Dopamine transporter density is decreased in parkinsonian patients with a history of manganese exposure: What does it mean?
Identifieur interne : 006503 ( Main/Merge ); précédent : 006502; suivant : 006504Dopamine transporter density is decreased in parkinsonian patients with a history of manganese exposure: What does it mean?
Auteurs : Y. Kim [Corée du Sud] ; J. Kim [Corée du Sud] ; J. Kim [Corée du Sud] ; C. Yoo [Corée du Sud] ; C. R. Lee [Corée du Sud] ; J. H. Lee [Corée du Sud] ; H. K. Kim [Corée du Sud] ; S. O. Yang [Corée du Sud] ; H. K. Chung [Corée du Sud] ; D. S. Lee [Corée du Sud] ; B. Jeon [Corée du Sud]Source :
- Movement Disorders [ 0885-3185 ] ; 2002-05.
English descriptors
- KwdEn :
- Causality, Cocaine (analogs & derivatives), Cocaine (diagnostic use), Corpus Striatum (metabolism), Corpus Striatum (pathology), Diagnosis, Differential, Dopamine (metabolism), Dopamine Plasma Membrane Transport Proteins, Humans, Iodine Radioisotopes (diagnostic use), Male, Manganese (adverse effects), Manganese (blood), Manganese (urine), Membrane Glycoproteins, Membrane Transport Proteins (analysis), Middle Aged, Nerve Tissue Proteins, Occupational Exposure (adverse effects), Parkinson Disease (etiology), Parkinson Disease (pathology), Parkinson Disease (radionuclide imaging), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (pathology), Parkinson Disease, Secondary (radionuclide imaging), Tomography, Emission-Computed, Single-Photon, dopamine transporter, idiopathic Parkinson disease, manganese, parkinsonism, β‐CIT SPECT.
- MESH :
- chemical , adverse effects : Manganese.
- chemical , analogs & derivatives : Cocaine.
- chemical , analysis : Membrane Transport Proteins.
- chemical , blood : Manganese.
- chemical , diagnostic use : Cocaine, Iodine Radioisotopes.
- adverse effects : Occupational Exposure.
- chemically induced : Parkinson Disease, Secondary.
- etiology : Parkinson Disease.
- metabolism : Corpus Striatum, Dopamine.
- pathology : Corpus Striatum, Parkinson Disease, Parkinson Disease, Secondary.
- radionuclide imaging : Parkinson Disease, Parkinson Disease, Secondary.
- chemical , urine : Manganese.
- Causality, Diagnosis, Differential, Dopamine Plasma Membrane Transport Proteins, Humans, Male, Membrane Glycoproteins, Middle Aged, Nerve Tissue Proteins, Tomography, Emission-Computed, Single-Photon.
Abstract
Manganese (Mn) exposure can cause parkinsonism. Pathological changes occur mostly in the pallidum and striatum. Two patients with a long history of occupational Mn exposure presented with Mn‐induced parkinsonism. In one patient, magnetic resonance imaging (MRI) showed findings consistent with Mn exposure, and Mn concentration was increased in the blood and urine. However, this patient's clinical features were typical of idiopathic Parkinson disease (PD). Previous pathological and positron emission tomography studies indicate that striatal dopamine transporter density is normal in Mn‐induced parkinsonism, whereas it is decreased in PD. Therefore, we performed [123I]‐(1r)‐2β‐carboxymethoxy‐3β‐(4‐iodophenyl)tropane ([123I]‐β‐CIT) single‐photon emission computed tomography. Severe reduction of striatal β‐CIT binding was indicated, which is consistent with PD. We propose three interpretations: (1) the patients have PD, and Mn exposure is incidental; (2) Mn induces selective degeneration of presynaptic dopaminergic nerve terminals, thereby causing parkinsonism; or (3) Mn exposure acts as a risk of PD in these patients. Our results and careful review of previous studies indicate that the axiom that Mn causes parkinsonism by pallidal lesion may be over‐simplified; Mn exposure and parkinsonism may be more complex than previously thought. Further studies are required to elucidate the relationship between Mn and various forms of parkinsonism. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10089
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Jeon</name><affiliation wicri:level="3"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Neurology, Seoul National University School of Medicine and Clinical Research Institute of Seoul National University Hospital, Seoul</wicri:regionArea><placeName><settlement type="city">Séoul</settlement></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="2002-05">2002-05</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="568">568</biblScope><biblScope unit="page" to="575">575</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">559B6DD2B7A35A89DEE343EE70E944B39BCDAAF2</idno><idno type="DOI">10.1002/mds.10089</idno><idno type="ArticleID">MDS10089</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Causality</term><term>Cocaine (analogs & derivatives)</term><term>Cocaine (diagnostic use)</term><term>Corpus Striatum (metabolism)</term><term>Corpus Striatum (pathology)</term><term>Diagnosis, Differential</term><term>Dopamine (metabolism)</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Humans</term><term>Iodine Radioisotopes (diagnostic use)</term><term>Male</term><term>Manganese (adverse effects)</term><term>Manganese (blood)</term><term>Manganese (urine)</term><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins (analysis)</term><term>Middle Aged</term><term>Nerve Tissue Proteins</term><term>Occupational Exposure (adverse effects)</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (radionuclide imaging)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (pathology)</term><term>Parkinson Disease, Secondary (radionuclide imaging)</term><term>Tomography, Emission-Computed, Single-Photon</term><term>dopamine transporter</term><term>idiopathic Parkinson disease</term><term>manganese</term><term>parkinsonism</term><term>β‐CIT SPECT</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Manganese</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Cocaine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Membrane Transport Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Manganese</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Cocaine</term><term>Iodine Radioisotopes</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Occupational Exposure</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Parkinson Disease</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" type="chemical" qualifier="urine" xml:lang="en"><term>Manganese</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Causality</term><term>Diagnosis, Differential</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Humans</term><term>Male</term><term>Membrane Glycoproteins</term><term>Middle Aged</term><term>Nerve Tissue Proteins</term><term>Tomography, Emission-Computed, Single-Photon</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Manganese (Mn) exposure can cause parkinsonism. Pathological changes occur mostly in the pallidum and striatum. Two patients with a long history of occupational Mn exposure presented with Mn‐induced parkinsonism. In one patient, magnetic resonance imaging (MRI) showed findings consistent with Mn exposure, and Mn concentration was increased in the blood and urine. However, this patient's clinical features were typical of idiopathic Parkinson disease (PD). Previous pathological and positron emission tomography studies indicate that striatal dopamine transporter density is normal in Mn‐induced parkinsonism, whereas it is decreased in PD. Therefore, we performed [123I]‐(1r)‐2β‐carboxymethoxy‐3β‐(4‐iodophenyl)tropane ([123I]‐β‐CIT) single‐photon emission computed tomography. Severe reduction of striatal β‐CIT binding was indicated, which is consistent with PD. We propose three interpretations: (1) the patients have PD, and Mn exposure is incidental; (2) Mn induces selective degeneration of presynaptic dopaminergic nerve terminals, thereby causing parkinsonism; or (3) Mn exposure acts as a risk of PD in these patients. Our results and careful review of previous studies indicate that the axiom that Mn causes parkinsonism by pallidal lesion may be over‐simplified; Mn exposure and parkinsonism may be more complex than previously thought. Further studies are required to elucidate the relationship between Mn and various forms of parkinsonism. © 2002 Movement Disorder Society</div></front></TEI><double doi="10.1002/mds.10089"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Dopamine transporter density is decreased in parkinsonian patients with a history of manganese exposure: What does it mean?</title><author><name sortKey="Kim, Y" sort="Kim, Y" uniqKey="Kim Y" first="Y." last="Kim">Y. Kim</name></author><author><name sortKey="Kim, J" sort="Kim, J" uniqKey="Kim J" first="J." last="Kim">J. Kim</name></author><author><name sortKey="Kim, J" sort="Kim, J" uniqKey="Kim J" first="J." last="Kim">J. Kim</name></author><author><name sortKey="Yoo, C" sort="Yoo, C" uniqKey="Yoo C" first="C." last="Yoo">C. Yoo</name></author><author><name sortKey="Lee, C R" sort="Lee, C R" uniqKey="Lee C" first="C. R." last="Lee">C. R. Lee</name></author><author><name sortKey="Lee, J H" sort="Lee, J H" uniqKey="Lee J" first="J. H." last="Lee">J. H. Lee</name></author><author><name sortKey="Kim, H K" sort="Kim, H K" uniqKey="Kim H" first="H. K." last="Kim">H. K. Kim</name></author><author><name sortKey="Yang, S O" sort="Yang, S O" uniqKey="Yang S" first="S. O." last="Yang">S. O. Yang</name></author><author><name sortKey="Chung, H K" sort="Chung, H K" uniqKey="Chung H" first="H. K." last="Chung">H. K. Chung</name></author><author><name sortKey="Lee, D S" sort="Lee, D S" uniqKey="Lee