ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000D01

Physiologic basis of dyskinesia. Discussion

Identifieur interne : 000D01 ( PascalFrancis/Corpus ); précédent : 000D00; suivant : 000D02

Physiologic basis of dyskinesia. Discussion

Auteurs : M. Filion ; OBESO ; BENABID ; OLANOW ; LANG ; HIRSCH ; NUTT

Source :

Annals of neurology [ 0364-5134 ] ; 2000.

RBID : Pascal:00-0263340

Descripteurs français

Pascal (Inist)
- Dyskinésie, Parkinson maladie, Lévodopa, Antiparkinsonien, Sélection, Attention, Modèle, Physiopathologie, Homme.

English descriptors

KwdEn :
- Antiparkinson agent, Attention, Dyskinesia, Human, Levodopa, Models, Parkinson disease, Pathophysiology, Selection.

Abstract

The current functional model of the basal ganglia suggests that dyskinesia results from abnormally low activity at the output of the system. This view appears incomplete. The recent literature suggests other factors. Thus, dyskinesia may result from disturbance of surround inhibition: a physiologic mechanism to select neuronal responses. A major criterion for selection in the basal ganglia is prediction of reward, materialized by release of dopamine. However, much of this release is independent of impulse flow, and controled presynaptically, at a myriad of terminals, whose presence is then essential. Thus, levodopa in parkinsonism is likely to exaggerate imbalance between regions of the basal ganglia more or less deprived of dopaminergic terminals. The cortex and thalamus may be viewed as equally important afferents to the basal ganglia. Each of them appears to influence preponderantly its own half of striatal projection neurons. Those of the indirect pathway would be part of a mainly transcortical loop, specialized for the precise weighing, and selection of cortical information. Those of the direct pathway would be part of a predominantly subcortical loop, more likely concerned by changes in alertness and attention. Dyskinesia could thus result from imbalance between cortical and thalamic functions, between selection and attention.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0364-5134`
A02	`01`			`@0 ANNED3`
A03		`1`		`@0 Ann. neurol.`
A05				`@2 47`
A06				`@2 4 @3 SUP1`
A08	`01`	`1`	`ENG`	`@1 Physiologic basis of dyskinesia. Discussion`
A09	`01`	`1`	`ENG`	`@1 Levodopa-induced dyskinesias`
A11	`01`	`1`		`@1 FILION (M.)`
A11	`02`	`1`		`@1 OBESO @9 comment.`
A11	`03`	`1`		`@1 BENABID @9 comment.`
A11	`04`	`1`		`@1 OLANOW @9 comment.`
A11	`05`	`1`		`@1 LANG @9 comment.`
A11	`06`	`1`		`@1 HIRSCH @9 comment.`
A11	`07`	`1`		`@1 NUTT @9 comment.`
A12	`01`	`1`		`@1 OLANOW (C. Warren) @9 ed.`
A14	`01`			`@1 Department of Anatomy and Physiology, Faculty of Medicine, Laval University and Neuroscience Unit, CHUL Research Center @2 Quebec @3 CAN @Z 1 aut.`
A15	`01`			`@1 Department of Neurology, Mount Sinai School of Medicine, 1 Gustave Levy Place, Annenburg 14-94 @2 New York, NY 10029 @3 USA @Z 1 aut.`
A20				`@2 S35-S41`
A21				`@1 2000`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 16555 @5 354000082146950040`
A44				`@0 0000 @1 © 2000 INIST-CNRS. All rights reserved.`
A45				`@0 44 ref.`
A47	`01`	`1`		`@0 00-0263340`
A60				`@1 P @3 AR @3 CT`
A61				`@0 A`
