Interhemispheric and ipsilateral connections in Parkinson's disease: Relation to mirror movements
Identifieur interne : 002D95 ( Main/Exploration ); précédent : 002D94; suivant : 002D96Interhemispheric 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 :
- Movement Disorders [ 0885-3185 ] ; 2007-04-30.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Brain (physiopathology), Corpus Callosum (anatomy & histology), Corpus Callosum (physiopathology), Electromyography, Female, Functional Laterality, Humans, Interhemispheric connection, Male, Middle Aged, Mirror, Motor Activity (physiology), Movement Disorders (physiopathology), Nervous system diseases, Parkinson Disease (physiopathology), Parkinson disease, Parkinson's disease, Reference Values, Transcranial magnetic stimulation, cortical inhibition, mirror movements, transcallosal inhibition, transcranial magnetic stimulation.
- MESH :
- anatomy & histology : Corpus Callosum.
- physiology : Motor Activity.
- physiopathology : Brain, Corpus Callosum, Movement Disorders, Parkinson Disease.
- Electromyography, Female, Functional Laterality, Humans, Male, Middle Aged, Reference Values.
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. © 2007 Movement Disorder Society
Url:
DOI: 10.1002/mds.21386
Affiliations:
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Le document en format XML
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<front><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. © 2007 Movement Disorder Society</div>
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