123I‐IBZM binding compared with long‐term clinical follow up in patients with de novo parkinsonism
Identifieur interne : 002898 ( Istex/Corpus ); précédent : 002897; suivant : 002899123I‐IBZM binding compared with long‐term clinical follow up in patients with de novo parkinsonism
Auteurs : Schwarz ; Klaus Tatsch ; Thomas Gasser ; Guy Arnold ; Oliver Pogarell ; Gais Künig ; Wolfgang H. OertelSource :
- Movement Disorders [ 0885-3185 ] ; 1998-01.
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Abstract
We performed a prospective clinical follow up (mean follow up, 36 months; range, 24–56 months) of 65 patients with de novo parkinsonism in whom imaging of dopamine D2 receptors was performed before the initiation of dopaminomimetic therapy by means of 123I‐iodobenzamidesingle‐photon‐emission computed tomography (IBZM‐SPECT). The results of IBZM‐SPECT were comared with the long‐term response to dopaminomimetic drugs, the development of motor fluctuations, and the development of clinical signs incompatible with Parkinson's disease (PD). A total of 55 patients had normal and 10 patients had reduced IBZM binding; 45 patients showed a good response to levodopa (L‐dopa), 11 showed an equivocal response, and nine did not respond; 31 patients developed a fluctuating response to dopaminomimetic drugs and seven patients developed clinical signs indicative of multiple‐system atrophy (n = 5), progressive supranuclear palsy (n = 1), or corticobasal ganglionic degeneration (n = 1). Chi‐squared analysis showed a significant correlation of the results of IBZM‐SPECT with the long‐term response to dopaminomimetic therapy (p < 0.0001) and the development of motor fluctuations (p < 0.0001) or clinical signs incompatible with PD (p < 0.0001). We conclude that IBZM‐SPECT can help to differentiate between patients who will show a good response to L‐dopa and will develop motor fluctuations (most likely patients with PD) and those patients who will not respond to L‐dopa and might develop clinical signs compatible with another hypokinetic disorder of the basal ganglia.
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DOI: 10.1002/mds.870130107
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Oertel</name><affiliation><mods:affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Current Address: Department of Neurology, Philipps University, D‐35033 Marburg, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</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="1998-01">1998-01</date><biblScope unit="vol">13</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="16">16</biblScope><biblScope unit="page" to="19">19</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">C82F777A0E968DC0CE551B41DF878389F9ED786F</idno><idno type="DOI">10.1002/mds.870130107</idno><idno type="ArticleID">MDS870130107</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apomorphine</term><term>IBZM‐SPECT</term><term>Levodopa</term><term>Parkinson's disease</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We performed a prospective clinical follow up (mean follow up, 36 months; range, 24–56 months) of 65 patients with de novo parkinsonism in whom imaging of dopamine D2 receptors was performed before the initiation of dopaminomimetic therapy by means of 123I‐iodobenzamidesingle‐photon‐emission computed tomography (IBZM‐SPECT). The results of IBZM‐SPECT were comared with the long‐term response to dopaminomimetic drugs, the development of motor fluctuations, and the development of clinical signs incompatible with Parkinson's disease (PD). A total of 55 patients had normal and 10 patients had reduced IBZM binding; 45 patients showed a good response to levodopa (L‐dopa), 11 showed an equivocal response, and nine did not respond; 31 patients developed a fluctuating response to dopaminomimetic drugs and seven patients developed clinical signs indicative of multiple‐system atrophy (n = 5), progressive supranuclear palsy (n = 1), or corticobasal ganglionic degeneration (n = 1). Chi‐squared analysis showed a significant correlation of the results of IBZM‐SPECT with the long‐term response to dopaminomimetic therapy (p < 0.0001) and the development of motor fluctuations (p < 0.0001) or clinical signs incompatible with PD (p < 0.0001). We conclude that IBZM‐SPECT can help to differentiate between patients who will show a good response to L‐dopa and will develop motor fluctuations (most likely patients with PD) and those patients who will not respond to L‐dopa and might develop clinical signs compatible with another hypokinetic disorder of the basal ganglia.