Pathological synchronization in Parkinson's disease : networks, models and treatments
Identifieur interne : 002A79 ( Main/Merge ); précédent : 002A78; suivant : 002A80Pathological synchronization in Parkinson's disease : networks, models and treatments
Auteurs : Constance Hammond [France] ; Hagai Bergman [Israël] ; Peter Brown [Royaume-Uni]Source :
- Trends in neurosciences : (Regular edition) [ 0166-2236 ] ; 2007.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
Abstract
Parkinson's disease is a common and disabling disorder of movement owing to dopaminergic denervation of the striatum. However, it is still unclear how this denervation perverts normal functioning to cause slowing of voluntary movements. Recent work using tissue slice preparations, animal models and in humans with Parkinson's disease has demonstrated abnormally synchronized oscillatory activity at multiple levels of the basal ganglia-cortical loop. This excessive synchronization correlates with motor deficit, and its suppression by dopaminergic therapies, ablative surgery or deep-brain stimulation might provide the basic mechanism whereby diverse therapeutic strategies ameliorate motor impairment in patients with Parkinson's disease. This review is part of the INMED/TINS special issue, Physiogenic and pathogenic oscillations: the beauty and the beast, based on presentations at the annual INMED/ TINS symposium (http://inmednet.com/).
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Pascal:07-0404923Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal model</term>
<term>Basal ganglion</term>
<term>Body movement</term>
<term>Corpus striatum</term>
<term>Deep brain stimulation</term>
<term>Human</term>
<term>Oscillation</term>
<term>Parkinson disease</term>
<term>Preparation</term>
<term>Review</term>
<term>Strategy</term>
<term>Suppression</term>
<term>Synchronization</term>
<term>Treatment</term>
<term>Voluntary movement</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Synchronisation</term>
<term>Modèle animal</term>
<term>Traitement</term>
<term>Corps strié</term>
<term>Mouvement volontaire</term>
<term>Mouvement corporel</term>
<term>Préparation</term>
<term>Noyau gris central</term>
<term>Parkinson maladie</term>
<term>Suppression</term>
<term>Stratégie</term>
<term>Article synthèse</term>
<term>Oscillation</term>
<term>Homme</term>
<term>Stimulation cérébrale profonde</term>
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<front><div type="abstract" xml:lang="en">Parkinson's disease is a common and disabling disorder of movement owing to dopaminergic denervation of the striatum. However, it is still unclear how this denervation perverts normal functioning to cause slowing of voluntary movements. Recent work using tissue slice preparations, animal models and in humans with Parkinson's disease has demonstrated abnormally synchronized oscillatory activity at multiple levels of the basal ganglia-cortical loop. This excessive synchronization correlates with motor deficit, and its suppression by dopaminergic therapies, ablative surgery or deep-brain stimulation might provide the basic mechanism whereby diverse therapeutic strategies ameliorate motor impairment in patients with Parkinson's disease. This review is part of the INMED/TINS special issue, Physiogenic and pathogenic oscillations: the beauty and the beast, based on presentations at the annual INMED/ TINS symposium (http://inmednet.com/).</div>
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