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Abstract
Background: Deep brain stimulation of the internal global pallidus (GPi) and the subthalamic nucleus (STN) has become a treatment alternative in advanced PD. Although the effects of GPi stimulation have been examined recently, little is known about STN stimulation effects on motor cortex excitability.
Methods: The effects of STN stimulation were studied in eight patients with advanced PD using paired-pulse transcranial magnetic stimulation (TMS) in comparison with healthy control subjects. Motor evoked potentials following paired-pulse TMS (interstimulus interval 3 ms to test for corticocortical inhibition vs 13 ms for facilitation) have been recorded from the extensor carpi radialis and its functional antagonist, the flexor carpi radialis muscle. Silent period (SP) was also determined. Patients were examined under four conditions: medication “off”/stimulator “off” vs medication “on”/stimulator “off” vs medication “off”/stimulator “on” vs medication “on”/stimulator “on.”
Results: Although the mean values for intracortical inhibition (ICI) were not significantly different, data variation was smaller and levels of significance higher with the STN stimulator switched “on,” suggesting that ICI was more consistent. SP during stimulator “on”/medication “on” was longer than during stimulator “off”/medication “off.” Motor performance as indicated by a finger-tapping test and Unified PD Rating Scale III was significantly better with dopaminergic medication and further improved with stimulator “on.”
Conclusions: Results suggest an effect of subthalamic nucleus stimulation on intracortical inhibitory mechanisms. This hypothesis could at least partially explain a more consistent depression of motor evoked potentials following inhibiting paired-pulse transcranial magnetic stimulation, a longer silent period (under stimulator “on”/medication “on”), and a reduction of akinesia and rigidity leading to a better motor performance in subthalamic nucleus–stimulated patients.
- Received January 20, 2002.
- Accepted May 16, 2002.
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