3H-spiperone binding to lymphocytes fails in the differential diagnosis of de novo Parkinson syndromes
Identifieur interne : 000208 ( Main/Corpus ); précédent : 000207; suivant : 0002093H-spiperone binding to lymphocytes fails in the differential diagnosis of de novo Parkinson syndromes
Auteurs : G. Arnold ; B. Bondy ; O. Bandmann ; Th. Gasser ; J. Schwarz ; C. Trenkwalder ; M. Wagner ; W. Poewe ; H. OertelSource :
- Journal of Neural Transmission - Parkinson's Disease and Dementia Section [ 0936-3076 ] ; 1993-06-01.
Abstract
Summary: In order to investigate the diagnostic value of3H-spiperone binding capacity to lymphocytes in the differential diagnosis of de novo Parkinson's disease (idiopathic Parkinson syndrome, PD), we performed a double blind prospective study of spiperone binding capacity of 123 patients and 23 healthy control persons, belonging to different diagnostic groups (PD, Parkinsonian syndrome due to vascular lesions, multiple system atrophy [MSA], essential tremor). Diagnoses were based on medical history, clinical examination, CT or MRI scan, acute response to dopamimetric drugs, one year follow up, and long term response to L-DOPA treatment. Spiperone binding was assayed using ten different concentrations (0.03–3 nmol) in absence or presence of 1μmol (+)-butaclamol to determine nonsepecific binding. There was no significant difference in spiperone binding between patients with PD not treated with L-DOPA, and patients with other basal ganglia disorders including parkinsonian syndrome due to vascular lesions, multiple system atrophy, or progressive supranuclear palsy, and age matched controls. Binding was significantly higher in parkinsonian patients with PD treated with L-DOPA and patients with essential tremor. It is concluded that at present3H-spiperone binding gives no further information in the differential diagnosis of de novo Parkinson's disease.
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DOI: 10.1007/BF02251201
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Arnold</name><affiliation><mods:affiliation>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Bondy, B" sort="Bondy, B" uniqKey="Bondy B" first="B." last="Bondy">B. Bondy</name><affiliation><mods:affiliation>Department of Psychiatry, Ludwig-Maximilians, Universität München, München, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Bandmann, O" sort="Bandmann, O" uniqKey="Bandmann O" first="O." last="Bandmann">O. Bandmann</name><affiliation><mods:affiliation>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Gasser, Th" sort="Gasser, Th" uniqKey="Gasser T" first="Th." last="Gasser">Th. 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Oertel</name><affiliation><mods:affiliation>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neural Transmission - Parkinson's Disease and Dementia Section</title><title level="j" type="abbrev">J Neural Transm Gen Sect</title><idno type="ISSN">0936-3076</idno><idno type="eISSN">1435-1463</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1993-06-01">1993-06-01</date><biblScope unit="volume">5</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="107">107</biblScope><biblScope unit="page" to="116">116</biblScope></imprint><idno type="ISSN">0936-3076</idno></series><idno type="istex">BFC8F1E56BC24079A5ED5661C3385A0B7A8646C3</idno><idno type="DOI">10.1007/BF02251201</idno><idno type="ArticleID">Art4</idno><idno type="ArticleID">BF02251201</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0936-3076</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: In order to investigate the diagnostic value of3H-spiperone binding capacity to lymphocytes in the differential diagnosis of de novo Parkinson's disease (idiopathic Parkinson syndrome, PD), we performed a double blind prospective study of spiperone binding capacity of 123 patients and 23 healthy control persons, belonging to different diagnostic groups (PD, Parkinsonian syndrome due to vascular lesions, multiple system atrophy [MSA], essential tremor). Diagnoses were based on medical history, clinical examination, CT or MRI scan, acute response to dopamimetric drugs, one year follow up, and long term response to L-DOPA treatment. Spiperone binding was assayed using ten different concentrations (0.03–3 nmol) in absence or presence of 1μmol (+)-butaclamol to determine nonsepecific binding. There was no significant difference in spiperone binding between patients with PD not treated with L-DOPA, and patients with other basal ganglia disorders including parkinsonian syndrome due to vascular lesions, multiple system atrophy, or progressive supranuclear palsy, and age matched controls. Binding was significantly higher in parkinsonian patients with PD treated with L-DOPA and patients with essential tremor. It is concluded that at present3H-spiperone binding gives no further information in the differential diagnosis of de novo Parkinson's disease.