Oral methylphenidate fails to elicit significant changes in extracellular putaminal dopamine levels in Parkinson's disease patients: positron emission tomographic studies.
Identifieur interne : 000633 ( Ncbi/Checkpoint ); précédent : 000632; suivant : 000634Oral methylphenidate fails to elicit significant changes in extracellular putaminal dopamine levels in Parkinson's disease patients: positron emission tomographic studies.
Auteurs : Kaveh M. Koochesfahani [Canada] ; Raúl De La Fuente-Fernández ; Vesna Sossi ; Michael Schulzer ; Lakshmi N. Yatham ; Thomas J. Ruth ; Stephan Blinder ; A Jon StoesslSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2006.
English descriptors
- KwdEn :
- Administration, Oral, Adult, Aged, Basal Ganglia (diagnostic imaging), Basal Ganglia (drug effects), Caudate Nucleus (diagnostic imaging), Caudate Nucleus (drug effects), Central Nervous System Stimulants (administration & dosage), Dopamine (metabolism), Dopamine D2 Receptor Antagonists, Dopamine Plasma Membrane Transport Proteins (antagonists & inhibitors), Extracellular Fluid (drug effects), Female, Humans, Image Processing, Computer-Assisted, Imaging, Three-Dimensional, Male, Methylphenidate (administration & dosage), Middle Aged, Parkinson Disease (diagnostic imaging), Parkinson Disease (drug therapy), Positron-Emission Tomography, Putamen (diagnostic imaging), Putamen (drug effects), Raclopride (pharmacokinetics), Treatment Failure.
- MESH :
- chemical , administration & dosage : Central Nervous System Stimulants, Methylphenidate.
- chemical , antagonists & inhibitors : Dopamine Plasma Membrane Transport Proteins.
- diagnostic imaging : Basal Ganglia, Caudate Nucleus, Parkinson Disease, Putamen.
- drug effects : Basal Ganglia, Caudate Nucleus, Extracellular Fluid, Putamen.
- drug therapy : Parkinson Disease.
- chemical , metabolism : Dopamine.
- chemical , pharmacokinetics : Raclopride.
- Administration, Oral, Adult, Aged, Dopamine D2 Receptor Antagonists, Female, Humans, Image Processing, Computer-Assisted, Imaging, Three-Dimensional, Male, Middle Aged, Positron-Emission Tomography, Treatment Failure.
Abstract
In this study, we assessed the changes of endogenous dopamine (DA) levels in response to methylphenidate in 5 patients with idiopathic Parkinson's disease (PD) and 6 healthy controls. Three-dimensional positron emission tomography was performed with the D2 receptor antagonist [11C]raclopride (RAC) at baseline and 1 hour following the administration of oral methylphenidate (0.8 mg/kg) to assess changes in dopamine levels indirectly. Oral methylphenidate produced no significant change in extracellular DA levels in the putamen, as estimated by comparing changes in RAC binding at baseline and 1 hour following its administration in PD subjects and healthy controls. However, there were small changes in RAC binding of opposite direction in caudate and ventral striatal regions compared between the two groups. Although there was no consistent improvement in motor function in the PD group, some patients did experience a subjective high in response to methylphenidate (MP). Failure of oral MP to alter extracellular DA levels in putamen could result from degeneration of presynaptic dopaminergic terminals, with consequent severe reductions in the levels of endogenous DA and dopamine transporter in PD subjects. Our data provide in vivo neurochemical support for the lack of clinical efficacy following MP in PD patients and are also in keeping with reduced DA release following amphetamine in PD subjects.
DOI: 10.1002/mds.20857
PubMed: 16570297
Affiliations:
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Koochesfahani</name><affiliation wicri:level="1"><nlm:affiliation>Pacific Parkinson's Research Centre, University of British Columbia, Vancouver, British Columbia, Canada. kavehm@interchange.ubc.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Pacific Parkinson's Research Centre, University of British Columbia, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation></author><author><name sortKey="De La Fuente Fernandez, Raul" sort="De La Fuente Fernandez, Raul" uniqKey="De La Fuente Fernandez R" first="Raúl" last="De La Fuente-Fernández">Raúl De La Fuente-Fernández</name></author><author><name sortKey="Sossi, Vesna" sort="Sossi, Vesna" uniqKey="Sossi V" first="Vesna" last="Sossi">Vesna Sossi</name></author><author><name sortKey="Schulzer, Michael" sort="Schulzer, Michael" uniqKey="Schulzer M" first="Michael" last="Schulzer">Michael Schulzer</name></author><author><name sortKey="Yatham, Lakshmi N" sort="Yatham, Lakshmi N" uniqKey="Yatham L" first="Lakshmi N" last="Yatham">Lakshmi N. 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Koochesfahani</name><affiliation wicri:level="1"><nlm:affiliation>Pacific Parkinson's Research Centre, University of British Columbia, Vancouver, British Columbia, Canada. kavehm@interchange.ubc.