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J Neurophysiol 92: 1937-1943, 2004. First published May 19, 2004; doi:10.1152/jn.00239.2004
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TRANSLATIONAL PHYSIOLOGY

Single Pulse Stimulation of the Human Subthalamic Nucleus Facilitates the Motor Cortex at Short Intervals

Ritsuko Hanajima1,2, Peter Ashby1,2, Andres M. Lozano1,3, Anthony E. Lang1,2 and Robert Chen1,2

1Toronto Western Research Institute, University Health Network; 2Division of Neurology, Department of Medicine and 3Division of Neurosurgery, Department of Surgery, University of Toronto, Toronto, Ontario M5T 2S8, Canada

Submitted 10 March 2004; accepted in final form 11 May 2004

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is an effective treatment for Parkinson's disease (PD). The mechanism is poorly understood. High-frequency STN DBS has been reported to affect motor cortex excitability in a complex way, but the timing between STN stimuli and changes in motor cortical (M1) excitability has not been investigated. We examined the time course of changes in motor cortical excitability following single pulse STN DBS. We studied 14 PD patients with implanted DBS electrodes in the STN, 2 patients with electrodes in internal globus pallidus (GPi), and 1 patient with an electrode in the sensory thalamus. Transcranial magnetic stimulation (TMS) was delivered to the M1 ipsilateral to the DBS with induced currents either in the anterior-posterior direction in the brain to evoke indirect (I) waves or in the lateral-medial direction to activate corticospinal axons directly. Single pulse stimulation through the DBS contacts preceded the TMS by 0–10 ms. Surface EMG was recorded from the contralateral first dorsal interosseous muscle. Three milliseconds after STN stimulation, the motor evoked potential (MEP) amplitudes produced by anterior-posterior current were significantly larger than control responses, while the responses to lateral-medial currents were unchanged. Similar facilitation also occurred after GPi stimulation, but not with thalamic stimulation. Single pulse STN stimulation facilitates the M1 at short latencies. The possible mechanisms include antidromic excitation of the cortico-STN fibers or transmission through the basal ganglia-thalamocortical pathway.

Address for reprint requests and other correspondence: R. Hanajima, Dept. of Neurology, Univ. of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan (E-mail: hanajima-tky{at}umin.ac.jp).




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