SPINAL CORD STIMULATION FAILED TO RELIEVE AKINESIA OR RESTORE LOCOMOTION IN PARKINSON DISEASE
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Dorsal column spinal stimulation in dopamine-depleted rodents was recently reported to disrupt pathologic corticostriatal synchronization, alleviate akinesia, and restore locomotion.1 This claim has prompted consideration that spinal stimulation “might become an efficient and less invasive alternative for treatment of Parkinson disease (PD) in the future.”
In this study, we investigated whether dorsal column stimulation was of therapeutic benefit in 2 patients with PD.
Level of evidence.
This study provides Class II evidence that for patients with moderate to severe motor impairment from PD, high-frequency epidural cervical spinal cord stimulation does not significantly improve motor function as measured by the motor subsection of the Unified Parkinson's Disease Rating Scale (UPDRS).
Methods.
Two patients with PD had spinal stimulators (Medtronic models 3487a or 3898) implanted surgically into the high cervical epidural space without complication, as described previously.2 Patient 1, 75 years old, had moderate motor impairment (off/on medication motor UPDRS = 30/18). Patient 2, 77 years old, had more severe motor impairment (off/on medication UPDRS = 51/38) and was unable to walk without dopaminergic medication. Both patients met UK Brain Bank criteria for PD.3
Ten days postoperatively, both patients participated in a double-blind crossover study of the motor effects of spinal stimulation. In an initial exploratory phase, an antiparkinsonian effect of spinal stimulation was sought over a range of frequencies (30–300 Hz) and intensities (up to 4.0 V and 240 μs). Having failed to establish a clear benefit for any particular set of parameters, for the purposes of the study, patient 1 was …
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Letters: Rapid online correspondence
- SPINAL CORD STIMULATION FAILED TO RELIEVE AKINESIA OR RESTORE LOCOMOTION IN PARKINSON DISEASE
- Miguel A. Nicolelis, Duke University, Box 3209 Dept. of Neurobiology, Duke University, Durham, NC 27710nicoleli@neuro.duke.edu
- Romulo Fuentes (Durham, NC; fuentes@ neuro.duke.edu), Per Petersson (Lund, Sweden; Per.Petersson@med.lu.se)
Submitted July 15, 2010 - Reply from the authors
- Wesley Thevathasan, Department of Experimental Neurology, University of Oxford, John Radcliffe Hospital, Oxford UK OX39DUwesley.thevathasan@nds.ox.ac.uk
- Peter Brown (Oxford, UK; peter.brown@clneuro.ox.ac.uk)
Submitted July 15, 2010
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