Olfactory deficits and cardiac 123I‐MIBG in Parkinson's disease related to the LRRK2 R1441G and G2019S mutations
Identifieur interne : 000795 ( Istex/Corpus ); précédent : 000794; suivant : 000796Olfactory deficits and cardiac 123I‐MIBG in Parkinson's disease related to the LRRK2 R1441G and G2019S mutations
Auteurs : Javier Ruiz-Martínez ; Ana Gorostidi ; Estibaliz Goyenechea ; Ainhoa Alzualde ; Juan José Poza ; Francisco Rodríguez ; Alberto Bergareche ; Fermín Moreno ; Adolfo L Pez De Munain ; José F. Martí MassSource :
- Movement Disorders [ 0885-3185 ] ; 2011-09.
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- KwdEn :
Abstract
It has been proposed that olfactory tests and metaiodobenzylguanidine cardiac scintigraphy may help diagnose idiopathic Parkinson's disease in the premotor phase. However, it is not clear what value these tests have in all patients with Parkinson's disease and, particularly, in those who carry mutations in LRRK2. The objective was to analyze olfactory dysfunction and the changes in cardiac I‐metaiodobenzylguanidine uptake in patients with Parkinson's disease carrying the R1441G and G2019S mutations in LRRK2, and in patients with Parkinson's disease with no known mutations. Patients with Parkinson's disease were screened for R1441G and G2019S LRRK2 gene mutations and classified as LRRK2 mutation carriers or noncarriers. A total of 190 patients with Parkinson's disease (44 LRRK2 mutation carriers) were tested for olfactory dysfunction using the Brief Smell Identification Test. Cardiac 123I‐metaiodobenzylguanidine scintigraphy was performed on 90 patients with Parkinson's disease (27 LRRK2 mutation carriers). Thirty‐six percent of patients with LRRK2 mutations have hyposmia, compared to 75% of noncarrier patients with Parkinson's disease (P < .001). Sixty‐six percent of LRRK2 mutation carriers have low early metaiodobenzylguanidine uptake, compared to 86% of noncarriers (P = .048). Similarly, the heart/mediastinum ratio in delayed metaiodobenzylguanidine images appeared to differ between these groups of patients with Parkinson's disease, although these results did not reach statistical significance. The data obtained indicate that olfactory and cardiac impairment is less prevalent when Parkinson's disease is associated with mutations in LRRK2, although the underlying mechanisms for this difference remain unclear. Thus, such screening would be less useful to detect the premotor phase in asymptomatic relatives who carry mutations in LRRK2 than in cases not associated with LRRK2. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23773
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Olfactory deficits and cardiac 123I‐MIBG in Parkinson's disease related to the LRRK2 R1441G and G2019S mutations</title><author><name sortKey="Ruiz Artinez, Javier" sort="Ruiz Artinez, Javier" uniqKey="Ruiz Artinez J" first="Javier" last="Ruiz-Martínez">Javier Ruiz-Martínez</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation><affiliation><mods:affiliation>Centro de Investigación Biomédica en Red para Enfermedades Neurodegenerativas (CIBERNED), Carlos III Health Institute, Madrid, Spain</mods:affiliation></affiliation></author><author><name sortKey="Gorostidi, Ana" sort="Gorostidi, Ana" uniqKey="Gorostidi A" first="Ana" last="Gorostidi">Ana Gorostidi</name><affiliation><mods:affiliation>Neurogenetics Laboratory, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Goyenechea, Estibaliz" sort="Goyenechea, Estibaliz" uniqKey="Goyenechea E" first="Estibaliz" last="Goyenechea">Estibaliz Goyenechea</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Alzualde, Ainhoa" sort="Alzualde, Ainhoa" uniqKey="Alzualde A" first="Ainhoa" last="Alzualde">Ainhoa Alzualde</name><affiliation><mods:affiliation>Neurogenetics Laboratory, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Poza, Juan Jose" sort="Poza, Juan Jose" uniqKey="Poza J" first="Juan José" last="Poza">Juan José Poza</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Rodriguez, Francisco" sort="Rodriguez, Francisco" uniqKey="Rodriguez F" first="Francisco" last="Rodríguez">Francisco Rodríguez</name><affiliation><mods:affiliation>Nuclear Medicine Department, Onkologikoa, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Bergareche, Alberto" sort="Bergareche, Alberto" uniqKey="Bergareche A" first="Alberto" last="Bergareche">Alberto Bergareche</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Moreno, Fermin" sort="Moreno, Fermin" uniqKey="Moreno F" first="Fermín" last="Moreno">Fermín Moreno</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="L Pez De Munain, Adolfo" sort="L Pez De Munain, Adolfo" uniqKey="L Pez De Munain A" first="Adolfo" last="L Pez De Munain">Adolfo