Levodopa is the most effective drug for treating Parkinson’s disease. However, long-term use of levodopa is often complicated by significantly disabling fluctuations and dyskinesias negating its beneficial effects. Younger age of Parkinson’s disease onset, disease severity, and high levodopa dose increase the risk of development of levodopa-induced dyskinesias (LID). The underlying mechanisms for LID are unclear though recent studies indicate the importance of pulsatile stimulation of striatal postsynaptic receptors in their pathogenesis. The non-human primates with MPTP-induced parkinsonism serve as a useful model to study dyskinesia. Once established, LID are difficult to treat and therefore efforts should be made to prevent them. The therapeutic and preventative strategies for LID include using a lower dosage of levodopa, employing dopamine agonists as initial therapy in Parkinson’s disease, amantadine, atypical neuroleptics, and neurosurgery. LID can adversely affect the quality of life and increase the cost of healthcare.
- COMT, catechol-O-methyl transferase
- D-I-D, dyskinesia-improvement-dyskinesia
- FRA, Fos-related proteins
- GABA, γ-aminobutyric acid
- GPDRS, Global Primate Dyskinesia Rating Scale
- GPi, internal globus pallidum
- 5-HT, 5-hydroxytryptamine
- LID, levodopa-induced dyskinesias
- MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
- NMDA, N-methyl-D-aspartate
- RAM, rapid alternating movements
- STN, subthalamic nucleus
- UPDRS, Unified Parkinson’s Disease Rating Scale
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