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>Dr. G. Arnold</name><affiliations><json:string>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>B. Bondy</name><affiliations><json:string>Department of Psychiatry, Ludwig-Maximilians, Universität München, München, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>O. Bandmann</name><affiliations><json:string>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>Th. Gasser</name><affiliations><json:string>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>J. Schwarz</name><affiliations><json:string>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>C. Trenkwalder</name><affiliations><json:string>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>M. Wagner</name><affiliations><json:string>Department of Neurology, University of Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>W. Poewe</name><affiliations><json:string>Department of Neurology, University of Innsbruck, Austria</json:string><json:string>Department of Neurology, Universitäts-Klinikum Rudolf Virchow, Berlin, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>W. H. Oertel</name><affiliations><json:string>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</json:string></affiliations></json:item></author><articleId><json:string>Art4</json:string><json:string>BF02251201</json:string></articleId><language><json:string>eng</json:string></language><abstract>Summary: In order to investigate the diagnostic value of3H-spiperone binding capacity to lymphocytes in the differential diagnosis of de novo Parkinson's disease (idiopathic Parkinson syndrome, PD), we performed a double blind prospective study of spiperone binding capacity of 123 patients and 23 healthy control persons, belonging to different diagnostic groups (PD, Parkinsonian syndrome due to vascular lesions, multiple system atrophy [MSA], essential tremor). Diagnoses were based on medical history, clinical examination, CT or MRI scan, acute response to dopamimetric drugs, one year follow up, and long term response to L-DOPA treatment. Spiperone binding was assayed using ten different concentrations (0.03–3 nmol) in absence or presence of 1μmol (+)-butaclamol to determine nonsepecific binding. There was no significant difference in spiperone binding between patients with PD not treated with L-DOPA, and patients with other basal ganglia disorders including parkinsonian syndrome due to vascular lesions, multiple system atrophy, or progressive supranuclear palsy, and age matched controls. Binding was significantly higher in parkinsonian patients with PD treated with L-DOPA and patients with essential tremor. It is concluded that at present3H-spiperone binding gives no further information in the differential diagnosis of de novo Parkinson's disease.</abstract><qualityIndicators><score>6.118</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 774 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1370</abstractCharCount><pdfWordCount>3838</pdfWordCount><pdfCharCount>21992</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>190</abstractWordCount></qualityIndicators><title>3H-spiperone binding to lymphocytes fails in the differential diagnosis of de novo Parkinson syndromes</title><genre><json:string>research-article</json:string></genre><host><volume>5</volume><pages><last>116</last><first>107</first></pages><issn><json:string>0936-3076</json:string></issn><issue>2</issue><subject><json:item><value>Pharmacology/Toxicology</value></json:item><json:item><value>Psychiatry</value></json:item><json:item><value>Neurology</value></json:item></subject><journalId><json:string>722</json:string></journalId><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1435-1463</json:string></eissn><title>Journal of Neural Transmission - 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Diagnoses were based on medical history, clinical examination, CT or MRI scan, acute response to dopamimetric drugs, one year follow up, and long term response to L-DOPA treatment. Spiperone binding was assayed using ten different concentrations (0.03–3 nmol) in absence or presence of 1μmol (+)-butaclamol to determine nonsepecific binding. There was no significant difference in spiperone binding between patients with PD not treated with L-DOPA, and patients with other basal ganglia disorders including parkinsonian syndrome due to vascular lesions, multiple system atrophy, or progressive supranuclear palsy, and age matched controls. Binding was significantly higher in parkinsonian patients with PD treated with L-DOPA and patients with essential tremor. It is concluded that at present3H-spiperone binding gives no further information in the differential diagnosis of de novo Parkinson's disease.