L Pez De Munain</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Marti Mass, Jose F" sort="Marti Mass, Jose F" uniqKey="Marti Mass J" first="José F." last="Martí Mass">José F. Martí Mass</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:31920B7096B87B810017537D1A39A1CACC347B6A</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/mds.23773</idno><idno type="url">https://api.istex.fr/document/31920B7096B87B810017537D1A39A1CACC347B6A/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000795</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Olfactory deficits and cardiac 123I‐MIBG in Parkinson's disease related to the LRRK2 R1441G and G2019S mutations</title><author><name sortKey="Ruiz Artinez, Javier" sort="Ruiz Artinez, Javier" uniqKey="Ruiz Artinez J" first="Javier" last="Ruiz-Martínez">Javier Ruiz-Martínez</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation><affiliation><mods:affiliation>Centro de Investigación Biomédica en Red para Enfermedades Neurodegenerativas (CIBERNED), Carlos III Health Institute, Madrid, Spain</mods:affiliation></affiliation></author><author><name sortKey="Gorostidi, Ana" sort="Gorostidi, Ana" uniqKey="Gorostidi A" first="Ana" last="Gorostidi">Ana Gorostidi</name><affiliation><mods:affiliation>Neurogenetics Laboratory, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Goyenechea, Estibaliz" sort="Goyenechea, Estibaliz" uniqKey="Goyenechea E" first="Estibaliz" last="Goyenechea">Estibaliz Goyenechea</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Alzualde, Ainhoa" sort="Alzualde, Ainhoa" uniqKey="Alzualde A" first="Ainhoa" last="Alzualde">Ainhoa Alzualde</name><affiliation><mods:affiliation>Neurogenetics Laboratory, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Poza, Juan Jose" sort="Poza, Juan Jose" uniqKey="Poza J" first="Juan José" last="Poza">Juan José Poza</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Rodriguez, Francisco" sort="Rodriguez, Francisco" uniqKey="Rodriguez F" first="Francisco" last="Rodríguez">Francisco Rodríguez</name><affiliation><mods:affiliation>Nuclear Medicine Department, Onkologikoa, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Bergareche, Alberto" sort="Bergareche, Alberto" uniqKey="Bergareche A" first="Alberto" last="Bergareche">Alberto Bergareche</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Moreno, Fermin" sort="Moreno, Fermin" uniqKey="Moreno F" first="Fermín" last="Moreno">Fermín Moreno</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="L Pez De Munain, Adolfo" sort="L Pez De Munain, Adolfo" uniqKey="L Pez De Munain A" first="Adolfo" last="L Pez De Munain">Adolfo L Pez De Munain</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</mods:affiliation></affiliation></author><author><name sortKey="Marti Mass, Jose F" sort="Marti Mass, Jose F" uniqKey="Marti Mass J" first="José F." last="Martí Mass">José F. Martí Mass</name><affiliation><mods:affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</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="2011-09">2011-09</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="2026">2026</biblScope><biblScope unit="page" to="2031">2031</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">31920B7096B87B810017537D1A39A1CACC347B6A</idno><idno type="DOI">10.1002/mds.23773</idno><idno type="ArticleID">MDS23773</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>LRRK2</term><term>Parkinson's disease</term><term>dardarin</term><term>hyposmia</term><term>metaiodobenzylguanidine</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">It has been proposed that olfactory tests and metaiodobenzylguanidine cardiac scintigraphy may help diagnose idiopathic Parkinson's disease in the premotor phase. However, it is not clear what value these tests have in all patients with Parkinson's disease and, particularly, in those who carry mutations in LRRK2. The objective was to analyze olfactory dysfunction and the changes in cardiac I‐metaiodobenzylguanidine uptake in patients with Parkinson's disease carrying the R1441G and G2019S mutations in LRRK2, and in patients with Parkinson's disease with no known mutations. Patients with Parkinson's disease were screened for R1441G and G2019S LRRK2 gene mutations and classified as LRRK2 mutation carriers or noncarriers. A total of 190 patients with Parkinson's disease (44 LRRK2 mutation carriers) were tested for olfactory dysfunction using the Brief Smell Identification Test. Cardiac 123I‐metaiodobenzylguanidine scintigraphy was performed on 90 patients with Parkinson's disease (27 LRRK2 mutation carriers). Thirty‐six percent of patients with LRRK2 mutations have hyposmia, compared to 75% of noncarrier patients with Parkinson's disease (P < .001). Sixty‐six