Background Deep brain stimulation electrodes can record oscillatory activity from deep brain structures, known as local field potentials. The authors’ objective was to evaluate and quantify the effects of dexmedetomidine (0.2 μg·kg-1·h-1) on local field potentials in patients with Parkinson disease undergoing deep brain stimulation surgery compared with control recording (primary outcome), as well as the effect of propofol at different estimated peak effect site concentrations (0.5, 1.0, 1.5, 2.0, and 2.5 μg/ml) from control recording. Methods A nonrandomized, nonblinded controlled clinical trial was carried out to assess the change in local field potentials activity over time in 10 patients with Parkinson disease who underwent deep brain stimulation placement surgery (18 subthalamic nuclei). The relationship was assessed between the activity in nuclei in the same patient at a given time and repeated measures from the same nucleus over time. Results No significant difference was observed between the relative beta power of local field potentials in dexmedetomidine and control recordings (−7.7; 95% CI, −18.9 to 7.6). By contrast, there was a significant decline of 12.7% (95% CI, −21.3 to −4.7) in the relative beta power of the local field potentials for each increment in the estimated peak propofol concentrations at the effect site relative to the control recordings. Conclusions Dexmedetomidine (0.2 μg·kg-1·h-1) did not show effect on local field potentials compared with control recording. A significant deep brain activity decline from control recording was observed with incremental doses of propofol.

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 mg kg À1 h À1 ) 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 (0.5e0.6 mg kg À1 h À1 ) 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: 0e9) min, showing full restoration of subthalamic activity. Dexmedetomidine dose administered and plasma levels showed a positive correlation (repeated measures correlation coefficient¼0.504; 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 mg kg À1 h À1 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.

Significant side effects appear to be uncommon. Blood count changes are likely multifactorial; surgical time may account for it partially, whereas 5-ALA role is not clear and may not be significant.

No author has a financial or proprietary interest in any material or method mentioned.