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Pacific Parkinson's Research Centre, University of British Columbia, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation></author><author><name sortKey="De La Fuente Fernandez, Raul" sort="De La Fuente Fernandez, Raul" uniqKey="De La Fuente Fernandez R" first="Raúl" last="De La Fuente-Fernández">Raúl De La Fuente-Fernández</name></author><author><name sortKey="Sossi, Vesna" sort="Sossi, Vesna" uniqKey="Sossi V" first="Vesna" last="Sossi">Vesna Sossi</name></author><author><name sortKey="Schulzer, Michael" sort="Schulzer, Michael" uniqKey="Schulzer M" first="Michael" last="Schulzer">Michael Schulzer</name></author><author><name sortKey="Yatham, Lakshmi N" sort="Yatham, Lakshmi N" uniqKey="Yatham L" first="Lakshmi N" last="Yatham">Lakshmi N. Yatham</name></author><author><name sortKey="Ruth, Thomas J" sort="Ruth, Thomas J" uniqKey="Ruth T" first="Thomas J" last="Ruth">Thomas J. Ruth</name></author><author><name sortKey="Blinder, Stephan" sort="Blinder, Stephan" uniqKey="Blinder S" first="Stephan" last="Blinder">Stephan Blinder</name></author><author><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A Jon" last="Stoessl">A Jon Stoessl</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Administration, Oral</term><term>Adult</term><term>Aged</term><term>Basal Ganglia (diagnostic imaging)</term><term>Basal Ganglia (drug effects)</term><term>Caudate Nucleus (diagnostic imaging)</term><term>Caudate Nucleus (drug effects)</term><term>Central Nervous System Stimulants (administration & dosage)</term><term>Dopamine (metabolism)</term><term>Dopamine D2 Receptor Antagonists</term><term>Dopamine Plasma Membrane Transport Proteins (antagonists & inhibitors)</term><term>Extracellular Fluid (drug effects)</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Imaging, Three-Dimensional</term><term>Male</term><term>Methylphenidate (administration & dosage)</term><term>Middle Aged</term><term>Parkinson Disease (diagnostic imaging)</term><term>Parkinson Disease (drug therapy)</term><term>Positron-Emission Tomography</term><term>Putamen (diagnostic imaging)</term><term>Putamen (drug effects)</term><term>Raclopride (pharmacokinetics)</term><term>Treatment Failure</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Central Nervous System Stimulants</term><term>Methylphenidate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Dopamine Plasma Membrane Transport Proteins</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Basal Ganglia</term><term>Caudate Nucleus</term><term>Parkinson Disease</term><term>Putamen</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Basal Ganglia</term><term>Caudate Nucleus</term><term>Extracellular Fluid</term><term>Putamen</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Raclopride</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Administration, Oral</term><term>Adult</term><term>Aged</term><term>Dopamine D2 Receptor Antagonists</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Imaging, Three-Dimensional</term><term>Male</term><term>Middle Aged</term><term>Positron-Emission Tomography</term><term>Treatment Failure</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In this study, we assessed the changes of endogenous dopamine (DA) levels in response to methylphenidate in 5 patients with idiopathic Parkinson's disease (PD) and 6 healthy controls. Three-dimensional positron emission tomography was performed with the D2 receptor antagonist [11C]raclopride (RAC) at baseline and 1 hour following the administration of oral methylphenidate (0.8 mg/kg) to assess changes in dopamine levels indirectly. Oral methylphenidate produced no significant change in extracellular DA levels in the putamen, as estimated by comparing changes in RAC binding at baseline and 1 hour following its administration in PD subjects and healthy controls. However, there were small changes in RAC binding of opposite direction in caudate and ventral striatal regions compared between the two groups. Although there was no consistent improvement in motor function in the PD group, some patients did experience a subjective high in response to methylphenidate (MP). Failure of oral MP to alter extracellular DA levels in putamen could result from degeneration of presynaptic dopaminergic terminals, with consequent severe reductions in the levels of endogenous DA and dopamine transporter in PD subjects. Our data provide in vivo neurochemical support for the lack of clinical efficacy following MP in PD patients and are also in keeping with reduced DA release following amphetamine in PD subjects.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Blinder, Stephan" sort="Blinder, Stephan" uniqKey="Blinder S" first="Stephan" last="Blinder">Stephan Blinder</name><name sortKey="De La Fuente Fernandez, Raul" sort="De La Fuente Fernandez, Raul" uniqKey="De La Fuente Fernandez R" first="Raúl" last="De La Fuente-Fernández">Raúl De La Fuente-Fernández</name><name sortKey="Ruth, Thomas J" sort="Ruth, Thomas J" uniqKey="Ruth T" first="Thomas J" last="Ruth">Thomas J. Ruth</name><name sortKey="Schulzer, Michael" sort="Schulzer, Michael" uniqKey="Schulzer M" first="Michael" last="Schulzer">Michael Schulzer</name><name sortKey="Sossi, Vesna" sort="Sossi, Vesna" uniqKey="Sossi V" first="Vesna" last="Sossi">Vesna Sossi</name><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A Jon" last="Stoessl">A Jon Stoessl</name><name sortKey="Yatham, Lakshmi N" sort="Yatham, Lakshmi N" uniqKey="Yatham L" first="Lakshmi N" last="Yatham">Lakshmi N. Yatham</name></noCountry><country name="Canada"><noRegion><name sortKey="Koochesfahani, Kaveh M" sort="Koochesfahani, Kaveh M" uniqKey="Koochesfahani K" first="Kaveh M" last="Koochesfahani">Kaveh M. Koochesfahani</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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