Association of olfactory dysfunction and brain. Metabolism in Parkinson's disease
Identifieur interne : 001935 ( Main/Corpus ); précédent : 001934; suivant : 001936Association of olfactory dysfunction and brain. Metabolism in Parkinson's disease
Auteurs : Toru Baba ; Atsushi Takeda ; Akio Kikuchi ; Yoshiyuki Nishio ; Yoshiyuki Hosokai ; Kazumi Hirayama ; Takafumi Hasegawa ; Naoto Sugeno ; Kyoko Suzuki ; Etsuro Mori ; Shoki Takahashi ; Hiroshi Fukuda ; Yasuto ItoyamaSource :
- Movement Disorders [ 0885-3185 ] ; 2011-03.
English descriptors
Abstract
Hyposmia is one of the cardinal early symptoms of Parkinson disease (PD). Accumulating clinical and pathological evidence suggests that dysfunction of the olfactory‐related cortices may be responsible for the impaired olfactory processing observed in PD; however, there are no clear data showing a direct association between altered brain metabolism and hyposmia in PD. In this study, we evaluated brain glucose metabolism and smell‐identification ability in 69 Japanese patients with nondemented PD. Olfactory function was assessed using the Odor Stick Identification Test for Japanese. The regional cerebral metabolic rate of glucose consumption at rest was measured using 18F‐fluorodeoxyglucose positron emission tomography and was analyzed using SPM‐based group comparisons and the brain–behavior partial least‐squares method. We found that olfactory dysfunction was closely related to cognitive dysfunction, including memory impairment. Moreover, brain–behavior partial least‐squares analysis revealed that odor‐identification performance was closely associated with broad cortical dysfunction, including dysfunction of the piriform cortex and amygdala. Our results suggest that the cognitive deficit in olfactory perception is an important aspect of hyposmia in PD and that this deficit is caused by altered brain metabolism in the amygdala and piriform cortex. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23602
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ISTEX:E7EF91B718D8B797727CF69D72E0EB6A3240F025Le document en format XML
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Metabolism in Parkinson's disease</title><author><name sortKey="Baba, Toru" sort="Baba, Toru" uniqKey="Baba T" first="Toru" last="Baba">Toru Baba</name><affiliation><mods:affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</mods:affiliation></affiliation></author><author><name sortKey="Takeda, Atsushi" sort="Takeda, Atsushi" uniqKey="Takeda A" first="Atsushi" last="Takeda">Atsushi Takeda</name><affiliation><mods:affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kikuchi, Akio" sort="Kikuchi, Akio" uniqKey="Kikuchi A" first="Akio" last="Kikuchi">Akio Kikuchi</name><affiliation><mods:affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nishio, Yoshiyuki" sort="Nishio, Yoshiyuki" uniqKey="Nishio Y" first="Yoshiyuki" last="Nishio">Yoshiyuki Nishio</name><affiliation><mods:affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hosokai, Yoshiyuki" sort="Hosokai, Yoshiyuki" uniqKey="Hosokai Y" first="Yoshiyuki" last="Hosokai">Yoshiyuki Hosokai</name><affiliation><mods:affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hirayama, Kazumi" sort="Hirayama, Kazumi" uniqKey="Hirayama K" first="Kazumi" last="Hirayama">Kazumi Hirayama</name><affiliation><mods:affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Occupational Therapy, Yamagata Prefectural University of Health Sciences, Yamagata, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hasegawa, Takafumi" sort="Hasegawa, Takafumi" uniqKey="Hasegawa T" first="Takafumi" last="Hasegawa">Takafumi Hasegawa</name><affiliation><mods:affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</mods:affiliation></affiliation></author><author><name sortKey="Sugeno, Naoto" sort="Sugeno, Naoto" uniqKey="Sugeno N" first="Naoto" last="Sugeno">Naoto Sugeno</name><affiliation><mods:affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</mods:affiliation></affiliation></author><author><name sortKey="Suzuki, Kyoko" sort="Suzuki, Kyoko" uniqKey="Suzuki K" first="Kyoko" last="Suzuki">Kyoko Suzuki</name><affiliation><mods:affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Clinical Neuroscience, Yamagata University, Graduate School of Medical Science, Yamagata, Japan</mods:affiliation></affiliation></author><author><name sortKey="Mori, Etsuro" sort="Mori, Etsuro" uniqKey="Mori E" first="Etsuro" last="Mori">Etsuro Mori</name><affiliation><mods:affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</mods:affiliation></affiliation></author><author><name sortKey="Takahashi, Shoki" sort="Takahashi, Shoki" uniqKey="Takahashi S" first="Shoki" last="Takahashi">Shoki Takahashi</name><affiliation><mods:affiliation>Department of Diagnostic Radiology, Tohoku University Graduate School of Medicine, Sendai, Japan</mods:affiliation></affiliation></author><author><name sortKey="Fukuda, Hiroshi" sort="Fukuda, Hiroshi" uniqKey="Fukuda H" first="Hiroshi" last="Fukuda">Hiroshi Fukuda</name><affiliation><mods:affiliation>Department of Nuclear Medicine and Radiology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan</mods:affiliation></affiliation></author><author><name sortKey="Itoyama, Yasuto" sort="Itoyama, Yasuto" uniqKey="Itoyama Y" first="Yasuto" last="Itoyama">Yasuto Itoyama</name><affiliation><mods:affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-03">2011-03</date><biblScope unit="volume">26</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="621">621</biblScope><biblScope