[123]IBZM Binding predicts dopaminergic responsiveness in patients with parkinsonism and previous dopaminomimetic therapy
Identifieur interne : 001962 ( Istex/Corpus ); précédent : 001961; suivant : 001963[123]IBZM Binding predicts dopaminergic responsiveness in patients with parkinsonism and previous dopaminomimetic therapy
Auteurs : Schwarz ; K. Tatsch ; T. Gasser ; G. Arnold ; OertelSource :
- Movement Disorders [ 0885-3185 ] ; 1997-11.
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Abstract
We investigated the cases of 55 patients with parkinsonism and prior dopaminomimetic therapy in whom the response to this treatment was questionable or reported to be negative. None of these patients had shown motor fluctuations prior to this study. We compared the results of imaging of dopamine‐D2 receptors by using [123l]iodobenzamide‐single‐photon‐emission computed tomography (IBZM‐SPECT) with the improvement in motor signs following a subcutaneous injection of apomorphine and a subsequent increase in oral dopaminomimetic therapy. IBZM‐SPECT accurately predicted a positive or negative response to apomorphine in 37 (84%) of 44 patients. The sensitivity/specificity was calculated as 96.3%/64.7%. The sensitivity/specificity of IBZM‐SPECT for the response to oral treatment with levodopa (L‐dopa) was calculated as 100%/75%. After a follow‐up period of 2–4 years, 25 patients developed motor fluctuations. All of these patients had normal IBZM binding. Nine developed clinical signs indicating a basal ganglia disorder other than Parkinson's disease. Eight of these nine patients had reduced, and one patient had normal, IBZM binding. We conclude that normal IBZM binding is a useful predictor of a good response to dopaminergic drugs in patients with parkinsonism and a questionable response to previous dopaminomimetic therapy. Reduced IBZM binding seems to exclude a diagnosis of Parkinson's disease, because none of the latter patients clearly benefited from L‐dopa and 66.7% developed clinical signs indicating another disorder of the basal ganglia.
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DOI: 10.1002/mds.870120610
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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>Hoboken</pubPlace><date type="published" when="1997-11">1997-11</date><biblScope unit="vol">12</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="898">898</biblScope><biblScope unit="page" to="902">902</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">507D526419C64997EB5E827665EEAA3AE79292F8</idno><idno type="DOI">10.1002/mds.870120610</idno><idno type="ArticleID">MDS870120610</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Computed tomography</term><term>Dopamine agonist</term><term>IBZM‐SPECT</term><term>Levodopa</term><term>Multiple‐system atrophy</term><term>Parkinson's disease</term><term>Single‐photon‐emission computed tomography</term><term>[123I]Iodobenzamide</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We investigated the cases of 55 patients with parkinsonism and prior dopaminomimetic therapy in whom the response to this treatment was questionable or reported to be negative. None of these patients had shown motor fluctuations prior to this study. We compared the results of imaging of dopamine‐D2 receptors by using [123l]iodobenzamide‐single‐photon‐emission computed tomography (IBZM‐SPECT) with the improvement in motor signs following a subcutaneous injection of apomorphine and a subsequent increase in oral dopaminomimetic therapy. IBZM‐SPECT accurately predicted a positive or negative response to apomorphine in 37 (84%) of 44 patients. The sensitivity/specificity was calculated as 96.3%/64.7%. The sensitivity/specificity of IBZM‐SPECT for the response to oral treatment with levodopa (L‐dopa) was calculated as 100%/75%. After a follow‐up period of 2–4 years, 25 patients developed motor fluctuations. All of these patients had normal IBZM binding. Nine developed clinical signs indicating a basal ganglia disorder other than Parkinson's disease. Eight of these nine patients had reduced, and one patient had normal, IBZM binding. We conclude that normal IBZM binding is a useful predictor of a good response to dopaminergic drugs in patients with parkinsonism and a questionable response to previous dopaminomimetic therapy. Reduced IBZM binding seems to exclude a diagnosis of Parkinson's disease, because none of the latter patients clearly benefited from L‐dopa and 66.7% developed clinical signs indicating another 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, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich, Germany</json:string></affiliations></json:item><json:item><name>K. Tatsch</name><affiliations><json:string>Department of Neucler Medicine, Klinikum Grosshadern, Ludwig‐Maximilian