Neuropathy as a potential complication of levodopa use in Parkinson's disease
Identifieur interne : 000564 ( Istex/Corpus ); précédent : 000563; suivant : 000565Neuropathy as a potential complication of levodopa use in Parkinson's disease
Auteurs : Cory Toth ; Martin Sutton Brown ; Sarah Furtado ; Oksana Suchowersky ; Douglas ZochodneSource :
- Movement Disorders [ 0885-3185 ] ; 2008-10-15.
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Abstract
The presence and potential etiologies of peripheral neuropathy (PN) in patients with Parkinson's Disease (PD) is unknown. We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD‐IPN) was compared to a group of PD patients without PN (PD‐only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD‐IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD‐IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime L‐dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD‐IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD. © 2008 Movement Disorder Society
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DOI: 10.1002/mds.22137
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ISTEX:5446F3CBE1DEE65F8B71BB768C0F06C4889691EFLe document en format XML
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We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD‐IPN) was compared to a group of PD patients without PN (PD‐only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD‐IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD‐IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime L‐dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD‐IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD. © 2008 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Cory Toth MD</name><affiliations><json:string>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</json:string><json:string>Department of Clinical Neurosciences, HMRB Room 155, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada</json:string></affiliations></json:item><json:item><name>Martin Sutton Brown MD</name><affiliations><json:string>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</json:string></affiliations></json:item><json:item><name>Sarah Furtado MD, PhD</name><affiliations><json:string>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</json:string></affiliations></json:item><json:item><name>Oksana Suchowersky MD</name><affiliations><json:string>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</json:string></affiliations></json:item><json:item><name>Douglas Zochodne MD</name><affiliations><json:string>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>peripheral neuropathy</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>levodopa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cobalamin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>homocysteine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>methylmalonic acid</value></json:item></subject><articleId><json:string>MDS22137</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>The presence and potential etiologies of peripheral neuropathy (PN) in patients with Parkinson's Disease (PD) is unknown. We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD‐IPN) was compared to a group of PD patients without PN (PD‐only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD‐IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD‐IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime L‐dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD‐IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD. © 2008 Movement Disorder Society</abstract><qualityIndicators><score>7.544</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1341</abstractCharCount><pdfWordCount>5758</pdfWordCount><pdfCharCount>37305</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>212</abstractWordCount></qualityIndicators><title>Neuropathy as a potential complication of levodopa use in Parkinson's disease</title><genre><json:string>article</json:string></genre><host><title>Movement Disorders</title><language><json:string>unknown</json:string></language><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi><issn><json:string>0885-3185</json:string></issn><eissn><json:string>1531-8257</json:string></eissn><publisherId><json:string>MDS</json:string></publisherId><volume>23</volume><issue>13</issue><pages><first>1850</first><last>1859</last><total>10</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Research Article</value></json:item></subject></host><categories><wos><json:string>science</json:string><json:string>clinical neurology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string></inist></categories><publicationDate>2008</publicationDate><copyrightDate>2008</copyrightDate><doi><json:string>10.1002/mds.22137</json:string></doi><id>5446F3CBE1DEE65F8B71BB768C0F06C4889691EF</id><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api-v5.istex.fr/document/5446F3CBE1DEE65F8B71BB768C0F06C4889691EF/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api-v5.istex.fr/document/5446F3CBE1DEE65F8B71BB768C0F06C4889691EF/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api-v5.istex.fr/document/5446F3CBE1DEE65F8B71BB768C0F06C4889691EF/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Neuropathy as a potential complication of levodopa use in Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Copyright © 2008 Movement Disorder Society</p></availability><date>2008</date></publicationStmt><notesStmt><note>Teva Neuroscience</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Neuropathy as a potential complication of levodopa use in Parkinson's disease</title><author xml:id="author-1"><persName><forename type="first">Cory</forename><surname>Toth</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</affiliation><affiliation>Department of Clinical Neurosciences, HMRB Room 155, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada</affiliation></author><author xml:id="author-2"><persName><forename type="first">Martin Sutton</forename><surname>Brown</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</affiliation></author><author xml:id="author-3"><persName><forename type="first">Sarah</forename><surname>Furtado</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</affiliation></author><author xml:id="author-4"><persName><forename type="first">Oksana</forename><surname>Suchowersky</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</affiliation></author><author xml:id="author-5"><persName><forename type="first">Douglas</forename><surname>Zochodne</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</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="2008-10-15"></date><biblScope unit="volume">23</biblScope><biblScope unit="issue">13</biblScope><biblScope unit="page" from="1850">1850</biblScope><biblScope unit="page" to="1859">1859</biblScope></imprint></monogr><idno type="istex">5446F3CBE1DEE65F8B71BB768C0F06C4889691EF</idno><idno type="DOI">10.1002/mds.22137</idno><idno type="ArticleID">MDS22137</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2008</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The