percent of LRRK2 mutation carriers have low early metaiodobenzylguanidine uptake, compared to 86% of noncarriers (P = .048). Similarly, the heart/mediastinum ratio in delayed metaiodobenzylguanidine images appeared to differ between these groups of patients with Parkinson's disease, although these results did not reach statistical significance. The data obtained indicate that olfactory and cardiac impairment is less prevalent when Parkinson's disease is associated with mutations in LRRK2, although the underlying mechanisms for this difference remain unclear. Thus, such screening would be less useful to detect the premotor phase in asymptomatic relatives who carry mutations in LRRK2 than in cases not associated with LRRK2. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Javier Ruiz‐Martínez MD</name><affiliations><json:string>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</json:string><json:string>Centro de Investigación Biomédica en Red para Enfermedades Neurodegenerativas (CIBERNED), Carlos III Health Institute, Madrid, Spain</json:string></affiliations></json:item><json:item><name>Ana Gorostidi PhD</name><affiliations><json:string>Neurogenetics Laboratory, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</json:string></affiliations></json:item><json:item><name>Estibaliz Goyenechea PhD</name><affiliations><json:string>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</json:string></affiliations></json:item><json:item><name>Ainhoa Alzualde PhD</name><affiliations><json:string>Neurogenetics Laboratory, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</json:string></affiliations></json:item><json:item><name>Juan José Poza MD, PhD</name><affiliations><json:string>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</json:string></affiliations></json:item><json:item><name>Francisco Rodríguez MD</name><affiliations><json:string>Nuclear Medicine Department, Onkologikoa, San Sebastián, Gipuzkoa, Spain</json:string></affiliations></json:item><json:item><name>Alberto Bergareche MD</name><affiliations><json:string>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</json:string></affiliations></json:item><json:item><name>Fermín Moreno MD</name><affiliations><json:string>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</json:string></affiliations></json:item><json:item><name>Adolfo López de Munain MD, PhD</name><affiliations><json:string>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</json:string></affiliations></json:item><json:item><name>José F. Martí Massó MD, PhD</name><affiliations><json:string>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>LRRK2</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dardarin</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>metaiodobenzylguanidine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hyposmia</value></json:item></subject><language><json:string>eng</json:string></language><abstract>It has been proposed that olfactory tests and metaiodobenzylguanidine cardiac scintigraphy may help diagnose idiopathic Parkinson's disease in the premotor phase. However, it is not clear what value these tests have in all patients with Parkinson's disease and, particularly, in those who carry mutations in LRRK2. The objective was to analyze olfactory dysfunction and the changes in cardiac I‐metaiodobenzylguanidine uptake in patients with Parkinson's disease carrying the R1441G and G2019S mutations in LRRK2, and in patients with Parkinson's disease with no known mutations. Patients with Parkinson's disease were screened for R1441G and G2019S LRRK2 gene mutations and classified as LRRK2 mutation carriers or noncarriers. A total of 190 patients with Parkinson's disease (44 LRRK2 mutation carriers) were tested for olfactory dysfunction using the Brief Smell Identification Test. Cardiac 123I‐metaiodobenzylguanidine scintigraphy was performed on 90 patients with Parkinson's disease (27 LRRK2 mutation carriers). Thirty‐six percent of patients with LRRK2 mutations have hyposmia, compared to 75% of noncarrier patients with Parkinson's disease (P > .001). Sixty‐six percent of LRRK2 mutation carriers have low early metaiodobenzylguanidine uptake, compared to 86% of noncarriers (P = .048). Similarly, the heart/mediastinum ratio in delayed metaiodobenzylguanidine images appeared to differ between these groups of patients with Parkinson's disease, although these results did not reach statistical significance. The data obtained indicate that olfactory and cardiac impairment is less prevalent when Parkinson's disease is associated with mutations in LRRK2, although the underlying mechanisms for this difference remain unclear. Thus, such screening would be less useful to detect the premotor phase in asymptomatic relatives who carry mutations in LRRK2 than in cases not associated with LRRK2. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>7.244</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1939</abstractCharCount><pdfWordCount>4244</pdfWordCount><pdfCharCount>27485</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>271</abstractWordCount></qualityIndicators><title>Olfactory deficits and cardiac 123I‐MIBG in Parkinson's disease related to the LRRK2 R1441G and G2019S mutations</title><genre><json:string>Serial article</json:string></genre><host><volume>26</volume><pages><total>6</total><last>2031</last><first>2026</first></pages><issn><json:string>0885-3185</json:string></issn><issue>11</issue><subject><json:item><value>Research Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/mds.23773</json:string></doi><id>31920B7096B87B810017537D1A39A1CACC347B6A</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/31920B7096B87B810017537D1A39A1CACC347B6A/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/31920B7096B87B810017537D1A39A1CACC347B6A/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/31920B7096B87B810017537D1A39A1CACC347B6A/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Olfactory deficits and cardiac 123I‐MIBG in Parkinson's disease related to the LRRK2 R1441G and G2019S mutations</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Funding agencies: This study was funded by the Ilundain Foundation, the Basque Government (Health Department: 2006111003), the Mutua Madrileña Medical Research Foundation, the Centro de Investigación Biomédica en Red para Enfermedades Neurodegenerativas (CIBERNED), and the Carlos III Health Institute (PI070660).</note><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></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Olfactory deficits and cardiac 123I‐MIBG in Parkinson's disease related to the LRRK2 R1441G and G2019S mutations</title><author><persName><forename type="first">Javier</forename><surname>Ruiz‐Martínez</surname><roleName type="degree">MD</roleName></persName><note type="correspondence"><p>Correspondence: Neurology Department, Donostia Hospital, Paseo Dr Beguiristain s/n, 20014 Donostia, San Sebastián, Gipuzkoa, Spain</p></note><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation><affiliation>Centro de Investigación Biomédica en Red para Enfermedades Neurodegenerativas (CIBERNED), Carlos III Health Institute, Madrid, Spain</affiliation></author><author><persName><forename type="first">Ana</forename><surname>Gorostidi</surname><roleName type="degree">PhD</roleName></persName><affiliation>Neurogenetics Laboratory, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation></author><author><persName><forename type="first">Estibaliz</forename><surname>Goyenechea</surname><roleName type="degree">PhD</roleName></persName><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation></author><author><persName><forename type="first">Ainhoa</forename><surname>Alzualde</surname><roleName type="degree">PhD</roleName></persName><affiliation>Neurogenetics Laboratory, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation></author><author><persName><forename type="first">Juan José</forename><surname>Poza</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation></author><author><persName><forename type="first">Francisco</forename><surname>Rodríguez</surname><roleName type="degree">MD</roleName></persName><affiliation>Nuclear Medicine Department, Onkologikoa, San Sebastián, Gipuzkoa, Spain</affiliation></author><author><persName><forename type="first">Alberto</forename><surname>Bergareche</surname><roleName type="degree">MD</roleName></persName><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation></author><author><persName><forename type="first">Fermín</forename><surname>Moreno</surname><roleName type="degree">MD</roleName></persName><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation></author><author><persName><forename type="first">Adolfo</forename><surname>López de Munain</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation></author><author><persName><forename type="first">José F.