[123]IBZM Binding predicts dopaminergic responsiveness in patients with parkinsonism and previous dopaminomimetic therapy
Identifieur interne : 005213 ( Main/Exploration ); précédent : 005212; suivant : 005214[123]IBZM Binding predicts dopaminergic responsiveness in patients with parkinsonism and previous dopaminomimetic therapy
Auteurs : Schwarz [Allemagne] ; K. Tatsch [Allemagne] ; T. Gasser [Allemagne] ; G. Arnold [Allemagne] ; Oertel [Allemagne]Source :
- Movement Disorders [ 0885-3185 ] ; 1997-11.
English descriptors
- KwdEn :
- Adult, Aged, Apomorphine (diagnostic use), Apomorphine (metabolism), Atrophy (pathology), Benzamides (pharmacokinetics), Binding Sites, Cerebral Cortex (pathology), Computed tomography, Dopamine (metabolism), Dopamine Agonists (metabolism), Dopamine Agonists (therapeutic use), Dopamine Antagonists (pharmacokinetics), Dopamine agonist, Follow-Up Studies, Humans, IBZM‐SPECT, Levodopa, Levodopa (therapeutic use), Magnetic Resonance Imaging, Middle Aged, Multiple‐system atrophy, Parkinson Disease (drug therapy), Parkinson Disease (pathology), Parkinson Disease (radionuclide imaging), Parkinson's disease, Predictive Value of Tests, Putamen (pathology), Pyrrolidines (pharmacokinetics), Receptors, Dopamine D2 (drug effects), Single‐photon‐emission computed tomography, Tomography, Emission-Computed, Single-Photon, [123I]Iodobenzamide.
- MESH :
- chemical , diagnostic use : Apomorphine.
- chemical , drug effects : Receptors, Dopamine D2.
- chemical , metabolism : Apomorphine, Dopamine, Dopamine Agonists.
- drug therapy : Parkinson Disease.
- pathology : Atrophy, Cerebral Cortex, Parkinson Disease, Putamen.
- chemical , pharmacokinetics : Benzamides, Dopamine Antagonists, Pyrrolidines.
- radionuclide imaging : Parkinson Disease.
- chemical , therapeutic use : Dopamine Agonists, Levodopa.
- Adult, Aged, Binding Sites, Follow-Up Studies, Humans, Magnetic Resonance Imaging, Middle Aged, Predictive Value of Tests, Tomography, Emission-Computed, Single-Photon.
Abstract
We investigated the cases of 55 patients with parkinsonism and prior dopaminomimetic therapy in whom the response to this treatment was questionable or reported to be negative. None of these patients had shown motor fluctuations prior to this study. We compared the results of imaging of dopamine‐D2 receptors by using [123l]iodobenzamide‐single‐photon‐emission computed tomography (IBZM‐SPECT) with the improvement in motor signs following a subcutaneous injection of apomorphine and a subsequent increase in oral dopaminomimetic therapy. IBZM‐SPECT accurately predicted a positive or negative response to apomorphine in 37 (84%) of 44 patients. The sensitivity/specificity was calculated as 96.3%/64.7%. The sensitivity/specificity of IBZM‐SPECT for the response to oral treatment with levodopa (L‐dopa) was calculated as 100%/75%. After a follow‐up period of 2–4 years, 25 patients developed motor fluctuations. All of these patients had normal IBZM binding. Nine developed clinical signs indicating a basal ganglia disorder other than Parkinson's disease. Eight of these nine patients had reduced, and one patient had normal, IBZM binding. We conclude that normal IBZM binding is a useful predictor of a good response to dopaminergic drugs in patients with parkinsonism and a questionable response to previous dopaminomimetic therapy. Reduced IBZM binding seems to exclude a diagnosis of Parkinson's disease, because none of the latter patients clearly benefited from L‐dopa and 66.7% developed clinical signs indicating another disorder of the basal ganglia.
