Neuropathy as a potential complication of levodopa use in Parkinson's disease
Identifieur interne : 003313 ( Main/Merge ); précédent : 003312; suivant : 003314Neuropathy as a potential complication of levodopa use in Parkinson's disease
Auteurs : Cory Toth [Canada] ; Martin Sutton Brown [Canada] ; Sarah Furtado [Canada] ; Oksana Suchowersky [Canada] ; Douglas Zochodne [Canada]Source :
- Movement Disorders [ 0885-3185 ] ; 2008-10-15.
English descriptors
- KwdEn :
- Analysis of Variance, Antiparkinson Agents (adverse effects), Female, Homocysteine (blood), Humans, Levodopa (adverse effects), Male, Methylmalonic Acid (blood), Parkinson Disease (complications), Parkinson Disease (drug therapy), Parkinson's disease, Peripheral Nervous System Diseases (etiology), Retrospective Studies, Vitamin B 12 (blood), cobalamin, homocysteine, levodopa, methylmalonic acid, peripheral neuropathy.
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , blood : Homocysteine, Methylmalonic Acid, Vitamin B 12.
- complications : Parkinson Disease.
- drug therapy : Parkinson Disease.
- etiology : Peripheral Nervous System Diseases.
- Analysis of Variance, Female, Humans, Male, Retrospective Studies.
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
Url:
DOI: 10.1002/mds.22137
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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="2008-10-15">2008-10-15</date><biblScope unit="vol">23</biblScope><biblScope unit="issue">13</biblScope><biblScope unit="page" from="1850">1850</biblScope><biblScope unit="page" to="1859">1859</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">5446F3CBE1DEE65F8B71BB768C0F06C4889691EF</idno><idno type="DOI">10.1002/mds.22137</idno><idno type="ArticleID">MDS22137</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Analysis of Variance</term><term>Antiparkinson Agents (adverse effects)</term><term>Female</term><term>Homocysteine (blood)</term><term>Humans</term><term>Levodopa (adverse effects)</term><term>Male</term><term>Methylmalonic Acid (blood)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson's disease</term><term>Peripheral Nervous System Diseases (etiology)</term><term>Retrospective Studies</term><term>Vitamin B 12 (blood)</term><term>cobalamin</term><term>homocysteine</term><term>levodopa</term><term>methylmalonic acid</term><term>peripheral neuropathy</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Homocysteine</term><term>Methylmalonic Acid</term><term>Vitamin B 12</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Peripheral Nervous System Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Female</term><term>Humans</term><term>Male</term><term>Retrospective Studies</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml: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</div></front></TEI><double doi="10.1002/mds.22137"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neuropathy as a potential complication of levodopa use in Parkinson's disease</title><author><name sortKey="Toth, Cory" sort="Toth, Cory" uniqKey="Toth C" first="Cory" last="Toth">Cory Toth</name></author><author><name sortKey="Brown, Martin Sutton" sort="Brown, Martin Sutton" uniqKey="Brown M" first="Martin Sutton" last="Brown">Martin Sutton Brown</name></author><author><name sortKey="Furtado, Sarah" sort="Furtado, Sarah" uniqKey="Furtado S" first="Sarah" last="Furtado">Sarah Furtado</name></author><author><name sortKey="Suchowersky, Oksana" sort="Suchowersky, Oksana" uniqKey="Suchowersky O" first="Oksana" last="Suchowersky">Oksana Suchowersky</name></author><author><name sortKey="Zochodne, Douglas" sort="Zochodne, Douglas" uniqKey="Zochodne D" first="Douglas" last="Zochodne">Douglas Zochodne</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:5446F3CBE1DEE65F8B71BB768C0F06C4889691EF</idno><date when="2008" year="2008">2008</date><idno type="doi">10.1002/mds.22137</idno><idno type="url">https://api.istex.fr/document/5446F3CBE1DEE65F8B71BB768C0F06C4889691EF/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000482</idno><idno type="wicri:Area/Istex/Curation">000482</idno><idno type="wicri:Area/Istex/Checkpoint">001291</idno><idno type="wicri:doubleKey">0885-3185:2008:Toth C:neuropathy:as:a</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Neuropathy as a potential complication of levodopa use in Parkinson's disease</title><author><name sortKey="Toth, Cory" sort="Toth, Cory" uniqKey="Toth C" first="Cory" last="Toth">Cory Toth</name><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta</wicri:regionArea><orgName type="university">Université de Calgary</orgName><placeName><settlement type="city">Calgary</settlement><region type="state">Alberta</region></placeName></affiliation></author><author><name sortKey="Brown, Martin Sutton" sort="Brown, Martin Sutton" uniqKey="Brown M" first="Martin Sutton" last="Brown">Martin Sutton Brown</name><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta</wicri:regionArea><orgName type="university">Université de Calgary</orgName><placeName><settlement type="city">Calgary</settlement><region type="state">Alberta</region></placeName></affiliation></author><author><name sortKey="Furtado, Sarah" sort="Furtado, Sarah" uniqKey="Furtado S" first="Sarah" last="Furtado">Sarah Furtado</name><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta</wicri:regionArea><orgName type="university">Université de Calgary</orgName><placeName><settlement type="city">Calgary</settlement><region type="state">Alberta</region></placeName></affiliation></author><author><name