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Schwarz</name><affiliations><json:string>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</json:string><json:string>Current Address: Department of Neurology, University of Ulm, D‐89081 Ulm, Germany</json:string></affiliations></json:item><json:item><name>Klaus Tatsch</name><affiliations><json:string>Department of Nuclear Medicine, Klinikum Grosshadern, Ludwig‐Maximilians University, Munich, Germany</json:string></affiliations></json:item><json:item><name>Thomas Gasser</name><affiliations><json:string>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</json:string></affiliations></json:item><json:item><name>Guy Arnold</name><affiliations><json:string>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</json:string></affiliations></json:item><json:item><name>Oliver Pogarell</name><affiliations><json:string>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</json:string></affiliations></json:item><json:item><name>Gais Künig</name><affiliations><json:string>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</json:string></affiliations></json:item><json:item><name>Wolfgang H. Oertel</name><affiliations><json:string>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</json:string><json:string>Current Address: Department of Neurology, Philipps University, D‐35033 Marburg, Germany</json:string></affiliations></json:item></author><subject><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>IBZM‐SPECT</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Apomorphine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Levodopa</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We performed a prospective clinical follow up (mean follow up, 36 months; range, 24–56 months) of 65 patients with de novo parkinsonism in whom imaging of dopamine D2 receptors was performed before the initiation of dopaminomimetic therapy by means of 123I‐iodobenzamidesingle‐photon‐emission computed tomography (IBZM‐SPECT). The results of IBZM‐SPECT were comared with the long‐term response to dopaminomimetic drugs, the development of motor fluctuations, and the development of clinical signs incompatible with Parkinson's disease (PD). A total of 55 patients had normal and 10 patients had reduced IBZM binding; 45 patients showed a good response to levodopa (L‐dopa), 11 showed an equivocal response, and nine did not respond; 31 patients developed a fluctuating response to dopaminomimetic drugs and seven patients developed clinical signs indicative of multiple‐system atrophy (n = 5), progressive supranuclear palsy (n = 1), or corticobasal ganglionic degeneration (n = 1). Chi‐squared analysis showed a significant correlation of the results of IBZM‐SPECT with the long‐term response to dopaminomimetic therapy (p > 0.0001) and the development of motor fluctuations (p > 0.0001) or clinical signs incompatible with PD (p > 0.0001). We conclude that IBZM‐SPECT can help to differentiate between patients who will show a good response to L‐dopa and will develop motor fluctuations (most likely patients with PD) and those patients who will not respond to L‐dopa and might develop clinical signs compatible with another hypokinetic disorder of the basal ganglia.</abstract><qualityIndicators><score>4.976</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1569</abstractCharCount><pdfWordCount>2204</pdfWordCount><pdfCharCount>13948</pdfCharCount><pdfPageCount>4</pdfPageCount><abstractWordCount>231</abstractWordCount></qualityIndicators><title>123I‐IBZM binding compared with long‐term clinical follow up in patients with de novo parkinsonism</title><genre><json:string>Serial 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parkinsonism</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>1998</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">123I‐IBZM binding compared with long‐term clinical follow up in patients with de novo parkinsonism</title><author><persName><surname>Schwarz</surname><roleName type="degree">Dr.</roleName></persName><note type="correspondence"><p>Correspondence: Department of Neurology, University of Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany</p></note><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</affiliation><affiliation>Current Address: Department of Neurology, University of Ulm, D‐89081 Ulm, Germany</affiliation></author><author><persName><forename type="first">Klaus</forename><surname>Tatsch</surname></persName><affiliation>Department of Nuclear Medicine, Klinikum Grosshadern, Ludwig‐Maximilians University, Munich, Germany</affiliation></author><author><persName><forename type="first">Thomas</forename><surname>Gasser</surname></persName><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</affiliation></author><author><persName><forename type="first">Guy</forename><surname>Arnold</surname></persName><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</affiliation></author><author><persName><forename type="first">Oliver</forename><surname>Pogarell</surname></persName><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</affiliation></author><author><persName><forename type="first">Gais</forename><surname>Künig</surname></persName><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</affiliation></author><author><persName><forename type="first">Wolfgang H.</forename><surname>Oertel</surname></persName><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</affiliation><affiliation>Current Address: Department of Neurology, Philipps University, D‐35033 Marburg, 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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="1998-01"></date><biblScope unit="vol">13</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="16">16</biblScope><biblScope unit="page" to="19">19</biblScope></imprint></monogr><idno type="istex">C82F777A0E968DC0CE551B41DF878389F9ED786F</idno><idno type="DOI">10.1002/mds.870130107</idno><idno type="ArticleID">MDS870130107</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We performed a prospective clinical follow up (mean follow up, 36 months; range, 24–56 months) of 65 patients with de novo parkinsonism in whom