Monosymptomatic resting tremor and Parkinson's disease: A multitracer positron emission tomographic study
Identifieur interne : 000595 ( Istex/Corpus ); précédent : 000594; suivant : 000596Monosymptomatic resting tremor and Parkinson's disease: A multitracer positron emission tomographic study
Auteurs : Mehran Ghaemi ; Jan Raethjen ; Rüdiger Hilker ; Jobst Rudolf ; Jan Sobesky ; Günther Deuschl ; Wolf-Dieter HeissSource :
- Movement Disorders [ 0885-3185 ] ; 2002-07.
English descriptors
Abstract
We sought to elucidate the relationship between monosymptomatic resting tremor (mRT) and Parkinson's disease (PD). We studied eight mRT patients (mean Hoehn and Yahr [H&Y], 1.1 ± 0.4), eight patients with PD (mean H&Y, 1.5 ± 0.8), who showed all three classic parkinsonian symptoms, and seven age‐matched healthy subjects. Subjects underwent cerebral magnetic resonance imaging (MRI) and multitracer positron emission tomography (PET) with 6‐[18F]fluoro‐L‐dopa (F‐dopa), [18F]fluorodeoxyglucose (FDG), and [11C]raclopride (RACLO). PD and mRT patients did not show significant differences in F‐dopa‐, RACLO‐, or FDG‐PET scans. In F‐dopa‐ and RACLO‐PET, significant differences between the pooled patient data and control subjects were found for the following regions: anterior and posterior putamen ipsilateral and contralateral to the more affected body side, and ipsilateral and contralateral putaminal gradients of the Ki values. Furthermore, we found a difference for the normalized glucose values of the whole cerebellum between the control group (0.94 ± 0.06) and PD patients (1.01 ± 0.04; P < 0.05) but not for the mRT group (0.97 ± 0.03). Our findings indicate that monosymptomatic resting tremor represents a phenotype of Parkinson's disease, with a nearly identical striatal dopaminergic deficit and postsynaptic D2‐receptor upregulation in both patient groups. We suggest that the cerebellar metabolic hyperactivity in PD is closer related to akinesia and rigidity rather than to tremor. © 2002 Movement Disorder Society
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DOI: 10.1002/mds.10125
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ISTEX:D078FB5AA9457D76B3CB7EE89CEF3CA587952298Le document en format XML
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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>New York</pubPlace><date type="published" when="2002-07">2002-07</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="782">782</biblScope><biblScope unit="page" to="788">788</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">D078FB5AA9457D76B3CB7EE89CEF3CA587952298</idno><idno type="DOI">10.1002/mds.10125</idno><idno type="ArticleID">MDS10125</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>monosymptomatic resting tremor</term><term>positron emission tomography</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We sought to elucidate the relationship between monosymptomatic resting tremor (mRT) and Parkinson's disease (PD). We studied eight mRT patients (mean Hoehn and Yahr [H&Y], 1.1 ± 0.4), eight patients with PD (mean H&Y, 1.5 ± 0.8), who showed all three classic parkinsonian symptoms, and seven age‐matched healthy subjects. Subjects underwent cerebral magnetic resonance imaging (MRI) and multitracer positron emission tomography (PET) with 6‐[18F]fluoro‐L‐dopa (F‐dopa), [18F]fluorodeoxyglucose (FDG), and [11C]raclopride (RACLO). PD and mRT patients did not show significant differences in F‐dopa‐, RACLO‐, or FDG‐PET scans. In F‐dopa‐ and RACLO‐PET, significant differences between the pooled patient data and control subjects were found for the following regions: anterior and posterior putamen ipsilateral and contralateral to the more affected body side, and ipsilateral and contralateral putaminal gradients of the Ki values. Furthermore, we found a difference for the normalized glucose values of the whole cerebellum between the control group (0.94 ± 0.06) and PD patients (1.01 ± 0.04; P < 0.05) but not for the mRT group (0.97 ± 0.03). Our findings indicate that monosymptomatic resting tremor represents a phenotype of Parkinson's disease, with a nearly identical striatal dopaminergic deficit and postsynaptic D2‐receptor upregulation in both patient groups. We suggest that the cerebellar metabolic hyperactivity in PD is closer related to akinesia and rigidity rather than to tremor. © 2002 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Mehran Ghaemi MD</name><affiliations><json:string>Klinik für Neurologie der Universität zu Köln, Köln, Germany</json:string></affiliations></json:item><json:item><name>Jan Raethjen MD</name><affiliations><json:string>Neurologische Klinik der Christian‐Albrechts‐Universität zu