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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ISTEX:559B6DD2B7A35A89DEE343EE70E944B39BCDAAF2Le document en format XML
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<term>Corpus Striatum (pathology)</term>
<term>Diagnosis, Differential</term>
<term>Dopamine (metabolism)</term>
<term>Dopamine Plasma Membrane Transport Proteins</term>
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<term>Manganese (adverse effects)</term>
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<term>Manganese (urine)</term>
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<term>Parkinson Disease (pathology)</term>
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<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>
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<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>
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<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>
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<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>
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<term>β‐CIT SPECT</term>
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<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>
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<author><name sortKey="Kim, Y" sort="Kim, Y" uniqKey="Kim Y" first="Y" last="Kim">Y. Kim</name>
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<wicri:regionArea>Department of Occupational and Environmental Medicine, University of Ulsan School of Medicine, Ulsan</wicri:regionArea>
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<author><name sortKey="Kim, J M" sort="Kim, J M" uniqKey="Kim J" first="J-M" last="Kim">J-M Kim</name>
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<author><name sortKey="Kim, J W" sort="Kim, J W" uniqKey="Kim J" first="J-W" last="Kim">J-W Kim</name>
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<author><name sortKey="Yoo, C I" sort="Yoo, C I" uniqKey="Yoo C" first="C-I" last="Yoo">C-I Yoo</name>
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<author><name sortKey="Lee, C R" sort="Lee, C R" uniqKey="Lee C" first="C R" last="Lee">C R Lee</name>
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<author><name sortKey="Lee, J H" sort="Lee, J H" uniqKey="Lee J" first="J H" last="Lee">J H Lee</name>
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<author><name sortKey="Kim, H K" sort="Kim, H K" uniqKey="Kim H" first="H K" last="Kim">H K Kim</name>
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<author><name sortKey="Yang, S O" sort="Yang, S O" uniqKey="Yang S" first="S O" last="Yang">S O Yang</name>
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<author><name sortKey="Chung, H K" sort="Chung, H K" uniqKey="Chung H" first="H K" last="Chung">H K Chung</name>
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<author><name sortKey="Lee, D S" sort="Lee, D S" uniqKey="Lee D" first="D S" last="Lee">D S Lee</name>
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<author><name sortKey="Jeon, B" sort="Jeon, B" uniqKey="Jeon B" first="B" last="Jeon">B. Jeon</name>
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<author><name sortKey="Kim, Y" sort="Kim, Y" uniqKey="Kim Y" first="Y" last="Kim">Y. Kim</name>
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<author><name sortKey="Kim, J M" sort="Kim, J M" uniqKey="Kim J" first="J-M" last="Kim">J-M Kim</name>
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<author><name sortKey="Kim, J W" sort="Kim, J W" uniqKey="Kim J" first="J-W" last="Kim">J-W Kim</name>
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<author><name sortKey="Yoo, C I" sort="Yoo, C I" uniqKey="Yoo C" first="C-I" last="Yoo">C-I Yoo</name>
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<author><name sortKey="Lee, C R" sort="Lee, C R" uniqKey="Lee C" first="C R" last="Lee">C R Lee</name>
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<author><name sortKey="Lee, J H" sort="Lee, J H" uniqKey="Lee J" first="J H" last="Lee">J H Lee</name>
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<author><name sortKey="Kim, H K" sort="Kim, H K" uniqKey="Kim H" first="H K" last="Kim">H K Kim</name>
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<author><name sortKey="Yang, S O" sort="Yang, S O" uniqKey="Yang S" first="S O" last="Yang">S O Yang</name>
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<author><name sortKey="Chung, H K" sort="Chung, H K" uniqKey="Chung H" first="H K" last="Chung">H K Chung</name>
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<author><name sortKey="Lee, D S" sort="Lee, D S" uniqKey="Lee D" first="D S" last="Lee">D S Lee</name>
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<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>
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<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>
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<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>
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<term>Male</term>
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<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>
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