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Pharmacology/Toxicology</term></item><item><term>Psychiatry</term></item><item><term>Neurology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1992-04-27">Created</change><change when="1993-06-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/BFC8F1E56BC24079A5ED5661C3385A0B7A8646C3/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" 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in the differential diagnosis of de novo Parkinson syndromes</ArticleTitle><ArticleCategory>Full Papers</ArticleCategory><ArticleFirstPage>107</ArticleFirstPage><ArticleLastPage>116</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2005</Year><Month>10</Month><Day>24</Day></RegistrationDate><Received><Year>1992</Year><Month>4</Month><Day>27</Day></Received><Accepted><Year>1992</Year><Month>7</Month><Day>23</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1993</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>722</JournalID><VolumeIDStart>5</VolumeIDStart><VolumeIDEnd>5</VolumeIDEnd><IssueIDStart>2</IssueIDStart><IssueIDEnd>2</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" PresentAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><Prefix>Dr.</Prefix><GivenName>G.</GivenName><FamilyName>Arnold</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>B.</GivenName><FamilyName>Bondy</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>O.</GivenName><FamilyName>Bandmann</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Th.</GivenName><FamilyName>Gasser</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>J.</GivenName><FamilyName>Schwarz</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>C.</GivenName><FamilyName>Trenkwalder</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>M.</GivenName><FamilyName>Wagner</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3 Aff4"><AuthorName DisplayOrder="Western"><GivenName>W.</GivenName><FamilyName>Poewe</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>W.</GivenName><GivenName>H.</GivenName><FamilyName>Oertel</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgName>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München</OrgName><OrgAddress><Street>Marchioninistrasse 15</Street><Postcode>D-W-8000</Postcode><City>München 70</City><Country>Federal Republic of Germany</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Department of Psychiatry, Ludwig-Maximilians</OrgDivision><OrgName>Universität München</OrgName><OrgAddress><City>München</City><Country>Federal Republic of Germany</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>Department of Neurology</OrgDivision><OrgName>University of Innsbruck</OrgName><OrgAddress><Country>Austria</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Department of Neurology</OrgDivision><OrgName>Universitäts-Klinikum Rudolf Virchow</OrgName><OrgAddress><City>Berlin</City><Country>Federal Republic of Germany</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>In order to investigate the diagnostic value of<Superscript>3</Superscript>H-spiperone binding capacity to lymphocytes in the differential diagnosis of de novo Parkinson's disease (idiopathic Parkinson syndrome, PD), we performed a double blind prospective study of spiperone binding capacity of 123 patients and 23 healthy control persons, belonging to different diagnostic groups (PD, Parkinsonian syndrome due to vascular lesions, multiple system atrophy [MSA], essential tremor). Diagnoses were based on medical history, clinical examination, CT or MRI scan, acute response to dopamimetric drugs, one year follow up, and long term response to L-DOPA treatment. Spiperone binding was assayed using ten different concentrations (0.03–3 nmol) in absence or presence of 1μmol (+)-butaclamol to determine nonsepecific binding. There was no significant difference in spiperone binding between patients with PD not treated with L-DOPA, and patients with other basal ganglia disorders including parkinsonian syndrome due to vascular lesions, multiple system atrophy, or progressive supranuclear palsy, and age matched controls. Binding was significantly higher in parkinsonian patients with PD treated with L-DOPA and patients with essential tremor. It is concluded that at present<Superscript>3</Superscript>H-spiperone binding gives no further information in the differential diagnosis of de novo Parkinson's disease.