Neurological impairment and recovery in Wilson's disease: evidence from PET and MRI
Identifieur interne : 002739 ( Main/Corpus ); précédent : 002738; suivant : 002740Neurological impairment and recovery in Wilson's disease: evidence from PET and MRI
Auteurs : Gottfried Schlaug ; Harald Hefter ; Volkher Engelbrecht ; Torsten Kuwert ; Stephan Arnold ; Gerhard Stöcklin ; Rüdiger J. SeitzSource :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1995.
Abstract
We studied the relationship of regional cerebral glucose consumption (rCMRGlc) and striatal dopamine D2 receptor binding as assessed with positron emission tomography (PET) with the structural abnormalities of the brain in magnetic resonance images (MR), and the degree of neurological impairment in 18 patients with Wilson's disease (WD). The rCMRGlc was determined in the. basal ganglia, the thalamus, the cerebral cortex, and the cerebellar hemispheres. The severity of neurological signs, defined by semiquantitative motor impairment scores, correlated highly (r = −0.80) with the reduction of striatal rCMRGlc. Clinical scores, striatal rCMRGlc, and the degree of MRI abnormalities showed no correlation with different indices of dopamine D2 receptor binding. Sequential PET measurements in three patients during treatment with chelating agents revealed a moderate increase of striatal rCMRGlc (in two patients) and a moderate to marked increase of striatal D2 receptor binding (in three patients) in association with clinical improvement. Our data suggest that the rCMRGlc represents a sensitive and objective measure for assessing and monitoring striatal and extrastriatal involvement in WD. The lack of correlation between the dopamine D2 receptor binding and striatal rCMRGlc and structural abnormalities may be explained by the wide spectrum of clinical manifestations and different responses to treatment in WD patients.
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DOI: 10.1016/0022-510X(95)00293-B
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Neurological impairment and recovery in Wilson's disease: evidence from PET and MRI</title><author><name sortKey="Schlaug, Gottfried" sort="Schlaug, Gottfried" uniqKey="Schlaug G" first="Gottfried" last="Schlaug">Gottfried Schlaug</name><affiliation><mods:affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hefter, Harald" sort="Hefter, Harald" uniqKey="Hefter H" first="Harald" last="Hefter">Harald Hefter</name><affiliation><mods:affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Engelbrecht, Volkher" sort="Engelbrecht, Volkher" uniqKey="Engelbrecht V" first="Volkher" last="Engelbrecht">Volkher Engelbrecht</name><affiliation><mods:affiliation>Department of Diagnostic Radiology, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Kuwert, Torsten" sort="Kuwert, Torsten" uniqKey="Kuwert T" first="Torsten" last="Kuwert">Torsten Kuwert</name><affiliation><mods:affiliation>Department of Nuclear Medicine, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Arnold, Stephan" sort="Arnold, Stephan" uniqKey="Arnold S" first="Stephan" last="Arnold">Stephan Arnold</name><affiliation><mods:affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Stocklin, Gerhard" sort="Stocklin, Gerhard" uniqKey="Stocklin G" first="Gerhard" last="Stöcklin">Gerhard Stöcklin</name><affiliation><mods:affiliation>Institute of Nuclear Chemistry, Research Center Jülich, Jülich, Germany</mods:affiliation></affiliation></author><author><name sortKey="Seitz, Rudiger J" sort="Seitz, Rudiger J" uniqKey="Seitz R" first="Rüdiger J." last="Seitz">Rüdiger J. Seitz</name><affiliation><mods:affiliation>Corresponding author. Tel.: 211/811-8974; Fax: 211/811-8469.</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A3071995EE0B39F7F12405783E8D15BED88ACC27</idno><date when="1996" year="1996">1996</date><idno type="doi">10.1016/0022-510X(95)00293-B</idno><idno type="url">https://api.istex.fr/document/A3071995EE0B39F7F12405783E8D15BED88ACC27/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002739</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Neurological impairment and recovery in Wilson's disease: evidence from PET and MRI</title><author><name sortKey="Schlaug, Gottfried" sort="Schlaug, Gottfried" uniqKey="Schlaug G" first="Gottfried" last="Schlaug">Gottfried Schlaug</name><affiliation><mods:affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hefter, Harald" sort="Hefter, Harald" uniqKey="Hefter H" first="Harald" last="Hefter">Harald Hefter</name><affiliation><mods:affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Engelbrecht, Volkher" sort="Engelbrecht, Volkher" uniqKey="Engelbrecht V" first="Volkher" last="Engelbrecht">Volkher Engelbrecht</name><affiliation><mods:affiliation>Department of Diagnostic Radiology, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Kuwert, Torsten" sort="Kuwert, Torsten" uniqKey="Kuwert T" first="Torsten" last="Kuwert">Torsten Kuwert</name><affiliation><mods:affiliation>Department of Nuclear Medicine, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Arnold, Stephan" sort="Arnold, Stephan" uniqKey="Arnold S" first="Stephan" last="Arnold">Stephan Arnold</name><affiliation><mods:affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</mods:affiliation></affiliation></author><author><name sortKey="Stocklin, Gerhard" sort="Stocklin, Gerhard" uniqKey="Stocklin G" first="Gerhard" last="Stöcklin">Gerhard Stöcklin</name><affiliation><mods:affiliation>Institute of Nuclear Chemistry, Research Center Jülich, Jülich, Germany</mods:affiliation></affiliation></author><author><name sortKey="Seitz, Rudiger J" sort="Seitz, Rudiger J" uniqKey="Seitz R" first="Rüdiger J." last="Seitz">Rüdiger J. Seitz</name><affiliation><mods:affiliation>Corresponding author. Tel.: 211/811-8974; Fax: 211/811-8469.