Odor identification deficits identify Parkinson's disease patients with poor cognitive performance
Identifieur interne : 001798 ( Main/Corpus ); précédent : 001797; suivant : 001799Odor identification deficits identify Parkinson's disease patients with poor cognitive performance
Auteurs : Malene Flensborg Damholdt ; Per Borghammer ; Lars Larsen ; Karen StergaardSource :
- Movement Disorders [ 0885-3185 ] ; 2011-09.
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- KwdEn :
Abstract
Olfactory dysfunction is a prodromal and prevalent nonmotor symptom of Parkinson's disease. Unlike olfactory dysfunction in Alzheimer's disease, it is believed to be unrelated to cognitive impairment. However, recent research has implicated cholinergic denervation in Parkinson's disease hyposmia and linked it to verbal memory. This research hypothesized that severe odor identification deficits may identify patients with Parkinson's disease at risk for cognitive impairment. The current study tested this hypothesis by comparing 24 functionally anosmic, nondemented patients with Parkinson's disease and 39 nonanosmic, nondemented patients with Parkinson's disease with 29 healthy control participants on composite scores of memory, processing speed, executive function, and language. The functionally anosmic group had significantly poorer visual and verbal memory than the nonanosmic group, which was indistinguishable from the control group. Furthermore, the functionally anosmic group had reduced processing speed compared with the nonanosmic patients with Parkinson's disease, who, in turn, were outperformed by the control group. On the composite language score, the score of the functionally anosmic group was significantly reduced compared with that of the control group, whereas the nonanosmic group scored in the medium range. The 2 patient groups did not differ on executive functioning. These findings demonstrate co‐occurrence between reduced cognitive function and olfactory deficits in functionally anosmic patients with Parkinson's disease and support the notion of more severe cognitive deficits in this group. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23782
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Unlike olfactory dysfunction in Alzheimer's disease, it is believed to be unrelated to cognitive impairment. However, recent research has implicated cholinergic denervation in Parkinson's disease hyposmia and linked it to verbal memory. This research hypothesized that severe odor identification deficits may identify patients with Parkinson's disease at risk for cognitive impairment. The current study tested this hypothesis by comparing 24 functionally anosmic, nondemented patients with Parkinson's disease and 39 nonanosmic, nondemented patients with Parkinson's disease with 29 healthy control participants on composite scores of memory, processing speed, executive function, and language. The functionally anosmic group had significantly poorer visual and verbal memory than the nonanosmic group, which was indistinguishable from the control group. Furthermore, the functionally anosmic group had reduced processing speed compared with the nonanosmic patients with Parkinson's disease, who, in turn, were outperformed by the control group. On the composite language score, the score of the functionally anosmic group was significantly reduced compared with that of the control group, whereas the nonanosmic group scored in the medium range. The 2 patient groups did not differ on executive functioning. These findings demonstrate co‐occurrence between reduced cognitive function and olfactory deficits in functionally anosmic patients with Parkinson's disease and support the notion of more severe cognitive deficits in this group. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Malene Flensborg Damholdt PhD, MSc</name><affiliations><json:string>Department of Psychology, Aarhus University, Aarhus, Denmark</json:string></affiliations></json:item><json:item><name>Per Borghammer MD, PhD</name><affiliations><json:string>Department of Nuclear Medicine, Aarhus University Hospitals, Aarhus, Denmark</json:string></affiliations></json:item><json:item><name>Lars Larsen PhD, MSc</name><affiliations><json:string>Department of Psychology, Aarhus University, Aarhus, Denmark</json:string></affiliations></json:item><json:item><name>Karen Østergaard MD, PhD, DMSc</name><affiliations><json:string>Department of Neurology, Aarhus University Hospitals, Aarhus, Denmark</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>cognition</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>odor identification</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>olfaction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item></subject><articleId><json:string>MDS23782</json:string></articleId><language><json:string>eng</json:string></language><abstract>Olfactory dysfunction is a prodromal and prevalent nonmotor symptom of Parkinson's disease. Unlike olfactory dysfunction in Alzheimer's disease, it is believed to be unrelated to cognitive impairment. However, recent research has implicated cholinergic denervation in Parkinson's disease hyposmia and linked it to verbal memory. This research hypothesized that severe odor identification deficits may identify patients with Parkinson's disease at risk for cognitive impairment. The current study tested this hypothesis by comparing 24 functionally anosmic, nondemented patients with Parkinson's disease and 39 nonanosmic, nondemented patients with Parkinson's disease with 29 healthy control participants on composite scores of memory, processing speed, executive function, and language. The functionally anosmic group had significantly poorer visual and verbal memory than the nonanosmic group, which was indistinguishable from the control group. Furthermore, the functionally anosmic group had reduced processing speed compared with the nonanosmic patients with Parkinson's disease, who, in turn, were outperformed by the control group. On the composite language score, the score of the functionally anosmic group was significantly reduced compared with that of the control group, whereas the nonanosmic group scored in the medium range. The 2 patient groups did not differ on executive functioning. 