ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000569

IMPACT OF PARKINSON'S DISEASE AND DOPAMINERGIC MEDICATION ON PROPRIOCEPTIVE PROCESSING

Identifieur interne : 000569 ( PascalFrancis/Corpus ); précédent : 000568; suivant : 000570

IMPACT OF PARKINSON'S DISEASE AND DOPAMINERGIC MEDICATION ON PROPRIOCEPTIVE PROCESSING

Auteurs : D. Mongeon ; P. Blanchet ; J. Messier

Source :

Neuroscience [ 0306-4522 ] ; 2009.

RBID : Pascal:09-0119781

Descripteurs français

Pascal (Inist)
- Dopamine, Proprioception, Coordination sensorimotrice, Noyau gris central, Maladie de Parkinson, Homme.

English descriptors

KwdEn :
- Basal ganglion, Dopamine, Human, Parkinson disease, Proprioception, Sensorimotor coordination.

Abstract

Increasing evidence suggests that the pathophysiology of movement disorders in Parkinson's disease (PD) includes deficits in sensory processing and integration. However, the exact nature of these deficits and the ability of dopamine medication to correct them have not been thoroughly examined in previous studies. For instance, it remains unclear whether PD patients have globally impaired sensorimotor integration functions or selective deficiencies in processing proprioception. We evaluated the specific deficits of PD patients in sensorimotor integration and proprioceptive processing by testing their ability to perform three-dimensional (3D) reaching movements in four conditions in which the sensory signals defining target and hand positions (visual and/or proprioceptive) varied. Ten healthy subjects and 11 PD patients, ON dopamine medication and in the OFF state, were tested. PD patients in the OFF state showed a greater mean level of 3D errors relative to controls when the only available sensory information about target and hand position came from proprioception, but this difference did not reach significance. This indicates that deficient proprioception is not an early key feature of PD. Interestingly, the inaccuracies of a number of PD subjects further increased in the ON medicated state relative to healthy controls when reaching to proprioceptively-defined targets, and this between group difference was statistically significant. However, dopamine medication did not consistently degrade the reaching accuracy of PD patients, with both negative and positive effects on accuracy of reaching to proprioceptive-defined targets. Together, these findings indicate that dopamine replacement therapy not only did not normalize sensorimotor performance to the level of controls, but also induced deficits in the processing of proprioceptive information in some of the PD patients tested. Furthermore, the diversity of effects of medication on accuracy of reaching to proprioceptively-defined targets supports the idea that dysfunction of dopaminergic circuits within the basal ganglia is not primarily responsible for the proprioceptive processing deficits of PD patients.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0306-4522`
A02	`01`			`@0 NRSCDN`
A03		`1`		`@0 Neuroscience`
A05				`@2 158`
A06				`@2 2`
A08	`01`	`1`	`ENG`	`@1 IMPACT OF PARKINSON'S DISEASE AND DOPAMINERGIC MEDICATION ON PROPRIOCEPTIVE PROCESSING`
A11	`01`	`1`		`@1 MONGEON (D.)`
A11	`02`	`1`		`@1 BLANCHET (P.)`
A11	`03`	`1`		`@1 MESSIER (J.)`
A14	`01`			`@1 Département de Kinésiologie, Université de Montréal, 2100, boul. Édouard-Montpetit, bureau 8225 @2 Montréal, Québec, QC H3T 1J4 @3 CAN @Z 1 aut. @Z 3 aut.`
A14	`02`			`@1 Institut universitaire de gériatrie de Montréal, Université de Montréal, 4545, Chemin Queen-Mary @2 Montréal, Québec, H3W 1W4 @3 CAN @Z 1 aut. @Z 3 aut.`
A14	`03`			`@1 Département de stomatologie, Université de Montréal, Pavillon Roger-Gaudry 2900, boul. Édouard-Montpetit @2 Montréal, Québec, H3T 1J4 @3 CAN @Z 2 aut.`
A14	`04`			`@1 Services de neurologie du Centre Hospitalier de l'Université de Montréal, Hôpital Notre-Dame, Pavillon DesChamps, 1560, rue Sherbrooke est @2 Montréal, Québec, H2L 4M1 @3 CAN @Z 2 aut.`
A20				`@1 426-440`
A21				`@1 2009`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 17194 @5 354000185405680070`
A44				`@0 0000 @1 © 2009 INIST-CNRS. All rights reserved.`
A45				`@0 1 p.3/4`
A47	`01`	`1`		`@0 09-0119781`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Neuroscience`
A66	`01`			`@0 GBR`