</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="ISSN">0022-510X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995">1995</date><biblScope unit="volume">136</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="129">129</biblScope><biblScope unit="page" to="139">139</biblScope></imprint><idno type="ISSN">0022-510X</idno></series><idno type="istex">A3071995EE0B39F7F12405783E8D15BED88ACC27</idno><idno type="DOI">10.1016/0022-510X(95)00293-B</idno><idno type="PII">0022-510X(95)00293-B</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-510X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We studied the relationship of regional cerebral glucose consumption (rCMRGlc) and striatal dopamine D2 receptor binding as assessed with positron emission tomography (PET) with the structural abnormalities of the brain in magnetic resonance images (MR), and the degree of neurological impairment in 18 patients with Wilson's disease (WD). The rCMRGlc was determined in the. basal ganglia, the thalamus, the cerebral cortex, and the cerebellar hemispheres. The severity of neurological signs, defined by semiquantitative motor impairment scores, correlated highly (r = −0.80) with the reduction of striatal rCMRGlc. Clinical scores, striatal rCMRGlc, and the degree of MRI abnormalities showed no correlation with different indices of dopamine D2 receptor binding. Sequential PET measurements in three patients during treatment with chelating agents revealed a moderate increase of striatal rCMRGlc (in two patients) and a moderate to marked increase of striatal D2 receptor binding (in three patients) in association with clinical improvement. Our data suggest that the rCMRGlc represents a sensitive and objective measure for assessing and monitoring striatal and extrastriatal involvement in WD. The lack of correlation between the dopamine D2 receptor binding and striatal rCMRGlc and structural abnormalities may be explained by the wide spectrum of clinical manifestations and different responses to treatment in WD patients.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Gottfried Schlaug</name><affiliations><json:string>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>Harald Hefter</name><affiliations><json:string>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>Volkher Engelbrecht</name><affiliations><json:string>Department of Diagnostic Radiology, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>Torsten Kuwert</name><affiliations><json:string>Department of Nuclear Medicine, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>Stephan Arnold</name><affiliations><json:string>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</json:string></affiliations></json:item><json:item><name>Gerhard Stöcklin</name><affiliations><json:string>Institute of Nuclear Chemistry, Research Center Jülich, Jülich, Germany</json:string></affiliations></json:item><json:item><name>Rüdiger J. Seitz</name><affiliations><json:string>Corresponding author. Tel.: 211/811-8974; Fax: 211/811-8469.</json:string><json:string>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Clinical section</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Wilson's disease</value></json:item><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>Regional cerebral glucose metabolism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dopamine D2 receptor, Magnetic resonance imaging</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We studied the relationship of regional cerebral glucose consumption (rCMRGlc) and striatal dopamine D2 receptor binding as assessed with positron emission tomography (PET) with the structural abnormalities of the brain in magnetic resonance images (MR), and the degree of neurological impairment in 18 patients with Wilson's disease (WD). The rCMRGlc was determined in the. basal ganglia, the thalamus, the cerebral cortex, and the cerebellar hemispheres. The severity of neurological signs, defined by semiquantitative motor impairment scores, correlated highly (r = −0.80) with the reduction of striatal rCMRGlc. Clinical scores, striatal rCMRGlc, and the degree of MRI abnormalities showed no correlation with different indices of dopamine D2 receptor binding. Sequential PET measurements in three patients during treatment with chelating agents revealed a moderate increase of striatal rCMRGlc (in two patients) and a moderate to marked increase of striatal D2 receptor binding (in three patients) in association with clinical improvement. Our data suggest that the rCMRGlc represents a sensitive and objective measure for assessing and monitoring striatal and extrastriatal involvement in WD. The lack of correlation between the dopamine D2 receptor binding and striatal rCMRGlc and structural abnormalities may be explained by the wide spectrum of clinical manifestations and different responses to treatment in WD patients.