</forename><surname>Martí Massó</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</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="2011-09"></date><biblScope unit="vol">26</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="2026">2026</biblScope><biblScope unit="page" to="2031">2031</biblScope></imprint></monogr><idno type="istex">31920B7096B87B810017537D1A39A1CACC347B6A</idno><idno type="DOI">10.1002/mds.23773</idno><idno type="ArticleID">MDS23773</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>It has been proposed that olfactory tests and metaiodobenzylguanidine cardiac scintigraphy may help diagnose idiopathic Parkinson's disease in the premotor phase. However, it is not clear what value these tests have in all patients with Parkinson's disease and, particularly, in those who carry mutations in LRRK2. The objective was to analyze olfactory dysfunction and the changes in cardiac I‐metaiodobenzylguanidine uptake in patients with Parkinson's disease carrying the R1441G and G2019S mutations in LRRK2, and in patients with Parkinson's disease with no known mutations. Patients with Parkinson's disease were screened for R1441G and G2019S LRRK2 gene mutations and classified as LRRK2 mutation carriers or noncarriers. A total of 190 patients with Parkinson's disease (44 LRRK2 mutation carriers) were tested for olfactory dysfunction using the Brief Smell Identification Test. Cardiac 123I‐metaiodobenzylguanidine scintigraphy was performed on 90 patients with Parkinson's disease (27 LRRK2 mutation carriers). Thirty‐six percent of patients with LRRK2 mutations have hyposmia, compared to 75% of noncarrier patients with Parkinson's disease (P < .001). Sixty‐six percent of LRRK2 mutation carriers have low early metaiodobenzylguanidine uptake, compared to 86% of noncarriers (P = .048). Similarly, the heart/mediastinum ratio in delayed metaiodobenzylguanidine images appeared to differ between these groups of patients with Parkinson's disease, although these results did not reach statistical significance. The data obtained indicate that olfactory and cardiac impairment is less prevalent when Parkinson's disease is associated with mutations in LRRK2, although the underlying mechanisms for this difference remain unclear. Thus, such screening would be less useful to detect the premotor phase in asymptomatic relatives who carry mutations in LRRK2 than in cases not associated with LRRK2. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>LRRK2</term></item><item><term>dardarin</term></item><item><term>Parkinson's disease</term></item><item><term>metaiodobenzylguanidine</term></item><item><term>hyposmia</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="2010-06-15">Received</change><change when="2011-04-04">Registration</change><change when="2011-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/31920B7096B87B810017537D1A39A1CACC347B6A/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="110"><doi origin="wiley" registered="yes">10.1002/mds.v26.11</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue">11</numbering></numberingGroup><coverDate startDate="2011-09">September 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="120" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23773</doi><idGroup><id type="unit" value="MDS23773"></id></idGroup><countGroup><count type="pageTotal" number="6"></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="2010-06-15"></event><event type="manuscriptRevised" date="2011-03-17"></event><event type="manuscriptAccepted" date="2011-04-04"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.10 mode:FullText" date="2011-09-19"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-05-24"></event><event type="firstOnline" date="2011-05-24"></event><event type="publishedOnlineFinalForm" date="2011-09-19"></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">2026</numbering><numbering type="pageLast">2031</numbering></numberingGroup><correspondenceTo>Neurology Department, Donostia Hospital, Paseo Dr Beguiristain s/n, 20014 Donostia, San Sebastián, Gipuzkoa, Spain</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23773.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="4"></count><count type="referenceTotal" number="38"></count><count type="wordTotal" number="5687"></count></countGroup><titleGroup><title type="main" xml:lang="en">Olfactory deficits and cardiac <sup>123</sup>I‐MIBG in Parkinson's disease related to the <i>LRRK2</i> R1441G and G2019S mutations<link href="#fn6"></link><link href="#fn7"></link><link href="#fn8"></link></title><title type="short" xml:lang="en">SMELL LOSS/CARDIAC <sup>123</sup>I‐MIBG AND <fi>LRRK2</fi></title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Javier</givenNames><familyName>Ruiz‐Martínez</familyName><degrees>MD</degrees></personName><contactDetails><email>javier.ruizmartinez@osakidetza.net</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Ana</givenNames><familyName>Gorostidi</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Estibaliz</givenNames><familyName>Goyenechea</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Ainhoa</givenNames><familyName>Alzualde</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Juan José</givenNames><familyName>Poza</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Francisco</givenNames><familyName>Rodríguez</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Alberto</givenNames><familyName>Bergareche</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Fermín</givenNames><familyName>Moreno</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Adolfo</givenNames><familyName>López de Munain</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af1"><personName><givenNames>José F.