C01	`01`		`ENG`	@0 Increasing evidence suggests that the pathophysiology of movement disorders in Parkinson's disease (PD) includes deficits in sensory processing and integration. However, the exact nature of these deficits and the ability of dopamine medication to correct them have not been thoroughly examined in previous studies. For instance, it remains unclear whether PD patients have globally impaired sensorimotor integration functions or selective deficiencies in processing proprioception. We evaluated the specific deficits of PD patients in sensorimotor integration and proprioceptive processing by testing their ability to perform three-dimensional (3D) reaching movements in four conditions in which the sensory signals defining target and hand positions (visual and/or proprioceptive) varied. Ten healthy subjects and 11 PD patients, ON dopamine medication and in the OFF state, were tested. PD patients in the OFF state showed a greater mean level of 3D errors relative to controls when the only available sensory information about target and hand position came from proprioception, but this difference did not reach significance. This indicates that deficient proprioception is not an early key feature of PD. Interestingly, the inaccuracies of a number of PD subjects further increased in the ON medicated state relative to healthy controls when reaching to proprioceptively-defined targets, and this between group difference was statistically significant. However, dopamine medication did not consistently degrade the reaching accuracy of PD patients, with both negative and positive effects on accuracy of reaching to proprioceptive-defined targets. Together, these findings indicate that dopamine replacement therapy not only did not normalize sensorimotor performance to the level of controls, but also induced deficits in the processing of proprioceptive information in some of the PD patients tested. Furthermore, the diversity of effects of medication on accuracy of reaching to proprioceptively-defined targets supports the idea that dysfunction of dopaminergic circuits within the basal ganglia is not primarily responsible for the proprioceptive processing deficits of PD patients.
C02	`01`	`X`		`@0 002A25`
C02	`02`	`X`		`@0 002B17G`
C03	`01`	`X`	`FRE`	`@0 Dopamine @2 NK @2 FR @5 01`
C03	`01`	`X`	`ENG`	`@0 Dopamine @2 NK @2 FR @5 01`
C03	`01`	`X`	`SPA`	`@0 Dopamina @2 NK @2 FR @5 01`
C03	`02`	`X`	`FRE`	`@0 Proprioception @5 02`
C03	`02`	`X`	`ENG`	`@0 Proprioception @5 02`
C03	`02`	`X`	`SPA`	`@0 Propiocepción @5 02`
C03	`03`	`X`	`FRE`	`@0 Coordination sensorimotrice @5 03`
C03	`03`	`X`	`ENG`	`@0 Sensorimotor coordination @5 03`
C03	`03`	`X`	`SPA`	`@0 Coordinación sensoriomotora @5 03`
C03	`04`	`X`	`FRE`	`@0 Noyau gris central @5 04`
C03	`04`	`X`	`ENG`	`@0 Basal ganglion @5 04`
C03	`04`	`X`	`SPA`	`@0 Núcleo basal @5 04`
C03	`05`	`X`	`FRE`	`@0 Maladie de Parkinson @2 NM @5 09`
C03	`05`	`X`	`ENG`	`@0 Parkinson disease @2 NM @5 09`
C03	`05`	`X`	`SPA`	`@0 Parkinson enfermedad @2 NM @5 09`
C03	`06`	`X`	`FRE`	`@0 Homme @5 54`
C03	`06`	`X`	`ENG`	`@0 Human @5 54`
C03	`06`	`X`	`SPA`	`@0 Hombre @5 54`
C07	`01`	`X`	`FRE`	`@0 Maladie dégénérative @5 20`
C07	`01`	`X`	`ENG`	`@0 Degenerative disease @5 20`
C07	`01`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 20`
C07	`02`	`X`	`FRE`	`@0 Pathologie du système nerveux @5 21`
C07	`02`	`X`	`ENG`	`@0 Nervous system diseases @5 21`
C07	`02`	`X`	`SPA`	`@0 Sistema nervioso patología @5 21`
C07	`03`	`X`	`FRE`	`@0 Pathologie de l'encéphale @5 22`
C07	`03`	`X`	`ENG`	`@0 Cerebral disorder @5 22`
C07	`03`	`X`	`SPA`	`@0 Encéfalo patología @5 22`
C07	`04`	`X`	`FRE`	`@0 Syndrome extrapyramidal @5 23`
C07	`04`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 23`
C07	`04`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 23`
C07	`05`	`X`	`FRE`	`@0 Pathologie du système nerveux central @5 24`
C07	`05`	`X`	`ENG`	`@0 Central nervous system disease @5 24`
C07	`05`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 24`
C07	`06`	`X`	`FRE`	`@0 Catécholamine @5 25`
C07	`06`	`X`	`ENG`	`@0 Catecholamine @5 25`
C07	`06`	`X`	`SPA`	`@0 Catecolamina @5 25`
C07	`07`	`X`	`FRE`	`@0 Neurotransmetteur @5 26`
C07	`07`	`X`	`ENG`	`@0 Neurotransmitter @5 26`
C07	`07`	`X`	`SPA`	`@0 Neurotransmisor @5 26`