imaging of dopamine D2 receptors was performed before the initiation of dopaminomimetic therapy by means of 123I‐iodobenzamidesingle‐photon‐emission computed tomography (IBZM‐SPECT). The results of IBZM‐SPECT were comared with the long‐term response to dopaminomimetic drugs, the development of motor fluctuations, and the development of clinical signs incompatible with Parkinson's disease (PD). A total of 55 patients had normal and 10 patients had reduced IBZM binding; 45 patients showed a good response to levodopa (L‐dopa), 11 showed an equivocal response, and nine did not respond; 31 patients developed a fluctuating response to dopaminomimetic drugs and seven patients developed clinical signs indicative of multiple‐system atrophy (n = 5), progressive supranuclear palsy (n = 1), or corticobasal ganglionic degeneration (n = 1). Chi‐squared analysis showed a significant correlation of the results of IBZM‐SPECT with the long‐term response to dopaminomimetic therapy (p < 0.0001) and the development of motor fluctuations (p < 0.0001) or clinical signs incompatible with PD (p < 0.0001). We conclude that IBZM‐SPECT can help to differentiate between patients who will show a good response to L‐dopa and will develop motor fluctuations (most likely patients with PD) and those patients who will not respond to L‐dopa and might develop clinical signs compatible with another hypokinetic disorder of the basal ganglia.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>IBZM‐SPECT</term></item><item><term>Apomorphine</term></item><item><term>Levodopa</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996-03-14">Received</change><change when="1997-01-24">Registration</change><change when="1998-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/C82F777A0E968DC0CE551B41DF878389F9ED786F/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="tocForm">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="10"><doi origin="wiley" registered="yes">10.1002/mds.v13:1</doi><numberingGroup><numbering type="journalVolume" number="13">13</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="1998-01">January 1998</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="7" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.870130107</doi><idGroup><id type="unit" value="MDS870130107"></id></idGroup><countGroup><count type="pageTotal" number="4"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 1998 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="1996-03-14"></event><event type="manuscriptRevised" date="1996-08-18"></event><event type="manuscriptAccepted" date="1997-01-24"></event><event type="firstOnline" date="2004-11-04"></event><event type="publishedOnlineFinalForm" date="2004-11-04"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-09"></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">16</numbering><numbering type="pageLast">19</numbering></numberingGroup><correspondenceTo>Department of Neurology, University of Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS870130107.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="12"></count></countGroup><titleGroup><title type="main" xml:lang="en"><sup>123</sup>I‐IBZM binding compared with long‐term clinical follow up in patients with de novo parkinsonism</title><title type="short" xml:lang="en">IBZM‐SPECT IN DE NOVO PARKINSONISM</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" currentRef="#curr2" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>Johannes</givenNames><familyName>Schwarz</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Klaus</givenNames><familyName>Tatsch</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Thomas</givenNames><familyName>Gasser</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Guy</givenNames><familyName>Arnold</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Oliver</givenNames><familyName>Pogarell</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Gais</givenNames><familyName>Künig</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1" currentRef="#curr1"><personName><givenNames>Wolfgang H.</givenNames><familyName>Oertel</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Department of Nuclear Medicine, Klinikum Grosshadern, Ludwig‐Maximilians University, Munich, Germany</unparsedAffiliation></affiliation><affiliation xml:id="curr1" countryCode="DE"><unparsedAffiliation>Department of Neurology, Philipps University, D‐35033 Marburg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="curr2" countryCode="DE"><unparsedAffiliation>Department of Neurology, University of Ulm, D‐89081 Ulm, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">IBZM‐SPECT</keyword><keyword xml:id="kwd3">Apomorphine</keyword><keyword xml:id="kwd4">Levodopa</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We performed a prospective clinical follow up (mean follow up, 36 months; range, 24–56 months) of 65 patients with de novo parkinsonism in whom imaging of dopamine D<sub>2</sub> receptors was performed before the initiation of dopaminomimetic therapy by means of <sup>123</sup>I‐iodobenzamidesingle‐photon‐emission computed tomography (IBZM‐SPECT). The results of IBZM‐SPECT were comared with the long‐term response to dopaminomimetic drugs, the development of motor fluctuations, and the development of clinical signs incompatible with Parkinson's disease (PD). A total of 55 patients had normal and 