Movement Disorders (revue)

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Interhemispheric and ipsilateral connections in Parkinson's disease : Relation to mirror movements

Identifieur interne : 001621 ( PascalFrancis/Curation ); précédent : 001620; suivant : 001622

Interhemispheric and ipsilateral connections in Parkinson's disease : Relation to mirror movements

Auteurs : Jie-Yuan Li [Canada, Taïwan] ; Alberto J. Espay [Canada] ; Carolyn A. Gunraj [Canada] ; Pramod K. Pal [Canada] ; Danny I. Cunic [Canada] ; Anthony E. Lang [Canada] ; Robert Chen [Canada]

Source :

RBID : Pascal:07-0263057

Descripteurs français

English descriptors

Abstract

Mirror movements (MM) occur in early, asymmetric Parkinson's disease (PD). To examine the pathophysiology of MM in PD, we studied 13 PD patients with MM (PD-MM), 7 PD patients without MM (PD-NM), and 14 normal subjects. Cross-correlogram did not detect common synaptic input to motoneuron pools innervating homologous hand muscles in PD-MM patients. Transcranial magnetic stimulation studies showed no significant difference in ipsilateral motor-evoked potentials between PD-MM patients and normal subjects. The MM side of PD-MM patients showed a slower increase in ipsilateral silent period area with higher level of muscle contraction than the non-MM side and normal subjects. There was less interhemispheric inhibition (IHI) at long interstimulus intervals of 20 to 50 ms in PD-MM than PD-NM. IHI reduced short interval intracortical inhibition in normal subjects and PD-NM, but not in PD-MM. IHI significantly increased intracortical facilitation in PD-MM and PD-NM patients, but not in normal subjects. Our results suggest that MM in PD is due to activation of the contralateral motor cortex. PD-MM patients had reduced transcallosal inhibitory effects on cortical output neurons and on intracortical inhibitory circuits compared to PD-NM patients and controls. These deficits in transcallosal inhibition may contribute to MM in PD patients.
pA  
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A05       @2 22
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A08 01  1  ENG  @1 Interhemispheric and ipsilateral connections in Parkinson's disease : Relation to mirror movements
A11 01  1    @1 LI (Jie-Yuan)
A11 02  1    @1 ESPAY (Alberto J.)
A11 03  1    @1 GUNRAJ (Carolyn A.)
A11 04  1    @1 PAL (Pramod K.)
A11 05  1    @1 CUNIC (Danny I.)
A11 06  1    @1 LANG (Anthony E.)
A11 07  1    @1 CHEN (Robert)
A14 01      @1 Division of Neurology, Department of Medicine, Toronto Western Research Institute, University of Toronto @2 Toronto, Ontario @3 CAN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 7 aut.
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A44       @0 0000 @1 © 2007 INIST-CNRS. All rights reserved.
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A47 01  1    @0 07-0263057
A60       @1 P
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C01 01    ENG  @0 Mirror movements (MM) occur in early, asymmetric Parkinson's disease (PD). To examine the pathophysiology of MM in PD, we studied 13 PD patients with MM (PD-MM), 7 PD patients without MM (PD-NM), and 14 normal subjects. Cross-correlogram did not detect common synaptic input to motoneuron pools innervating homologous hand muscles in PD-MM patients. Transcranial magnetic stimulation studies showed no significant difference in ipsilateral motor-evoked potentials between PD-MM patients and normal subjects. The MM side of PD-MM patients showed a slower increase in ipsilateral silent period area with higher level of muscle contraction than the non-MM side and normal subjects. There was less interhemispheric inhibition (IHI) at long interstimulus intervals of 20 to 50 ms in PD-MM than PD-NM. IHI reduced short interval intracortical inhibition in normal subjects and PD-NM, but not in PD-MM. IHI significantly increased intracortical facilitation in PD-MM and PD-NM patients, but not in normal subjects. Our results suggest that MM in PD is due to activation of the contralateral motor cortex. PD-MM patients had reduced transcallosal inhibitory effects on cortical output neurons and on intracortical inhibitory circuits compared to PD-NM patients and controls. These deficits in transcallosal inhibition may contribute to MM in PD patients.
C02 01  X    @0 002B17
C02 02  X    @0 002B17G
C02 03  X    @0 002B17A03
C03 01  X  FRE  @0 Système nerveux pathologie @5 01
C03 01  X  ENG  @0 Nervous system diseases @5 01
C03 01  X  SPA  @0 Sistema nervioso patología @5 01
C03 02  X  FRE  @0 Parkinson maladie @5 02
C03 02  X  ENG  @0 Parkinson disease @5 02
C03 02  X  SPA  @0 Parkinson enfermedad @5 02
C03 03  X  FRE  @0 Connexion interhémisphérique @5 09
C03 03  X  ENG  @0 Interhemispheric connection @5 09
C03 03  X  SPA  @0 Conexión interhemisférica @5 09
C03 04  X  FRE  @0 Miroir @5 10
C03 04  X  ENG  @0 Mirror @5 10
C03 04  X  SPA  @0 Espejo @5 10
C03 05  X  FRE  @0 Stimulation magnétique transcrânienne @4 CD @5 96
C03 05  X  ENG  @0 Transcranial magnetic stimulation @4 CD @5 96
C07 01  X  FRE  @0 Encéphale pathologie @5 37
C07 01  X  ENG  @0 Cerebral disorder @5 37
C07 01  X  SPA  @0 Encéfalo patología @5 37
C07 02  X  FRE  @0 Extrapyramidal syndrome @5 38
C07 02  X  ENG  @0 Extrapyramidal syndrome @5 38
C07 02  X  SPA  @0 Extrapiramidal síndrome @5 38
C07 03  X  FRE  @0 Maladie dégénérative @5 39
C07 03  X  ENG  @0 Degenerative disease @5 39
C07 03  X  SPA  @0 Enfermedad degenerativa @5 39
C07 04  X  FRE  @0 Système nerveux central pathologie @5 40
C07 04  X  ENG  @0 Central nervous system disease @5 40
C07 04  X  SPA  @0 Sistema nervosio central patología @5 40
N21       @1 176
N44 01      @1 OTO
N82       @1 OTO

