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Subthalamic nucleus stimulation modulates afferent inhibition in Parkinson disease

From the Divisions of Neurology (A.S., D.I.C., G.O.P., C.A.G., A.W-S., E.M., A.E.L., R.C.) and Neurosurgery (A.M.L.), Krembil Neuroscience Centre and Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada; and Department of Pharmacology and Clinical Neuroscience, Division of Clinical Neurophysiology, Umeå University, Sweden (A.S.)

Address correspondence and reprint requests to Dr. Robert Chen, Division of Neurology, Room 7MC411, Toronto Western Hospital, 399 Bathurst St., Toronto, Ontario, M5T 1S8, Canada; e-mail: robert.chen{at}uhn.on.ca

Background: Peripheral sensory stimulation at the wrist inhibits the motor cortex as measured by transcranial magnetic stimulation at interstimulus intervals of approximately 20 ms (short latency afferent inhibition [SAI]) and 200 ms (long latency afferent inhibition [LAI]). Previous studies suggested that reduced SAI in Parkinson disease (PD) reflects adverse effect of dopaminergic medications and reduced LAI may be related to nondopaminergic manifestations of PD. We hypothesize that subthalamic nucleus (STN) deep brain stimulation (DBS) may correct these deficiencies.

Methods: We studied the effects of STN DBS on SAI and LAI in seven PD patients and age-matched controls. PD patients were studied in an off medication followed by an on medication session, with the stimulator switched on or off in random order in each session.

Results: In the on medication session, SAI was reduced in the stimulator off condition and was restored by STN DBS. LAI was partially normalized by STN DBS in the medication on condition.

Conclusions: Subthalamic nucleus (STN) stimulation improves short latency afferent inhibition, suggesting that it could normalize pathways that are adversely affected by dopaminergic medications. The effect of STN stimulation on long latency afferent inhibition suggests that it may influence nondopaminergic pathways involved in sensorimotor integration.

The study was funded by the Michael J. Fox Foundation for Parkinson Research and the Canadian Institutes of Health Research. The Movement Disorders Center at the Toronto Western Hospital is supported by a Center of Excellence grant from the National Parkinson Foundation.

Disclosure: Dr. Lang received research grant support from Medtronic Inc. in excess of $10,000. Dr. Lozano received consulting fees and research grant support from Medtronic Inc. in excess of $10,000. Dr. Moro received honorarium for speaking from Medtronic Inc.

Received May 8, 2006. Accepted in final form October 6, 2006.

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