Anticardiolipin antibody in vascular parkinsonism
Identifieur interne : 006580 ( Main/Merge ); précédent : 006579; suivant : 006581Anticardiolipin antibody in vascular parkinsonism
Auteurs : Zhigao Huang [États-Unis] ; Michael Jacewicz [États-Unis] ; Ronald F. Pfeiffer [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2002-09.
English descriptors
- KwdEn :
- Aged, Antibodies, Anticardiolipin (immunology), Antiparkinson Agents (therapeutic use), Brain (blood supply), Brain (pathology), Brain Ischemia (pathology), Cerebrovascular Circulation (physiology), Cognition Disorders (diagnosis), Female, Gait, Humans, Levodopa (therapeutic use), Lower Extremity (physiopathology), Male, Neuropsychological Tests, Parkinson Disease, Secondary (drug therapy), Parkinson Disease, Secondary (immunology), Parkinson Disease, Secondary (physiopathology), Posture, Risk Factors, anticardiolipin antibody, gait disorder, vascular parkinsonism.
- MESH :
- chemical , immunology : Antibodies, Anticardiolipin.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- blood supply : Brain.
- diagnosis : Cognition Disorders.
- drug therapy : Parkinson Disease, Secondary.
- immunology : Parkinson Disease, Secondary.
- pathology : Brain, Brain Ischemia.
- physiology : Cerebrovascular Circulation.
- physiopathology : Lower Extremity, Parkinson Disease, Secondary.
- Aged, Female, Gait, Humans, Male, Neuropsychological Tests, Posture, Risk Factors.
Abstract
Vascular parkinsonism (VP) is characterized by predominantly lower body involvement with gait impairment and postural instability, often without tremor, and by relative levodopa unresponsiveness. Neuroimaging studies demonstrate multiple infarcts or ischemic changes in periventricular white matter. Anticardiolipin antibodies (ACLA) are associated with hypercoagulable states and increased stroke risk. Review of our Movement Disorders Clinic records identified 44 individuals with a diagnosis of VP. ACLA have been obtained in 22 of these patients (mean age, 78.3 years; mean Mini‐Mental Status Exam score, 25.8). Gait disturbance was the initial clinical feature in 82% of the patients, and levodopa responsiveness was present in 18% of those treated. In 9 of the 22 (40.9%), ACLA immunoglobulin G was positive. No significant differences in clinical features or risk factors (hypertension, diabetes, coronary artery disease, and clinical stroke) were evident between ACLA+ and ACLA− groups. Since the presence of ACLA in individuals with stroke is usually treated by full‐scale anticoagulation with warfarin, our findings raise the question whether such treatment should also be used in persons with VP who are ACLA positive. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10219
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Pfeiffer</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, University of Tennessee Health Science Center, Memphis, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</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>New York</pubPlace><date type="published" when="2002-09">2002-09</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="992">992</biblScope><biblScope unit="page" to="997">997</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">6858F2E6B9C2BFBE0FC2634FAB1BAFD064989F99</idno><idno type="DOI">10.1002/mds.10219</idno><idno type="ArticleID">MDS10219</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Antibodies, Anticardiolipin (immunology)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Brain (blood supply)</term><term>Brain (pathology)</term><term>Brain Ischemia (pathology)</term><term>Cerebrovascular Circulation (physiology)</term><term>Cognition Disorders (diagnosis)</term><term>Female</term><term>Gait</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Lower Extremity (physiopathology)</term><term>Male</term><term>Neuropsychological Tests</term><term>Parkinson Disease, Secondary (drug therapy)</term><term>Parkinson Disease, Secondary (immunology)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Posture</term><term>Risk Factors</term><term>anticardiolipin antibody</term><term>gait disorder</term><term>vascular parkinsonism</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antibodies, Anticardiolipin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Brain Ischemia</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cerebrovascular Circulation</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lower Extremity</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Female</term><term>Gait</term><term>Humans</term><term>Male</term><term>Neuropsychological Tests</term><term>Posture</term><term>Risk Factors</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Vascular parkinsonism (VP) is characterized by predominantly lower body involvement with gait impairment and postural