presence and potential etiologies of peripheral neuropathy (PN) in patients with Parkinson's Disease (PD) is unknown. We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD‐IPN) was compared to a group of PD patients without PN (PD‐only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD‐IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD‐IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime L‐dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD‐IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD. © 2008 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>peripheral neuropathy</term></item><item><term>Parkinson's disease</term></item><item><term>levodopa</term></item><item><term>cobalamin</term></item><item><term>homocysteine</term></item><item><term>methylmalonic acid</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article-category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-05-27">Received</change><change when="2008-04-23">Registration</change><change when="2008-10-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/5446F3CBE1DEE65F8B71BB768C0F06C4889691EF/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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type="manuscriptAccepted" date="2008-04-23"></event><event type="firstOnline" date="2008-09-10"></event><event type="publishedOnlineFinalForm" date="2008-10-27"></event><event type="publishedOnlineAcceptedOrEarlyUnpaginated" date="2008-09-10"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.4.7 mode:FullText source:FullText result:FullText" date="2011-02-24"></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">1850</numbering><numbering type="pageLast">1859</numbering></numberingGroup><correspondenceTo>Department of Clinical Neurosciences, HMRB Room 155, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS22137.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="4"></count><count type="referenceTotal" number="40"></count><count type="wordTotal" number="6966"></count></countGroup><titleGroup><title type="main" xml:lang="en">Neuropathy as a potential complication of levodopa use in Parkinson's disease</title><title type="short" xml:lang="en">Peripheral Neuropathy in PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Cory</givenNames><familyName>Toth</familyName><degrees>MD</degrees></personName><contactDetails><email>corytoth@shaw.ca</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Martin Sutton</givenNames><familyName>Brown</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Sarah</givenNames><familyName>Furtado</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Oksana</givenNames><familyName>Suchowersky</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Douglas</givenNames><familyName>Zochodne</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">peripheral neuropathy</keyword><keyword xml:id="kwd2">Parkinson's disease</keyword><keyword xml:id="kwd3">levodopa</keyword><keyword xml:id="kwd4">cobalamin</keyword><keyword xml:id="kwd5">homocysteine</keyword><keyword xml:id="kwd6">methylmalonic acid</keyword></keywordGroup><fundingInfo><fundingAgency>Teva Neuroscience</fundingAgency></fundingInfo><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds22137:mds_22137_sm_SuppTab1"></mediaResource><caption>Supplementary Table 1</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds22137:mds_22137_sm_SuppTab2"></mediaResource><caption>Supplementary Table 2</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds22137:mds_22137_sm_SuppTab3"></mediaResource><caption>Supplementary Table 3</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The presence and potential etiologies of peripheral neuropathy (PN) in patients with Parkinson's Disease (PD) is unknown. We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD‐IPN) was compared to a group of PD patients without PN (PD‐only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD‐IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD‐IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime <sc>L</sc>‐dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD‐IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD. © 2008 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Neuropathy as a potential complication of levodopa use in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Peripheral Neuropathy in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Neuropathy as a potential complication of levodopa use in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Cory</namePart><namePart type="family">Toth</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</affiliation><affiliation>Department of Clinical Neurosciences, HMRB Room 155, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Martin Sutton</namePart><namePart type="family">Brown</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sarah</namePart><namePart type="family">Furtado</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Oksana</namePart><namePart type="family">Suchowersky</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Douglas</namePart><namePart type="family">Zochodne</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2008-10-15</dateIssued><dateCaptured encoding="w3cdtf">2007-05-27</dateCaptured><dateValid encoding="w3cdtf">2008-04-23</dateValid><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">4</extent><extent unit="references">40</extent><extent unit="words">6966</extent></physicalDescription><abstract lang="en">The presence and potential etiologies of peripheral neuropathy (PN) in patients with Parkinson's Disease (PD) is unknown. We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD‐IPN) was compared to a group of PD patients without PN (PD‐only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD‐IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD‐IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime L‐dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD‐IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD. © 2008 Movement Disorder Society</abstract><note type="funding">Teva Neuroscience</note><subject lang="en"><genre>keywords</genre><topic>peripheral neuropathy</topic><topic>Parkinson's disease</topic><topic>levodopa</topic><topic>cobalamin</topic><topic>homocysteine</topic><topic>methylmalonic acid</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="journal">journal</genre><note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supplementary Table 1 - Supplementary Table 2 - Supplementary Table 3 - </note><subject><genre>article-category</genre><topic>Research 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>2008</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>13</number></detail><extent unit="pages"><start>1850</start><end>1859</end><total>10</total></extent></part></relatedItem><identifier type="istex">5446F3CBE1DEE65F8B71BB768C0F06C4889691EF</identifier><identifier type="DOI">10.1002/mds.22137</identifier><identifier type="ArticleID">MDS22137</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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