Url:
DOI: 10.1002/mds.870120610
Affiliations:
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Gasser</name><affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich</wicri:regionArea><placeName><region type="land" nuts="1">Bavière</region><region type="district" nuts="2">District de Haute-Bavière</region><settlement type="city">Munich</settlement></placeName></affiliation></author><author><name sortKey="Arnold, G" sort="Arnold, G" uniqKey="Arnold G" first="G." last="Arnold">G. Arnold</name><affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich</wicri:regionArea><placeName><region type="land" nuts="1">Bavière</region><region type="district" nuts="2">District de Haute-Bavière</region><settlement type="city">Munich</settlement></placeName></affiliation></author><author><name sortKey="Oertel" sort="Oertel" uniqKey="Oertel" last="Oertel">Oertel</name><affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurology, Klinikum Grosshadern, Ludwig–Maximilian University; and Munich BMFT Research Program, Parkinson's Disease and Other Basal Ganglia Disorder, Munich</wicri:regionArea><placeName><region type="land" nuts="1">Bavière</region><region type="district" nuts="2">District de Haute-Bavière</region><settlement type="city">Munich</settlement></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Current Address: Department of Neurology, Philipps University, D‐35033 Marburg</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Giessen</region><settlement type="city">Marbourg</settlement></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="1997-11">1997-11</date><biblScope unit="vol">12</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="898">898</biblScope><biblScope unit="page" to="902">902</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">507D526419C64997EB5E827665EEAA3AE79292F8</idno><idno type="DOI">10.1002/mds.870120610</idno><idno type="ArticleID">MDS870120610</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Apomorphine (diagnostic use)</term><term>Apomorphine (metabolism)</term><term>Atrophy (pathology)</term><term>Benzamides (pharmacokinetics)</term><term>Binding Sites</term><term>Cerebral Cortex (pathology)</term><term>Computed tomography</term><term>Dopamine (metabolism)</term><term>Dopamine Agonists (metabolism)</term><term>Dopamine Agonists (therapeutic use)</term><term>Dopamine Antagonists (pharmacokinetics)</term><term>Dopamine agonist</term><term>Follow-Up Studies</term><term>Humans</term><term>IBZM‐SPECT</term><term>Levodopa</term><term>Levodopa (therapeutic use)</term><term>Magnetic Resonance Imaging</term><term>Middle Aged</term><term>Multiple‐system atrophy</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (radionuclide imaging)</term><term>Parkinson's disease</term><term>Predictive Value of Tests</term><term>Putamen (pathology)</term><term>Pyrrolidines (pharmacokinetics)</term><term>Receptors, Dopamine D2 (drug effects)</term><term>Single‐photon‐emission computed tomography</term><term>Tomography, Emission-Computed, Single-Photon</term><term>[123I]Iodobenzamide</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Apomorphine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Apomorphine</term><term>Dopamine</term><term>Dopamine Agonists</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Atrophy</term><term>Cerebral Cortex</term><term>Parkinson Disease</term><term>Putamen</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Benzamides</term><term>Dopamine Antagonists</term><term>Pyrrolidines</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Dopamine Agonists</term><term>Levodopa</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Binding Sites</term><term>Follow-Up Studies</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Middle Aged</term><term>Predictive Value of Tests</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">We investigated the cases of 55 patients with parkinsonism and prior dopaminomimetic therapy in whom the response to this treatment was questionable or reported to be negative. None of these patients had shown motor fluctuations prior to this study. We compared the results of imaging of dopamine‐D2 receptors by using [123l]iodobenzamide‐single‐photon‐emission computed tomography (IBZM‐SPECT) with the improvement in motor signs following a subcutaneous injection of apomorphine and a subsequent increase in oral dopaminomimetic therapy. IBZM‐SPECT accurately predicted a positive or negative response to apomorphine in 37 (84%) of 44 patients. The sensitivity/specificity was calculated as 96.3%/64.7%. The sensitivity/specificity of IBZM‐SPECT for the response to oral treatment with levodopa (L‐dopa) was calculated as 100%/75%. After a follow‐up period of 2–4 years, 25 patients developed motor fluctuations. All of these patients had normal IBZM binding. Nine developed clinical signs indicating a basal ganglia disorder other than Parkinson's disease. Eight of these nine patients had reduced, and one patient had normal, IBZM binding. We conclude that normal IBZM binding is a useful predictor of a good response to dopaminergic drugs in patients with parkinsonism and a questionable response to previous dopaminomimetic therapy. Reduced IBZM binding seems to exclude a diagnosis of Parkinson's disease, because none of the latter patients clearly benefited from L‐dopa and 66.7% developed clinical signs indicating another disorder of the basal ganglia.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country><region><li>Bavière</li><li>District de Giessen</li><li>District de Haute-Bavière</li><li>Hesse (Land)</li></region><settlement><li>Marbourg</li><li>Munich</li></settlement></list><tree><country name="Allemagne"><region name="Bavière"><name sortKey="Schwarz" sort="Schwarz" uniqKey="Schwarz" last="Schwarz">Schwarz</name></region><name sortKey="Arnold, G" sort="Arnold, G" uniqKey="Arnold G" first="G." last="Arnold">G. Arnold</name><name sortKey="Gasser, T" sort="Gasser, T" uniqKey="Gasser T" first="T." last="Gasser">T. Gasser</name><name sortKey="Oertel" sort="Oertel" uniqKey="Oertel" last="Oertel">Oertel</name><name sortKey="Oertel" sort="Oertel" uniqKey="Oertel" last="Oertel">Oertel</name><name sortKey="Tatsch, K" sort="Tatsch, K" uniqKey="Tatsch K" first="K." last="Tatsch">K. Tatsch</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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