University, Munich, Germany</json:string></affiliations></json:item><json:item><name>T. Gasser</name><affiliations><json:string>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich, Germany</json:string></affiliations></json:item><json:item><name>G. Arnold</name><affiliations><json:string>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich, Germany</json:string></affiliations></json:item><json:item><name>Dr. Oertel</name><affiliations><json:string>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, 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>Computed tomography</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dopamine agonist</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>[123I]Iodobenzamide</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Levodopa</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>Multiple‐system atrophy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Single‐photon‐emission computed tomography</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We investigated the cases of 55 patients with parkinsonism and prior dopaminomimetic therapy in whom the response to this treatment was questionable or reported to be negative. None of these patients had shown motor fluctuations prior to this study. We compared the results of imaging of dopamine‐D2 receptors by using [123l]iodobenzamide‐single‐photon‐emission computed tomography (IBZM‐SPECT) with the improvement in motor signs following a subcutaneous injection of apomorphine and a subsequent increase in oral dopaminomimetic therapy. IBZM‐SPECT accurately predicted a positive or negative response to apomorphine in 37 (84%) of 44 patients. The sensitivity/specificity was calculated as 96.3%/64.7%. The sensitivity/specificity of IBZM‐SPECT for the response to oral treatment with levodopa (L‐dopa) was calculated as 100%/75%. After a follow‐up period of 2–4 years, 25 patients developed motor fluctuations. All of these patients had normal IBZM binding. Nine developed clinical signs indicating a basal ganglia disorder other than Parkinson's disease. Eight of these nine patients had reduced, and one patient had normal, IBZM binding. We conclude that normal IBZM binding is a useful predictor of a good response to dopaminergic drugs in patients with parkinsonism and a questionable response to previous dopaminomimetic therapy. Reduced IBZM binding seems to exclude a diagnosis of Parkinson's disease, because none of the latter patients clearly benefited from L‐dopa and 66.7% developed clinical signs indicating another disorder of the basal ganglia.</abstract><qualityIndicators><score>5.861</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 827.759 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1563</abstractCharCount><pdfWordCount>3197</pdfWordCount><pdfCharCount>20248</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>222</abstractWordCount></qualityIndicators><title>[123]IBZM Binding predicts dopaminergic responsiveness in patients with parkinsonism and previous dopaminomimetic therapy</title><genre><json:string>Serial article</json:string></genre><host><volume>12</volume><pages><total>5</total><last>902</last><first>898</first></pages><issn><json:string>0885-3185</json:string></issn><issue>6</issue><subject><json:item><value>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>1997</publicationDate><copyrightDate>1997</copyrightDate><doi><json:string>10.1002/mds.870120610</json:string></doi><id>507D526419C64997EB5E827665EEAA3AE79292F8</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/507D526419C64997EB5E827665EEAA3AE79292F8/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/507D526419C64997EB5E827665EEAA3AE79292F8/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/507D526419C64997EB5E827665EEAA3AE79292F8/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">[123]IBZM Binding predicts dopaminergic responsiveness in patients with parkinsonism and previous dopaminomimetic therapy</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>1997</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">[123]IBZM Binding predicts dopaminergic responsiveness in patients with parkinsonism and previous dopaminomimetic therapy</title><author><persName><surname>Schwarz</surname><roleName type="degree">Dr.</roleName></persName><note type="correspondence"><p>Correspondence: Department of Neurology, University of Ulm, RKU, Oberer Eselsberg 45, 89081 Ulm, Germany (current address)</p></note><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich, Germany</affiliation></author><author><persName><forename type="first">K.</forename><surname>Tatsch</surname></persName><affiliation>Department of Neucler Medicine, Klinikum Grosshadern, Ludwig‐Maximilian University, Munich, Germany</affiliation></author><author><persName><forename type="first">T.</forename><surname>Gasser</surname></persName><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich, Germany</affiliation></author><author><persName><forename type="first">G.