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Related Experiment Video

Updated: Jun 22, 2026

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Published on: October 4, 2021

Drug-induced dyskinesias.

Philippe Damier¹

¹CHU Nantes, CIC 04, Pôle neurosciences, Nantes, France. philippe.damier@chu-nantes.fr

Current Opinion in Neurology

|June 4, 2009

Summary

New research identifies factors contributing to Parkinson's disease dyskinesias and suggests deep brain stimulation for tardive dyskinesias. Understanding these mechanisms can improve future treatment strategies.

Area of Science:

Neurology
Movement Disorders
Neuropharmacology

Background:

Parkinson's disease (PD) is often treated with levodopa, which can lead to motor complications like dyskinesias.
Antipsychotic medications can also induce dyskinesias, a separate but related condition.
Deep brain stimulation (DBS) is an established treatment for severe, medication-refractory movement disorders.

Purpose of the Study:

To review recent findings on the pathophysiology and contributing factors of levodopa-induced dyskinesias (LID) in Parkinson's disease.
To highlight advancements in understanding antipsychotic-induced dyskinesias.
To discuss the efficacy of deep brain stimulation for severe tardive dyskinesias.

Main Methods:

Review of recent scientific literature on PD, LID, and tardive dyskinesias.

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Last Updated: Jun 22, 2026

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Published on: November 21, 2013

Analysis of findings from neuroimaging (PET) and neurophysiological studies.

Evaluation of clinical outcomes for deep brain stimulation in tardive dyskinesias.

Main Results:

Long-term benefits of initial dopamine agonist therapy for preventing PD dyskinesias are less clear than previously thought.
Increased synaptic dopamine in the striatum and abnormal cortico-subcortical loop activity are associated with LID.
Bilateral pallidal stimulation is effective and safe for managing severe tardive dyskinesias.

Conclusions:

Emerging factors related to PD pathogenesis and patient endophenotypes are crucial for understanding dyskinesias.
Dysfunction in compensatory mechanisms may underlie treatment-induced brain changes.
These insights promise improved strategies for preventing and treating PD dyskinesias and offer a vital option for severe tardive dyskinesias.