instability, often without tremor, and by relative levodopa unresponsiveness. Neuroimaging studies demonstrate multiple infarcts or ischemic changes in periventricular white matter. Anticardiolipin antibodies (ACLA) are associated with hypercoagulable states and increased stroke risk. Review of our Movement Disorders Clinic records identified 44 individuals with a diagnosis of VP. ACLA have been obtained in 22 of these patients (mean age, 78.3 years; mean Mini‐Mental Status Exam score, 25.8). Gait disturbance was the initial clinical feature in 82% of the patients, and levodopa responsiveness was present in 18% of those treated. In 9 of the 22 (40.9%), ACLA immunoglobulin G was positive. No significant differences in clinical features or risk factors (hypertension, diabetes, coronary artery disease, and clinical stroke) were evident between ACLA+ and ACLA− groups. Since the presence of ACLA in individuals with stroke is usually treated by full‐scale anticoagulation with warfarin, our findings raise the question whether such treatment should also be used in persons with VP who are ACLA positive. © 2002 Movement Disorder Society</div></front></TEI><double doi="10.1002/mds.10219"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Anticardiolipin antibody in vascular parkinsonism</title><author><name sortKey="Huang, Zhigao" sort="Huang, Zhigao" uniqKey="Huang Z" first="Zhigao" last="Huang">Zhigao Huang</name></author><author><name sortKey="Jacewicz, Michael" sort="Jacewicz, Michael" uniqKey="Jacewicz M" first="Michael" last="Jacewicz">Michael Jacewicz</name></author><author><name sortKey="Pfeiffer, Ronald F" sort="Pfeiffer, Ronald F" uniqKey="Pfeiffer R" first="Ronald F." last="Pfeiffer">Ronald F. Pfeiffer</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:6858F2E6B9C2BFBE0FC2634FAB1BAFD064989F99</idno><date when="2002" year="2002">2002</date><idno type="doi">10.1002/mds.10219</idno><idno type="url">https://api.istex.fr/document/6858F2E6B9C2BFBE0FC2634FAB1BAFD064989F99/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001282</idno><idno type="wicri:Area/Istex/Curation">001282</idno><idno type="wicri:Area/Istex/Checkpoint">002E66</idno><idno type="wicri:doubleKey">0885-3185:2002:Huang Z:anticardiolipin:antibody:in</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Anticardiolipin antibody in vascular parkinsonism</title><author><name sortKey="Huang, Zhigao" sort="Huang, Zhigao" uniqKey="Huang Z" first="Zhigao" last="Huang">Zhigao Huang</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, University of Tennessee Health Science Center, Memphis, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Jacewicz, Michael" sort="Jacewicz, Michael" uniqKey="Jacewicz M" first="Michael" last="Jacewicz">Michael Jacewicz</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, University of Tennessee Health Science Center, Memphis, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Pfeiffer, Ronald F" sort="Pfeiffer, Ronald F" uniqKey="Pfeiffer R" first="Ronald F." last="Pfeiffer">Ronald F. Pfeiffer</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, University of Tennessee Health Science Center, Memphis, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</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>New York</pubPlace><date type="published" when="2002-09">2002-09</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="992">992</biblScope><biblScope unit="page" to="997">997</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">6858F2E6B9C2BFBE0FC2634FAB1BAFD064989F99</idno><idno type="DOI">10.1002/mds.10219</idno><idno type="ArticleID">MDS10219</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>anticardiolipin antibody</term><term>gait disorder</term><term>vascular parkinsonism</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Vascular parkinsonism (VP) is characterized by predominantly lower body involvement with gait impairment and postural instability, often without tremor, and by relative levodopa unresponsiveness. Neuroimaging studies demonstrate multiple infarcts or ischemic changes in periventricular white matter. Anticardiolipin antibodies (ACLA) are associated with hypercoagulable states and increased stroke risk. Review of our Movement Disorders Clinic records identified 44 individuals with a diagnosis of VP. ACLA have been obtained in 22 of these patients (mean age, 78.3 years; mean Mini‐Mental Status Exam score, 25.8). Gait disturbance was the initial clinical feature in 82% of the patients, and levodopa responsiveness was present in 18% of those treated. In 9 of the 22 (40.9%), ACLA immunoglobulin G was positive. No significant differences in clinical features or risk factors (hypertension, diabetes, coronary artery disease, and clinical stroke) were evident between ACLA+ and ACLA− groups. Since the presence of ACLA in individuals with stroke is usually treated by full‐scale anticoagulation with warfarin, our findings raise the question whether such treatment should also be used in persons with VP who are ACLA positive. © 2002 Movement Disorder Society</div></front></TEI></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Anticardiolipin antibody in vascular parkinsonism.