</abstract><qualityIndicators><score>7.448</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1431</abstractCharCount><pdfWordCount>6642</pdfWordCount><pdfCharCount>43489</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>204</abstractWordCount></qualityIndicators><title>Neurological impairment and recovery in Wilson's disease: evidence from PET and MRI</title><pii><json:string>0022-510X(95)00293-B</json:string></pii><genre><json:string>research-article</json:string></genre><serie><pages><last>34</last><first>19</first></pages><genre></genre><language><json:string>unknown</json:string></language><title>Parkinson's disease</title></serie><host><volume>136</volume><pii><json:string>S0022-510X(00)X0005-6</json:string></pii><pages><last>139</last><first>129</first></pages><issn><json:string>0022-510X</json:string></issn><issue>1–2</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><title>Journal of the Neurological Sciences</title><publicationDate>1996</publicationDate></host><categories><wos><json:string>CLINICAL NEUROLOGY</json:string><json:string>NEUROIMAGING</json:string><json:string>NEUROSCIENCES</json:string></wos></categories><publicationDate>1995</publicationDate><copyrightDate>1996</copyrightDate><doi><json:string>10.1016/0022-510X(95)00293-B</json:string></doi><id>A3071995EE0B39F7F12405783E8D15BED88ACC27</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/A3071995EE0B39F7F12405783E8D15BED88ACC27/fulltext/pdf</uri></json:item><json:item><original>true</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/A3071995EE0B39F7F12405783E8D15BED88ACC27/fulltext/txt</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/A3071995EE0B39F7F12405783E8D15BED88ACC27/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/A3071995EE0B39F7F12405783E8D15BED88ACC27/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Neurological impairment and recovery in Wilson's disease: evidence from PET and MRI</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1996</date></publicationStmt><notesStmt><note type="content">Section title: Research article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Neurological impairment and recovery in Wilson's disease: evidence from PET and MRI</title><author><persName><forename type="first">Gottfried</forename><surname>Schlaug</surname></persName><affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</affiliation></author><author><persName><forename type="first">Harald</forename><surname>Hefter</surname></persName><affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</affiliation></author><author><persName><forename type="first">Volkher</forename><surname>Engelbrecht</surname></persName><affiliation>Department of Diagnostic Radiology, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany</affiliation></author><author><persName><forename type="first">Torsten</forename><surname>Kuwert</surname></persName><affiliation>Department of Nuclear Medicine, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany</affiliation></author><author><persName><forename type="first">Stephan</forename><surname>Arnold</surname></persName><affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</affiliation></author><author><persName><forename type="first">Gerhard</forename><surname>Stöcklin</surname></persName><affiliation>Institute of Nuclear Chemistry, Research Center Jülich, Jülich, Germany</affiliation></author><author><persName><forename type="first">Rüdiger J.</forename><surname>Seitz</surname></persName><affiliation>Corresponding author. Tel.: 211/811-8974; Fax: 211/811-8469.</affiliation><affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</affiliation></author></analytic><monogr><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="pISSN">0022-510X</idno><idno type="PII">S0022-510X(00)X0005-6</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995"></date><biblScope unit="volume">136</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="129">129</biblScope><biblScope unit="page" to="139">139</biblScope></imprint></monogr><idno type="istex">A3071995EE0B39F7F12405783E8D15BED88ACC27</idno><idno type="DOI">10.1016/0022-510X(95)00293-B</idno><idno type="PII">0022-510X(95)00293-B</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1996</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We studied the relationship of regional cerebral glucose consumption (rCMRGlc) and striatal dopamine D2 receptor binding as assessed with positron emission tomography (PET) with the