Kiel, Germany</json:string></affiliations></json:item><json:item><name>Rüdiger Hilker MD</name><affiliations><json:string>Klinik für Neurologie der Universität zu Köln, Köln, Germany</json:string></affiliations></json:item><json:item><name>Jobst Rudolf MD</name><affiliations><json:string>Klinik für Neurologie der Universität zu Köln, Köln, Germany</json:string></affiliations></json:item><json:item><name>Jan Sobesky MD</name><affiliations><json:string>Klinik für Neurologie der Universität zu Köln, Köln, Germany</json:string></affiliations></json:item><json:item><name>Günther Deuschl MD</name><affiliations><json:string>Neurologische Klinik der Christian‐Albrechts‐Universität zu Kiel, Germany</json:string></affiliations></json:item><json:item><name>Wolf‐Dieter Heiss MD</name><affiliations><json:string>Klinik für Neurologie der Universität zu Köln, Köln, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>positron emission tomography</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>monosymptomatic resting tremor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We sought to elucidate the relationship between monosymptomatic resting tremor (mRT) and Parkinson's disease (PD). We studied eight mRT patients (mean Hoehn and Yahr [H&Y], 1.1 ± 0.4), eight patients with PD (mean H&Y, 1.5 ± 0.8), who showed all three classic parkinsonian symptoms, and seven age‐matched healthy subjects. Subjects underwent cerebral magnetic resonance imaging (MRI) and multitracer positron emission tomography (PET) with 6‐[18F]fluoro‐L‐dopa (F‐dopa), [18F]fluorodeoxyglucose (FDG), and [11C]raclopride (RACLO). PD and mRT patients did not show significant differences in F‐dopa‐, RACLO‐, or FDG‐PET scans. In F‐dopa‐ and RACLO‐PET, significant differences between the pooled patient data and control subjects were found for the following regions: anterior and posterior putamen ipsilateral and contralateral to the more affected body side, and ipsilateral and contralateral putaminal gradients of the Ki values. Furthermore, we found a difference for the normalized glucose values of the whole cerebellum between the control group (0.94 ± 0.06) and PD patients (1.01 ± 0.04; P > 0.05) but not for the mRT group (0.97 ± 0.03). Our findings indicate that monosymptomatic resting tremor represents a phenotype of Parkinson's disease, with a nearly identical striatal dopaminergic deficit and postsynaptic D2‐receptor upregulation in both patient groups. We suggest that the cerebellar metabolic hyperactivity in PD is closer related to akinesia and rigidity rather than to tremor. © 2002 Movement Disorder Society</abstract><qualityIndicators><score>7.478</score><pdfVersion>1.4</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1530</abstractCharCount><pdfWordCount>4338</pdfWordCount><pdfCharCount>27430</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>220</abstractWordCount></qualityIndicators><title>Monosymptomatic resting tremor and Parkinson's disease: A multitracer positron emission tomographic study</title><genre><json:string>Serial article</json:string></genre><host><volume>17</volume><pages><total>7</total><last>788</last><first>782</first></pages><issn><json:string>0885-3185</json:string></issn><issue>4</issue><subject><json:item><value>Brief Report</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>2002</publicationDate><copyrightDate>2002</copyrightDate><doi><json:string>10.1002/mds.10125</json:string></doi><id>D078FB5AA9457D76B3CB7EE89CEF3CA587952298</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/D078FB5AA9457D76B3CB7EE89CEF3CA587952298/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/D078FB5AA9457D76B3CB7EE89CEF3CA587952298/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/D078FB5AA9457D76B3CB7EE89CEF3CA587952298/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Monosymptomatic resting tremor and Parkinson's disease: A multitracer positron emission tomographic study</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2002</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Monosymptomatic resting tremor and Parkinson's disease: A multitracer positron emission tomographic study</title><author><persName><forename type="first">Mehran</forename><surname>Ghaemi</surname><roleName type="degree">MD</roleName></persName><affiliation>Klinik für Neurologie der Universität zu Köln, Köln, Germany</affiliation></author><author><persName><forename type="first">Jan</forename><surname>Raethjen</surname><roleName type="degree">MD</roleName></persName><affiliation>Neurologische Klinik der Christian‐Albrechts‐Universität zu Kiel, Germany</affiliation></author><author><persName><forename type="first">Rüdiger</forename><surname>Hilker</surname><roleName