L-Dopa Doesn't Hasten Parkinson's Disease
Study Eases Concerns About Possible Negative Effects of Parkinson's Disease Treatment
WebMD News Archive
Dec. 7, 2004 -- A new study helps put to rest worries that the drug L-dopa might speed Parkinson's disease.
L-dopa is the gold standard treatment for Parkinson's disease. It helps reduce many of the disease's most troubling symptoms: trembling, slow motion, rigidity, unstable posture, and frozen gait.
But there's recent experimental laboratory evidence that the helpful drug might kill nerve cells similar to those shown to degenerate in the brain of people with Parkinson's disease -- thus speeding Parkinson's brain degeneration. To test this theory, Columbia University researcher Stanley Fahn, MD, led a study of patients with early Parkinson's disease.
The 361 patients received low, medium, and high doses of L-dopa or inactive placebo pills for 9.5 months. Fahn and colleagues examined them before and after treatment.
"We can assure both patients with early Parkinson's disease and their physicians that, from a clinical perspective, our study did not find that [L-dopa] hastens the progression of Parkinson's disease," the researchers conclude.
Fahn and colleagues report their findings in the Dec. 9 issue of The New England Journal of Medicine.
The researchers also performed brain-function scans on 116 of the patients. They did find that the brain cells of patients taking L-dopa took in less dopamine than untreated patients. In the past, researchers have said that this meant worse Parkinson's disease.
But there was no evidence these patients were getting worse. In fact, those taking the highest L-dopa doses did the best. Fahn and colleagues say their findings question the traditional interpretation of these functional brain scans.
For now, the biggest problem for Parkinson's patients taking L-dopa is finding a dosage that controls their symptoms but limits the drug's side effects.
"Until more evidence is available, we recommend customizing the dose of [L-dopa] to the needs of the individual patient on the basis of the clinical response and the profile of adverse events," Fahn and colleagues write.