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| Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represent the opinions of the authors and are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology. |
From the Department of Neurology, Psychiatry and Behavioral Neuroscience, Wayne State University School of Medicine, Detroit, Michigan (Dr. LeWitt); Clinical Neuroscience Program, William Beaumont Hospital Research Institute, Southfield, Michigan (Dr. LeWitt); and Department of Neurosciences and Neurology, Uppsala University Hospital, Uppsala, Sweden (Dr. Nyholm).
Address correspondence and reprint requests to Dr. Peter A. LeWitt, Clinical Neuroscience Center, 26400 West Twelve Mile Road, Suite 110, Southfield, MI 48034.
More than 30 years after its development, levodopa is still the most effective treatment for the symptomatic control of Parkinsons disease (PD). Although a number of therapies have been developed in an attempt to improve PD management, such as dopaminergic agonists and inhibitors of COMT and MAO-B, most patients still depend on levodopa alone because of its superior ability to control PD symptoms. The issue of toxicity has been raised by in vitro studies suggesting that levodopa might be toxic to dopaminergic neurons, but this has since been answered by in vivo studies finding no evidence of toxicity and possibly even neurotrophic-like effects. A more pressing concern regarding levodopa is its association with the development of motor complications after long-term use. Pulsatile dopaminergic stimulation as a result of erratic absorption and the short half-life of levodopa have been central issues in attempts to explain this occurrence. Evidence suggests that altering the delivery of levodopa to provide a more continuous supply of this drug to the brain may result in improved control of PD symptoms.
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