</forename><surname>Arnold</surname></persName><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich, Germany</affiliation></author><author><persName><surname>Oertel</surname><roleName type="degree">Dr.</roleName></persName><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich, Germany</affiliation><affiliation>Current Address: Department of Neurology, Philipps University, D‐35033 Marburg, 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>Hoboken</pubPlace><date type="published" when="1997-11"></date><biblScope unit="vol">12</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="898">898</biblScope><biblScope unit="page" to="902">902</biblScope></imprint></monogr><idno type="istex">507D526419C64997EB5E827665EEAA3AE79292F8</idno><idno type="DOI">10.1002/mds.870120610</idno><idno type="ArticleID">MDS870120610</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1997</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We investigated the cases of 55 patients with parkinsonism and prior dopaminomimetic therapy in whom the response to this treatment was questionable or reported to be negative. None of these patients had shown motor fluctuations prior to this study. We compared the results of imaging of dopamine‐D2 receptors by using [123l]iodobenzamide‐single‐photon‐emission computed tomography (IBZM‐SPECT) with the improvement in motor signs following a subcutaneous injection of apomorphine and a subsequent increase in oral dopaminomimetic therapy. IBZM‐SPECT accurately predicted a positive or negative response to apomorphine in 37 (84%) of 44 patients. The sensitivity/specificity was calculated as 96.3%/64.7%. The sensitivity/specificity of IBZM‐SPECT for the response to oral treatment with levodopa (L‐dopa) was calculated as 100%/75%. After a follow‐up period of 2–4 years, 25 patients developed motor fluctuations. All of these patients had normal IBZM binding. Nine developed clinical signs indicating a basal ganglia disorder other than Parkinson's disease. Eight of these nine patients had reduced, and one patient had normal, IBZM binding. We conclude that normal IBZM binding is a useful predictor of a good response to dopaminergic drugs in patients with parkinsonism and a questionable response to previous dopaminomimetic therapy. Reduced IBZM binding seems to exclude a diagnosis of Parkinson's disease, because none of the latter patients clearly benefited from L‐dopa and 66.7% developed clinical signs indicating another disorder of the basal ganglia.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Computed tomography</term></item><item><term>Dopamine agonist</term></item><item><term>IBZM‐SPECT</term></item><item><term>[123I]Iodobenzamide</term></item><item><term>Levodopa</term></item><item><term>Parkinson's disease</term></item><item><term>Multiple‐system atrophy</term></item><item><term>Single‐photon‐emission computed tomography</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="1996-01-31">Received</change><change when="1997-01-21">Registration</change><change when="1997-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/507D526419C64997EB5E827665EEAA3AE79292F8/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. 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H.</givenNames><familyName>Oertel</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neucler Medicine, Klinikum Grosshadern, Ludwig‐Maximilian University, Munich, Germany</unparsedAffiliation></affiliation><affiliation xml:id="curr1" countryCode="DE"><unparsedAffiliation>Department of Neurology, Philipps University, D‐35033 Marburg, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Computed tomography</keyword><keyword xml:id="kwd2">Dopamine agonist</keyword><keyword xml:id="kwd3">IBZM‐SPECT</keyword><keyword xml:id="kwd4">[<sup>123</sup>I]Iodobenzamide</keyword><keyword xml:id="kwd5">Levodopa</keyword><keyword xml:id="kwd6">Parkinson's disease</keyword><keyword xml:id="kwd7">Multiple‐system atrophy</keyword><keyword xml:id="kwd8">Single‐photon‐emission computed tomography</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We investigated the cases of 55 patients with parkinsonism and prior dopaminomimetic therapy in whom the response to this treatment was questionable or reported to be negative. None of these patients had shown motor fluctuations prior to this study. We compared the results of imaging of dopamine‐D2 receptors by using [<sup>123</sup>l]iodobenzamide‐single‐photon‐emission computed tomography (IBZM‐SPECT) with the improvement in motor signs following a subcutaneous injection of apomorphine and a subsequent increase in oral dopaminomimetic therapy. IBZM‐SPECT accurately predicted a positive or negative response to apomorphine in 37 (84%) of 44 patients. The sensitivity/specificity was calculated