Copyright © 2017, the American Society of Anesthesiologists, Inc. Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited. <zdoi;10.1097/ALN.0000000000001620> Anesthesiology, V 126 • No 6 1033 June 2017 D EEP brain stimulation (DBS) is a standard treatment to combat the symptoms of Parkinson disease (PD). 1–3 In most centers with surgery for PD, the surgical implan- tation of the electrodes for DBS follows a well-established technique that combines microelectrode recordings (MERs), microstimulation, and neurologic intraoperative testing to localize the target nuclei. 4–8 A variety of anesthetic approaches are used when DBS electrodes are implanted, including local anesthesia, con- scious sedation, “asleep-awake,” or “asleep-awake-asleep” protocols. 6,9,10 With the exception of local anesthesia, one important drawback is that all the sedative drugs used to achieve anesthesia in this surgery afect the quality of MERs, lowering the fring rate of basal ganglia neurons while simul- taneously suppressing or altering symptoms of PD. 11–13 What We Already Know about This Topic • In patients undergoing implantation of deep brain stimulation electrodes for Parkinson disease, microelectrode recordings from the target nuclei are used to guide proper electrode placement. The selection of anesthetic agents that have the least impact on microelectrode recordings is therefore important. • The effect of dexmedetomidine on activity of subthalamic nuclei was compared with that of graded doses of propofol in patients undergoing placement of deep brain stimulation electrodes. What This Article Tells Us That Is New • Activity in the subthalamic nuclei was similar to the control, unsedated state in patients who received dexmedetomidine. By contrast, propofol produced a dose-dependent reduction in neuronal activity, especially in the beta frequency range. • The data support the use of dexmedetomidine for sedation in patients undergoing deep brain stimulator implantation. Copyright © 2017, the American Society of Anesthesiologists, Inc. Wolters Kluwer Health, Inc. All Rights Reserved. Anesthesiology 2017; 126:1033-42 ABSTRACT Background: Deep brain stimulation electrodes can record oscillatory activity from deep brain structures, known as local feld potentials. Te authors’ objective was to evaluate and quantify the efects of dexmedetomidine (0.2 μg∙kg -1 ∙h -1 ) on local feld potentials in patients with Parkinson disease undergoing deep brain stimulation surgery compared with control recording (primary outcome), as well as the efect of propofol at diferent estimated peak efect 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 feld potentials activity over time in 10 patients with Parkinson disease who underwent deep brain stimulation placement surgery (18 sub- thalamic nuclei). Te 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 signifcant diference was observed between the relative beta power of local feld potentials in dexmedetomidine and control recordings (−7.7; 95% CI, −18.9 to 7.6). By contrast, there was a signifcant decline of 12.7% (95% CI, −21.3 to −4.7) in the relative beta power of the local feld potentials for each increment in the estimated peak propofol concentra- tions at the efect site relative to the control recordings. Conclusions: Dexmedetomidine (0.2 μg∙kg -1 ∙h -1 ) did not show efect on local feld potentials compared with control recording. A signifcant deep brain activity decline from control recording was observed with incremental doses of propofol. (ANESTHESIOLOGY 2017; 126:1033-42) This article is featured in “This Month in Anesthesiology,” page 1A. Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are available in both the HTML and PDF versions of this article. Links to the digital files are provided in the HTML text of this article on the Journal’s Web site (www.anesthesiology.org). Submitted for publication June 30, 2016. Accepted for publication February 21, 2017. From the Department of Anesthesia, Perioperative Medicine and Critical Care (A.M.-S., C.H-C., E.C.-A.), Department of Neurophysiology (M.A.), Research Support Service, Central Clinical Trials Unit (J.M.N.-C), Department of Neurology (M.C.-A.), and Department of Neurosurgery (J.G.), University of Navarra Clinic, Pamplona, Spain; and Department of Pharmacy and Pharmaceutical Technology, School of Pharmacy and Nutrition (I.F.T.) and Neurophysiology Laboratory, Center for Applied Medical Research (M.V.), University of Navarra, Pamplona, Spain. Effect of Dexmedetomidine and Propofol on Basal Ganglia Activity in Parkinson Disease A Controlled Clinical Trial Antonio Martinez-Simon, M.D., Ph.D., Manuel Alegre, M.D., Ph.D., Cristina Honorato-Cia, M.D., Ph.D., Jorge M. Nuñez-Cordoba, M.D., Ph.D., M.P.H., Elena Cacho-Asenjo, M.D., Ph.D., Iñaki F. Trocóniz, Ph.D., Mar Carmona-Abellán, M.D., Ph.D., Miguel Valencia, Ph.D., Jorge Guridi, M.D., Ph.D. Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/126/6/1033/519244/20170600_0-00013.pdf by guest on 14 June 2022