C07	`08`	`X`	`FRE`	`@0 Encéphale @5 27`
C07	`08`	`X`	`ENG`	`@0 Encephalon @5 27`
C07	`08`	`X`	`SPA`	`@0 Encéfalo @5 27`
C07	`09`	`X`	`FRE`	`@0 Système nerveux central @5 28`
C07	`09`	`X`	`ENG`	`@0 Central nervous system @5 28`
C07	`09`	`X`	`SPA`	`@0 Sistema nervioso central @5 28`
N21				`@1 082`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 09-0119781 INIST
ET :	IMPACT OF PARKINSON'S DISEASE AND DOPAMINERGIC MEDICATION ON PROPRIOCEPTIVE PROCESSING
AU :	MONGEON (D.); BLANCHET (P.); MESSIER (J.)
AF :	Département de Kinésiologie, Université de Montréal, 2100, boul. Édouard-Montpetit, bureau 8225/Montréal, Québec, QC H3T 1J4/Canada (1 aut., 3 aut.); Institut universitaire de gériatrie de Montréal, Université de Montréal, 4545, Chemin Queen-Mary/Montréal, Québec, H3W 1W4/Canada (1 aut., 3 aut.); Département de stomatologie, Université de Montréal, Pavillon Roger-Gaudry 2900, boul. Édouard-Montpetit/Montréal, Québec, H3T 1J4/Canada (2 aut.); Services de neurologie du Centre Hospitalier de l'Université de Montréal, Hôpital Notre-Dame, Pavillon DesChamps, 1560, rue Sherbrooke est/Montréal, Québec, H2L 4M1/Canada (2 aut.)
DT :	Publication en série; Niveau analytique
SO :	Neuroscience; ISSN 0306-4522; Coden NRSCDN; Royaume-Uni; Da. 2009; Vol. 158; No. 2; Pp. 426-440; Bibl. 1 p.3/4
LA :	Anglais
EA :	Increasing evidence suggests that the pathophysiology of movement disorders in Parkinson's disease (PD) includes deficits in sensory processing and integration. However, the exact nature of these deficits and the ability of dopamine medication to correct them have not been thoroughly examined in previous studies. For instance, it remains unclear whether PD patients have globally impaired sensorimotor integration functions or selective deficiencies in processing proprioception. We evaluated the specific deficits of PD patients in sensorimotor integration and proprioceptive processing by testing their ability to perform three-dimensional (3D) reaching movements in four conditions in which the sensory signals defining target and hand positions (visual and/or proprioceptive) varied. Ten healthy subjects and 11 PD patients, ON dopamine medication and in the OFF state, were tested. PD patients in the OFF state showed a greater mean level of 3D errors relative to controls when the only available sensory information about target and hand position came from proprioception, but this difference did not reach significance. This indicates that deficient proprioception is not an early key feature of PD. Interestingly, the inaccuracies of a number of PD subjects further increased in the ON medicated state relative to healthy controls when reaching to proprioceptively-defined targets, and this between group difference was statistically significant. However, dopamine medication did not consistently degrade the reaching accuracy of PD patients, with both negative and positive effects on accuracy of reaching to proprioceptive-defined targets. Together, these findings indicate that dopamine replacement therapy not only did not normalize sensorimotor performance to the level of controls, but also induced deficits in the processing of proprioceptive information in some of the PD patients tested. Furthermore, the diversity of effects of medication on accuracy of reaching to proprioceptively-defined targets supports the idea that dysfunction of dopaminergic circuits within the basal ganglia is not primarily responsible for the proprioceptive processing deficits of PD patients.
CC :	002A25; 002B17G
FD :	Dopamine; Proprioception; Coordination sensorimotrice; Noyau gris central; Maladie de Parkinson; Homme
FG :	Maladie dégénérative; Pathologie du système nerveux; Pathologie de l'encéphale; Syndrome extrapyramidal; Pathologie du système nerveux central; Catécholamine; Neurotransmetteur; Encéphale; Système nerveux central
ED :	Dopamine; Proprioception; Sensorimotor coordination; Basal ganglion; Parkinson disease; Human
EG :	Degenerative disease; Nervous system diseases; Cerebral disorder; Extrapyramidal syndrome; Central nervous system disease; Catecholamine; Neurotransmitter; Encephalon; Central nervous system
SD :	Dopamina; Propiocepción; Coordinación sensoriomotora; Núcleo basal; Parkinson enfermedad; Hombre
LO :	INIST-17194.354000185405680070
ID :	09-0119781