A64	`01`	`1`		`@0 Annals of neurology`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 The current functional model of the basal ganglia suggests that dyskinesia results from abnormally low activity at the output of the system. This view appears incomplete. The recent literature suggests other factors. Thus, dyskinesia may result from disturbance of surround inhibition: a physiologic mechanism to select neuronal responses. A major criterion for selection in the basal ganglia is prediction of reward, materialized by release of dopamine. However, much of this release is independent of impulse flow, and controled presynaptically, at a myriad of terminals, whose presence is then essential. Thus, levodopa in parkinsonism is likely to exaggerate imbalance between regions of the basal ganglia more or less deprived of dopaminergic terminals. The cortex and thalamus may be viewed as equally important afferents to the basal ganglia. Each of them appears to influence preponderantly its own half of striatal projection neurons. Those of the indirect pathway would be part of a mainly transcortical loop, specialized for the precise weighing, and selection of cortical information. Those of the direct pathway would be part of a predominantly subcortical loop, more likely concerned by changes in alertness and attention. Dyskinesia could thus result from imbalance between cortical and thalamic functions, between selection and attention.
C02	`01`	`X`		`@0 002B17G`
C03	`01`	`X`	`FRE`	`@0 Dyskinésie @5 01`
C03	`01`	`X`	`ENG`	`@0 Dyskinesia @5 01`
C03	`01`	`X`	`SPA`	`@0 Disquinesia @5 01`
C03	`02`	`X`	`FRE`	`@0 Parkinson maladie @5 04`
C03	`02`	`X`	`ENG`	`@0 Parkinson disease @5 04`
C03	`02`	`X`	`SPA`	`@0 Parkinson enfermedad @5 04`
C03	`03`	`X`	`FRE`	`@0 Lévodopa @5 07`
C03	`03`	`X`	`ENG`	`@0 Levodopa @5 07`
C03	`03`	`X`	`SPA`	`@0 Levodopa @5 07`
C03	`04`	`X`	`FRE`	`@0 Antiparkinsonien @5 08`
C03	`04`	`X`	`ENG`	`@0 Antiparkinson agent @5 08`
C03	`04`	`X`	`SPA`	`@0 Antiparkinsoniano @5 08`
C03	`05`	`X`	`FRE`	`@0 Sélection @5 10`
C03	`05`	`X`	`ENG`	`@0 Selection @5 10`
C03	`05`	`X`	`SPA`	`@0 Selección @5 10`
C03	`06`	`X`	`FRE`	`@0 Attention @5 13`
C03	`06`	`X`	`ENG`	`@0 Attention @5 13`
C03	`06`	`X`	`SPA`	`@0 Atención @5 13`
C03	`07`	`X`	`FRE`	`@0 Modèle @5 16`
C03	`07`	`X`	`ENG`	`@0 Models @5 16`
C03	`07`	`X`	`SPA`	`@0 Modelo @5 16`
C03	`08`	`X`	`FRE`	`@0 Physiopathologie @5 17`
C03	`08`	`X`	`ENG`	`@0 Pathophysiology @5 17`
C03	`08`	`X`	`SPA`	`@0 Fisiopatología @5 17`
C03	`09`	`X`	`FRE`	`@0 Homme @5 20`
C03	`09`	`X`	`ENG`	`@0 Human @5 20`
C03	`09`	`X`	`SPA`	`@0 Hombre @5 20`
C07	`01`	`X`	`FRE`	`@0 Système nerveux pathologie @5 37`
C07	`01`	`X`	`ENG`	`@0 Nervous system diseases @5 37`
C07	`01`	`X`	`SPA`	`@0 Sistema nervioso patología @5 37`
C07	`02`	`X`	`FRE`	`@0 Trouble neurologique @5 38`
C07	`02`	`X`	`ENG`	`@0 Neurological disorder @5 38`
C07	`02`	`X`	`SPA`	`@0 Trastorno neurológico @5 38`
C07	`03`	`X`	`FRE`	`@0 Mouvement involontaire @5 39`
C07	`03`	`X`	`ENG`	`@0 Involuntary movement @5 39`
C07	`03`	`X`	`SPA`	`@0 Movimiento involuntario @5 39`
C07	`04`	`X`	`FRE`	`@0 Extrapyramidal syndrome @5 40`
C07	`04`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 40`
C07	`04`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 40`
C07	`05`	`X`	`FRE`	`@0 Système nerveux central pathologie @5 46`
C07	`05`	`X`	`ENG`	`@0 Central nervous system disease @5 46`
C07	`05`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 46`
C07	`06`	`X`	`FRE`	`@0 Encéphale pathologie @5 47`
C07	`06`	`X`	`ENG`	`@0 Cerebral disorder @5 47`
C07	`06`	`X`	`SPA`	`@0 Encéfalo patología @5 47`
C07	`07`	`X`	`FRE`	`@0 Maladie dégénérative @5 49`
C07	`07`	`X`	`ENG`	`@0 Degenerative disease @5 49`
C07	`07`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 49`
N21				`@1 178`