10 patients had reduced IBZM binding; 45 patients showed a good response to levodopa (<sc>L</sc>‐dopa), 11 showed an equivocal response, and nine did not respond; 31 patients developed a fluctuating response to dopaminomimetic drugs and seven patients developed clinical signs indicative of multiple‐system atrophy (n = 5), progressive supranuclear palsy (n = 1), or corticobasal ganglionic degeneration (n = 1). Chi‐squared analysis showed a significant correlation of the results of IBZM‐SPECT with the long‐term response to dopaminomimetic therapy (p < 0.0001) and the development of motor fluctuations (p < 0.0001) or clinical signs incompatible with PD (p < 0.0001). We conclude that IBZM‐SPECT can help to differentiate between patients who will show a good response to <sc>L</sc>‐dopa and will develop motor fluctuations (most likely patients with PD) and those patients who will not respond to <sc>L</sc>‐dopa and might develop clinical signs compatible with another hypokinetic disorder of the basal ganglia.</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>123I‐IBZM binding compared with long‐term clinical follow up in patients with de novo parkinsonism</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>IBZM‐SPECT IN DE NOVO PARKINSONISM</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>I‐IBZM binding compared with long‐term clinical follow up in patients with de novo parkinsonism</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Schwarz</namePart><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</affiliation><affiliation>Current Address: Department of Neurology, University of Ulm, D‐89081 Ulm, Germany</affiliation><description>Correspondence: Department of Neurology, University of Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Klaus</namePart><namePart type="family">Tatsch</namePart><affiliation>Department of Nuclear Medicine, Klinikum Grosshadern, Ludwig‐Maximilians University, Munich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Gasser</namePart><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Guy</namePart><namePart type="family">Arnold</namePart><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Oliver</namePart><namePart type="family">Pogarell</namePart><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gais</namePart><namePart type="family">Künig</namePart><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wolfgang H.</namePart><namePart type="family">Oertel</namePart><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwing‐Maximilians University, and “Parkinson's Disease and Other Basal Ganglia Disorders” BMFT Research Program, Munich, Germany</affiliation><affiliation>Current Address: Department of Neurology, Philipps University, D‐35033 Marburg, Germany</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">1998-01</dateIssued><dateCaptured encoding="w3cdtf">1996-03-14</dateCaptured><dateValid encoding="w3cdtf">1997-01-24</dateValid><copyrightDate encoding="w3cdtf">1998</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">1</extent><extent unit="references">12</extent></physicalDescription><abstract lang="en">We performed a prospective clinical follow up (mean follow up, 36 months; range, 24–56 months) of 65 patients with de novo parkinsonism in whom imaging of dopamine D2 receptors was performed before the initiation of dopaminomimetic therapy by means of 123I‐iodobenzamidesingle‐photon‐emission computed tomography (IBZM‐SPECT). The results of IBZM‐SPECT were comared with the long‐term response to dopaminomimetic drugs, the development of motor fluctuations, and the development of clinical signs incompatible with Parkinson's disease (PD). A total of 55 patients had normal and 10 patients had reduced IBZM binding; 45 patients showed a good response to levodopa (L‐dopa), 11 showed an equivocal response, and nine did not respond; 31 patients developed a fluctuating response to dopaminomimetic drugs and seven patients developed clinical signs indicative of multiple‐system atrophy (n = 5), progressive supranuclear palsy (n = 1), or corticobasal ganglionic degeneration (n = 1). Chi‐squared analysis showed a significant correlation of the results of IBZM‐SPECT with the long‐term response to dopaminomimetic therapy (p < 0.0001) and the development of motor fluctuations (p < 0.0001) or clinical signs incompatible with PD (p < 0.0001). We conclude that IBZM‐SPECT can help to differentiate between patients who will show a good response to L‐dopa and will develop motor fluctuations (most likely patients with PD) and those patients who will not respond to L‐dopa and might develop clinical signs compatible with another hypokinetic disorder of the basal ganglia.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>IBZM‐SPECT</topic><topic>Apomorphine</topic><topic>Levodopa</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>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>1998</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>16</start><end>19</end><total>4</total></extent></part></relatedItem><identifier type="istex">C82F777A0E968DC0CE551B41DF878389F9ED786F</identifier><identifier type="DOI">10.1002/mds.870130107</identifier><identifier type="ArticleID">MDS870130107</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1998 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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