Deep Brain Stimulation

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Motor cortex stimulation in patients with Parkinson disease: 12-month follow-up in 4 patients

Jeffrey E. Arle, Diana Apetauerova, Janet Zani, D. Vedran Deletis, Dana L. Penney, Daniel Hoit, Christine Gould, and Jay L. Shils


Since the initial 1991 report by Tsubokawa et al., stimulation of the M1 region of cortex has been used to treat chronic pain conditions and a variety of movement disorders.


A Medline search of the literature published between 1991 and the beginning of 2007 revealed 459 cases in which motor cortex stimulation (MCS) was used. Of these, 72 were related to a movement disorder. More recently, up to 16 patients specifically with Parkinson disease were treated with MCS, and a variety of results were reported. In this report the authors describe 4 patients who were treated with extradural MCS.


Although there were benefits seen within the first 6 months in Unified Parkinson's Disease Rating Scale Part III scores (decreased by 60%), tremor was only modestly managed with MCS in this group, and most benefits seen initially were lost by the end of 12 months.


Although there have been some positive findings using MCS for Parkinson disease, a larger study may be needed to better determine if it should be pursued as an alternative surgical treatment to DBS.

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Immediate and sustained relief of levodopa-induced dyskinesias after dorsal relocation of a deep brain stimulation lead

Case report

Ron L. Alterman, Jay L. Shils, Mark Gudesblatt, and Michele Tagliati

The authors demonstrate that high-frequency electrical stimulation dorsal to the subthalamic nucleus (STN) can directly suppress levodopa-induced dyskinesias. This 63-year-old woman with idiopathic Parkinson disease underwent surgery for placement of bilateral subthalamic deep brain stimulation (DBS) electrodes to control progressive rigidity, motor fluctuations, and levodopa-induced dyskinesias. The model 3389 DBS leads were implanted with microelectrode guidance. Magnetic resonance imaging confirmed proper placement of the leads. Postoperatively the patient exhibited improvement in all of her parkinsonian symptoms; however, her right leg dyskinesias had not improved. Based on their previous experiences treating levodopa-induced dyskinesias with subthalamic stimulation through the more dorsally located contacts of the model 3387 lead, the authors withdrew the implanted 3389 lead 3 mm. Following relocation of the lead they were able to suppress the right leg dyskinesias by using the most dorsal contacts. The patient's dopaminergic medication intake increased slightly. These findings indicate that electrical stimulation dorsal to the STN can directly suppress levodopa-induced dyskinesias independent of dopaminergic medication changes. The 3389 lead may provide inadequate coverage of the subthalamic region for some patients.