Effects of dexmedetomidine on subthalamic local field potentials in parkinson's disease
Keywords: 
Parkinson's disease
Deep brain stimulation
Dexmedetomidine
Local field potentials
Sedation
Subthalamic activity
Issue Date: 
2021
Publisher: 
Elsevier
ISSN: 
0007-0912
Note: 
This is an open access article under the CC BY-NC-ND license
Citation: 
Martinez-Simon, A. (Antonio); Cacho-Asenjo, E. (Elena); Honorato-Cía, C. (Cristina); et al. "Effects of dexmedetomidine on subthalamic local field potentials in parkinson's disease". British Journal of Anaesthesia. 127 (2), 2021, 245 - 253
Abstract
Background: Dexmedetomidine is frequently used for sedation during deep brain stimulator implantation in patients with Parkinson's disease, but its effect on subthalamic nucleus activity is not well known. The aim of this study was to quantify the effect of increasing doses of dexmedetomidine in this population. Methods: Controlled clinical trial assessing changes in subthalamic activity with increasing doses of dexmedetomidine (from 0.2 to 0.6 μg kg-1 h-1) in a non-operating theatre setting. We recorded local field potentials in 12 patients with Parkinson's disease with bilateral deep brain stimulators (24 nuclei) and compared basal activity in the nuclei of each patient and activity recorded with different doses. Plasma levels of dexmedetomidine were obtained and correlated with the dose administered. Results: With dexmedetomidine infusion, patients became clinically sedated, and at higher doses (0.5-0.6 μg kg-1 h-1) a significant decrease in the characteristic Parkinsonian subthalamic activity was observed (P<0.05 in beta activity). All subjects awoke to external stimulus over a median of 1 (range: 0-9) min, showing full restoration of subthalamic activity. Dexmedetomidine dose administered and plasma levels showed a positive correlation (repeated measures correlation coefficient=0.504; P<0.001). Conclusions: Patients needing some degree of sedation throughout subthalamic deep brain stimulator implantation for Parkinson's disease can probably receive dexmedetomidine up to 0.6 μg kg-1 h-1 without significant alteration of their characteristic subthalamic activity. If patients achieve a 'sedated' state, subthalamic activity decreases, but they can be easily awakened with a non-pharmacological external stimulus and recover baseline subthalamic activity patterns in less than 10 min.

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