daytime sleepiness</kwd><kwd>hypocretin-1</kwd><kwd>sleep architecture</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Cerebrospinal hypocretin, daytime sleepiness and sleep architecture in Parkinson's disease dementia</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Cerebrospinal hypocretin, daytime sleepiness and sleep architecture in Parkinson's disease dementia</title></titleInfo><name type="personal"><namePart type="given">Yaroslau</namePart><namePart type="family">Compta</namePart><affiliation>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joan</namePart><namePart type="family">Santamaria</namePart><affiliation>2 Multidisciplinary Sleep Disorders Unit and Neurology Service, ICN, IDIBAPS, CIBERNED, Hospital Clnic, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Luca</namePart><namePart type="family">Ratti</namePart><affiliation>2 Multidisciplinary Sleep Disorders Unit and Neurology Service, ICN, IDIBAPS, CIBERNED, Hospital Clnic, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eduardo</namePart><namePart type="family">Tolosa</namePart><affiliation>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alex</namePart><namePart type="family">Iranzo</namePart><affiliation>2 Multidisciplinary Sleep Disorders Unit and Neurology Service, ICN, IDIBAPS, CIBERNED, Hospital Clnic, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Esteban</namePart><namePart type="family">Muoz</namePart><affiliation>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Francesc</namePart><namePart type="family">Valldeoriola</namePart><affiliation>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Roser</namePart><namePart type="family">Casamitjana</namePart><affiliation>3 Biochemistry and Molecular Genetics Laboratory, Centre de Diagnstic Biomdic (CDB), IDIBAPS, Hospital Clnic, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jose</namePart><namePart type="family">Ros</namePart><affiliation>4 Statistics and Methodologic Support Unit, Unitat dAvaluaci, Suport i Prevenci (UASP), Hospital Clnic, IDIBAPS, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Maria J.</namePart><namePart type="family">Marti</namePart><affiliation>1 Parkinson disease and Movement Disorders Unit, Neurology Service, Institut Clnic de Neurocincies (ICN), Institut dInvestigacions Biomdiques August Pi i Sunyer (IDIBAPS), Centro de Investigacin en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clnic, c./Villarroel 170, 08036, Barcelona, Catalonia, Spain</affiliation><affiliation>E-mail: mjmarti@clinic.ub.es</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><topic>Original Articles</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2009-12</dateIssued><dateCreated encoding="w3cdtf">2009-10-24</dateCreated><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Excessive daytime sleepiness is common in Parkinson's disease and has been associated with Parkinson's disease-related dementia. Narcoleptic features have been observed in Parkinson's disease patients with excessive daytime sleepiness and hypocretin cell loss has been found in the hypothalamus of Parkinson's disease patients, in association with advanced disease. However, studies on cerebrospinal fluid levels of hypocretin-1 (orexin A) in Parkinson's disease have been inconclusive. Reports of sleep studies in Parkinson's disease patients with and without excessive daytime sleepiness have also been disparate, pointing towards a variety of causes underlying excessive daytime sleepiness. In this study, we aimed to measure cerebrospinal fluid hypocretin-1 levels in Parkinson's disease patients with and without dementia and to study their relationship to dementia and clinical excessive daytime sleepiness, as well as to describe potentially related sleep architecture changes. Twenty-one Parkinson's disease patients without dementia and 20 Parkinson's disease patients with dementia, along with 22 control subjects without sleep complaints, were included. Both Epworth sleepiness scale, obtained with the help of the caregivers, and mini-mental state examination were recorded. Lumbar cerebrospinal fluid hypocretin-1 levels were measured in all individuals using a radio-immunoassay technique. Additionally, eight Parkinson's disease patients without dementia and seven Parkinson's disease patients with dementia underwent video-polysomnogram and multiple sleep latencies test. Epworth sleepiness scale scores were higher in Parkinson's disease patients without dementia and Parkinson's disease patients with dementia than controls (P < 0.01) and scores >10 were more frequent in Parkinson's disease patients with dementia than in Parkinson's disease patients without dementia (P 0.04). Cerebrospinal fluid hypocretin-1 levels were similar among groups (controls 321.15 47.15 pg/ml; without dementia 300.99 58.68 pg/ml; with dementia 309.94 65.95 pg/ml; P 0.67), and unrelated to either epworth sleepiness scale or mini-mental state examination. Dominant occipital frequency awake was slower in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia (P 0.05). Presence of slow dominant occipital frequency and/or loss of normal non-rapid eye movement sleep architecture was more frequent among Parkinson's disease patients with dementia (P 0.029). Thus, excessive daytime sleepiness is more frequent in Parkinson's disease patients with dementia than Parkinson's disease patients without dementia, but lumbar cerebrospinal fluid hypocretin-1 levels are normal and unrelated to severity of sleepiness or the cognitive status. Lumbar cerebrospinal fluid does not accurately reflect the hypocretin cell loss known to occur in the hypothalamus of advanced Parkinson's disease. Alternatively, mechanisms other than hypocretin cells dysfunction may be responsible for excessive daytime sleepiness and the sleep architecture alterations seen in these patients.</abstract><subject><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>dementia</topic><topic>excessive daytime sleepiness</topic><topic>hypocretin-1</topic><topic>sleep architecture</topic></subject><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0006-8950</identifier><identifier type="eISSN">1460-2156</identifier><identifier type="PublisherID">brainj</identifier><identifier type="PublisherID-hwp">brain</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>132</number></detail><detail type="issue"><caption>no.</caption><number>12</number></detail><extent unit="pages"><start>3308</start><end>3317</end></extent></part></relatedItem><identifier type="istex">6A9494669245A5370D71D959BFCD659160A5BDA1</identifier><identifier type="DOI">10.1093/brain/awp263</identifier><identifier type="ArticleID">awp263</identifier><accessCondition type="use and reproduction" contentType="copyright">The Author (2009). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. 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