</Para></Abstract><KeywordGroup Language="En"><Heading>Keywords</Heading><Keyword>Spiperone binding</Keyword><Keyword>Parkinson's disease</Keyword><Keyword>multiple system atrophy</Keyword><Keyword>vascular lesions</Keyword><Keyword>differential diagnosis</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>3H-spiperone binding to lymphocytes fails in the differential diagnosis of de novo Parkinson syndromes</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>3H-spiperone binding to lymphocytes fails in the differential diagnosis of de novo Parkinson syndromes</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="given">G.</namePart><namePart type="family">Arnold</namePart><affiliation>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B.</namePart><namePart type="family">Bondy</namePart><affiliation>Department of Psychiatry, Ludwig-Maximilians, Universität München, München, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O.</namePart><namePart type="family">Bandmann</namePart><affiliation>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Th.</namePart><namePart type="family">Gasser</namePart><affiliation>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Schwarz</namePart><affiliation>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Trenkwalder</namePart><affiliation>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Wagner</namePart><affiliation>Department of Neurology, University of Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.</namePart><namePart type="family">Poewe</namePart><affiliation>Department of Neurology, University of Innsbruck, Austria</affiliation><affiliation>Department of Neurology, Universitäts-Klinikum Rudolf Virchow, Berlin, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.</namePart><namePart type="given">H.</namePart><namePart type="family">Oertel</namePart><affiliation>Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität München, Marchioninistrasse 15, D-W-8000, München 70, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Vienna</placeTerm></place><dateCreated encoding="w3cdtf">1992-04-27</dateCreated><dateIssued encoding="w3cdtf">1993-06-01</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Summary: In order to investigate the diagnostic value of3H-spiperone binding capacity to lymphocytes in the differential diagnosis of de novo Parkinson's disease (idiopathic Parkinson syndrome, PD), we performed a double blind prospective study of spiperone binding capacity of 123 patients and 23 healthy control persons, belonging to different diagnostic groups (PD, Parkinsonian syndrome due to vascular lesions, multiple system atrophy [MSA], essential tremor). Diagnoses were based on medical history, clinical examination, CT or MRI scan, acute response to dopamimetric drugs, one year follow up, and long term response to L-DOPA treatment. Spiperone binding was assayed using ten different concentrations (0.03–3 nmol) in absence or presence of 1μmol (+)-butaclamol to determine nonsepecific binding. There was no significant difference in spiperone binding between patients with PD not treated with L-DOPA, and patients with other basal ganglia disorders including parkinsonian syndrome due to vascular lesions, multiple system atrophy, or progressive supranuclear palsy, and age matched controls. Binding was significantly higher in parkinsonian patients with PD treated with L-DOPA and patients with essential tremor. It is concluded that at present3H-spiperone binding gives no further information in the differential diagnosis of de novo Parkinson's disease.</abstract><note>Full Papers</note><relatedItem type="host"><titleInfo><title>Journal of Neural Transmission - Parkinson's Disease and Dementia Section</title></titleInfo><titleInfo type="abbreviated"><title>J Neural Transm Gen Sect</title></titleInfo><genre type="Journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1993-06-01</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Pharmacology/Toxicology</topic><topic>Psychiatry</topic><topic>Neurology</topic></subject><identifier type="ISSN">0936-3076</identifier><identifier type="eISSN">1435-1463</identifier><identifier type="JournalID">722</identifier><identifier type="IssueArticleCount">10</identifier><identifier type="VolumeIssueCount">3</identifier><part><date>1993</date><detail type="volume"><number>5</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="pages"><start>107</start><end>116</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1993</recordOrigin></recordInfo></relatedItem><identifier type="istex">BFC8F1E56BC24079A5ED5661C3385A0B7A8646C3</identifier><identifier type="DOI">10.1007/BF02251201</identifier><identifier type="ArticleID">Art4</identifier><identifier type="ArticleID">BF02251201</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag</accessCondition><recordInfo><recordContentSource>SPRINGER</recordContentSource><recordOrigin>Springer-Verlag, 1993</recordOrigin></recordInfo></mods></metadata><enrichments><istex:refBibTEI 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