Background: A low-dose bolus or infusion of ketamine does not affect transcranial electrical motor-evoked potential (MEP) amplitude, but a dose ≥ 1 mg/kg may reduce MEP amplitude. We conducted a randomized, double-blinded, placebo-controlled study to evaluate the effect of ketamine (1 mg/kg) on transcranial electrical MEP.Methods: Twenty female patients (aged 12 to 18 y) with adolescent idiopathic scoliosis scheduled to undergo posterior spinal fusion were randomly allocated to receive ketamine or saline. General anesthesia was induced and maintained with continuous infusions of propofol and remifentanil. MEP was elicited by supramaximal transcranial electrical stimulation. MEP recordings were obtained at baseline and then at 2, 4, 6, 8, and 10 minutes after administration of ketamine (1 mg/kg) or saline (0.1 ml/kg). The primary endpoint was the minimum relative MEP amplitude (peak-to-peak amplitude, % of baseline value) recorded from the left tibialis anterior muscle. The baseline amplitude recorded before test drug administration was defined as 100%.Results: Medians (interquartile range) minimum MEP amplitudes in the left tibialis anterior muscle in the ketamine and saline groups were 26% (9% to 34%) and 87% (55% to 103%) of the baseline value, respectively (P < 0.001). MEP amplitudes in other muscles were significantly reduced by ketamine. The suppressive effect of ketamine lasted for at least 10 minutes in each muscle. Conclusion:A 1-mg/kg bolus dose of ketamine can reduce MEP amplitude. Anesthesiologists should consider the dosage and timing of intravenous ketamine administration during MEP monitoring.

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BackgroundIt is believed that ketamine does not affect motor-evoked potential amplitude, whereas various anesthetic drugs attenuate the amplitude of transcranial motor-evoked potential. However, we encountered a patient with marked attenuation of motor-evoked potential amplitude after intravenous bolus administration of ketamine.Case presentationA 15-year-old Japanese girl with a diagnosis of adolescent idiopathic scoliosis was admitted to our hospital to undergo posterior spinal fusion at T4–L3. After induction of general anesthesia using a continuous infusion of propofol and remifentanil, we confirmed that transcranial electrical motor-evoked potentials were being recorded correctly. Ketamine 1.25 mg/kg was administered intravenously for intraoperative and postoperative analgesia. About 3 minutes later, the motor-evoked potential amplitude was markedly attenuated. No other drugs were administered except for ketamine. The patient’s vital signs were stable, and the surgery had not yet started. The motor-evoked potential amplitude was recovered at about 6 minutes after administration of ketamine. The surgery was performed uneventfully, and the patient had no neurologic deficit when she emerged from general anesthesia.ConclusionsAlthough there is a widely held belief in the field of anesthesiology that ketamine does not affect motor-evoked potential amplitude, it has been suggested that ketamine could affect its monitoring.