Format Inist (serveur)

NO :	PASCAL 00-0263340 INIST
ET :	Physiologic basis of dyskinesia. Discussion
AU :	FILION (M.); OBESO; BENABID; OLANOW; LANG; HIRSCH; NUTT; OLANOW (C. Warren)
AF :	Department of Anatomy and Physiology, Faculty of Medicine, Laval University and Neuroscience Unit, CHUL Research Center/Quebec/Canada (1 aut.); Department of Neurology, Mount Sinai School of Medicine, 1 Gustave Levy Place, Annenburg 14-94/New York, NY 10029/Etats-Unis (1 aut.)
DT :	Publication en série; Article; Commentaire; Niveau analytique
SO :	Annals of neurology; ISSN 0364-5134; Coden ANNED3; Etats-Unis; Da. 2000; Vol. 47; No. 4 SUP1; S35-S41; Bibl. 44 ref.
LA :	Anglais
EA :	The current functional model of the basal ganglia suggests that dyskinesia results from abnormally low activity at the output of the system. This view appears incomplete. The recent literature suggests other factors. Thus, dyskinesia may result from disturbance of surround inhibition: a physiologic mechanism to select neuronal responses. A major criterion for selection in the basal ganglia is prediction of reward, materialized by release of dopamine. However, much of this release is independent of impulse flow, and controled presynaptically, at a myriad of terminals, whose presence is then essential. Thus, levodopa in parkinsonism is likely to exaggerate imbalance between regions of the basal ganglia more or less deprived of dopaminergic terminals. The cortex and thalamus may be viewed as equally important afferents to the basal ganglia. Each of them appears to influence preponderantly its own half of striatal projection neurons. Those of the indirect pathway would be part of a mainly transcortical loop, specialized for the precise weighing, and selection of cortical information. Those of the direct pathway would be part of a predominantly subcortical loop, more likely concerned by changes in alertness and attention. Dyskinesia could thus result from imbalance between cortical and thalamic functions, between selection and attention.
CC :	002B17G
FD :	Dyskinésie; Parkinson maladie; Lévodopa; Antiparkinsonien; Sélection; Attention; Modèle; Physiopathologie; Homme
FG :	Système nerveux pathologie; Trouble neurologique; Mouvement involontaire; Extrapyramidal syndrome; Système nerveux central pathologie; Encéphale pathologie; Maladie dégénérative
ED :	Dyskinesia; Parkinson disease; Levodopa; Antiparkinson agent; Selection; Attention; Models; Pathophysiology; Human
EG :	Nervous system diseases; Neurological disorder; Involuntary movement; Extrapyramidal syndrome; Central nervous system disease; Cerebral disorder; Degenerative disease
SD :	Disquinesia; Parkinson enfermedad; Levodopa; Antiparkinsoniano; Selección; Atención; Modelo; Fisiopatología; Hombre
LO :	INIST-16555.354000082146950040
ID :	00-0263340