sortKey="Suchowersky, Oksana" sort="Suchowersky, Oksana" uniqKey="Suchowersky O" first="Oksana" last="Suchowersky">Oksana Suchowersky</name><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta</wicri:regionArea><orgName type="university">Université de Calgary</orgName><placeName><settlement type="city">Calgary</settlement><region type="state">Alberta</region></placeName></affiliation></author><author><name sortKey="Zochodne, Douglas" sort="Zochodne, Douglas" uniqKey="Zochodne D" first="Douglas" last="Zochodne">Douglas Zochodne</name><affiliation wicri:level="4"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary, Calgary, Alberta</wicri:regionArea><orgName type="university">Université de Calgary</orgName><placeName><settlement type="city">Calgary</settlement><region type="state">Alberta</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2008-10-15">2008-10-15</date><biblScope unit="vol">23</biblScope><biblScope unit="issue">13</biblScope><biblScope unit="page" from="1850">1850</biblScope><biblScope unit="page" to="1859">1859</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">5446F3CBE1DEE65F8B71BB768C0F06C4889691EF</idno><idno type="DOI">10.1002/mds.22137</idno><idno type="ArticleID">MDS22137</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>cobalamin</term><term>homocysteine</term><term>levodopa</term><term>methylmalonic acid</term><term>peripheral neuropathy</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml: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</div></front></TEI></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neuropathy as a potential complication of levodopa use in Parkinson's disease.</title><author><name sortKey="Toth, Cory" sort="Toth, Cory" uniqKey="Toth C" first="Cory" last="Toth">Cory Toth</name><affiliation wicri:level="4"><nlm:affiliation>Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada. corytoth@shaw.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta</wicri:regionArea><orgName type="university">Université de Calgary</orgName><placeName><settlement type="city">Calgary</settlement><region type="state">Alberta</region></placeName></affiliation></author><author><name sortKey="Brown, Martin Sutton" sort="Brown, Martin Sutton" uniqKey="Brown M" first="Martin Sutton" last="Brown">Martin Sutton Brown</name></author><author><name sortKey="Furtado, Sarah" sort="Furtado, Sarah" uniqKey="Furtado S" first="Sarah" last="Furtado">Sarah Furtado</name></author><author><name sortKey="Suchowersky, Oksana" sort="Suchowersky, Oksana" uniqKey="Suchowersky O" first="Oksana" last="Suchowersky">Oksana Suchowersky</name></author><author><name sortKey="Zochodne, Douglas" sort="Zochodne, Douglas" uniqKey="Zochodne D" first="Douglas" last="Zochodne">Douglas Zochodne</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="doi">10.1002/mds.22137</idno><idno type="RBID">pubmed:18785232</idno><idno type="pmid">18785232</idno><idno type="wicri:Area/PubMed/Corpus">002039</idno><idno type="wicri:Area/PubMed/Curation">002039</idno><idno type="wicri:Area/PubMed/Checkpoint">002186</idno><idno type="wicri:Area/Ncbi/Merge">002324</idno><idno type="wicri:Area/Ncbi/Curation">002324</idno><idno type="wicri:Area/Ncbi/Checkpoint">002324</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Neuropathy as a potential complication of levodopa use in Parkinson's disease.</title><author><name sortKey="Toth, Cory" sort="Toth, Cory" uniqKey="Toth C" first="Cory" last="Toth">Cory Toth</name><affiliation wicri:level="4"><nlm:affiliation>Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada. corytoth@shaw.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta</wicri:regionArea><orgName type="university">Université de Calgary</orgName><placeName><settlement type="city">Calgary</settlement><region type="state">Alberta</region></placeName></affiliation></author><author><name sortKey="Brown, Martin Sutton" sort="Brown, Martin Sutton" uniqKey="Brown M" first="Martin Sutton" last="Brown">Martin Sutton Brown</name></author><author><name sortKey="Furtado, Sarah" sort="Furtado, Sarah" uniqKey="Furtado S" first="Sarah" last="Furtado">Sarah Furtado</name></author><author><name sortKey="Suchowersky, Oksana" sort="Suchowersky, Oksana" uniqKey="Suchowersky O" first="Oksana" last="Suchowersky">Oksana Suchowersky</name></author><author><name sortKey="Zochodne, Douglas" sort="Zochodne, Douglas" uniqKey="Zochodne D" first="Douglas" last="Zochodne">Douglas Zochodne</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Analysis of Variance</term><term>Antiparkinson Agents (adverse effects)</term><term>Female</term><term>Homocysteine (blood)</term><term>Humans</term><term>Levodopa (adverse effects)</term><term>Male</term><term>Methylmalonic Acid (blood)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (drug therapy)</term><term>Peripheral Nervous System Diseases (etiology)</term><term>Retrospective Studies</term><term>Vitamin B 12 (blood)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Homocysteine</term><term>Methylmalonic Acid</term><term>Vitamin B 12</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Peripheral Nervous System Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Female</term><term>Humans</term><term>Male</term><term>Retrospective Studies</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml: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.</div></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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