D" first="D. S." last="Lee">D. S. Lee</name></author><author><name sortKey="Jeon, B" sort="Jeon, B" uniqKey="Jeon B" first="B." last="Jeon">B. Jeon</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:559B6DD2B7A35A89DEE343EE70E944B39BCDAAF2</idno><date when="2002" year="2002">2002</date><idno type="doi">10.1002/mds.10089</idno><idno type="url">https://api.istex.fr/document/559B6DD2B7A35A89DEE343EE70E944B39BCDAAF2/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000404</idno><idno type="wicri:Area/Istex/Curation">000404</idno><idno type="wicri:Area/Istex/Checkpoint">002D89</idno><idno type="wicri:doubleKey">0885-3185:2002:Kim Y:dopamine:transporter:density</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Dopamine transporter density is decreased in parkinsonian patients with a history of manganese exposure: What does it mean?</title><author><name sortKey="Kim, Y" sort="Kim, Y" uniqKey="Kim Y" first="Y." last="Kim">Y. Kim</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Occupational and Environmental Medicine, University of Ulsan School of Medicine, Ulsan</wicri:regionArea><wicri:noRegion>Ulsan</wicri:noRegion></affiliation></author><author><name sortKey="Kim, J" sort="Kim, J" uniqKey="Kim J" first="J." last="Kim">J. Kim</name><affiliation wicri:level="3"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Neurology, Seoul National University School of Medicine and Clinical Research Institute of Seoul National University Hospital, Seoul</wicri:regionArea><placeName><settlement type="city">Séoul</settlement></placeName></affiliation></author><author><name sortKey="Kim, J" sort="Kim, J" uniqKey="Kim J" first="J." last="Kim">J. Kim</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Neurology, Dong‐A University School of Medicine, Pusan</wicri:regionArea><wicri:noRegion>Pusan</wicri:noRegion></affiliation></author><author><name sortKey="Yoo, C" sort="Yoo, C" uniqKey="Yoo C" first="C." last="Yoo">C. Yoo</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Occupational and Environmental Medicine, University of Ulsan School of Medicine, Ulsan</wicri:regionArea><wicri:noRegion>Ulsan</wicri:noRegion></affiliation></author><author><name sortKey="Lee, C R" sort="Lee, C R" uniqKey="Lee C" first="C. R." last="Lee">C. R. Lee</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Occupational and Environmental Medicine, University of Ulsan School of Medicine, Ulsan</wicri:regionArea><wicri:noRegion>Ulsan</wicri:noRegion></affiliation></author><author><name sortKey="Lee, J H" sort="Lee, J H" uniqKey="Lee J" first="J. H." last="Lee">J. H. Lee</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Occupational and Environmental Medicine, University of Ulsan School of Medicine, Ulsan</wicri:regionArea><wicri:noRegion>Ulsan</wicri:noRegion></affiliation></author><author><name sortKey="Kim, H K" sort="Kim, H K" uniqKey="Kim H" first="H. K." last="Kim">H. K. Kim</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Neurology, University of Ulsan School of Medicine, Ulsan</wicri:regionArea><wicri:noRegion>Ulsan</wicri:noRegion></affiliation></author><author><name sortKey="Yang, S O" sort="Yang, S O" uniqKey="Yang S" first="S. O." last="Yang">S. O. Yang</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Radiology, University of Ulsan School of Medicine, Ulsan</wicri:regionArea><wicri:noRegion>Ulsan</wicri:noRegion></affiliation></author><author><name sortKey="Chung, H K" sort="Chung, H K" uniqKey="Chung H" first="H. K." last="Chung">H. K. Chung</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Industrial Safety and Health Research Institute, Korea Industrial Safety Corporation, Inchon</wicri:regionArea><wicri:noRegion>Inchon</wicri:noRegion></affiliation></author><author><name sortKey="Lee, D S" sort="Lee, D S" uniqKey="Lee D" first="D. S." last="Lee">D. S. Lee</name><affiliation wicri:level="3"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Nuclear Medicine, Seoul National University School of Medicine and Clinical Research Institute of Seoul National University Hospital, Seoul</wicri:regionArea><placeName><settlement type="city">Séoul</settlement></placeName></affiliation></author><author><name sortKey="Jeon, B" sort="Jeon, B" uniqKey="Jeon B" first="B." last="Jeon">B. Jeon</name><affiliation wicri:level="3"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Neurology, Seoul National University School of Medicine and Clinical Research Institute of Seoul National University Hospital, Seoul</wicri:regionArea><placeName><settlement type="city">Séoul</settlement></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="2002-05">2002-05</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="568">568</biblScope><biblScope