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ANESTHETIC PHARMACOLOGY

The Effect of Dexmedetomidine on Electrocorticography in Patients with Temporal Lobe Epilepsy Under Sevoflurane Anesthesia

Yutaka Oda, MD, PhD^*, Sumiko Toriyama, MD^*, Katsuaki Tanaka, MD, PhD^*, Tadashi Matsuura, MD^*, Naoya Hamaoka, MD, PhD^*, Michiharu Morino, MD, PhD, and Akira Asada, MD, PhD^*

From the Departments of *Anesthesiology and Intensive Care Medicine and Neurosurgery, Graduate School of Medicine, Osaka City University, Osaka, Japan.

Address correspondence and reprint requests to Yutaka Oda, MD, PhD, Department of Anesthesiology and Intensive Care Medicine, Graduate School of Medicine, Osaka City University, 1-5-7 Asahimachi, Abeno-ku, Osaka 545-8586, Japan. Address e-mail to odayou{at}msic.med.osaka-cu.ac.jp.

BACKGROUND: Although dexmedetomidine is often used in neuroanesthesia and neuronal critical care practice, its effect on cerebral electrical activity in those with an abnormal electroencephalogram is not known. The electrocorticogram (ECoG), a sensitive method for examining the effect of drugs on cerebral electrical activity and surgical treatment for epilepsy, is usually guided by monitoring of the ECoG. We investigated the effect of dexmedetomidine on ECoG in patients with epilepsy undergoing surgery with sevoflurane.

METHODS: Patients with medically intractable temporal lobe epilepsy undergoing resection of the epileptic foci (n = 11) were enrolled. Under general anesthesia with 2.5% sevoflurane and end-tidal carbon dioxide tension at 30 mm Hg, ECoG was recorded by strip electrodes with eight contacts placed on the mesial temporal lobe ipsilateral to the epilepsy foci. Dexmedetomidine was given as a computer-controlled infusion to achieve target plasma concentrations of 0.5 and 1.5 ng/mL. Each concentration was maintained for 20 min and ECoG was recorded before infusion of dexmedetomidine and between the 10th and 20th min after starting infusion. The median frequency of ECoG, spectral power density of each spectral band, and number of spikes at each concentration of dexmedetomidine were compared by Kruskal–Wallis test, followed by Student–Newman–Keuls test.

RESULTS: The median frequency of ECoG in 88 leads from all leads from all patients was significantly decreased by 1.5 ng/mL of dexmedetomidine compared with those at baseline and 0.5 ng/mL (P = 0.003 and 0.03, respectively); however, spectral power densities in the frequency bands: (<4 Hz), (4 and <8 Hz), (8 and <13 Hz), and ß (13 Hz), were not changed. Neither the number of leads with spikes nor the number of spikes in all leads and in the lead with highest number of spikes at baseline was affected by dexmedetomidine.

CONCLUSIONS: Dexmedetomidine at plasma concentrations of 0.48 and 1.60 ng/mL decreased the median frequency of ECoG, but did not affect spike activity in patients with temporal lobe epilepsy anesthetized with 2.5% sevoflurane.