Links to Exploration step

Pascal:09-0119781

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">IMPACT OF PARKINSON'S DISEASE AND DOPAMINERGIC MEDICATION ON PROPRIOCEPTIVE PROCESSING</title>
<author><name sortKey="Mongeon, D" sort="Mongeon, D" uniqKey="Mongeon D" first="D." last="Mongeon">D. Mongeon</name>
<affiliation><inist:fA14 i1="01"><s1>Département de Kinésiologie, Université de Montréal, 2100, boul. Édouard-Montpetit, bureau 8225</s1>
<s2>Montréal, Québec, QC H3T 1J4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Institut universitaire de gériatrie de Montréal, Université de Montréal, 4545, Chemin Queen-Mary</s1>
<s2>Montréal, Québec, H3W 1W4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Blanchet, P" sort="Blanchet, P" uniqKey="Blanchet P" first="P." last="Blanchet">P. Blanchet</name>
<affiliation><inist:fA14 i1="03"><s1>Département de stomatologie, Université de Montréal, Pavillon Roger-Gaudry 2900, boul. Édouard-Montpetit</s1>
<s2>Montréal, Québec, H3T 1J4</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="04"><s1>Services de neurologie du Centre Hospitalier de l'Université de Montréal, Hôpital Notre-Dame, Pavillon DesChamps, 1560, rue Sherbrooke est</s1>
<s2>Montréal, Québec, H2L 4M1</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Messier, J" sort="Messier, J" uniqKey="Messier J" first="J." last="Messier">J. Messier</name>
<affiliation><inist:fA14 i1="01"><s1>Département de Kinésiologie, Université de Montréal, 2100, boul. Édouard-Montpetit, bureau 8225</s1>
<s2>Montréal, Québec, QC H3T 1J4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Institut universitaire de gériatrie de Montréal, Université de Montréal, 4545, Chemin Queen-Mary</s1>
<s2>Montréal, Québec, H3W 1W4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">09-0119781</idno>
<date when="2009">2009</date>
<idno type="stanalyst">PASCAL 09-0119781 INIST</idno>
<idno type="RBID">Pascal:09-0119781</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000569</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">IMPACT OF PARKINSON'S DISEASE AND DOPAMINERGIC MEDICATION ON PROPRIOCEPTIVE PROCESSING</title>
<author><name sortKey="Mongeon, D" sort="Mongeon, D" uniqKey="Mongeon D" first="D." last="Mongeon">D. Mongeon</name>
<affiliation><inist:fA14 i1="01"><s1>Département de Kinésiologie, Université de Montréal, 2100, boul. Édouard-Montpetit, bureau 8225</s1>
<s2>Montréal, Québec, QC H3T 1J4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Institut universitaire de gériatrie de Montréal, Université de Montréal, 4545, Chemin Queen-Mary</s1>
<s2>Montréal, Québec, H3W 1W4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Blanchet, P" sort="Blanchet, P" uniqKey="Blanchet P" first="P." last="Blanchet">P. Blanchet</name>
<affiliation><inist:fA14 i1="03"><s1>Département de stomatologie, Université de Montréal, Pavillon Roger-Gaudry 2900, boul. Édouard-Montpetit</s1>
<s2>Montréal, Québec, H3T 1J4</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="04"><s1>Services de neurologie du Centre Hospitalier de l'Université de Montréal, Hôpital Notre-Dame, Pavillon DesChamps, 1560, rue Sherbrooke est</s1>
<s2>Montréal, Québec, H2L 4M1</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Messier, J" sort="Messier, J" uniqKey="Messier J" first="J." last="Messier">J. Messier</name>
<affiliation><inist:fA14 i1="01"><s1>Département de Kinésiologie, Université de Montréal, 2100, boul. Édouard-Montpetit, bureau 8225</s1>
<s2>Montréal, Québec, QC H3T 1J4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Institut universitaire de gériatrie de Montréal, Université de Montréal, 4545, Chemin Queen-Mary</s1>
<s2>Montréal, Québec, H3W 1W4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Neuroscience</title>
<title level="j" type="abbreviated">Neuroscience</title>
<idno type="ISSN">0306-4522</idno>
<imprint><date when="2009">2009</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Neuroscience</title>
<title level="j" type="abbreviated">Neuroscience</title>
<idno type="ISSN">0306-4522</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Basal ganglion</term>
<term>Dopamine</term>
<term>Human</term>
<term>Parkinson disease</term>
<term>Proprioception</term>
<term>Sensorimotor coordination</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Dopamine</term>
<term>Proprioception</term>
<term>Coordination sensorimotrice</term>
<term>Noyau gris central</term>
<term>Maladie de Parkinson</term>
