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Deceased.
From the Departments of Neurology (Drs. Kühn, Meyer, Trottenberg, Brandt, and Kupsch) and Neurosurgery (Dr. Schneider), Charité, Campus Virchow Klinikum, Humboldt University Berlin, Germany.
Address correspondence and reprint requests to PD Dr. A. Kupsch, Department of Neurology, Charité, Campus Virchow Klinikum, Augustenburger Platz 1, 13353 Berlin, Germany; e-mail: andreas.kupsch{at}charite.de
Objective: To study the influence of continuous high-frequency electrical stimulation with electrodes implanted in the globus pallidus internus (GPi) on motor cortex excitability in nine patients with dystonia.
Methods: Short-term effects related to switching off and on the deep brain stimulator were investigated >3 months after electrode implantation. Activation of motor cortical excitatory and inhibitory neurons was examined with transcranial magnetic stimulation (TMS) by analysis of electromyographic activity in the hand muscles. Parameters of corticospinally mediated excitatory motor responses included latency, threshold, and response sizes with increasing stimulus intensities (stimulus–response curves). Other measures of motor cortex excitability comprised the duration of the contralateral silent period and intracortical inhibition and facilitation in a paired-pulse paradigm.
Results: Switching off GPi stimulation led to a decrease of motor cortex excitability, as reflected by an increase in motor thresholds (GPi stimulation on 37.5 ± 6.1%, mean ± SD; GPi stimulation off for 15 to 120 minutes, 40.5 ± 6.7% of maximum stimulator output), and reduced the size of contralateral responses in the stimulus–response curves established for relaxed muscles. The changes were reversible within minutes after switching on GPi stimulation. They were associated with mild changes of dystonia. By contrast, measures of intracortical inhibition were not altered by switching off GPi stimulation. Spinal excitability did not change as assessed by H-reflex.
Conclusion: GPi stimulation influences motor cortex excitability by a rapid modulation of thalamocortical outputs.
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