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

Mov Disord. 2001 Mar;16(2):208-16. doi: 10.1002/mds.1046.

Abstract

A 69-year-old woman with Parkinson's disease and levodopa-induced dyskinesias had a deep brain stimulation (DBS) electrode inserted into the right globus pallidus internus (GPi). During the operation, the GPi was mapped with dual microelectrode recordings. Stimulation through one microelectrode in GPi inhibited the firing of GPi neurons recorded with another microelectrode 600--1,000 microm distant. The inhibition could be obtained with pulse widths of 150 micros and intensities as low as 10 microA. Single stimuli inhibited GPi neurons for approximately 50 ms. Trains of 300 Hz stimuli inhibited GPi neuron firing almost completely. Postoperatively, stimulation through macroelectrode contacts located in the posterior ventral pallidum controlled the patient's dyskinesias. The effect could be obtained with pulse widths of 50 micros and frequencies as low as 70--80 Hz. We postulate stimulation of the ventral pallidum controls dyskinesias by activating large axons which inhibit GPi neurons.

Publication types

  • Case Reports

MeSH terms

  • Action Potentials / physiology
  • Aged
  • Antiparkinson Agents / administration & dosage
  • Antiparkinson Agents / therapeutic use*
  • Axons / physiology*
  • Dyskinesia, Drug-Induced / diagnosis*
  • Dyskinesia, Drug-Induced / therapy*
  • Electric Stimulation / methods
  • Electrodes, Implanted
  • Evoked Potentials, Visual / physiology
  • Female
  • Functional Laterality / physiology
  • Globus Pallidus / physiology*
  • Globus Pallidus / surgery
  • Humans
  • Levodopa / administration & dosage
  • Levodopa / therapeutic use*
  • Microelectrodes
  • Monitoring, Intraoperative
  • Neural Inhibition / physiology*
  • Parkinson Disease / drug therapy*
  • Periodicity

Substances

  • Antiparkinson Agents
  • Levodopa