<term>Homme</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Increasing evidence suggests that the pathophysiology of movement disorders in Parkinson's disease (PD) includes deficits in sensory processing and integration. However, the exact nature of these deficits and the ability of dopamine medication to correct them have not been thoroughly examined in previous studies. For instance, it remains unclear whether PD patients have globally impaired sensorimotor integration functions or selective deficiencies in processing proprioception. We evaluated the specific deficits of PD patients in sensorimotor integration and proprioceptive processing by testing their ability to perform three-dimensional (3D) reaching movements in four conditions in which the sensory signals defining target and hand positions (visual and/or proprioceptive) varied. Ten healthy subjects and 11 PD patients, ON dopamine medication and in the OFF state, were tested. PD patients in the OFF state showed a greater mean level of 3D errors relative to controls when the only available sensory information about target and hand position came from proprioception, but this difference did not reach significance. This indicates that deficient proprioception is not an early key feature of PD. Interestingly, the inaccuracies of a number of PD subjects further increased in the ON medicated state relative to healthy controls when reaching to proprioceptively-defined targets, and this between group difference was statistically significant. However, dopamine medication did not consistently degrade the reaching accuracy of PD patients, with both negative and positive effects on accuracy of reaching to proprioceptive-defined targets. Together, these findings indicate that dopamine replacement therapy not only did not normalize sensorimotor performance to the level of controls, but also induced deficits in the processing of proprioceptive information in some of the PD patients tested. Furthermore, the diversity of effects of medication on accuracy of reaching to proprioceptively-defined targets supports the idea that dysfunction of dopaminergic circuits within the basal ganglia is not primarily responsible for the proprioceptive processing deficits of PD patients.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0306-4522</s0>
</fA01>
<fA02 i1="01"><s0>NRSCDN</s0>
</fA02>
<fA03 i2="1"><s0>Neuroscience</s0>
</fA03>
<fA05><s2>158</s2>
</fA05>
<fA06><s2>2</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>IMPACT OF PARKINSON'S DISEASE AND DOPAMINERGIC MEDICATION ON PROPRIOCEPTIVE PROCESSING</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>MONGEON (D.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>BLANCHET (P.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>MESSIER (J.)</s1>
</fA11>
<fA14 i1="01"><s1>Département de Kinésiologie, Université de Montréal, 2100, boul. Édouard-Montpetit, bureau 8225</s1>
<s2>Montréal, Québec, QC H3T 1J4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Institut universitaire de gériatrie de Montréal, Université de Montréal, 4545, Chemin Queen-Mary</s1>
<s2>Montréal, Québec, H3W 1W4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Département de stomatologie, Université de Montréal, Pavillon Roger-Gaudry 2900, boul. Édouard-Montpetit</s1>
<s2>Montréal, Québec, H3T 1J4</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Services de neurologie du Centre Hospitalier de l'Université de Montréal, Hôpital Notre-Dame, Pavillon DesChamps, 1560, rue Sherbrooke est</s1>
<s2>Montréal, Québec, H2L 4M1</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA20><s1>426-440</s1>
</fA20>
<fA21><s1>2009</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>17194</s2>
<s5>354000185405680070</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2009 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>1 p.3/4</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>09-0119781</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Neuroscience</s0>
</fA64>