unit="page" to="628">628</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">E7EF91B718D8B797727CF69D72E0EB6A3240F025</idno><idno type="DOI">10.1002/mds.23602</idno><idno type="ArticleID">MDS23602</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>PET, amygdala</term><term>cluster analysis</term><term>hyposmia</term><term>piriform cortex</term><term>spatial covariance analysis</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Hyposmia is one of the cardinal early symptoms of Parkinson disease (PD). Accumulating clinical and pathological evidence suggests that dysfunction of the olfactory‐related cortices may be responsible for the impaired olfactory processing observed in PD; however, there are no clear data showing a direct association between altered brain metabolism and hyposmia in PD. In this study, we evaluated brain glucose metabolism and smell‐identification ability in 69 Japanese patients with nondemented PD. Olfactory function was assessed using the Odor Stick Identification Test for Japanese. The regional cerebral metabolic rate of glucose consumption at rest was measured using 18F‐fluorodeoxyglucose positron emission tomography and was analyzed using SPM‐based group comparisons and the brain–behavior partial least‐squares method. We found that olfactory dysfunction was closely related to cognitive dysfunction, including memory impairment. Moreover, brain–behavior partial least‐squares analysis revealed that odor‐identification performance was closely associated with broad cortical dysfunction, including dysfunction of the piriform cortex and amygdala. Our results suggest that the cognitive deficit in olfactory perception is an important aspect of hyposmia in PD and that this deficit is caused by altered brain metabolism in the amygdala and piriform cortex. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Toru Baba MD</name><affiliations><json:string>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</json:string></affiliations></json:item><json:item><name>Atsushi Takeda MD</name><affiliations><json:string>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</json:string></affiliations></json:item><json:item><name>Akio Kikuchi MD</name><affiliations><json:string>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</json:string></affiliations></json:item><json:item><name>Yoshiyuki Nishio MD</name><affiliations><json:string>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</json:string></affiliations></json:item><json:item><name>Yoshiyuki Hosokai MD</name><affiliations><json:string>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</json:string></affiliations></json:item><json:item><name>Kazumi Hirayama MD</name><affiliations><json:string>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</json:string><json:string>Department of Occupational Therapy, Yamagata Prefectural University of Health Sciences, Yamagata, Japan</json:string></affiliations></json:item><json:item><name>Takafumi Hasegawa MD</name><affiliations><json:string>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</json:string></affiliations></json:item><json:item><name>Naoto Sugeno MD</name><affiliations><json:string>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</json:string></affiliations></json:item><json:item><name>Kyoko Suzuki MD</name><affiliations><json:string>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</json:string><json:string>Department of Clinical Neuroscience, Yamagata University, Graduate School of Medical Science, Yamagata, Japan</json:string></affiliations></json:item><json:item><name>Etsuro Mori MD</name><affiliations><json:string>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</json:string></affiliations></json:item><json:item><name>Shoki Takahashi MD</name><affiliations><json:string>Department of Diagnostic Radiology, Tohoku University Graduate School of Medicine, Sendai, Japan</json:string></affiliations></json:item><json:item><name>Hiroshi Fukuda MD</name><affiliations><json:string>Department of Nuclear Medicine and Radiology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan</json:string></affiliations></json:item><json:item><name>Yasuto Itoyama MD</name><affiliations><json:string>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>hyposmia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>spatial covariance analysis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cluster analysis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PET, amygdala</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>piriform cortex</value></json:item></subject><articleId><json:string>MDS23602</json:string></articleId><language><json:string>eng</json:string></language><abstract>Hyposmia is one of the cardinal early symptoms of Parkinson disease (PD). Accumulating clinical and pathological evidence suggests that dysfunction of the olfactory‐related cortices may be responsible for the impaired olfactory processing observed in PD; however, there are no clear data showing a direct association between altered brain metabolism and hyposmia in PD. In this study, we evaluated brain glucose metabolism and smell‐identification ability in 69 Japanese patients with nondemented PD. Olfactory function was assessed using the Odor Stick Identification Test for Japanese. The regional cerebral metabolic rate of glucose consumption at rest was measured using 18F‐fluorodeoxyglucose positron emission tomography and was analyzed using SPM‐based group comparisons and the brain–behavior partial least‐squares method. We found that olfactory dysfunction was closely related to cognitive dysfunction, including memory impairment. Moreover, brain–behavior partial least‐squares analysis revealed that odor‐identification performance was closely associated with broad cortical dysfunction, including dysfunction of the piriform cortex and amygdala. Our results suggest that the cognitive deficit in olfactory perception is an important aspect of hyposmia in PD and that this deficit is caused by altered brain metabolism in the amygdala and piriform cortex. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>6.744</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1400</abstractCharCount><pdfWordCount>4464</pdfWordCount><pdfCharCount>29198</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>190</abstractWordCount></qualityIndicators><title>Association of olfactory dysfunction and brain. 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Metabolism in Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: Nothing to report.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Association of olfactory dysfunction and brain. Metabolism in Parkinson's disease</title><author><persName><forename type="first">Toru</forename><surname>Baba</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation></author><author><persName><forename type="first">Atsushi</forename><surname>Takeda</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Department of Neurology, Tohoku University Graduate School of Medicine, 1‐1 Seiryo‐machi, Aoba‐ku, Sendai 980‐8575, Japan</p></note><affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation></author><author><persName><forename type="first">Akio</forename><surname>Kikuchi</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation></author><author><persName><forename type="first">Yoshiyuki</forename><surname>Nishio</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation></author><author><persName><forename type="first">Yoshiyuki</forename><surname>Hosokai</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation></author><author><persName><forename type="first">Kazumi</forename><surname>Hirayama</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><affiliation>Department of Occupational Therapy, Yamagata Prefectural University of Health Sciences, Yamagata, Japan</affiliation></author><author><persName><forename type="first">Takafumi</forename><surname>Hasegawa</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation></author><author><persName><forename type="first">Naoto</forename><surname>Sugeno</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation></author><author><persName><forename type="first">Kyoko</forename><surname>Suzuki</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><affiliation>Department of Clinical Neuroscience, Yamagata University, Graduate School of Medical Science, Yamagata, Japan</affiliation></author><author><persName><forename type="first">Etsuro</forename><surname>Mori</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation></author><author><persName><forename type="first">Shoki</forename><surname>Takahashi</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Diagnostic Radiology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation></author><author><persName><forename type="first">Hiroshi</forename><surname>Fukuda</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Nuclear Medicine and Radiology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan</affiliation></author><author><persName><forename type="first">Yasuto</forename><surname>Itoyama</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-03"></date><biblScope unit="volume">26</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="621">621</biblScope><biblScope unit="page" to="628">628</biblScope></imprint></monogr><idno type="istex">E7EF91B718D8B797727CF69D72E0EB6A3240F025</idno><idno type="DOI">10.1002/mds.23602</idno><idno type="ArticleID">MDS23602</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Hyposmia is one of the cardinal early symptoms of Parkinson disease (PD). Accumulating clinical and pathological evidence suggests that dysfunction of the olfactory‐related cortices may be responsible for the impaired olfactory processing observed in PD; however, there are no clear data showing a direct association between altered brain metabolism and hyposmia in PD. In this study, we evaluated brain glucose metabolism and smell‐identification ability in 69 Japanese patients with nondemented PD. Olfactory function was assessed using the Odor Stick Identification Test for Japanese. The regional cerebral metabolic rate of glucose consumption at rest was measured using 18F‐fluorodeoxyglucose positron emission tomography and was analyzed using SPM‐based group comparisons and the brain–behavior partial least‐squares method. We found that olfactory dysfunction was closely related to cognitive dysfunction, including memory impairment. Moreover, brain–behavior partial least‐squares analysis revealed that odor‐identification performance was closely associated with broad cortical dysfunction, including dysfunction of the piriform cortex and amygdala. Our results suggest that the cognitive deficit in olfactory perception is an important aspect of hyposmia in PD and that this deficit is caused by altered brain metabolism in the amygdala and piriform cortex. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>hyposmia</term></item><item><term>spatial covariance analysis</term></item><item><term>cluster analysis</term></item><item><term>PET, amygdala</term></item><item><term>piriform cortex</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-08-31">Received</change><change when="2010-11-29">Registration</change><change when="2011-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/E7EF91B718D8B797727CF69D72E0EB6A3240F025/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="40"><doi origin="wiley" registered="yes">10.1002/mds.v26.4</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue">4</numbering></numberingGroup><coverDate startDate="2011-03">March 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="110" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23602</doi><idGroup><id type="unit" value="MDS23602"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2011 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2010-08-31"></event><event type="manuscriptRevised" date="2010-11-24"></event><event type="manuscriptAccepted" date="2010-11-29"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.5.2 mode:FullText" date="2011-07-19"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-01-31"></event><event type="publishedOnlineFinalForm" date="2011-04-19"></event><event type="firstOnline" date="2011-01-31"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">621</numbering><numbering type="pageLast">628</numbering></numberingGroup><correspondenceTo>Department of Neurology, Tohoku University Graduate School of Medicine, 1‐1 Seiryo‐machi, Aoba‐ku, Sendai 980‐8575, Japan</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23602.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="39"></count><count type="wordTotal" number="5249"></count></countGroup><titleGroup><title type="main" xml:lang="en">Association of olfactory dysfunction and brain. Metabolism in Parkinson's disease<link href="#fn2"></link></title><title type="short" xml:lang="en">Hyposmia and Brain Metabolism in PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Toru</givenNames><familyName>Baba</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Atsushi</givenNames><familyName>Takeda</familyName><degrees>MD</degrees></personName><contactDetails><email>atakeda@em.neurol.med.tohoku.ac.jp</email></contactDetails></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Akio</givenNames><familyName>Kikuchi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Yoshiyuki</givenNames><familyName>Nishio</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Yoshiyuki</givenNames><familyName>Hosokai</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af2 #af3"><personName><givenNames>Kazumi</givenNames><familyName>Hirayama</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Takafumi</givenNames><familyName>Hasegawa</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Naoto</givenNames><familyName>Sugeno</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af2 #af4"><personName><givenNames>Kyoko</givenNames><familyName>Suzuki</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Etsuro</givenNames><familyName>Mori</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Shoki</givenNames><familyName>Takahashi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au12" creatorRole="author" affiliationRef="#af6"><personName><givenNames>Hiroshi</givenNames><familyName>Fukuda</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au13" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Yasuto</givenNames><familyName>Itoyama</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="JP" type="organization"><unparsedAffiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="JP" type="organization"><unparsedAffiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="JP" type="organization"><unparsedAffiliation>Department of Occupational Therapy, Yamagata Prefectural University of Health Sciences, Yamagata, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="JP" type="organization"><unparsedAffiliation>Department of Clinical Neuroscience, Yamagata University, Graduate School of Medical Science, Yamagata, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="JP" type="organization"><unparsedAffiliation>Department of Diagnostic Radiology, Tohoku University Graduate School of Medicine, Sendai, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="JP" type="organization"><unparsedAffiliation>Department of Nuclear Medicine and Radiology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">hyposmia</keyword><keyword xml:id="kwd2">spatial covariance analysis</keyword><keyword xml:id="kwd3">cluster analysis</keyword><keyword xml:id="kwd4">PET, amygdala</keyword><keyword xml:id="kwd5">piriform cortex</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Hyposmia is one of the cardinal early symptoms of Parkinson disease (PD). Accumulating clinical and pathological evidence suggests that dysfunction of the olfactory‐related cortices may be responsible for the impaired olfactory processing observed in PD; however, there are no clear data showing a direct association between altered brain metabolism and hyposmia in PD. In this study, we evaluated brain glucose metabolism and smell‐identification ability in 69 Japanese patients with nondemented PD. Olfactory function was assessed using the Odor Stick Identification Test for Japanese. The regional cerebral metabolic rate of glucose consumption at rest was measured using <sup>18</sup>F‐fluorodeoxyglucose positron emission tomography and was analyzed using SPM‐based group comparisons and the brain–behavior partial least‐squares method. We found that olfactory dysfunction was closely related to cognitive dysfunction, including memory impairment. Moreover, brain–behavior partial least‐squares analysis revealed that odor‐identification performance was closely associated with broad cortical dysfunction, including dysfunction of the piriform cortex and amygdala. Our results suggest that the cognitive deficit in olfactory perception is an important aspect of hyposmia in PD and that this deficit is caused by altered brain metabolism in the amygdala and piriform cortex. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn2"><p><b>Potential conflict of interest:</b> Nothing to report.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Association of olfactory dysfunction and brain. Metabolism in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Hyposmia and Brain Metabolism in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Association of olfactory dysfunction and brain. Metabolism in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Toru</namePart><namePart type="family">Baba</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Atsushi</namePart><namePart type="family">Takeda</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><description>Correspondence: Department of Neurology, Tohoku University Graduate School of Medicine, 1‐1 Seiryo‐machi, Aoba‐ku, Sendai 980‐8575, Japan</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Akio</namePart><namePart type="family">Kikuchi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yoshiyuki</namePart><namePart type="family">Nishio</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yoshiyuki</namePart><namePart type="family">Hosokai</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kazumi</namePart><namePart type="family">Hirayama</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><affiliation>Department of Occupational Therapy, Yamagata Prefectural University of Health Sciences, Yamagata, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takafumi</namePart><namePart type="family">Hasegawa</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Naoto</namePart><namePart type="family">Sugeno</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kyoko</namePart><namePart type="family">Suzuki</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><affiliation>Department of Clinical Neuroscience, Yamagata University, Graduate School of Medical Science, Yamagata, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Etsuro</namePart><namePart type="family">Mori</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Behavioral Neurology and Cognitive Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shoki</namePart><namePart type="family">Takahashi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Diagnostic Radiology, Tohoku University Graduate School of Medicine, Sendai, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hiroshi</namePart><namePart type="family">Fukuda</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Nuclear Medicine and Radiology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yasuto</namePart><namePart type="family">Itoyama</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan</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">2011-03</dateIssued><dateCaptured encoding="w3cdtf">2010-08-31</dateCaptured><dateValid encoding="w3cdtf">2010-11-29</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="figures">4</extent><extent unit="tables">1</extent><extent unit="references">39</extent><extent unit="words">5249</extent></physicalDescription><abstract lang="en">Hyposmia is one of the cardinal early symptoms of Parkinson disease (PD). Accumulating clinical and pathological evidence suggests that dysfunction of the olfactory‐related cortices may be responsible for the impaired olfactory processing observed in PD; however, there are no clear data showing a direct association between altered brain metabolism and hyposmia in PD. In this study, we evaluated brain glucose metabolism and smell‐identification ability in 69 Japanese patients with nondemented PD. Olfactory function was assessed using the Odor Stick Identification Test for Japanese. The regional cerebral metabolic rate of glucose consumption at rest was measured using 18F‐fluorodeoxyglucose positron emission tomography and was analyzed using SPM‐based group comparisons and the brain–behavior partial least‐squares method. We found that olfactory dysfunction was closely related to cognitive dysfunction, including memory impairment. Moreover, brain–behavior partial least‐squares analysis revealed that odor‐identification performance was closely associated with broad cortical dysfunction, including dysfunction of the piriform cortex and amygdala. Our results suggest that the cognitive deficit in olfactory perception is an important aspect of hyposmia in PD and that this deficit is caused by altered brain metabolism in the amygdala and piriform cortex. © 2011 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Nothing to report.</note><subject lang="en"><genre>Keywords</genre><topic>hyposmia</topic><topic>spatial covariance analysis</topic><topic>cluster analysis</topic><topic>PET, amygdala</topic><topic>piriform cortex</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. 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