Both L-DOPA and HFS-STN restore the enhanced group II spinal reflex excitation to a normal level in patients with Parkinson's disease.
Identifieur interne : 000937 ( PubMed/Curation ); précédent : 000936; suivant : 000938Both L-DOPA and HFS-STN restore the enhanced group II spinal reflex excitation to a normal level in patients with Parkinson's disease.
Auteurs : V. Marchand-Pauvert [France] ; A. Gerdelat-Mas ; F. Ory-Magne ; F. Calvas ; D. Mazevet ; S. Meunier ; C. Brefel-Courbon ; M. Vidailhet ; M. Simonetta-MoreauSource :
- Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology [ 1872-8952 ] ; 2011.
English descriptors
- KwdEn :
- Adult, Aged, Analysis of Variance, Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Deep Brain Stimulation, Electromyography, Female, Humans, Levodopa (pharmacology), Levodopa (therapeutic use), Male, Middle Aged, Muscle Rigidity (therapy), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Reflex (drug effects), Reflex (physiology).
- MESH :
- chemical , pharmacology : Antiparkinson Agents, Levodopa.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- drug effects : Reflex.
- physiology : Reflex.
- physiopathology : Parkinson Disease.
- therapy : Muscle Rigidity, Parkinson Disease.
- Adult, Aged, Analysis of Variance, Deep Brain Stimulation, Electromyography, Female, Humans, Male, Middle Aged.
Abstract
To investigate the contribution of group II spinal pathways in Parkinsonian upper limb rigidity and the modulation of spinal excitability of group I and group II pathways by L-DOPA and subthalamic nucleus-high-frequency stimulation (STN-HFS).
DOI: 10.1016/j.clinph.2010.08.015
PubMed: 20943434
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pubmed:20943434Le document en format XML
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<front><div type="abstract" xml:lang="en">To investigate the contribution of group II spinal pathways in Parkinsonian upper limb rigidity and the modulation of spinal excitability of group I and group II pathways by L-DOPA and subthalamic nucleus-high-frequency stimulation (STN-HFS).</div>
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<Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To investigate the contribution of group II spinal pathways in Parkinsonian upper limb rigidity and the modulation of spinal excitability of group I and group II pathways by L-DOPA and subthalamic nucleus-high-frequency stimulation (STN-HFS).</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">The effect of ulnar nerve electrical stimulation on Flexor Carpi Radialis Electromyogram (FCR EMG) was investigated in two groups of patients: patients receiving medication (MED group) and chronically surgically implanted patients (DBS group). Results were compared in patients ON and OFF treatment, and between patients and control subjects.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">The resulting long-lasting facilitation in FCR EMG had similar characteristics in all groups, and surface area was assessed in analysis windows corresponding to the parts supposed to be mediated by non-monosynaptic spinal pathways to FCR motoneurones, fed by hand muscle group I and group II afferents (Lourenço et al., 2006). In both the MED and DBS groups, the group I excitation was not altered but the group II excitation was particularly enhanced when OFF treatment, compared to controls, and both L-DOPA and STN-HFS restored the group II spinal excitation to normal level.</AbstractText>
<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Both L-DOPA and STN-HFS influence the metabolism of monoamines in the midbrain, and restore the descending neuromodulation on group II spinal reflex.</AbstractText>
<AbstractText Label="SIGNIFICANCE" NlmCategory="CONCLUSIONS">These results further support a group II contribution to the enhanced long latency response (LLR) to muscle stretch observed in wrist muscles of rigid Parkinson's disease (PD) patients.</AbstractText>
<CopyrightInformation>Copyright © 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation>
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