structural abnormalities of the brain in magnetic resonance images (MR), and the degree of neurological impairment in 18 patients with Wilson's disease (WD). The rCMRGlc was determined in the. basal ganglia, the thalamus, the cerebral cortex, and the cerebellar hemispheres. The severity of neurological signs, defined by semiquantitative motor impairment scores, correlated highly (r = −0.80) with the reduction of striatal rCMRGlc. Clinical scores, striatal rCMRGlc, and the degree of MRI abnormalities showed no correlation with different indices of dopamine D2 receptor binding. Sequential PET measurements in three patients during treatment with chelating agents revealed a moderate increase of striatal rCMRGlc (in two patients) and a moderate to marked increase of striatal D2 receptor binding (in three patients) in association with clinical improvement. Our data suggest that the rCMRGlc represents a sensitive and objective measure for assessing and monitoring striatal and extrastriatal involvement in WD. The lack of correlation between the dopamine D2 receptor binding and striatal rCMRGlc and structural abnormalities may be explained by the wide spectrum of clinical manifestations and different responses to treatment in WD patients.</p></abstract><textClass><keywords scheme="keyword"><list><head>Article category</head><item><term>Clinical section</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Wilson's disease</term></item><item><term>Positron emission tomography</term></item><item><term>Regional cerebral glucose metabolism</term></item><item><term>Dopamine D2 receptor, Magnetic resonance imaging</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-09-08">Registration</change><change when="1995-08-29">Modified</change><change when="1995">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>JNS</jid><aid>9500293B</aid><ce:pii>0022-510X(95)00293-B</ce:pii><ce:doi>10.1016/0022-510X(95)00293-B</ce:doi><ce:copyright type="unknown" year="1996"></ce:copyright><ce:doctopics><ce:doctopic><ce:text>Clinical section</ce:text></ce:doctopic></ce:doctopics></item-info><head><ce:dochead><ce:textfn>Research article</ce:textfn></ce:dochead><ce:title>Neurological impairment and recovery in Wilson's disease: evidence from PET and MRI</ce:title><ce:author-group><ce:author><ce:given-name>Gottfried</ce:given-name><ce:surname>Schlaug</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Harald</ce:given-name><ce:surname>Hefter</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Volkher</ce:given-name><ce:surname>Engelbrecht</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Torsten</ce:given-name><ce:surname>Kuwert</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>c</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Stephan</ce:given-name><ce:surname>Arnold</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Gerhard</ce:given-name><ce:surname>Stöcklin</ce:surname><ce:cross-ref refid="AFF4"><ce:sup>d</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Rüdiger J.</ce:given-name><ce:surname>Seitz</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Diagnostic Radiology, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Department of Nuclear Medicine, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany</ce:textfn></ce:affiliation><ce:affiliation id="AFF4"><ce:label>d</ce:label><ce:textfn>Institute of Nuclear Chemistry, Research Center Jülich, Jülich, Germany</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Corresponding author. Tel.: 211/811-8974; Fax: 211/811-8469.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="2" month="5" year="1995"></ce:date-received><ce:date-revised day="29" month="8" year="1995"></ce:date-revised><ce:date-accepted day="8" month="9" year="1995"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>We studied the relationship of regional cerebral glucose consumption (rCMRGlc) and striatal dopamine D2 receptor binding as assessed with positron emission tomography (PET) with the structural abnormalities of the brain in magnetic resonance images (MR), and the degree of neurological impairment in 18 patients with Wilson's disease (WD). The rCMRGlc was determined in the. basal ganglia, the thalamus, the cerebral cortex, and the cerebellar hemispheres. The severity of neurological signs, defined by semiquantitative motor impairment scores, correlated highly (<ce:italic>r</ce:italic> = −0.80) with the reduction of striatal rCMRGlc. Clinical scores, striatal rCMRGlc, and the degree of MRI abnormalities showed no correlation with different indices of dopamine D2 receptor binding. Sequential PET measurements in three patients during treatment with chelating agents revealed a moderate increase of striatal rCMRGlc (in two patients) and a moderate to marked increase of striatal D2 receptor binding (in three patients) in association with clinical improvement. Our data suggest that the rCMRGlc represents a sensitive and objective measure for assessing and monitoring striatal and extrastriatal involvement in WD. The lack of correlation between the dopamine D2 receptor binding and striatal rCMRGlc and structural abnormalities may be explained by the wide spectrum of clinical manifestations and different responses to treatment in WD patients.