123I‐IBZM binding compared with long‐term clinical follow up in patients with de novo parkinsonism
Identifieur interne : 002898 ( Istex/Curation ); précédent : 002897; suivant : 002899123I‐IBZM binding compared with long‐term clinical follow up in patients with de novo parkinsonism
Auteurs : Schwarz [Allemagne] ; Klaus Tatsch [Allemagne] ; Thomas Gasser [Allemagne] ; Guy Arnold [Allemagne] ; Oliver Pogarell [Allemagne] ; Gais Künig [Allemagne] ; Wolfgang H. Oertel [Allemagne]Source :
- Movement Disorders [ 0885-3185 ] ; 1998-01.
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Abstract
We performed a prospective clinical follow up (mean follow up, 36 months; range, 24–56 months) of 65 patients with de novo parkinsonism in whom imaging of dopamine D2 receptors was performed before the initiation of dopaminomimetic therapy by means of 123I‐iodobenzamidesingle‐photon‐emission computed tomography (IBZM‐SPECT). The results of IBZM‐SPECT were comared with the long‐term response to dopaminomimetic drugs, the development of motor fluctuations, and the development of clinical signs incompatible with Parkinson's disease (PD). A total of 55 patients had normal and 10 patients had reduced IBZM binding; 45 patients showed a good response to levodopa (L‐dopa), 11 showed an equivocal response, and nine did not respond; 31 patients developed a fluctuating response to dopaminomimetic drugs and seven patients developed clinical signs indicative of multiple‐system atrophy (n = 5), progressive supranuclear palsy (n = 1), or corticobasal ganglionic degeneration (n = 1). Chi‐squared analysis showed a significant correlation of the results of IBZM‐SPECT with the long‐term response to dopaminomimetic therapy (p < 0.0001) and the development of motor fluctuations (p < 0.0001) or clinical signs incompatible with PD (p < 0.0001). We conclude that IBZM‐SPECT can help to differentiate between patients who will show a good response to L‐dopa and will develop motor fluctuations (most likely patients with PD) and those patients who will not respond to L‐dopa and might develop clinical signs compatible with another hypokinetic disorder of the basal ganglia.
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DOI: 10.1002/mds.870130107
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Basal Ganglia Disorders” BMFT Research Program, Munich</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>Current Address: Department of Neurology, University of Ulm, D‐89081 Ulm, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Current Address: Department of Neurology, University of Ulm, D‐89081 Ulm</wicri:regionArea></affiliation></author><author><name sortKey="Tatsch, Klaus" sort="Tatsch, Klaus" uniqKey="Tatsch K" first="Klaus" last="Tatsch">Klaus Tatsch</name><affiliation wicri:level="1"><mods:affiliation>Department of Nuclear Medicine, Klinikum Grosshadern, Ludwig‐Maximilians University, Munich, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Nuclear Medicine, Klinikum Grosshadern, Ludwig‐Maximilians University, Munich</wicri:regionArea></affiliation></author><author><name sortKey="Gasser, Thomas" sort="Gasser, Thomas" uniqKey="Gasser T" first="Thomas" 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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="1998-01">1998-01</date><biblScope unit="vol">13</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="16">16</biblScope><biblScope unit="page" to="19">19</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">C82F777A0E968DC0CE551B41DF878389F9ED786F</idno><idno type="DOI">10.1002/mds.870130107</idno><idno type="ArticleID">MDS870130107</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apomorphine</term><term>IBZM‐SPECT</term><term>Levodopa</term><term>Parkinson's disease</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We performed a prospective clinical follow up (mean follow up, 36 months; range, 24–56 months) of 65 patients with de novo parkinsonism in whom imaging of dopamine D2 receptors was performed before the initiation of dopaminomimetic therapy by means of 123I‐iodobenzamidesingle‐photon‐emission computed tomography (IBZM‐SPECT). The results of IBZM‐SPECT were comared with the long‐term response to dopaminomimetic drugs, the development of motor fluctuations, and the development of clinical signs incompatible with Parkinson's disease (PD). A total of 55 patients had normal and 10 patients had reduced IBZM binding; 45 patients showed a good response to levodopa (L‐dopa), 11 showed an equivocal response, and nine did not respond; 31 patients developed a fluctuating response to dopaminomimetic drugs and seven patients developed clinical signs indicative of multiple‐system atrophy (n = 5), progressive supranuclear palsy (n = 1), or corticobasal ganglionic degeneration (n = 1). Chi‐squared analysis showed a significant correlation of the results of IBZM‐SPECT with the long‐term response to dopaminomimetic therapy (p < 0.0001) and the development of motor fluctuations (p < 0.0001) or clinical signs incompatible with PD (p < 0.0001). We conclude that IBZM‐SPECT can help to differentiate between patients who will show a good response to L‐dopa and will develop motor fluctuations (most likely patients with PD) and those patients who will not respond to L‐dopa and might develop clinical signs compatible with another hypokinetic disorder of the basal ganglia.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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