</title><author><name sortKey="Huang, Zhigao" sort="Huang, Zhigao" uniqKey="Huang Z" first="Zhigao" last="Huang">Zhigao Huang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, University of Tennessee Health Science Center, Memphis, Tennessee 38163</wicri:regionArea><wicri:noRegion>Tennessee 38163</wicri:noRegion></affiliation></author><author><name sortKey="Jacewicz, Michael" sort="Jacewicz, Michael" uniqKey="Jacewicz M" first="Michael" last="Jacewicz">Michael Jacewicz</name></author><author><name sortKey="Pfeiffer, Ronald F" sort="Pfeiffer, Ronald F" uniqKey="Pfeiffer R" first="Ronald F" last="Pfeiffer">Ronald F. Pfeiffer</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:12360548</idno><idno type="pmid">12360548</idno><idno type="doi">10.1002/mds.10219</idno><idno type="wicri:Area/PubMed/Corpus">003953</idno><idno type="wicri:Area/PubMed/Curation">003953</idno><idno type="wicri:Area/PubMed/Checkpoint">003B95</idno><idno type="wicri:Area/Ncbi/Merge">000898</idno><idno type="wicri:Area/Ncbi/Curation">000898</idno><idno type="wicri:Area/Ncbi/Checkpoint">000898</idno><idno type="wicri:doubleKey">0885-3185:2002:Huang Z:anticardiolipin:antibody:in</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Anticardiolipin antibody in vascular parkinsonism.</title><author><name sortKey="Huang, Zhigao" sort="Huang, Zhigao" uniqKey="Huang Z" first="Zhigao" last="Huang">Zhigao Huang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, University of Tennessee Health Science Center, Memphis, Tennessee 38163</wicri:regionArea><wicri:noRegion>Tennessee 38163</wicri:noRegion></affiliation></author><author><name sortKey="Jacewicz, Michael" sort="Jacewicz, Michael" uniqKey="Jacewicz M" first="Michael" last="Jacewicz">Michael Jacewicz</name></author><author><name sortKey="Pfeiffer, Ronald F" sort="Pfeiffer, Ronald F" uniqKey="Pfeiffer R" first="Ronald F" last="Pfeiffer">Ronald F. Pfeiffer</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Antibodies, Anticardiolipin (immunology)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Brain (blood supply)</term><term>Brain (pathology)</term><term>Brain Ischemia (pathology)</term><term>Cerebrovascular Circulation (physiology)</term><term>Cognition Disorders (diagnosis)</term><term>Female</term><term>Gait</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Lower Extremity (physiopathology)</term><term>Male</term><term>Neuropsychological Tests</term><term>Parkinson Disease, Secondary (drug therapy)</term><term>Parkinson Disease, Secondary (immunology)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Posture</term><term>Risk Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antibodies, Anticardiolipin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Brain Ischemia</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cerebrovascular Circulation</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lower Extremity</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Female</term><term>Gait</term><term>Humans</term><term>Male</term><term>Neuropsychological Tests</term><term>Posture</term><term>Risk Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Vascular parkinsonism (VP) is characterized by predominantly lower body involvement with gait impairment and postural instability, often without tremor, and by relative levodopa unresponsiveness. Neuroimaging studies demonstrate multiple infarcts or ischemic changes in periventricular white matter. Anticardiolipin antibodies (ACLA) are associated with hypercoagulable states and increased stroke risk. Review of our Movement Disorders Clinic records identified 44 individuals with a diagnosis of VP. ACLA have been obtained in 22 of these patients (mean age, 78.3 years; mean Mini-Mental Status Exam score, 25.8). Gait disturbance was the initial clinical feature in 82% of the patients, and levodopa responsiveness was present in 18% of those treated. In 9 of the 22 (40.9%), ACLA immunoglobulin G was positive. No significant differences in clinical features or risk factors (hypertension, diabetes, coronary artery disease, and clinical stroke) were evident between ACLA+ and ACLA- groups. Since the presence of ACLA in individuals with stroke is usually treated by full-scale anticoagulation with warfarin, our findings raise the question whether such treatment should also be used in persons with VP who are ACLA positive.</div></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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