Apr. 17, 2005 CHICAGO – Deep brain stimulation of two different areas of the brain appears to improve problems with uncontrolled movements (dyskinesia) in patients with Parkinson disease (PD), according to an article in the April issue of Archives of Neurology, one of the JAMA/Archives journals.
Deep brain stimulation with electrical impulses delivered to structures deep within the brain is being intensively investigated for the management of advanced Parkinson disease, according to background information in the article. Although a number of studies have shown that stimulation of two different areas of the brain, the globus pallidus interna (GPi) and the subthalmic nucleus (STN), can be achieved safely and effectively, STN has been thought to be the preferred target. At the same time, the authors note, there does seem to be some evidence that the STN is more vulnerable during surgery and that STN patients may have more postoperative problems.
Valerie C. Anderson, Ph.D., of the Oregon Health and Science University, Portland, and colleagues compared 23 patients with Parkinson disease and problems with medication-induced uncontrolled movement who were randomly assigned to implantation of deep brain stimulators in either the GPi or the STN areas of the brain. Patients' Parkinson symptoms were evaluated with and without medication using a standard rating scale at three, six and 12 months after surgery.
"Off-medication Unified Parkinson's Disease Rating Scale motor scores were improved after 12 months of both GPi and STN stimulation (39 vs 48 percent)," the authors write. "Bradykinesia [extremely slow movement] tended to improve more with STN than GPi stimulation. No improvement in on-medication function was observed in either group. Levodopa [Parkinson medication] dose was reduced by 38 percent in STN stimulation patients compared with three percent in GPi stimulation patients. … Dyskinesia was reduced by stimulation at both GPi and STN ( 89 v 62 percent). Cognitive and behavioral complications were observed only in combination with STN stimulation."
"At this point, it appears that stimulation at either STN or GPi improves off-medication motor scores and levodopa-induced dyskinesia for at least one year, and there is no clear superiority of STN over GPi stimulation," the authors conclude. "Indeed, our comparison of GPi vs STN stimulation suggests that selection of a stimulation site should be influenced by symptom profile. Although GPi stimulation may be better for the patient with dose-limiting dyskinesia, STN stimulation may be better for the younger patient with prominent bradykinesia."
(Arch Neurol. 2005; 62:554-560. Available post-embargo at www.archneurol.com.)
Editor's Note: This study was supported in part by a grant from the Public Health Service.
Editorial: Will Pallidal Deep Brain Stimulation Make a Triumphant Return?
In an editorial accompanying this study, Michael S. Okun, M.D., and Kelly D. Foote, M.D., of the University of Florida, Gainesville, write, "Dyskinesia improves dramatically with both GPi and STN DBS [deep brain stimulation]. As suggested by the authors of this article and by others, the mechanism underlying this improvement may be different for each target. The majority of the anti-dyskinetic benefit of GPi DBS may be due to active stimulation, and the benefits in STN may be primarily a result of medication reduction. … the antidyskinetic effects of GPi DBS seem to be greater than those of STN DBS."
"One important and perhaps deciding factor in the rematch between GPi and STN DBS will be the incidence of surgical and postoperative complications," the authors suggest. "Assuming that the rates of the procedure-related and device complications are equal, then long-term cognitive, mood, and behavioral problems may lead to a victory of one target over the other."
"The unanswered questions regarding target selection will require several more head-to-head rematches between GPi and STN," the authors conclude. "Future improvements in implantation technique and in lead design may also enhance the benefit in each target. Studies may prove that STN is a better target than GPi or that there is no clear winner. Studies may also prove that STN is superior for certain features of the disease such as tremor, bradykinesia, and medication reduction. Alternatively, studies may show that GPi is equal to STN with regard to motor improvements, and is better antidyskinesia treatment, but has fewer cognitive, mood, and behavioral adverse effects. Whatever the outcome of these rematches, we should be open to changes in our current practices and recognize the possibility that we should match individual patient needs with the strengths and weaknesses of individual targets."
(Arch Neurol. 2005; 62:533-536. Available post-embargo at www.archneurol.com.)
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