Levodopa-induced dyskinesia in Parkinson's disease: epidemiology, etiology, and treatment.

Parkinson's Disease and Movement Disorders Center, University of South Florida, Tampa, Florida 33612, USA.
Current Neurology and Neuroscience Reports (Impact Factor: 3.78). 08/2007; 7(4):302-10. DOI: 10.1007/s11910-007-0046-y
Source: PubMed

ABSTRACT Although levodopa is the gold standard for treating motor symptoms of Parkinson's disease (PD), long-term therapy leads to levodopa-induced dyskinesia (LID). Dyskinesia refers to involuntary movements other than tremor and most commonly consists of chorea that occurs when levodopa-derived dopamine is peaking in the brain ("peak-dose dyskinesia"). However, dyskinesia can also consist of dystonia or myoclonus and occur during other parts of the levodopa dosing cycle. New validated rating scales and home diaries can better help the health care provider assess the timing and severity of dyskinesia. The exact etiology of LID is unknown, but there is evidence that abnormal pulsatile stimulation of dopamine receptors may be contributory. Treatment of LID includes adjustment of PD medications to maximize "on" time without troublesome dyskinesia. Amantadine is the only medication available with demonstrated ability to reduce the expression of established LID without reducing antiparkinsonian benefit. Other medications that are currently being studied to treat established LID include antiepileptics and serotonergic medications. Deep brain stimulation of the subthalamic nucleus is now the most commonly used surgical procedure for PD patients, and it is very effective in treating LID.

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    Journal of central nervous system disease. 01/2011; 3:169-78.
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    ABSTRACT: Spontaneous involuntary dystonic and choreatic movements induced by L-DOPA (L-DOPA-induced dyskinesias (LID)) represent a severe complication of long-time pharmacotherapy in Parkinson's disease that deserves novel therapeutics. Previous studies demonstrated antidyskinetics effect of the KV7.2-7.5 channel opener retigabine after acute and chronic treatment in a rat model of LID. We hypothesized that this effect was mainly mediated by KV7.2/3 channels located on striatal projection neurons, as an increased activity of these neurons seems to be involved in the pathophysiology of LID. We therefore examined the acute effects of the KV7.2/3 preferring channel opener ICA 27243 (N-(6-Chloro-pyridin-3-yl)-3,4-difluoro-benzamide, 5-15mg/kg i.p.) on LID in this animal model. Ten and 15mg ICA 27243 significantly reduced abnormal involuntary movements (AIM) while no negative impact on the antiparkinsonian effect of L-DOPA was observed. However, at the end of the testing session (180min) AIM scores increased after application of both doses. Further studies have to clarify if this can be avoided by a different application regime. Nevertheless, the present results suggest that selective openers of KV7.2/3 channels might be interesting candidates for the treatment of LID as antidyskinetic effects occurred at well tolerated doses and did not interfere with the antiparkinsonian effect of L-DOPA.
    Neuroscience Letters 04/2013; · 2.03 Impact Factor
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    PLoS ONE 01/2009; 4(2). · 3.53 Impact Factor