as 96.3%/64.7%. The sensitivity/specificity of IBZM‐SPECT for the response to oral treatment with levodopa (L‐dopa) was calculated as 100%/75%. After a follow‐up period of 2–4 years, 25 patients developed motor fluctuations. All of these patients had normal IBZM binding. Nine developed clinical signs indicating a basal ganglia disorder other than Parkinson's disease. Eight of these nine patients had reduced, and one patient had normal, IBZM binding. We conclude that normal IBZM binding is a useful predictor of a good response to dopaminergic drugs in patients with parkinsonism and a questionable response to previous dopaminomimetic therapy. Reduced IBZM binding seems to exclude a diagnosis of Parkinson's disease, because none of the latter patients clearly benefited from L‐dopa and 66.7% developed clinical signs indicating another disorder of the basal ganglia.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>[123]IBZM Binding predicts dopaminergic responsiveness in patients with parkinsonism and previous dopaminomimetic therapy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>IBZM‐SPECT AND THERAPY FOR PARKINSONISM</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>[</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Schwarz</namePart><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich, Germany</affiliation><description>Correspondence: Department of Neurology, University of Ulm, RKU, Oberer Eselsberg 45, 89081 Ulm, Germany (current address)</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Tatsch</namePart><affiliation>Department of Neucler Medicine, Klinikum Grosshadern, Ludwig‐Maximilian University, Munich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T.</namePart><namePart type="family">Gasser</namePart><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Arnold</namePart><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Oertel</namePart><affiliation>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, 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">1997-11</dateIssued><dateCaptured encoding="w3cdtf">1996-01-31</dateCaptured><dateValid encoding="w3cdtf">1997-01-21</dateValid><copyrightDate encoding="w3cdtf">1997</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="tables">2</extent><extent unit="references">17</extent></physicalDescription><abstract lang="en">We investigated the cases of 55 patients with parkinsonism and prior dopaminomimetic therapy in whom the response to this treatment was questionable or reported to be negative. None of these patients had shown motor fluctuations prior to this study. We compared the results of imaging of dopamine‐D2 receptors by using [123l]iodobenzamide‐single‐photon‐emission computed tomography (IBZM‐SPECT) with the improvement in motor signs following a subcutaneous injection of apomorphine and a subsequent increase in oral dopaminomimetic therapy. IBZM‐SPECT accurately predicted a positive or negative response to apomorphine in 37 (84%) of 44 patients. The sensitivity/specificity was calculated as 96.3%/64.7%. The sensitivity/specificity of IBZM‐SPECT for the response to oral treatment with levodopa (L‐dopa) was calculated as 100%/75%. After a follow‐up period of 2–4 years, 25 patients developed motor fluctuations. All of these patients had normal IBZM binding. Nine developed clinical signs indicating a basal ganglia disorder other than Parkinson's disease. Eight of these nine patients had reduced, and one patient had normal, IBZM binding. We conclude that normal IBZM binding is a useful predictor of a good response to dopaminergic drugs in patients with parkinsonism and a questionable response to previous dopaminomimetic therapy. Reduced IBZM binding seems to exclude a diagnosis of Parkinson's disease, because none of the latter patients clearly benefited from L‐dopa and 66.7% developed clinical signs indicating another disorder of the basal ganglia.</abstract><subject lang="en"><genre>Keywords</genre><topic>Computed tomography</topic><topic>Dopamine agonist</topic><topic>IBZM‐SPECT</topic><topic>[123I]Iodobenzamide</topic><topic>Levodopa</topic><topic>Parkinson's disease</topic><topic>Multiple‐system atrophy</topic><topic>Single‐photon‐emission computed tomography</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>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>1997</date><detail type="volume"><caption>vol.</caption><number>12</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>898</start><end>902</end><total>5</total></extent></part></relatedItem><identifier type="istex">507D526419C64997EB5E827665EEAA3AE79292F8</identifier><identifier type="DOI">10.1002/mds.870120610</identifier><identifier type="ArticleID">MDS870120610</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1997 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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