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Pascal:00-0263340

Le document en format XML

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<front><div type="abstract" xml:lang="en">The current functional model of the basal ganglia suggests that dyskinesia results from abnormally low activity at the output of the system. This view appears incomplete. The recent literature suggests other factors. Thus, dyskinesia may result from disturbance of surround inhibition: a physiologic mechanism to select neuronal responses. A major criterion for selection in the basal ganglia is prediction of reward, materialized by release of dopamine. However, much of this release is independent of impulse flow, and controled presynaptically, at a myriad of terminals, whose presence is then essential. Thus, levodopa in parkinsonism is likely to exaggerate imbalance between regions of the basal ganglia more or less deprived of dopaminergic terminals. The cortex and thalamus may be viewed as equally important afferents to the basal ganglia. Each of them appears to influence preponderantly its own half of striatal projection neurons. Those of the indirect pathway would be part of a mainly transcortical loop, specialized for the precise weighing, and selection of cortical information. Those of the direct pathway would be part of a predominantly subcortical loop, more likely concerned by changes in alertness and attention. Dyskinesia could thus result from imbalance between cortical and thalamic functions, between selection and attention.</div>
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<fC01 i1="01" l="ENG"><s0>The current functional model of the basal ganglia suggests that dyskinesia results from abnormally low activity at the output of the system. This view appears incomplete. The recent literature suggests other factors. Thus, dyskinesia may result from disturbance of surround inhibition: a physiologic mechanism to select neuronal responses. A major criterion for selection in the basal ganglia is prediction of reward, materialized by release of dopamine. However, much of this release is independent of impulse flow, and controled presynaptically, at a myriad of terminals, whose presence is then essential. Thus, levodopa in parkinsonism is likely to exaggerate imbalance between regions of the basal ganglia more or less deprived of dopaminergic terminals. The cortex and thalamus may be viewed as equally important afferents to the basal ganglia. Each of them appears to influence preponderantly its own half of striatal projection neurons. Those of the indirect pathway would be part of a mainly transcortical loop, specialized for the precise weighing, and selection of cortical information. Those of the direct pathway would be part of a predominantly subcortical loop, more likely concerned by changes in alertness and attention. Dyskinesia could thus result from imbalance between cortical and thalamic functions, between selection and attention.</s0>
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<server><NO>PASCAL 00-0263340 INIST</NO>
<ET>Physiologic basis of dyskinesia. Discussion</ET>
<AU>FILION (M.); OBESO; BENABID; OLANOW; LANG; HIRSCH; NUTT; OLANOW (C. Warren)</AU>
<AF>Department of Anatomy and Physiology, Faculty of Medicine, Laval University and Neuroscience Unit, CHUL Research Center/Quebec/Canada (1 aut.); Department of Neurology, Mount Sinai School of Medicine, 1 Gustave Levy Place, Annenburg 14-94/New York, NY 10029/Etats-Unis (1 aut.)</AF>
<DT>Publication en série; Article; Commentaire; Niveau analytique</DT>
<SO>Annals of neurology; ISSN 0364-5134; Coden ANNED3; Etats-Unis; Da. 2000; Vol. 47; No. 4 SUP1; S35-S41; Bibl. 44 ref.</SO>
<LA>Anglais</LA>
<EA>The current functional model of the basal ganglia suggests that dyskinesia results from abnormally low activity at the output of the system. This view appears incomplete. The recent literature suggests other factors. Thus, dyskinesia may result from disturbance of surround inhibition: a physiologic mechanism to select neuronal responses. A major criterion for selection in the basal ganglia is prediction of reward, materialized by release of dopamine. However, much of this release is independent of impulse flow, and controled presynaptically, at a myriad of terminals, whose presence is then essential. Thus, levodopa in parkinsonism is likely to exaggerate imbalance between regions of the basal ganglia more or less deprived of dopaminergic terminals. The cortex and thalamus may be viewed as equally important afferents to the basal ganglia. Each of them appears to influence preponderantly its own half of striatal projection neurons. Those of the indirect pathway would be part of a mainly transcortical loop, specialized for the precise weighing, and selection of cortical information. Those of the direct pathway would be part of a predominantly subcortical loop, more likely concerned by changes in alertness and attention. Dyskinesia could thus result from imbalance between cortical and thalamic functions, between selection and attention.</EA>
<CC>002B17G</CC>
<FD>Dyskinésie; Parkinson maladie; Lévodopa; Antiparkinsonien; Sélection; Attention; Modèle; Physiopathologie; Homme</FD>
<FG>Système nerveux pathologie; Trouble neurologique; Mouvement involontaire; Extrapyramidal syndrome; Système nerveux central pathologie; Encéphale pathologie; Maladie dégénérative</FG>
<ED>Dyskinesia; Parkinson disease; Levodopa; Antiparkinson agent; Selection; Attention; Models; Pathophysiology; Human</ED>
<EG>Nervous system diseases; Neurological disorder; Involuntary movement; Extrapyramidal syndrome; Central nervous system disease; Cerebral disorder; Degenerative disease</EG>
<SD>Disquinesia; Parkinson enfermedad; Levodopa; Antiparkinsoniano; Selección; Atención; Modelo; Fisiopatología; Hombre</SD>
<LO>INIST-16555.354000082146950040</LO>
<ID>00-0263340</ID>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

Physiologic basis of dyskinesia. Discussion

Physiologic basis of dyskinesia. Discussion

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