unit="page" to="575">575</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">559B6DD2B7A35A89DEE343EE70E944B39BCDAAF2</idno><idno type="DOI">10.1002/mds.10089</idno><idno type="ArticleID">MDS10089</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>dopamine transporter</term><term>idiopathic Parkinson disease</term><term>manganese</term><term>parkinsonism</term><term>β‐CIT SPECT</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Manganese (Mn) exposure can cause parkinsonism. Pathological changes occur mostly in the pallidum and striatum. Two patients with a long history of occupational Mn exposure presented with Mn‐induced parkinsonism. In one patient, magnetic resonance imaging (MRI) showed findings consistent with Mn exposure, and Mn concentration was increased in the blood and urine. However, this patient's clinical features were typical of idiopathic Parkinson disease (PD). Previous pathological and positron emission tomography studies indicate that striatal dopamine transporter density is normal in Mn‐induced parkinsonism, whereas it is decreased in PD. Therefore, we performed [123I]‐(1r)‐2β‐carboxymethoxy‐3β‐(4‐iodophenyl)tropane ([123I]‐β‐CIT) single‐photon emission computed tomography. Severe reduction of striatal β‐CIT binding was indicated, which is consistent with PD. We propose three interpretations: (1) the patients have PD, and Mn exposure is incidental; (2) Mn induces selective degeneration of presynaptic dopaminergic nerve terminals, thereby causing parkinsonism; or (3) Mn exposure acts as a risk of PD in these patients. Our results and careful review of previous studies indicate that the axiom that Mn causes parkinsonism by pallidal lesion may be over‐simplified; Mn exposure and parkinsonism may be more complex than previously thought. Further studies are required to elucidate the relationship between Mn and various forms of parkinsonism. © 2002 Movement Disorder Society</div></front></TEI></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Dopamine transporter density is decreased in parkinsonian patients with a history of manganese exposure: what does it mean?</title><author><name sortKey="Kim, Y" sort="Kim, Y" uniqKey="Kim Y" first="Y" last="Kim">Y. Kim</name><affiliation wicri:level="1"><nlm:affiliation>Department of Occupational and Environmental Medicine, University of Ulsan School of Medicine, Ulsan, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Occupational and Environmental Medicine, University of Ulsan School of Medicine, Ulsan</wicri:regionArea><wicri:noRegion>Ulsan</wicri:noRegion></affiliation></author><author><name sortKey="Kim, J M" sort="Kim, J M" uniqKey="Kim J" first="J-M" last="Kim">J-M Kim</name></author><author><name sortKey="Kim, J W" sort="Kim, J W" uniqKey="Kim J" first="J-W" last="Kim">J-W Kim</name></author><author><name sortKey="Yoo, C I" sort="Yoo, C I" uniqKey="Yoo C" first="C-I" last="Yoo">C-I Yoo</name></author><author><name sortKey="Lee, C R" sort="Lee, C R" uniqKey="Lee C" first="C R" last="Lee">C R Lee</name></author><author><name sortKey="Lee, J H" sort="Lee, J H" uniqKey="Lee J" first="J H" last="Lee">J H Lee</name></author><author><name sortKey="Kim, H K" sort="Kim, H K" uniqKey="Kim H" first="H K" last="Kim">H K Kim</name></author><author><name sortKey="Yang, S O" sort="Yang, S O" uniqKey="Yang S" first="S O" last="Yang">S O Yang</name></author><author><name sortKey="Chung, H K" sort="Chung, H K" uniqKey="Chung H" first="H K" last="Chung">H K Chung</name></author><author><name sortKey="Lee, D S" sort="Lee, D S" uniqKey="Lee D" first="D S" last="Lee">D S Lee</name></author><author><name sortKey="Jeon, B" sort="Jeon, B" uniqKey="Jeon B" first="B" last="Jeon">B. Jeon</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:12112209</idno><idno type="pmid">12112209</idno><idno type="doi">10.1002/mds.10089</idno><idno type="wicri:Area/PubMed/Corpus">003A49</idno><idno type="wicri:Area/PubMed/Curation">003A49</idno><idno type="wicri:Area/PubMed/Checkpoint">003B21</idno><idno type="wicri:Area/Ncbi/Merge">000802</idno><idno type="wicri:Area/Ncbi/Curation">000802</idno><idno type="wicri:Area/Ncbi/Checkpoint">000802</idno><idno type="wicri:doubleKey">0885-3185:2002:Kim Y:dopamine:transporter:density</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Dopamine transporter density is decreased in parkinsonian patients with a history of manganese exposure: what does it mean?