Related Experiment Video
Updated: Aug 21, 2026

Recording Gamma Band Oscillations in Pedunculopontine Nucleus Neurons
Published on: September 14, 2016
Target-specific modulation of cortical narrowband gamma by basal ganglia nuclei: a case report
Mallory L S Eisel1,2, Jackson N Cagle1,3, Kara A Johnson1,3
1Department of Neurology, University of Florida, Gainesville, FL, United States.
Introduction:
Narrow-band gamma (NBG) is an oscillatory activity in the gamma band (60-90 Hz) that has been observed in the subthalamic nucleus (STN), the motor cortex, and, more recently, the globus pallidus internus (GPi) of Parkinson's disease (PD) patients, often in the on-medication state. Therapeutic DBS has been shown to modulate NBG, often entraining cortical and subcortical NBG to half the stimulation frequency, often referred to as finely tuned gamma (FTG). However, the differential effect of STN, GPi, and GPe DBS on cortical NBG has never been explored in the same patient.
Method:
We report a case of a 54-year-old female patient with early-onset PD harboring PRKN variants, who underwent GPi-DBS implantation to supplement the effect of a prior STN lead. During surgery, cortical potentials were recorded via a temporary electrocorticography (ECoG) strip placed over the sensorimotor cortex while sequentially stimulating the STN, GPi, and GPe using the same DBS parameters (bipolar mode, 3 V, 180 Hz, 60 μs). Given the severity of symptoms, the participant took medication before surgery. Therefore, all recordings were done in the on-medication state in the presence of leg dyskinesia.
Result:
At baseline, the primary motor cortex (M1) exhibited prominent NBG activity at 68 Hz. Both STN and GPi DBS induced similar effects, leading to NBG suppression. These neurophysiological changes were accompanied by modest clinical improvements in rigidity and dystonia. In contrast, GPe DBS did not suppress NBG and was not associated with any clinical benefit.
Discussion:
Our results show that therapeutic and nontherapeutic basal ganglia stimulation differentially modulated M1 NBG, supporting the potential utility of this activity as a biomarker for therapeutic stimulation. The absence of entrainment during STN and GPi stimulation might be due to high frequency (180 Hz) exceeding the range of cortical synchronization and FTG emergence.