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Wilson's disease</ce:text></ce:keyword><ce:keyword><ce:text>Positron emission tomography</ce:text></ce:keyword><ce:keyword><ce:text>Regional cerebral glucose metabolism</ce:text></ce:keyword><ce:keyword><ce:text>Dopamine D2 receptor, Magnetic resonance imaging</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Neurological impairment and recovery in Wilson's disease: evidence from PET and MRI</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Neurological impairment and recovery in Wilson's disease: evidence from PET and MRI</title></titleInfo><name type="personal"><namePart type="given">Gottfried</namePart><namePart type="family">Schlaug</namePart><affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Harald</namePart><namePart type="family">Hefter</namePart><affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Volkher</namePart><namePart type="family">Engelbrecht</namePart><affiliation>Department of Diagnostic Radiology, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Torsten</namePart><namePart type="family">Kuwert</namePart><affiliation>Department of Nuclear Medicine, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stephan</namePart><namePart type="family">Arnold</namePart><affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gerhard</namePart><namePart type="family">Stöcklin</namePart><affiliation>Institute of Nuclear Chemistry, Research Center Jülich, Jülich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rüdiger J.</namePart><namePart type="family">Seitz</namePart><affiliation>Corresponding author. Tel.: 211/811-8974; Fax: 211/811-8469.</affiliation><affiliation>Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1995</dateIssued><dateValid encoding="w3cdtf">1995-09-08</dateValid><dateModified encoding="w3cdtf">1995-08-29</dateModified><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">We studied the relationship of regional cerebral glucose consumption (rCMRGlc) and striatal dopamine D2 receptor binding as assessed with positron emission tomography (PET) with the structural abnormalities of the brain in magnetic resonance images (MR), and the degree of neurological impairment in 18 patients with Wilson's disease (WD). The rCMRGlc was determined in the. basal ganglia, the thalamus, the cerebral cortex, and the cerebellar hemispheres. The severity of neurological signs, defined by semiquantitative motor impairment scores, correlated highly (r = −0.80) with the reduction of striatal rCMRGlc. Clinical scores, striatal rCMRGlc, and the degree of MRI abnormalities showed no correlation with different indices of dopamine D2 receptor binding. Sequential PET measurements in three patients during treatment with chelating agents revealed a moderate increase of striatal rCMRGlc (in two patients) and a moderate to marked increase of striatal D2 receptor binding (in three patients) in association with clinical improvement. Our data suggest that the rCMRGlc represents a sensitive and objective measure for assessing and monitoring striatal and extrastriatal involvement in WD. The lack of correlation between the dopamine D2 receptor binding and striatal rCMRGlc and structural abnormalities may be explained by the wide spectrum of clinical manifestations and different responses to treatment in WD patients.</abstract><note type="content">Section title: Research article</note><subject><genre>Article category</genre><topic>Clinical section</topic></subject><subject><genre>Keywords</genre><topic>Wilson's disease</topic><topic>Positron emission tomography</topic><topic>Regional cerebral glucose metabolism</topic><topic>Dopamine D2 receptor, Magnetic resonance imaging</topic></subject><relatedItem type="host"><titleInfo><title>Journal of the Neurological Sciences</title></titleInfo><titleInfo type="abbreviated"><title>JNS</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">199603</dateIssued></originInfo><identifier type="ISSN">0022-510X</identifier><identifier type="PII">S0022-510X(00)X0005-6</identifier><part><date>199603</date><detail type="volume"><number>136</number><caption>vol.</caption></detail><detail type="issue"><number>1–2</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>202</end></extent><extent unit="pages"><start>129</start><end>139</end></extent></part></relatedItem><identifier type="istex">A3071995EE0B39F7F12405783E8D15BED88ACC27</identifier><identifier type="DOI">10.1016/0022-510X(95)00293-B</identifier><identifier type="PII">0022-510X(95)00293-B</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/A3071995EE0B39F7F12405783E8D15BED88ACC27/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROIMAGING</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments></istex></record>Pour manipuler ce document sous Unix (Dilib)
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