Modulation of Subthalamic Low Beta and Finely Tuned Gamma Activity with Parkinson's Therapy: Placebo Control Single-blind Study
Hikaru Kamo1, Jackson Cagle1, kara Johnson1, Joshua Wong2, Genko Oyama3, Hirokazu Iwamuro4, Atsushi Umemura3, Nobutaka Hattori3, Coralie Hemptinne1
1Department of Neurology, Fixel Institute for Neurological Diseases, University of Florida, Gainesville, Florida, United States of America, 2University of Florida College of Medicine - Neurology, 3Juntendo University School of Medicine, 4Department of Neurology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan
Objective:
To investigate the deep brain stimulation (DBS), levodopa, and placebo on subthalamic nucleus (STN) physiology and clinical symptoms in patients with Parkinson’s disease (PD).
Background:
Beta power (13-30Hz) and finely tuned gamma (FTG, 65-90Hz) can be modulated by PD therapies. However, how DBS and medication influence STN activity at a patient specific level, compared to a placebo is still unknown.
Design/Methods:
Fourteen PD patients with bilateral STN-DBS leads, had local field potentials (LFPs) recorded 1-year after surgery, in 5-conditions: Medication ON/OFF, DBS ON/OFF, and placebo. Levodopa (1.5 times the morning dose) and saline as a placebo were administered intravenously. Symptoms were assessed with a clinical rating scale (MDS-UPDRS part III) while participants were blinded to the therapeutic condition. Five minutes of artifact-free data were selected at the end of each condition and averaged across multiple frequency bands: Alpha (8-12Hz), Low beta (LB, 13-20Hz), High beta (HB, 20-30Hz), and FTG (60-100Hz).
Results:
LB and HB bands were the largest in the OFF medication and were significantly reduced by DBS. Levodopa perfusion significantly reduced LB (62%) but not HB. The emergence of FTG was observed during L-dopa infusion in 46% of the recordings and was often preceded by a reduction in LB power. Adding DBS resulted in the entrainment of FTG to half the stimulation frequency (58%). Similar FTG entrainment was found in the OFF medication ON DBS (19%). The changes in both LB and FTG were correlated with the improvement rate of the symptoms, especially the akinesia and rigidity sub-scores, and were not consistently associated with dyskinesia. Interestingly, placebo administration reduced LB (36%) but did not modulate FTG.
Conclusions:
This study demonstrated treatment-induced changes in STN beta power and FTG in an individualized fashions. LB and FTG correlate with symptom improvement suggesting FTG and LB as biomarkers of ‘ON state’ in PD.
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