Does stimulation of the GPi control dyskinesia by activating inhibitory axons?

Citation
Yr. Wu et al., Does stimulation of the GPi control dyskinesia by activating inhibitory axons?, MOVEMENT D, 16(2), 2001, pp. 208-216
Citations number
22
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
MOVEMENT DISORDERS
ISSN journal
08853185 → ACNP
Volume
16
Issue
2
Year of publication
2001
Pages
208 - 216
Database
ISI
SICI code
0885-3185(200103)16:2<208:DSOTGC>2.0.ZU;2-H
Abstract
A 69-year-old woman with Parkinson's disease and levodopa-induced dyskinesi as had a deep brain stimulation (DBS) electrode inserted into the right glo bus pallidus internus (GPi). During the operation, the GPI was mapped with dual microelectrode recordings. Stimulation through one microelectrode in G PI inhibited the firing of GPi neurons recorded with another microelectrode 600-1.000 mum distant. The inhibition could be obtained with pulse widths of 150 mus and intensities as low as 10 muA. Single stimuli inhibited GPI n eurons for similar to 50 ms. Trains of 300 Hz stimuli inhibited GPi neuron firing almost completely. Postoperatively. stimulation through macroelectro de contacts located in the posterior ventral pallidum controlled the patien t's dyskinesias. The effect could be obtained with pulse widths of 50 mus a nd frequencies as low as 70-80 Hz. We postulate stimulation of the ventral pallidum controls dyskinesias by activating large axons which inhibit GPi n eurons. (C) 2001 Movement Disorder Society.