<fA66 i1="01"><s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Increasing evidence suggests that the pathophysiology of movement disorders in Parkinson's disease (PD) includes deficits in sensory processing and integration. However, the exact nature of these deficits and the ability of dopamine medication to correct them have not been thoroughly examined in previous studies. For instance, it remains unclear whether PD patients have globally impaired sensorimotor integration functions or selective deficiencies in processing proprioception. We evaluated the specific deficits of PD patients in sensorimotor integration and proprioceptive processing by testing their ability to perform three-dimensional (3D) reaching movements in four conditions in which the sensory signals defining target and hand positions (visual and/or proprioceptive) varied. Ten healthy subjects and 11 PD patients, ON dopamine medication and in the OFF state, were tested. PD patients in the OFF state showed a greater mean level of 3D errors relative to controls when the only available sensory information about target and hand position came from proprioception, but this difference did not reach significance. This indicates that deficient proprioception is not an early key feature of PD. Interestingly, the inaccuracies of a number of PD subjects further increased in the ON medicated state relative to healthy controls when reaching to proprioceptively-defined targets, and this between group difference was statistically significant. However, dopamine medication did not consistently degrade the reaching accuracy of PD patients, with both negative and positive effects on accuracy of reaching to proprioceptive-defined targets. Together, these findings indicate that dopamine replacement therapy not only did not normalize sensorimotor performance to the level of controls, but also induced deficits in the processing of proprioceptive information in some of the PD patients tested. Furthermore, the diversity of effects of medication on accuracy of reaching to proprioceptively-defined targets supports the idea that dysfunction of dopaminergic circuits within the basal ganglia is not primarily responsible for the proprioceptive processing deficits of PD patients.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A25</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Proprioception</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Proprioception</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Propiocepción</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Coordination sensorimotrice</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Sensorimotor coordination</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Coordinación sensoriomotora</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Noyau gris central</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Basal ganglion</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Núcleo basal</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Homme</s0>
<s5>54</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Human</s0>
<s5>54</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Hombre</s0>
<s5>54</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Pathologie du   système nerveux</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie du   système nerveux central</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>25</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Neurotransmetteur</s0>
<s5>26</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Neurotransmitter</s0>
<s5>26</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Neurotransmisor</s0>
<s5>26</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>27</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Encephalon</s0>
<s5>27</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>27</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>28</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>28</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>28</s5>
</fC07>
<fN21><s1>082</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 09-0119781 INIST</NO>
<ET>IMPACT OF PARKINSON'S DISEASE AND DOPAMINERGIC MEDICATION ON PROPRIOCEPTIVE PROCESSING</ET>
<AU>MONGEON (D.); BLANCHET (P.); MESSIER (J.)</AU>
<AF>Département de Kinésiologie, Université de Montréal, 2100, boul. Édouard-Montpetit, bureau 8225/Montréal, Québec, QC H3T 1J4/Canada (1 aut., 3 aut.); Institut universitaire de gériatrie de Montréal, Université de Montréal, 4545, Chemin Queen-Mary/Montréal, Québec, H3W 1W4/Canada (1 aut., 3 aut.); Département de stomatologie, Université de Montréal, Pavillon Roger-Gaudry 2900, boul. Édouard-Montpetit/Montréal, Québec, H3T 1J4/Canada (2 aut.); Services de neurologie du Centre Hospitalier de l'Université de Montréal, Hôpital Notre-Dame, Pavillon DesChamps, 1560, rue Sherbrooke est/Montréal, Québec, H2L 4M1/Canada (2 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neuroscience; ISSN 0306-4522; Coden NRSCDN; Royaume-Uni; Da. 2009; Vol. 158; No. 2; Pp. 426-440; Bibl. 1 p.3/4</SO>