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Unlike olfactory dysfunction in Alzheimer's disease, it is believed to be unrelated to cognitive impairment. However, recent research has implicated cholinergic denervation in Parkinson's disease hyposmia and linked it to verbal memory. This research hypothesized that severe odor identification deficits may identify patients with Parkinson's disease at risk for cognitive impairment. The current study tested this hypothesis by comparing 24 functionally anosmic, nondemented patients with Parkinson's disease and 39 nonanosmic, nondemented patients with Parkinson's disease with 29 healthy control participants on composite scores of memory, processing speed, executive function, and language. The functionally anosmic group had significantly poorer visual and verbal memory than the nonanosmic group, which was indistinguishable from the control group. Furthermore, the functionally anosmic group had reduced processing speed compared with the nonanosmic patients with Parkinson's disease, who, in turn, were outperformed by the control group. On the composite language score, the score of the functionally anosmic group was significantly reduced compared with that of the control group, whereas the nonanosmic group scored in the medium range. The 2 patient groups did not differ on executive functioning. 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Unlike olfactory dysfunction in Alzheimer's disease, it is believed to be unrelated to cognitive impairment. However, recent research has implicated cholinergic denervation in Parkinson's disease hyposmia and linked it to verbal memory. This research hypothesized that severe odor identification deficits may identify patients with Parkinson's disease at risk for cognitive impairment. The current study tested this hypothesis by comparing 24 functionally anosmic, nondemented patients with Parkinson's disease and 39 nonanosmic, nondemented patients with Parkinson's disease with 29 healthy control participants on composite scores of memory, processing speed, executive function, and language. The functionally anosmic group had significantly poorer visual and verbal memory than the nonanosmic group, which was indistinguishable from the control group. Furthermore, the functionally anosmic group had reduced processing speed compared with the nonanosmic patients with Parkinson's disease, who, in turn, were outperformed by the control group. On the composite language score, the score of the functionally anosmic group was significantly reduced compared with that of the control group, whereas the nonanosmic group scored in the medium range. The 2 patient groups did not differ on executive functioning. These findings demonstrate co‐occurrence between reduced cognitive function and olfactory deficits in functionally anosmic patients with Parkinson's disease and support the notion of more severe cognitive deficits in this group. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Relevant conflicts of interest/financial disclosures:</b> Nothing to report.</p></note><note xml:id="fn2"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Odor identification deficits identify Parkinson's disease patients with poor cognitive performance</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Odor Id Deficits and Poor Cognition in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Odor identification deficits identify Parkinson's disease patients with poor cognitive performance</title></titleInfo><name type="personal"><namePart type="given">Malene Flensborg</namePart><namePart type="family">Damholdt</namePart><namePart type="termsOfAddress">PhD, MSc</namePart><affiliation>Department of Psychology, Aarhus University, Aarhus, Denmark</affiliation><description>Correspondence: Department of Psychology, Aarhus University, Jens Chr. Skous Vej 4, 8000 Aarhus C, Denmark</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Per</namePart><namePart type="family">Borghammer</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Nuclear Medicine, Aarhus University Hospitals, Aarhus, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lars</namePart><namePart type="family">Larsen</namePart><namePart type="termsOfAddress">PhD, MSc</namePart><affiliation>Department of Psychology, Aarhus University, Aarhus, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karen</namePart><namePart type="family">Østergaard</namePart><namePart type="termsOfAddress">MD, PhD, DMSc</namePart><affiliation>Department of Neurology, Aarhus University Hospitals, Aarhus, Denmark</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">2011-09</dateIssued><dateCaptured encoding="w3cdtf">2010-12-17</dateCaptured><dateValid encoding="w3cdtf">2011-04-11</dateValid><copyrightDate encoding="w3cdtf">2011</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="tables">2</extent><extent unit="references">44</extent><extent unit="words">5916</extent></physicalDescription><abstract lang="en">Olfactory dysfunction is a prodromal and prevalent nonmotor symptom of Parkinson's disease. Unlike olfactory dysfunction in Alzheimer's disease, it is believed to be unrelated to cognitive impairment. However, recent research has implicated cholinergic denervation in Parkinson's disease hyposmia and linked it to verbal memory. This research hypothesized that severe odor identification deficits may identify patients with Parkinson's disease at risk for cognitive impairment. The current study tested this hypothesis by comparing 24 functionally anosmic, nondemented patients with Parkinson's disease and 39 nonanosmic, nondemented patients with Parkinson's disease with 29 healthy control participants on composite scores of memory, processing speed, executive function, and language. The functionally anosmic group had significantly poorer visual and verbal memory than the nonanosmic group, which was indistinguishable from the control group. Furthermore, the functionally anosmic group had reduced processing speed compared with the nonanosmic patients with Parkinson's disease, who, in turn, were outperformed by the control group. On the composite language score, the score of the functionally anosmic group was significantly reduced compared with that of the control group, whereas the nonanosmic group scored in the medium range. The 2 patient groups did not differ on executive functioning. These findings demonstrate co‐occurrence between reduced cognitive function and olfactory deficits in functionally anosmic patients with Parkinson's disease and support the notion of more severe cognitive deficits in this group. © 2011 Movement Disorder Society</abstract><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>cognition</topic><topic>odor identification</topic><topic>olfaction</topic><topic>Parkinson's disease</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</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>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>2045</start><end>2050</end><total>6</total></extent></part></relatedItem><identifier type="istex">AFAC657F8CFEB08DC807877D649F79D1ECBA4AAF</identifier><identifier type="DOI">10.1002/mds.23782</identifier><identifier type="ArticleID">MDS23782</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 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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