type="degree">MD</roleName></persName><affiliation>Klinik für Neurologie der Universität zu Köln, Köln, Germany</affiliation></author><author><persName><forename type="first">Jobst</forename><surname>Rudolf</surname><roleName type="degree">MD</roleName></persName><affiliation>Klinik für Neurologie der Universität zu Köln, Köln, Germany</affiliation></author><author><persName><forename type="first">Jan</forename><surname>Sobesky</surname><roleName type="degree">MD</roleName></persName><affiliation>Klinik für Neurologie der Universität zu Köln, Köln, Germany</affiliation></author><author><persName><forename type="first">Günther</forename><surname>Deuschl</surname><roleName type="degree">MD</roleName></persName><affiliation>Neurologische Klinik der Christian‐Albrechts‐Universität zu Kiel, Germany</affiliation></author><author><persName><forename type="first">Wolf‐Dieter</forename><surname>Heiss</surname><roleName type="degree">MD</roleName></persName><note type="correspondence"><p>Correspondence: Klinik für Neurologie der Universität zu Köln, Joseph‐Stelzmann Strasse 9, 50924 Köln, Germany</p></note><affiliation>Klinik für Neurologie der Universität zu Köln, Köln, Germany</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>New York</pubPlace><date type="published" when="2002-07"></date><biblScope unit="vol">17</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="782">782</biblScope><biblScope unit="page" to="788">788</biblScope></imprint></monogr><idno type="istex">D078FB5AA9457D76B3CB7EE89CEF3CA587952298</idno><idno type="DOI">10.1002/mds.10125</idno><idno type="ArticleID">MDS10125</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2002</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We sought to elucidate the relationship between monosymptomatic resting tremor (mRT) and Parkinson's disease (PD). We studied eight mRT patients (mean Hoehn and Yahr [H&Y], 1.1 ± 0.4), eight patients with PD (mean H&Y, 1.5 ± 0.8), who showed all three classic parkinsonian symptoms, and seven age‐matched healthy subjects. Subjects underwent cerebral magnetic resonance imaging (MRI) and multitracer positron emission tomography (PET) with 6‐[18F]fluoro‐L‐dopa (F‐dopa), [18F]fluorodeoxyglucose (FDG), and [11C]raclopride (RACLO). PD and mRT patients did not show significant differences in F‐dopa‐, RACLO‐, or FDG‐PET scans. In F‐dopa‐ and RACLO‐PET, significant differences between the pooled patient data and control subjects were found for the following regions: anterior and posterior putamen ipsilateral and contralateral to the more affected body side, and ipsilateral and contralateral putaminal gradients of the Ki values. Furthermore, we found a difference for the normalized glucose values of the whole cerebellum between the control group (0.94 ± 0.06) and PD patients (1.01 ± 0.04; P < 0.05) but not for the mRT group (0.97 ± 0.03). Our findings indicate that monosymptomatic resting tremor represents a phenotype of Parkinson's disease, with a nearly identical striatal dopaminergic deficit and postsynaptic D2‐receptor upregulation in both patient groups. 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We studied eight mRT patients (mean Hoehn and Yahr [H&Y], 1.1 ± 0.4), eight patients with PD (mean H&Y, 1.5 ± 0.8), who showed all three classic parkinsonian symptoms, and seven age‐matched healthy subjects. Subjects underwent cerebral magnetic resonance imaging (MRI) and multitracer positron emission tomography (PET) with 6‐[<sup>18</sup>F]fluoro‐<sc>L</sc>‐dopa (<sc>F</sc>‐dopa), [<sup>18</sup>F]fluorodeoxyglucose (FDG), and [<sup>11</sup>C]raclopride (RACLO). PD and mRT patients did not show significant differences in <sc>F</sc>‐dopa‐, RACLO‐, or FDG‐PET scans. In <sc>F</sc>‐dopa‐ and RACLO‐PET, significant differences between the pooled patient data and control subjects were found for the following regions: anterior and posterior putamen ipsilateral and contralateral to the more affected body side, and ipsilateral and contralateral putaminal gradients of the K<sub>i</sub> values. Furthermore, we found a difference for the normalized glucose values of the whole cerebellum between the control group (0.94 ± 0.06) and PD patients (1.01 ± 0.04; <i>P</i> < 0.05) but not for the mRT group (0.97 ± 0.03). Our findings indicate that monosymptomatic resting tremor represents a phenotype of Parkinson's disease, with a nearly identical striatal dopaminergic deficit and postsynaptic D2‐receptor upregulation in both patient groups. We suggest that the cerebellar metabolic hyperactivity in PD is closer related to akinesia and rigidity rather than to tremor. © 2002 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Monosymptomatic resting tremor and