[Management of levodopa-induced dyskinesia].
Identifieur interne : 000323 ( Ncbi/Checkpoint ); précédent : 000322; suivant : 000324[Management of levodopa-induced dyskinesia].
Auteurs : O. Rascol [France] ; J J Ferreira ; P. Payoux ; Ch Brefel-Courbon ; J L MontastrucSource :
- Revue neurologique [ 0035-3787 ] ; 2002.
English descriptors
- KwdEn :
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- drug therapy : Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced.
- prevention & control : Dyskinesia, Drug-Induced.
- Algorithms, Humans.
Abstract
There are three main therapeutic strategies to manage levodopa-induced dyskinesias in parkinsonian patients: (1) prevent the occurrence of the priming phenomenon which generates the abnormal movements, (2) avoid the expression of dyskinesias in already primed brain with antidyskinetic symptomatic interventions and (3) reverse, once primed, the changes that occurred in the basal ganglia to induce dyskinesias. To prevent, at least partly, priming for dyskinesias is attempted by the early use of dopamine D2 agonists, which delays the need for levodopa. To avoid the expression of dyskinesias in already primed patients, amantadine is presently the most efficacious symptomatic medication, while functional stereotactic surgery is required in the most severe cases. There are several ways to try to reverse, at least partly, dyskinesia priming. The strategy is to reduce as much as possible (ideally completely) the daily dose of levodopa, by the mean of adjunct interventions like high doses of oral agonists, or more efficiently, with apormorphine subcutaneous infusion or subthalamic deep brain stimulation.
PubMed: 12690671
Affiliations:
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pubmed:12690671Le document en format XML
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<front><div type="abstract" xml:lang="en">There are three main therapeutic strategies to manage levodopa-induced dyskinesias in parkinsonian patients: (1) prevent the occurrence of the priming phenomenon which generates the abnormal movements, (2) avoid the expression of dyskinesias in already primed brain with antidyskinetic symptomatic interventions and (3) reverse, once primed, the changes that occurred in the basal ganglia to induce dyskinesias. To prevent, at least partly, priming for dyskinesias is attempted by the early use of dopamine D2 agonists, which delays the need for levodopa. To avoid the expression of dyskinesias in already primed patients, amantadine is presently the most efficacious symptomatic medication, while functional stereotactic surgery is required in the most severe cases. There are several ways to try to reverse, at least partly, dyskinesia priming. The strategy is to reduce as much as possible (ideally completely) the daily dose of levodopa, by the mean of adjunct interventions like high doses of oral agonists, or more efficiently, with apormorphine subcutaneous infusion or subthalamic deep brain stimulation.</div>
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