[123I] FP‐CIT spect study in vascular parkinsonism and Parkinson's disease
Identifieur interne : 002998 ( Main/Curation ); précédent : 002997; suivant : 002999[123I] FP‐CIT spect study in vascular parkinsonism and Parkinson's disease
Auteurs : Jan Zijlmans [Royaume-Uni, Pays-Bas] ; Andrew Evans [Royaume-Uni] ; Flavia Fontes [Royaume-Uni] ; Regina Katzenschlager [Royaume-Uni, Autriche] ; Svetoslav Gacinovic [Royaume-Uni] ; Andrew J. Lees [Royaume-Uni] ; Durval Costa [Royaume-Uni, Portugal]Source :
- Movement Disorders [ 0885-3185 ] ; 2007-07-15.
English descriptors
Abstract
There is substantial evidence to support a role for small vessel disease (SVD) as a cause for vascular parkinsonism (VP). Using [123I] FP‐CIT SPECT (single photon emission computed tomography), we have tried to determine whether VP patients have pre‐synaptic dopaminergic function similar to PD patients, and whether the severity of parkinsonian symptoms as well as the levodopa response in VP patients are correlated with pre‐synaptic dopaminergic dysfunction. Thirteen patients fulfilling operational clinical criteria for VP had [123I] FP‐CIT scans. Mean [123I] FP‐CIT uptake in the basal ganglia was significantly lower in VP patients than in healthy controls, and the asymmetry index was not significantly different between these groups. In contrast, compared with the PD group, only the mean asymmetry index was significantly lower in VP patients. None of the parameters measured was significantly different between VP patients who had an insidious onset of parkinsonism (VPi) and those who had an acute onset (VPa). There was a significant correlation between the bilateral basal ganglia FP‐CIT uptake reduction in the VP patients and UPDRS motor scores, but not with the mean % reduction in motor UPDRS after levodopa. We suggest that in the majority of VP patients, pre‐synaptic dopaminergic function is reduced. The presence of a rather symmetrical FP‐CIT uptake in the basal ganglia may help to distinguish VP from PD and could therefore be used as a criterion for the clinical diagnosis of VP. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21479
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first="Andrew" last="Evans">Andrew Evans</name><affiliation wicri:level="1"><mods:affiliation>National Hospital for Neurology and Neurosurgery, London, United Kingdom</mods:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>National Hospital for Neurology and Neurosurgery, London</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom</mods:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Reta Lila Weston Institute of Neurological Studies, University College London</wicri:regionArea></affiliation></author><author><name sortKey="Fontes, Flavia" sort="Fontes, Flavia" uniqKey="Fontes F" first="Flavia" last="Fontes">Flavia Fontes</name><affiliation wicri:level="1"><mods:affiliation>Institute of Nuclear Medicine, UCL, London, United Kingdom</mods:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute 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Lees</name><affiliation wicri:level="1"><mods:affiliation>National Hospital for Neurology and Neurosurgery, London, United Kingdom</mods:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>National Hospital for Neurology and Neurosurgery, London</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, United Kingdom</mods:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Reta Lila Weston Institute of Neurological Studies, University College London</wicri:regionArea></affiliation></author><author><name sortKey="Costa, Durval" sort="Costa, Durval" uniqKey="Costa D" first="Durval" last="Costa">Durval Costa</name><affiliation wicri:level="1"><mods:affiliation>Institute of Nuclear Medicine, UCL, London, United Kingdom</mods:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Nuclear Medicine, UCL, London</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>HPP Medicina Molecular, SA, Porto, Portugal</mods:affiliation><country xml:lang="fr">Portugal</country><wicri:regionArea>HPP Medicina Molecular, SA, Porto</wicri:regionArea></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>Hoboken</pubPlace><date type="published" when="2007-07-15">2007-07-15</date><biblScope unit="volume">22</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1278">1278</biblScope><biblScope unit="page" to="1285">1285</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">E079B40BEFB56C7F11BEB352B18840E6DBD7BFAD</idno><idno type="DOI">10.1002/mds.21479</idno><idno type="ArticleID">MDS21479</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>FP‐CIT SPECT</term><term>L‐dopa challenge</term><term>criteria</term><term>vascular parkinsonism</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">There is substantial evidence to support a role for small vessel disease (SVD) as a cause for vascular parkinsonism (VP). Using [123I] FP‐CIT SPECT (single photon emission computed tomography), we have tried to determine whether VP patients have pre‐synaptic dopaminergic function similar to PD patients, and whether the severity of parkinsonian symptoms as well as the levodopa response in VP patients are correlated with pre‐synaptic dopaminergic dysfunction. Thirteen patients fulfilling operational clinical criteria for VP had [123I] FP‐CIT scans. Mean [123I] FP‐CIT uptake in the basal ganglia was significantly lower in VP patients than in healthy controls, and the asymmetry index was not significantly different between these groups. In contrast, compared with the PD group, only the mean asymmetry index was significantly lower in VP patients. None of the parameters measured was significantly different between VP patients who had an insidious onset of parkinsonism (VPi) and those who had an acute onset (VPa). There was a significant correlation between the bilateral basal ganglia FP‐CIT uptake reduction in the VP patients and UPDRS motor scores, but not with the mean % reduction in motor UPDRS after levodopa. We suggest that in the majority of VP patients, pre‐synaptic dopaminergic function is reduced. The presence of a rather symmetrical FP‐CIT uptake in the basal ganglia may help to distinguish VP from PD and could therefore be used as a criterion for the clinical diagnosis of VP. © 2007 Movement Disorder Society</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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