Effect of Subthalamic Deep Brain Stimulation on Levodopa-Induced Dyskinesia in Parkinson's Disease.
10.3349/ymj.2015.56.5.1316
- Author:
Ji Hee KIM
1
;
Won Seok CHANG
;
Hyun Ho JUNG
;
Jin Woo CHANG
Author Information
1. Division of Stereotactic and Functional Neurosurgery, Department of Neurosurgery, Brain Research Institute, Yonsei University College of Medicine, Seoul, Korea. JCHANG@yuhs.ac
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Deep brain stimulation;
dyskinesias;
Parkinson disease;
subthalamic nucleus
- MeSH:
Aged;
Aged, 80 and over;
Antiparkinson Agents/administration & dosage/*adverse effects;
*Deep Brain Stimulation;
Dyskinesia, Drug-Induced/*therapy;
Female;
Humans;
Levodopa/administration & dosage/*adverse effects;
Male;
Middle Aged;
Outcome Assessment (Health Care);
Parkinson Disease/*drug therapy;
Postoperative Period;
Retrospective Studies;
Subthalamic Nucleus;
Treatment Outcome
- From:Yonsei Medical Journal
2015;56(5):1316-1321
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: To evaluate the effect of bilateral subthalamic nucleus (STN) deep brain stimulation (DBS) on levodopa-induced peakdose dyskinesia in patients with Parkinson's disease (PD). MATERIALS AND METHODS: A retrospective review was conducted on patients who underwent STN DBS for PD from May 2000 to July 2012. Only patients with levodopa-induced dyskinesia prior to surgery and more than 1 year of available follow-up data after DBS were included. The outcome measures included the dyskinesia subscore of the Unified Parkinson's Disease Rating Scale (UPDRS) part IV (items 32 to 34 of UPDRS part IV) and the levodopa equivalent daily dose (LEDD). The patients were divided into two groups based on preoperative to postoperative LEDD change at 12 months after the surgery: Group 1, LEDD decrease >15%; Group 2, all other patients. Group 2 was further divided by the location of DBS leads. RESULTS: Of the 100 patients enrolled, 67 were in Group 1, while those remaining were in Group 2. Twelve months after STN DBS, Groups 1 and 2 showed improvements of 61.90% and 57.14%, respectively, in the dyskinesia subscore. Group 1 was more likely to experience dyskinesia suppression; however, the association between the groups and dyskinesia suppression was not statistically significant (p=0.619). In Group 2, dyskinesia was significantly decreased by stimulation of the area above the STN in 18 patients compared to stimulation of the STN in 15 patients (p=0.048). CONCLUSION: Levodopa-induced dyskinesia is attenuated by STN DBS without reducing the levodopa dosage.
