Abstract |
Involuntary movements, or dyskinesias, represent a debilitating complication of levodopa therapy for Parkinson's disease. Dyskinesia is, ultimately, experienced by the vast majority of the patients. Despite the importance of this problem, little was known about the cause of dyskinesia, a situation that has dramatically evolved in the last few years. The present review presents: 1) the current understanding of dyskinesia pathophysiology and 2) the therapeutic modalities, mainly non-dopaminergic, available or in development. We here show that the questions raised by the dyskinesia may have a clinically-driven pharmacological answer: the symptomatic treatment of dyskinesia, the prevention of the priming and the de-priming of the neural networks.
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Authors | A Hadj Tahar, E Bézard, R Grondin, C E Gross, P J Bédard |
Journal | Revue neurologique
(Rev Neurol (Paris))
Vol. 159
Issue 12
Pg. 1125-42
(Dec 2003)
ISSN: 0035-3787 [Print] France |
Vernacular Title | Physiopathologie et modalités thérapeutiques des dyskinésies induites à la L-Dopa. |
PMID | 14978413
(Publication Type: English Abstract, Journal Article, Review)
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Chemical References |
- Dopamine Agents
- Receptors, Adrenergic
- Receptors, Dopamine
- Receptors, Glutamate
- Receptors, Opioid
- Receptors, Purinergic P1
- Levodopa
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Topics |
- Animals
- Basal Ganglia
(anatomy & histology, physiology)
- Disease Models, Animal
- Dopamine Agents
(adverse effects)
- Dyskinesia, Drug-Induced
(drug therapy, physiopathology, prevention & control)
- Humans
- Levodopa
(adverse effects)
- Receptors, Adrenergic
(drug effects, physiology)
- Receptors, Dopamine
(drug effects, physiology)
- Receptors, Glutamate
(drug effects, physiology)
- Receptors, Opioid
(drug effects, physiology)
- Receptors, Purinergic P1
(drug effects, physiology)
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