ST. PAUL, MN – Electrical brain stimulation can reduce the problems Parkinson's patients develop after long-term use of the drug levodopa, the main treatment for Parkinson's, according to a study published in the November 27 issue of Neurology, the scientific journal of the American Academy of Neurology.
After years of use, levodopa becomes less effective, causing fluctuations in Parkinson's motor symptoms such as tremor and poor balance, called the "on/off" phenomenon.
Electrical brain stimulation increased the "on" motor function when medication was working by 29 percent, and improved the "off" motor function by 38 percent in the study. The process, also called deep brain stimulation, uses a surgical implant similar to a cardiac pacemaker to block brain signals that cause tremors and other signs of the disease.
The study examined 12 people who had stimulating electrodes implanted one to three years prior. They were monitored hourly for two days while taking their normal medications. One day the stimulators were turned on; one day they were turned off.
Six of the patients received stimulation in the globus pallidus interna nuclei of the brain; six were stimulated in the subthalamic nuclei. The patients were also able to complete a walking test 13 percent faster when the stimulator was on. And patients improved by 23 percent on a finger-tapping test, which measures bradykinesia, or the slowness in initiating movement that affects Parkinson's patients.
Other studies citing improvements from deep brain stimulation on levodopa-induced symptoms have been based on reports from patients, not on objective tests, according to study author and neurologist John Nutt, MD, of Oregon Health & Science University in Portland.
The study was also designed to help researchers determine how deep brain stimulation changes the body's response to levodopa. To that end, patients were studied for another two days, during which they received their levodopa doses intravenously rather than orally -- once while the stimulators were on and once while they were off.
"The hypothesis has been that the improvement occurs because the body's response to levodopa is prolonged by the stimulation," Nutt said. "But we saw no evidence of this. Instead, we found that improvement is determined more by the decrease in the amount of disability patients experience when they are in their 'off' state when the drug is not working."
Nutt said this finding may give researchers a new strategy for developing therapies to reduce the motor fluctuations in advanced Parkinson's patients. "Most new therapies have focused on extending the response of each dose of levodopa," he said. "These findings suggest that we should focus on improving the 'off' disability level."
The study was supported in part by the National Parkinson Foundation, Willamette-Columbia Parkinsonian Society, National Institute of Neurological Disorders and Stroke and Oregon Health Sciences University General Clinical Research Center.
The American Academy of Neurology, an association of more than 17,500 neurologists and neuroscience professionals, is dedicated to improving patient care through education and research. For more information about the American Academy of Neurology, visit its web site at http://www.aan.com