</givenNames><familyName>Martí Massó</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="ES" type="organization"><unparsedAffiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="ES" type="organization"><unparsedAffiliation>Centro de Investigación Biomédica en Red para Enfermedades Neurodegenerativas (CIBERNED), Carlos III Health Institute, Madrid, Spain</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="ES" type="organization"><unparsedAffiliation>Neurogenetics Laboratory, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="ES" type="organization"><unparsedAffiliation>Nuclear Medicine Department, Onkologikoa, San Sebastián, Gipuzkoa, Spain</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1"><i>LRRK2</i></keyword><keyword xml:id="kwd2">dardarin</keyword><keyword xml:id="kwd3">Parkinson's disease</keyword><keyword xml:id="kwd4">metaiodobenzylguanidine</keyword><keyword xml:id="kwd5">hyposmia</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>It has been proposed that olfactory tests and metaiodobenzylguanidine cardiac scintigraphy may help diagnose idiopathic Parkinson's disease in the premotor phase. However, it is not clear what value these tests have in all patients with Parkinson's disease and, particularly, in those who carry mutations in <i>LRRK2</i>. The objective was to analyze olfactory dysfunction and the changes in cardiac I‐metaiodobenzylguanidine uptake in patients with Parkinson's disease carrying the R1441G and G2019S mutations in <i>LRRK2</i>, and in patients with Parkinson's disease with no known mutations. Patients with Parkinson's disease were screened for R1441G and G2019S <i>LRRK2</i> gene mutations and classified as <i>LRRK2</i> mutation carriers or noncarriers. A total of 190 patients with Parkinson's disease (44 <i>LRRK2</i> mutation carriers) were tested for olfactory dysfunction using the Brief Smell Identification Test. Cardiac <sup>123</sup>I‐metaiodobenzylguanidine scintigraphy was performed on 90 patients with Parkinson's disease (27 <i>LRRK2</i> mutation carriers). Thirty‐six percent of patients with <i>LRRK2</i> mutations have hyposmia, compared to 75% of noncarrier patients with Parkinson's disease (<i>P</i> < .001). Sixty‐six percent of <i>LRRK2</i> mutation carriers have low early metaiodobenzylguanidine uptake, compared to 86% of noncarriers (<i>P</i> = .048). Similarly, the heart/mediastinum ratio in delayed metaiodobenzylguanidine images appeared to differ between these groups of patients with Parkinson's disease, although these results did not reach statistical significance. The data obtained indicate that olfactory and cardiac impairment is less prevalent when Parkinson's disease is associated with mutations in <i>LRRK2</i>, although the underlying mechanisms for this difference remain unclear. Thus, such screening would be less useful to detect the premotor phase in asymptomatic relatives who carry mutations in <i>LRRK2</i> than in cases not associated with <i>LRRK2</i>. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn6"><p><b>Funding agencies:</b> This study was funded by the Ilundain Foundation, the Basque Government (Health Department: 2006111003), the Mutua Madrileña Medical Research Foundation, the Centro de Investigación Biomédica en Red para Enfermedades Neurodegenerativas (CIBERNED), and the Carlos III Health Institute (PI070660).</p></note><note xml:id="fn7"><p><b>Relevant conflicts of interest/financial disclosures:</b> Nothing to report.</p></note><note xml:id="fn8"><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><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Olfactory deficits and cardiac 123I‐MIBG in Parkinson's disease related to the LRRK2 R1441G and G2019S mutations</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>SMELL LOSS/CARDIAC 123I‐MIBG AND LRRK2</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Olfactory deficits and cardiac</title></titleInfo><name type="personal"><namePart type="given">Javier</namePart><namePart type="family">Ruiz‐Martínez</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation><affiliation>Centro de Investigación Biomédica en Red para Enfermedades Neurodegenerativas (CIBERNED), Carlos III Health Institute, Madrid, Spain</affiliation><description>Correspondence: Neurology