The relation of putamen and caudate nucleus 18F-Dopa uptake to motor and cognitive performances in Parkinson's disease.
Identifieur interne : 000058 ( Ncbi/Curation ); précédent : 000057; suivant : 000059The relation of putamen and caudate nucleus 18F-Dopa uptake to motor and cognitive performances in Parkinson's disease.
Auteurs : E. Broussolle [France] ; C. Dentresangle ; P. Landais ; L. Garcia-Larrea ; P. Pollak ; B. Croisile ; O. Hibert ; F. Bonnefoi ; G. Galy ; J C Froment ; D. ComarSource :
- Journal of the neurological sciences [ 0022-510X ] ; 1999.
English descriptors
- KwdEn :
- Adult, Affect (physiology), Aged, Analysis of Variance, Case-Control Studies, Caudate Nucleus (diagnostic imaging), Caudate Nucleus (metabolism), Caudate Nucleus (physiopathology), Cognition (physiology), Dopamine Agents (pharmacology), Event-Related Potentials, P300, Female, Humans, Levodopa (pharmacokinetics), Male, Middle Aged, Motor Skills Disorders (physiopathology), Parkinson Disease (diagnostic imaging), Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Putamen (diagnostic imaging), Putamen (metabolism), Putamen (physiopathology), Tomography, Emission-Computed.
- MESH :
- chemical , pharmacokinetics : Levodopa.
- chemical , pharmacology : Dopamine Agents.
- diagnostic imaging : Caudate Nucleus, Parkinson Disease, Putamen.
- metabolism : Caudate Nucleus, Parkinson Disease, Putamen.
- physiology : Affect, Cognition.
- physiopathology : Caudate Nucleus, Motor Skills Disorders, Parkinson Disease, Putamen.
- Adult, Aged, Analysis of Variance, Case-Control Studies, Event-Related Potentials, P300, Female, Humans, Male, Middle Aged, Tomography, Emission-Computed.
Abstract
The contribution of striatal (caudate nucleus-putamen) dopaminergic deficiency to the severity of motor signs is well established in Parkinson's disease (PD), while its role in the occurrence of cognitive and mood changes remains unresolved. We therefore measured in 27 non-demented PD patients and 10 age-matched controls striatal uptake of [18F]-6-fluoro-L-Dopa (F-Dopa) with PET, and mood (Beck depression), memory (Grober-Buschke), frontal executive functions (verbal fluency and Wisconsin card sorting), and attentional processing of sensory stimuli (N2-P3 auditory event-related potentials--ERPs). Locomotor disability of patients was assessed by Hoehn and Yahr score and Unified Parkinson's Disease Rating Scale (UPDRS). ANOVA showed that memory, but neither frontal lobe functions nor ERPs, was significantly altered in PD patients, whereas indices of depression were found only in advanced PD. The F-Dopa rate constant Ki was significantly reduced in the striatum, more in putamen than caudate nucleus, and inversely correlated with disease duration. A significant inverse correlation was found between both putamen and caudate nucleus Ki and Hoehn and Yahr score, and between putamen--but not caudate nucleus Ki --and UPDRS motor score. Principal components analysis (PCA) of PD patients Ki values and mood, cognitive and ERP parameters gave a three-factor solution. Variables contributing to factor 1 were memory score and N2-P3 ERP latencies, those to factor 2 were striatal Ki values, and those to factor 3 frontal executive performances. Depression did not segregate with any variable. Our findings suggest that unlike locomotor disability, cognitive abilities and mood state of non-demented PD patients are for the most part unrelated to striatal dopaminergic depletion and may result from dysfunction of extra-striatal dopaminergic or from non-dopaminergic systems.