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Pascal:07-0263057

Le document en format XML

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<div type="abstract" xml:lang="en">Mirror movements (MM) occur in early, asymmetric Parkinson's disease (PD). To examine the pathophysiology of MM in PD, we studied 13 PD patients with MM (PD-MM), 7 PD patients without MM (PD-NM), and 14 normal subjects. Cross-correlogram did not detect common synaptic input to motoneuron pools innervating homologous hand muscles in PD-MM patients. Transcranial magnetic stimulation studies showed no significant difference in ipsilateral motor-evoked potentials between PD-MM patients and normal subjects. The MM side of PD-MM patients showed a slower increase in ipsilateral silent period area with higher level of muscle contraction than the non-MM side and normal subjects. There was less interhemispheric inhibition (IHI) at long interstimulus intervals of 20 to 50 ms in PD-MM than PD-NM. IHI reduced short interval intracortical inhibition in normal subjects and PD-NM, but not in PD-MM. IHI significantly increased intracortical facilitation in PD-MM and PD-NM patients, but not in normal subjects. Our results suggest that MM in PD is due to activation of the contralateral motor cortex. PD-MM patients had reduced transcallosal inhibitory effects on cortical output neurons and on intracortical inhibitory circuits compared to PD-NM patients and controls. These deficits in transcallosal inhibition may contribute to MM in PD patients.</div>
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<s0>Mirror movements (MM) occur in early, asymmetric Parkinson's disease (PD). To examine the pathophysiology of MM in PD, we studied 13 PD patients with MM (PD-MM), 7 PD patients without MM (PD-NM), and 14 normal subjects. Cross-correlogram did not detect common synaptic input to motoneuron pools innervating homologous hand muscles in PD-MM patients. Transcranial magnetic stimulation studies showed no significant difference in ipsilateral motor-evoked potentials between PD-MM patients and normal subjects. The MM side of PD-MM patients showed a slower increase in ipsilateral silent period area with higher level of muscle contraction than the non-MM side and normal subjects. There was less interhemispheric inhibition (IHI) at long interstimulus intervals of 20 to 50 ms in PD-MM than PD-NM. IHI reduced short interval intracortical inhibition in normal subjects and PD-NM, but not in PD-MM. IHI significantly increased intracortical facilitation in PD-MM and PD-NM patients, but not in normal subjects. Our results suggest that MM in PD is due to activation of the contralateral motor cortex. PD-MM patients had reduced transcallosal inhibitory effects on cortical output neurons and on intracortical inhibitory circuits compared to PD-NM patients and controls. These deficits in transcallosal inhibition may contribute to MM in PD patients.</s0>
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<s0>002B17</s0>
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