Idiopathic hyposmia as a preclinical sign of Parkinson's disease
Identifieur interne : 000A71 ( Main/Corpus ); précédent : 000A70; suivant : 000A72Idiopathic hyposmia as a preclinical sign of Parkinson's disease
Auteurs : Mirthe M. Ponsen ; Diederick Stoffers ; Jan Booij ; Berthe L. F. Van Eck-Smit ; Erik Ch. Wolters ; Henk W. BerendseSource :
- Annals of Neurology [ 0364-5134 ] ; 2004-08.
Abstract
Olfactory dysfunction is an early and common symptom in Parkinson's disease (PD). In an effort to determine whether otherwise unexplained (idiopathic) olfactory dysfunction is associated with an increased risk of developing PD, we designed a prospective study in a cohort of 361 asymptomatic relatives (parents, siblings, or children) of PD patients. A combination of olfactory detection, identification, and discrimination tasks was used to select groups of hyposmic (n = 40) and normosmic (n = 38) individuals for a 2‐year clinical follow‐up evaluation and sequential single‐photon emission computed tomography (SPECT), using [123I]β‐CIT as a dopamine transporter ligand, to assess nigrostriatal dopaminergic function at baseline and 2 years from baseline. A validated questionnaire, sensitive to the presence of parkinsonism, was used in the follow‐up of the remaining 283 relatives. Two years from baseline, 10% of the individuals with idiopathic hyposmia, who also had strongly reduced [123I]β‐CIT binding at baseline, had developed clinical PD as opposed to none of the other relatives in the cohort. In the remaining nonparkinsonian hyposmic relatives, the average rate of decline in dopamine transporter binding was significantly higher than in the normosmic relatives. These results indicate that idiopathic olfactory dysfunction is associated with an increased risk of developing PD of at least 10%. Ann Neurol 2004
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DOI: 10.1002/ana.20160
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In an effort to determine whether otherwise unexplained (idiopathic) olfactory dysfunction is associated with an increased risk of developing PD, we designed a prospective study in a cohort of 361 asymptomatic relatives (parents, siblings, or children) of PD patients. A combination of olfactory detection, identification, and discrimination tasks was used to select groups of hyposmic (n = 40) and normosmic (n = 38) individuals for a 2‐year clinical follow‐up evaluation and sequential single‐photon emission computed tomography (SPECT), using [123I]β‐CIT as a dopamine transporter ligand, to assess nigrostriatal dopaminergic function at baseline and 2 years from baseline. A validated questionnaire, sensitive to the presence of parkinsonism, was used in the follow‐up of the remaining 283 relatives. Two years from baseline, 10% of the individuals with idiopathic hyposmia, who also had strongly reduced [123I]β‐CIT binding at baseline, had developed clinical PD as opposed to none of the other relatives in the cohort. In the remaining nonparkinsonian hyposmic relatives, the average rate of decline in dopamine transporter binding was significantly higher than in the normosmic relatives. These results indicate that idiopathic olfactory dysfunction is associated with an increased risk of developing PD of at least 10%. Ann Neurol 2004</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Mirthe M. Ponsen MD</name><affiliations><json:string>Research Institute Neurosciences Vrije Universiteit, Department of Neurology, VU University Medical Center Amsterdam, The Netherlands</json:string></affiliations></json:item><json:item><name>Diederick Stoffers MA</name><affiliations><json:string>Research Institute Neurosciences Vrije Universiteit, Department of Neurology, VU University Medical Center Amsterdam, The Netherlands</json:string><json:string>Department of Clinical Neuropsychology, Vrije Universiteit, Amsterdam, The Netherlands</json:string></affiliations></json:item><json:item><name>Jan Booij MD, PhD</name><affiliations><json:string>Department of Nuclear Medicine, Academic Medical Center, Amsterdam, The Netherlands</json:string></affiliations></json:item><json:item><name>Berthe L. 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Two years from baseline, 10% of the individuals with idiopathic hyposmia, who also had strongly reduced [123I]β‐CIT binding at baseline, had developed clinical PD as opposed to none of the other relatives in the cohort. In the remaining nonparkinsonian hyposmic relatives, the average rate of decline in dopamine transporter binding was significantly higher than in the normosmic relatives. These results indicate that idiopathic olfactory dysfunction is associated with an increased risk of developing PD of at least 10%. 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In an effort to determine whether otherwise unexplained (idiopathic) olfactory dysfunction is associated with an increased risk of developing PD, we designed a prospective study in a cohort of 361 asymptomatic relatives (parents, siblings, or children) of PD patients. A combination of olfactory detection, identification, and discrimination tasks was used to select groups of hyposmic (n = 40) and normosmic (n = 38) individuals for a 2‐year clinical follow‐up evaluation and sequential single‐photon emission computed tomography (SPECT), using [123I]β‐CIT as a dopamine transporter ligand, to assess nigrostriatal dopaminergic function at baseline and 2 years from baseline. A validated questionnaire, sensitive to the presence of parkinsonism, was used in the follow‐up of the remaining 283 relatives. Two years from baseline, 10% of the individuals with idiopathic hyposmia, who also had strongly reduced [123I]β‐CIT binding at baseline, had developed clinical PD as opposed to none of the other relatives in the cohort. In the remaining nonparkinsonian hyposmic relatives, the average rate of decline in dopamine transporter binding was significantly higher than in the normosmic relatives. These results indicate that idiopathic olfactory dysfunction is associated with an increased risk of developing PD of at least 10%. 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F.</givenNames><familyName>van Eck‐Smit</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Erik Ch.</givenNames><familyName>Wolters</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Henk W.</givenNames><familyName>Berendse</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="NL" type="organization"><unparsedAffiliation>Research Institute Neurosciences Vrije Universiteit, Department of Neurology, VU University Medical Center Amsterdam, The Netherlands</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="NL" type="organization"><unparsedAffiliation>Department of Clinical Neuropsychology, Vrije Universiteit, Amsterdam, The Netherlands</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="NL" type="organization"><unparsedAffiliation>Department of Nuclear Medicine, Academic Medical Center, Amsterdam, The Netherlands</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>ZorgOnderzoek Nederland</fundingAgency><fundingNumber>28‐3062‐1</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Olfactory dysfunction is an early and common symptom in Parkinson's disease (PD). In an effort to determine whether otherwise unexplained (idiopathic) olfactory dysfunction is associated with an increased risk of developing PD, we designed a prospective study in a cohort of 361 asymptomatic relatives (parents, siblings, or children) of PD patients. A combination of olfactory detection, identification, and discrimination tasks was used to select groups of hyposmic (n = 40) and normosmic (n = 38) individuals for a 2‐year clinical follow‐up evaluation and sequential single‐photon emission computed tomography (SPECT), using [<sup>123</sup>I]β‐CIT as a dopamine transporter ligand, to assess nigrostriatal dopaminergic function at baseline and 2 years from baseline. A validated questionnaire, sensitive to the presence of parkinsonism, was used in the follow‐up of the remaining 283 relatives. Two years from baseline, 10% of the individuals with idiopathic hyposmia, who also had strongly reduced [<sup>123</sup>I]β‐CIT binding at baseline, had developed clinical PD as opposed to none of the other relatives in the cohort. In the remaining nonparkinsonian hyposmic relatives, the average rate of decline in dopamine transporter binding was significantly higher than in the normosmic relatives. These results indicate that idiopathic olfactory dysfunction is associated with an increased risk of developing PD of at least 10%. Ann Neurol 2004</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Idiopathic hyposmia as a preclinical sign of Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Hyposmia Increases Risk of PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Idiopathic hyposmia as a preclinical sign of Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Mirthe M.</namePart><namePart type="family">Ponsen</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Research Institute Neurosciences Vrije Universiteit, Department of Neurology, VU University Medical Center Amsterdam, The Netherlands</affiliation><description>Correspondence: Research Institute Neurosciences VU, Department of Neurology, VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Diederick</namePart><namePart type="family">Stoffers</namePart><namePart type="termsOfAddress">MA</namePart><affiliation>Research Institute Neurosciences Vrije Universiteit, Department of Neurology, VU University Medical Center Amsterdam, The Netherlands</affiliation><affiliation>Department of Clinical Neuropsychology, Vrije Universiteit, Amsterdam, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan</namePart><namePart type="family">Booij</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Nuclear Medicine, Academic Medical Center, Amsterdam, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Berthe L. F.</namePart><namePart type="family">van Eck‐Smit</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Nuclear Medicine, Academic Medical Center, Amsterdam, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Erik Ch.</namePart><namePart type="family">Wolters</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Research Institute Neurosciences Vrije Universiteit, Department of Neurology, VU University Medical Center Amsterdam, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Henk W.</namePart><namePart type="family">Berendse</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Research Institute Neurosciences Vrije Universiteit, Department of Neurology, VU University Medical Center Amsterdam, The Netherlands</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">2004-08</dateIssued><dateCaptured encoding="w3cdtf">2003-12-08</dateCaptured><dateValid encoding="w3cdtf">2004-04-18</dateValid><copyrightDate encoding="w3cdtf">2004</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">4</extent><extent unit="tables">4</extent><extent unit="references">38</extent><extent unit="words">5737</extent></physicalDescription><abstract lang="en">Olfactory dysfunction is an early and common symptom in Parkinson's disease (PD). In an effort to determine whether otherwise unexplained (idiopathic) olfactory dysfunction is associated with an increased risk of developing PD, we designed a prospective study in a cohort of 361 asymptomatic relatives (parents, siblings, or children) of PD patients. A combination of olfactory detection, identification, and discrimination tasks was used to select groups of hyposmic (n = 40) and normosmic (n = 38) individuals for a 2‐year clinical follow‐up evaluation and sequential single‐photon emission computed tomography (SPECT), using [123I]β‐CIT as a dopamine transporter ligand, to assess nigrostriatal dopaminergic function at baseline and 2 years from baseline. A validated questionnaire, sensitive to the presence of parkinsonism, was used in the follow‐up of the remaining 283 relatives. Two years from baseline, 10% of the individuals with idiopathic hyposmia, who also had strongly reduced [123I]β‐CIT binding at baseline, had developed clinical PD as opposed to none of the other relatives in the cohort. In the remaining nonparkinsonian hyposmic relatives, the average rate of decline in dopamine transporter binding was significantly higher than in the normosmic relatives. These results indicate that idiopathic olfactory dysfunction is associated with an increased risk of developing PD of at least 10%. Ann Neurol 2004</abstract><note type="funding">ZorgOnderzoek Nederland - No. 28‐3062‐1; </note><relatedItem type="host"><titleInfo><title>Annals of Neurology</title><subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>56</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>173</start><end>181</end><total>9</total></extent></part></relatedItem><identifier type="istex">2CFD60A7F4B38A6BC5CE517081EBCB0B056A68EB</identifier><identifier type="DOI">10.1002/ana.20160</identifier><identifier type="ArticleID">ANA20160</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 American Neurological Association</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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