Parkinson's disease: A multitracer positron emission tomographic study</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Monosymptomatic Resting Tremor and PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Monosymptomatic resting tremor and Parkinson's disease: A multitracer positron emission tomographic study</title></titleInfo><name type="personal"><namePart type="given">Mehran</namePart><namePart type="family">Ghaemi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Klinik für Neurologie der Universität zu Köln, Köln, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan</namePart><namePart type="family">Raethjen</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurologische Klinik der Christian‐Albrechts‐Universität zu Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rüdiger</namePart><namePart type="family">Hilker</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Klinik für Neurologie der Universität zu Köln, Köln, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jobst</namePart><namePart type="family">Rudolf</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Klinik für Neurologie der Universität zu Köln, Köln, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan</namePart><namePart type="family">Sobesky</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Klinik für Neurologie der Universität zu Köln, Köln, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Günther</namePart><namePart type="family">Deuschl</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurologische Klinik der Christian‐Albrechts‐Universität zu Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wolf‐Dieter</namePart><namePart type="family">Heiss</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Klinik für Neurologie der Universität zu Köln, Köln, Germany</affiliation><description>Correspondence: Klinik für Neurologie der Universität zu Köln, Joseph‐Stelzmann Strasse 9, 50924 Köln, Germany</description><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">New York</placeTerm></place><dateIssued encoding="w3cdtf">2002-07</dateIssued><dateCaptured encoding="w3cdtf">2001-06-12</dateCaptured><dateValid encoding="w3cdtf">2001-11-26</dateValid><copyrightDate encoding="w3cdtf">2002</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">1</extent><extent unit="tables">2</extent><extent unit="references">30</extent><extent unit="words">3917</extent></physicalDescription><abstract lang="en">We sought to elucidate the relationship between monosymptomatic resting tremor (mRT) and Parkinson's disease (PD). We studied eight mRT patients (mean Hoehn and Yahr [H&Y], 1.1 ± 0.4), eight patients with PD (mean H&Y, 1.5 ± 0.8), who showed all three classic parkinsonian symptoms, and seven age‐matched healthy subjects. Subjects underwent cerebral magnetic resonance imaging (MRI) and multitracer positron emission tomography (PET) with 6‐[18F]fluoro‐L‐dopa (F‐dopa), [18F]fluorodeoxyglucose (FDG), and [11C]raclopride (RACLO). PD and mRT patients did not show significant differences in F‐dopa‐, RACLO‐, or FDG‐PET scans. In F‐dopa‐ and RACLO‐PET, significant differences between the pooled patient data and control subjects were found for the following regions: anterior and posterior putamen ipsilateral and contralateral to the more affected body side, and ipsilateral and contralateral putaminal gradients of the Ki values. Furthermore, we found a difference for the normalized glucose values of the whole cerebellum between the control group (0.94 ± 0.06) and PD patients (1.01 ± 0.04; P < 0.05) but not for the mRT group (0.97 ± 0.03). Our findings indicate that monosymptomatic resting tremor represents a phenotype of Parkinson's disease, with a nearly identical striatal dopaminergic deficit and postsynaptic D2‐receptor upregulation in both patient groups. We suggest that the cerebellar metabolic hyperactivity in PD is closer related to akinesia and rigidity rather than to tremor. © 2002 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>positron emission tomography</topic><topic>monosymptomatic resting tremor</topic><topic>Parkinson's disease</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>Brief Report</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>2002</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>782</start><end>788</end><total>7</total></extent></part></relatedItem><identifier type="istex">D078FB5AA9457D76B3CB7EE89CEF3CA587952298</identifier><identifier type="DOI">10.1002/mds.10125</identifier><identifier type="ArticleID">MDS10125</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2002 Movement Disorders 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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