</title><author><name sortKey="Kim, Y" sort="Kim, Y" uniqKey="Kim Y" first="Y" last="Kim">Y. Kim</name><affiliation wicri:level="1"><nlm:affiliation>Department of Occupational and Environmental Medicine, University of Ulsan School of Medicine, Ulsan, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Occupational and Environmental Medicine, University of Ulsan School of Medicine, Ulsan</wicri:regionArea><wicri:noRegion>Ulsan</wicri:noRegion></affiliation></author><author><name sortKey="Kim, J M" sort="Kim, J M" uniqKey="Kim J" first="J-M" last="Kim">J-M Kim</name></author><author><name sortKey="Kim, J W" sort="Kim, J W" uniqKey="Kim J" first="J-W" last="Kim">J-W Kim</name></author><author><name sortKey="Yoo, C I" sort="Yoo, C I" uniqKey="Yoo C" first="C-I" last="Yoo">C-I Yoo</name></author><author><name sortKey="Lee, C R" sort="Lee, C R" uniqKey="Lee C" first="C R" last="Lee">C R Lee</name></author><author><name sortKey="Lee, J H" sort="Lee, J H" uniqKey="Lee J" first="J H" last="Lee">J H Lee</name></author><author><name sortKey="Kim, H K" sort="Kim, H K" uniqKey="Kim H" first="H K" last="Kim">H K Kim</name></author><author><name sortKey="Yang, S O" sort="Yang, S O" uniqKey="Yang S" first="S O" last="Yang">S O Yang</name></author><author><name sortKey="Chung, H K" sort="Chung, H K" uniqKey="Chung H" first="H K" last="Chung">H K Chung</name></author><author><name sortKey="Lee, D S" sort="Lee, D S" uniqKey="Lee D" first="D S" last="Lee">D S Lee</name></author><author><name sortKey="Jeon, B" sort="Jeon, B" uniqKey="Jeon B" first="B" last="Jeon">B. Jeon</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>Causality</term><term>Cocaine (analogs & derivatives)</term><term>Cocaine (diagnostic use)</term><term>Corpus Striatum (metabolism)</term><term>Corpus Striatum (pathology)</term><term>Diagnosis, Differential</term><term>Dopamine (metabolism)</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Humans</term><term>Iodine Radioisotopes (diagnostic use)</term><term>Male</term><term>Manganese (adverse effects)</term><term>Manganese (blood)</term><term>Manganese (urine)</term><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins (analysis)</term><term>Middle Aged</term><term>Nerve Tissue Proteins</term><term>Occupational Exposure (adverse effects)</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (radionuclide imaging)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (pathology)</term><term>Parkinson Disease, Secondary (radionuclide imaging)</term><term>Tomography, Emission-Computed, Single-Photon</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Manganese</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Cocaine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Membrane Transport Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Manganese</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Cocaine</term><term>Iodine Radioisotopes</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Occupational Exposure</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Parkinson Disease</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" type="chemical" qualifier="urine" xml:lang="en"><term>Manganese</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Causality</term><term>Diagnosis, Differential</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Humans</term><term>Male</term><term>Membrane Glycoproteins</term><term>Middle Aged</term><term>Nerve Tissue Proteins</term><term>Tomography, Emission-Computed, Single-Photon</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Manganese (Mn) exposure can cause parkinsonism. Pathological changes occur mostly in the pallidum and striatum. Two patients with a long history of occupational Mn exposure presented with Mn-induced parkinsonism. In one patient, magnetic resonance imaging (MRI) showed findings consistent with Mn exposure, and Mn concentration was increased in the blood and urine. However, this patient's clinical features were typical of idiopathic Parkinson disease (PD). Previous pathological and positron emission tomography studies indicate that striatal dopamine transporter density is normal in Mn-induced parkinsonism, whereas it is decreased in PD. Therefore, we performed [(123)I]-(1r)-2 beta-carboxymethoxy-3beta-(4-iodophenyl)tropane ([(123)I]-beta-CIT) single-photon emission computed tomography. Severe reduction of striatal beta-CIT binding was indicated, which is consistent with PD. We propose three interpretations: (1) the patients have PD, and Mn exposure is incidental; (2) Mn induces selective degeneration of presynaptic dopaminergic nerve terminals, thereby causing parkinsonism; or (3) Mn exposure acts as a risk of PD in these patients. Our results and careful review of previous studies indicate that the axiom that Mn causes parkinsonism by pallidal lesion may be over-simplified; Mn exposure and parkinsonism may be more complex than previously thought. Further studies are required to elucidate the relationship between Mn and various forms of parkinsonism.</div></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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