Neurophysiological modulation of the subthalamic nucleus by pallidal stimulation in Parkinson's disease
- 1Department of Neurosurgery, NYU School of Medicine, NY, USA
- 2Department of Neurology, NYU School of Medicine, NY, USA
- 3Department of Neurology, Mount Sinai School of Medicine, NY, USA
- 4Department of Neurosurgery, Weill Medical College of Cornell University, NY, USA
- 5Department of Anesthesiology, Hospital for Joint Diseases, New York, NY, USA
- Correspondence to: Dr A Berić, Department of Neurology, Hospital for Joint Diseases, 301 East 17th Street, New York, NY 10003, USA;
- Received 11 July 2001
- Accepted 5 November 2001
- Revised 30 October 2001
Abstract
Objectives: Current models of basal ganglia dysfunction in Parkinson's disease suggest a pivotal role of subthalamic nucleus (STN) hyperactivity. There is a direct excitatory output to the globus pallidus internus (GPi), which in turn hyperinhibits the motor thalamus and leads to a lack of cortical facilitation. The model, however, does not address the reciprocal influence of GPi on STN activity.
Methods: Measurement of immediate changes in STN single cell activity after GPi deep brain stimulation (DBS).
Results: An opposite effect of GPi DBS in the dorsal versus ventral STN was found. There was an almost exclusive reduction of firing rate in the dorsal region of the STN, whereas the cells in the ventral region exhibited facilitation similar to the recordings from the substantia nigra pars reticulata.
Conclusion: Although these findings require confirmation, they suggest that the current theories of GPi DBS action, which do not include a GPi-STN modulation, are most likely incomplete.
- STN, subthalamic nucleus
- GPi, globus pallidus internus
- GPe, globus pallidus externus
- DBS, deep brain stimulator
- AC, anterior commissure
- PC, posterior commissure
- ISI, interspike interval
