Abstracts

Rationale: Dexmedetomidine is a highly selective α-2 adrenoreceptor agonist with sedative effects useful for induction of sedation and immobility for imaging studies children. Dexmedetomidine has been described as inducing a cardiovascular and respiratory state similar to natural sleep in children, though little is known of the effects of this agent on the pediatric EEG. We set out to study the effects of dexmedetomidine sedation on EEG background and epileptiform activity in children. Methods: Selected EEG samples from 16 consecutive pediatric patients undergoing dexmedetomidine sedation for nuclear medicine scanning as candidates for epilepsy surgery were studied. All children underwent continuous EEG monitoring during these admissions, including during administration of sedation. Because, based on adult data, EEG background during dexmedetomidine sedation resembles onset of stage II (spindle) sleep, EEG samples during sedation were compared to comparable samples of stage II sleep: a sample following the appearance of the second sleep spindle during dexmedetomidine sedation was compared to a sample following the appearance of the second sleep spindle during natural sleep. RMS EEG power in the delta, theta, alpha, beta, and total power bandwidths were compared on a patient by patient basis. Likewise, the frequency of EEG spikes in each dexmedetomidine sample was compared to a corresponding sample in each patient during natural sleep. Results: Visual analysis of the EEG during dexmedetomidine sedation showed a pattern consistent with stage II sleep. In comparing EEG samples during dexmedetomidine sedation to natural sleep samples obtained during the same admission, no significant differences were found in slow wave (delta and theta) or midrange (alpha) frequencies. A 44% increase in fast activity (beta) was statistically significant (p = 0.05, Student’s paired t-test). A 26% average increase in spike frequency was seen in sedation samples compared to natural sleep samples (p = 0.01, Student’s paired t-test). No new spike foci were noted during dexmedetomidine sedation. Conclusions: The EEG of children undergoing dexmedetomidine sedation resembles onset of stage II sleep. EEG power analysis during dexmedetomidine sedation showed a mild increase in fast activity and a modest increase in spike frequency when compared to naturally-occurring stage II sleep. These features make dexmedetomidine a uniquely attractive agent for performing diagnostic EEG studies during sedation in pediatric patients in whom such tracings cannot be performed in the awake state.