Drug-induced dyskinesias

Recent studies have improved our knowledge of the factors responsible for the development of dyskinesias in Parkinson's disease and the associated pathophysiology. Deep brain stimulation has been shown to be effective to treat severe tardive dyskinesias. This review highlights some recent findings related to levodopa-induced and antipsychotic-induced dyskinesias.

The reported advantage of using a dopamine agonist as an initial treatment to prevent the development of dyskinesias in Parkinson's disease appears to be less evident after a long-term follow-up. Other factors, related to the etiopathogenesis of Parkinson's disease or to patients' endophenotypes, are beginning to be identified. Several brain changes have been found to be associated with levodopa-induced dyskinesias. PET studies have evidenced an increased level of synaptic dopamine in the striatum. Neurophysiological studies have suggested that dyskinesias might reflect abnormal skill memorization processes within the cortico-subcortical loops. A dysfunction of the mechanisms trying to compensate for dopamine deficiency and its brain consequences could be responsible for these changes induced by the dopaminergic treatment. Bilateral pallidal stimulation has been shown to be an effective and safe treatment for severe tardive dyskinesias.

These findings will improve future strategies to prevent and treat Parkinson's disease dyskinesias and offer a much needed treatment for severe tardive dyskinesias.