Department, Donostia Hospital, Paseo Dr Beguiristain s/n, 20014 Donostia, San Sebastián, Gipuzkoa, Spain</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ana</namePart><namePart type="family">Gorostidi</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurogenetics Laboratory, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Estibaliz</namePart><namePart type="family">Goyenechea</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ainhoa</namePart><namePart type="family">Alzualde</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurogenetics Laboratory, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Juan José</namePart><namePart type="family">Poza</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Francisco</namePart><namePart type="family">Rodríguez</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Nuclear Medicine Department, Onkologikoa, San Sebastián, Gipuzkoa, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alberto</namePart><namePart type="family">Bergareche</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Fermín</namePart><namePart type="family">Moreno</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Adolfo</namePart><namePart type="family">López de Munain</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">José F.</namePart><namePart type="family">Martí Massó</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Neurology Department, Donostia Hospital, San Sebastián, Gipuzkoa, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">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">2010-06-15</dateCaptured><dateValid encoding="w3cdtf">2011-04-04</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">4</extent><extent unit="references">38</extent><extent unit="words">5687</extent></physicalDescription><abstract lang="en">It has been proposed that olfactory tests and metaiodobenzylguanidine cardiac scintigraphy may help diagnose idiopathic Parkinson's disease in the premotor phase. However, it is not clear what value these tests have in all patients with Parkinson's disease and, particularly, in those who carry mutations in LRRK2. The objective was to analyze olfactory dysfunction and the changes in cardiac I‐metaiodobenzylguanidine uptake in patients with Parkinson's disease carrying the R1441G and G2019S mutations in LRRK2, and in patients with Parkinson's disease with no known mutations. Patients with Parkinson's disease were screened for R1441G and G2019S LRRK2 gene mutations and classified as LRRK2 mutation carriers or noncarriers. A total of 190 patients with Parkinson's disease (44 LRRK2 mutation carriers) were tested for olfactory dysfunction using the Brief Smell Identification Test. Cardiac 123I‐metaiodobenzylguanidine scintigraphy was performed on 90 patients with Parkinson's disease (27 LRRK2 mutation carriers). Thirty‐six percent of patients with LRRK2 mutations have hyposmia, compared to 75% of noncarrier patients with Parkinson's disease (P < .001). Sixty‐six percent of LRRK2 mutation carriers have low early metaiodobenzylguanidine uptake, compared to 86% of noncarriers (P = .048). Similarly, the heart/mediastinum ratio in delayed metaiodobenzylguanidine images appeared to differ between these groups of patients with Parkinson's disease, although these results did not reach statistical significance. The data obtained indicate that olfactory and cardiac impairment is less prevalent when Parkinson's disease is associated with mutations in LRRK2, although the underlying mechanisms for this difference remain unclear. Thus, such screening would be less useful to detect the premotor phase in asymptomatic relatives who carry mutations in LRRK2 than in cases not associated with LRRK2. © 2011 Movement Disorder Society</abstract><note type="content">*Funding agencies: This study was funded by the Ilundain Foundation, the Basque Government (Health Department: 2006111003), the Mutua Madrileña Medical Research Foundation, the Centro de Investigación Biomédica en Red para Enfermedades Neurodegenerativas (CIBERNED), and the Carlos III Health Institute (PI070660).</note><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>LRRK2</topic><topic>dardarin</topic><topic>Parkinson's disease</topic><topic>metaiodobenzylguanidine</topic><topic>hyposmia</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><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>2026</start><end>2031</end><total>6</total></extent></part></relatedItem><identifier type="istex">31920B7096B87B810017537D1A39A1CACC347B6A</identifier><identifier type="DOI">10.1002/mds.23773</identifier><identifier type="ArticleID">MDS23773</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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