<LA>Anglais</LA>
<EA>Increasing evidence suggests that the pathophysiology of movement disorders in Parkinson's disease (PD) includes deficits in sensory processing and integration. However, the exact nature of these deficits and the ability of dopamine medication to correct them have not been thoroughly examined in previous studies. For instance, it remains unclear whether PD patients have globally impaired sensorimotor integration functions or selective deficiencies in processing proprioception. We evaluated the specific deficits of PD patients in sensorimotor integration and proprioceptive processing by testing their ability to perform three-dimensional (3D) reaching movements in four conditions in which the sensory signals defining target and hand positions (visual and/or proprioceptive) varied. Ten healthy subjects and 11 PD patients, ON dopamine medication and in the OFF state, were tested. PD patients in the OFF state showed a greater mean level of 3D errors relative to controls when the only available sensory information about target and hand position came from proprioception, but this difference did not reach significance. This indicates that deficient proprioception is not an early key feature of PD. Interestingly, the inaccuracies of a number of PD subjects further increased in the ON medicated state relative to healthy controls when reaching to proprioceptively-defined targets, and this between group difference was statistically significant. However, dopamine medication did not consistently degrade the reaching accuracy of PD patients, with both negative and positive effects on accuracy of reaching to proprioceptive-defined targets. Together, these findings indicate that dopamine replacement therapy not only did not normalize sensorimotor performance to the level of controls, but also induced deficits in the processing of proprioceptive information in some of the PD patients tested. Furthermore, the diversity of effects of medication on accuracy of reaching to proprioceptively-defined targets supports the idea that dysfunction of dopaminergic circuits within the basal ganglia is not primarily responsible for the proprioceptive processing deficits of PD patients.</EA>
<CC>002A25; 002B17G</CC>
<FD>Dopamine; Proprioception; Coordination sensorimotrice; Noyau gris central; Maladie de Parkinson; Homme</FD>
<FG>Maladie dégénérative; Pathologie du système nerveux; Pathologie de l'encéphale; Syndrome extrapyramidal; Pathologie du   système nerveux central; Catécholamine; Neurotransmetteur; Encéphale; Système nerveux central</FG>
<ED>Dopamine; Proprioception; Sensorimotor coordination; Basal ganglion; Parkinson disease; Human</ED>
<EG>Degenerative disease; Nervous system diseases; Cerebral disorder; Extrapyramidal syndrome; Central nervous system disease; Catecholamine; Neurotransmitter; Encephalon; Central nervous system</EG>
<SD>Dopamina; Propiocepción; Coordinación sensoriomotora; Núcleo basal; Parkinson enfermedad; Hombre</SD>
<LO>INIST-17194.354000185405680070</LO>
<ID>09-0119781</ID>
</server>
</inist>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/PascalFrancis/Corpus

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000569 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 000569 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Canada
   |area=    ParkinsonCanadaV1
   |flux=    PascalFrancis
   |étape=   Corpus
   |type=    RBID
   |clé=     Pascal:09-0119781
   |texte=   IMPACT OF PARKINSON'S DISEASE AND DOPAMINERGIC MEDICATION ON PROPRIOCEPTIVE PROCESSING
}}

This area was generated with Dilib version V0.6.29.
Data generation: Thu May 4 22:20:19 2017. Site generation: Fri Dec 23 23:17:26 2022

	La maladie de Parkinson au Canada (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

La maladie de Parkinson au Canada (serveur d'exploration)

IMPACT OF PARKINSON'S DISEASE AND DOPAMINERGIC MEDICATION ON PROPRIOCEPTIVE PROCESSING

IMPACT OF PARKINSON'S DISEASE AND DOPAMINERGIC MEDICATION ON PROPRIOCEPTIVE PROCESSING

Source :

Descripteurs français

English descriptors

Abstract

Notice en format standard (ISO 2709)

Format Inist (serveur)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri