• Mohamed Mahmoud, Senthilkumar Sadhasivam, Shelia Salisbury, Todd G Nick, Beverly Schnell, Anthony K Sestokas, Cheryl Wiggins, Paul Samuels, Thomas Kabalin, and John McAuliffe.
• Department of Anesthesiology, Division of Biostatistics and Epidemiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA. mohamed.mahmoud@cchmc.org
• Anesthesiology. 2010 Jun 1; 112 (6): 1364-73.

BackgroundDexmedetomidine has been increasingly used as an adjunct to opioid-propofol total intravenous anesthesia (TIVA). The authors tested the hypothesis and found that clinically relevant blood levels of dexmedetomidine do not produce significant attenuation of the amplitude of transcranial electric motor-evoked potentials either independently or by interaction with propofol in a dose-dependent manner.MethodsThe authors planned to recruit 72 patients with idiopathic scoliosis who had posterior spine fusion surgery during propofol and remifentanil TIVA with dexmedetomidine as an adjunct. However, the authors terminated the study after enrolling 44 patients because of change in surgical technique. Before administering dexmedetomidine, baseline transcranial electric motor-evoked potentials were acquired during TIVA with remifentanil and propofol. Patients were randomized to varying targeted blood levels of dexmedetomidine (0.4, 0.6, and 0.8 ng/ml) and propofol (2.5, 3.75, and 5 microg/ml) using a factorial design. The primary outcome variable was amplitude of transcranial electric motor-evoked potential. The secondary outcome was amplitude of cortical somatosensory-evoked potentials.ResultsOf the 44 recruited patients, 40 completed the study, and their data were analyzed. The administration of dexmedetomidine in increasing doses as an adjunct to propofol-based TIVA caused a clinically and statistically significant attenuation of amplitudes of transcranial electric motor-evoked potentials.ConclusionThe authors conclude that under the stimulation conditions used, dexmedetomidine as an anesthetic adjunct to propofol-based TIVA at clinically relevant target plasma concentrations (0.6-0.8 ng/ml) can significantly attenuate the amplitude of transcranial electric motor-evoked potentials.

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