PubMed: 10475108
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Dentresangle</name></author><author><name sortKey="Landais, P" sort="Landais, P" uniqKey="Landais P" first="P" last="Landais">P. Landais</name></author><author><name sortKey="Garcia Larrea, L" sort="Garcia Larrea, L" uniqKey="Garcia Larrea L" first="L" last="Garcia-Larrea">L. Garcia-Larrea</name></author><author><name sortKey="Pollak, P" sort="Pollak, P" uniqKey="Pollak P" first="P" last="Pollak">P. Pollak</name></author><author><name sortKey="Croisile, B" sort="Croisile, B" uniqKey="Croisile B" first="B" last="Croisile">B. Croisile</name></author><author><name sortKey="Hibert, O" sort="Hibert, O" uniqKey="Hibert O" first="O" last="Hibert">O. Hibert</name></author><author><name sortKey="Bonnefoi, F" sort="Bonnefoi, F" uniqKey="Bonnefoi F" first="F" last="Bonnefoi">F. Bonnefoi</name></author><author><name sortKey="Galy, G" sort="Galy, G" uniqKey="Galy G" first="G" last="Galy">G. 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Broussolle</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurology, Hôpital Neurologique Pierre Wertheimer, Lyon, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Department of Neurology, Hôpital Neurologique Pierre Wertheimer, Lyon</wicri:regionArea><placeName><region type="region">Auvergne-Rhône-Alpes</region><region type="old region">Rhône-Alpes</region><settlement type="city">Lyon</settlement></placeName></affiliation></author><author><name sortKey="Dentresangle, C" sort="Dentresangle, C" uniqKey="Dentresangle C" first="C" last="Dentresangle">C. Dentresangle</name></author><author><name sortKey="Landais, P" sort="Landais, P" uniqKey="Landais P" first="P" last="Landais">P. Landais</name></author><author><name sortKey="Garcia Larrea, L" sort="Garcia Larrea, L" uniqKey="Garcia Larrea L" first="L" last="Garcia-Larrea">L. Garcia-Larrea</name></author><author><name sortKey="Pollak, P" sort="Pollak, P" uniqKey="Pollak P" first="P" last="Pollak">P. Pollak</name></author><author><name sortKey="Croisile, B" sort="Croisile, B" uniqKey="Croisile B" first="B" last="Croisile">B. Croisile</name></author><author><name sortKey="Hibert, O" sort="Hibert, O" uniqKey="Hibert O" first="O" last="Hibert">O. Hibert</name></author><author><name sortKey="Bonnefoi, F" sort="Bonnefoi, F" uniqKey="Bonnefoi F" first="F" last="Bonnefoi">F. Bonnefoi</name></author><author><name sortKey="Galy, G" sort="Galy, G" uniqKey="Galy G" first="G" last="Galy">G. Galy</name></author><author><name sortKey="Froment, J C" sort="Froment, J C" uniqKey="Froment J" first="J C" last="Froment">J C Froment</name></author><author><name sortKey="Comar, D" sort="Comar, D" uniqKey="Comar D" first="D" last="Comar">D. Comar</name></author></analytic><series><title level="j">Journal of the neurological sciences</title><idno type="ISSN">0022-510X</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Affect (physiology)</term><term>Aged</term><term>Analysis of Variance</term><term>Case-Control Studies</term><term>Caudate Nucleus (diagnostic imaging)</term><term>Caudate Nucleus (metabolism)</term><term>Caudate Nucleus (physiopathology)</term><term>Cognition (physiology)</term><term>Dopamine Agents (pharmacology)</term><term>Event-Related Potentials, P300</term><term>Female</term><term>Humans</term><term>Levodopa (pharmacokinetics)</term><term>Male</term><term>Middle Aged</term><term>Motor Skills Disorders (physiopathology)</term><term>Parkinson Disease (diagnostic imaging)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (physiopathology)</term><term>Putamen (diagnostic imaging)</term><term>Putamen (metabolism)</term><term>Putamen (physiopathology)</term><term>Tomography, Emission-Computed</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Dopamine Agents</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Caudate Nucleus</term><term>Parkinson Disease</term><term>Putamen</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Caudate Nucleus</term><term>Parkinson Disease</term><term>Putamen</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Affect</term><term>Cognition</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Caudate Nucleus</term><term>Motor Skills Disorders</term><term>Parkinson Disease</term><term>Putamen</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Analysis of Variance</term><term>Case-Control Studies</term><term>Event-Related Potentials, P300</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Tomography, Emission-Computed</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The contribution of striatal (caudate nucleus-putamen) dopaminergic deficiency to the severity of motor signs is well established in Parkinson's disease (PD), while its role in the occurrence of cognitive and mood changes remains unresolved. We therefore measured in 27 non-demented PD patients and 10 age-matched controls striatal uptake of [18F]-6-fluoro-L-Dopa (F-Dopa) with PET, and mood (Beck depression), memory (Grober-Buschke), frontal executive functions (verbal fluency and Wisconsin card sorting), and attentional processing of sensory stimuli (N2-P3 auditory event-related potentials--ERPs). Locomotor disability of patients was assessed by Hoehn and Yahr score and Unified Parkinson's Disease Rating Scale (UPDRS). ANOVA showed that memory, but neither frontal lobe functions nor ERPs, was significantly altered in PD patients, whereas indices of depression were found only in advanced PD. The F-Dopa rate constant Ki was significantly reduced in the striatum, more in putamen than caudate nucleus, and inversely correlated with disease duration. A significant inverse correlation was found between both putamen and caudate nucleus Ki and Hoehn and Yahr score, and between putamen--but not caudate nucleus Ki --and UPDRS motor score. Principal components analysis (PCA) of PD patients Ki values and mood, cognitive and ERP parameters gave a three-factor solution. Variables contributing to factor 1 were memory score and N2-P3 ERP latencies, those to factor 2 were striatal Ki values, and those to factor 3 frontal executive performances. Depression did not segregate with any variable. Our findings suggest that unlike locomotor disability, cognitive abilities and mood state of non-demented PD patients are for the most part unrelated to striatal dopaminergic depletion and may result from dysfunction of extra-striatal dopaminergic or from non-dopaminergic systems.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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