Browsing by Author "Shinnar, Shlomo"

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    Decreased Electroencephalographic Alpha Power During Anesthesia Induction Is Associated With EEG Discontinuity in Human Infants
    (International Anesthesia Research Society, 2022-12) Chao, Jerry Y.; Gutiérrez, Rodrigo; Legatt , Alan D.; Yozawitz , Elissa G.; Lo , Yungtai; Adams , David C.; Delphin , Ellise S.; Shinnar, Shlomo; Purdon, Patrick L.; Anesthesia, School of Medicine
    Background: Electroencephalogram (EEG) discontinuity can occur at high concentrations of anesthetic drugs, reflecting suppression of electrocortical activity. This EEG pattern has been reported in children and reflects a deep state of anesthesia. Isoelectric events on the EEG, a more extreme degree of voltage suppression, have been shown to be associated with worse long-term neurologic outcomes in neonates undergoing cardiac surgery. However, the clinical significance of EEG discontinuities during pediatric anesthesia for non-cardiac surgery is not yet known and merits further research. In this study, we assessed the incidence of EEG discontinuity during anesthesia induction in neurologically normal infants and the clinical factors associated with its development. We hypothesized that EEG discontinuity would be associated with sevoflurane-induced alpha (8 to 12 Hz) power during the period of anesthesia induction in infants. Methods: We prospectively recorded 26 channels of EEG during anesthesia induction in an observational cohort of 54 infants (median age 7.6 IQR [4.9, 9.8] months). We identified EEG discontinuity, defined as voltage amplitude <25 microvolts for >2 seconds, and assessed its association with sevoflurane-induced alpha power using spectral analysis and multivariable logistic regression adjusting for clinically important variables. Results: EEG discontinuity was observed in 20 of 54 subjects (37%), with a total of 25 discrete events. Sevoflurane-induced alpha power in the posterior regions of the head (e.g., parietal or occipital regions) was significantly lower in the EEG discontinuity group (midline parietal channel [Pz], 8.3 vs. 11.2 dBs, p = 0.004), and this association remained after multivariable adjustment (adjusted odds ratio [aOR] = 0.51 per dB increase in alpha power [95% CI: 0.30 – 0.89], p = 0.02). There were no differences in the baseline (unanesthetized) EEG between groups in alpha power, or power in any other frequency band. Conclusions: We demonstrate that EEG discontinuity is common during anesthesia induction and is related to the level of sevoflurane-induced posterior alpha power, a putative marker of cortical-thalamic circuit development in the first year of life. This association persisted even after adjusting for age and propofol co-administration. The fact that this difference was only observed during anesthesia and not in the baseline EEG suggests that otherwise hidden brain circuit properties are unmasked by general anesthesia. These neurophysiologic markers observed during anesthesia may be useful in identifying patients who may have a greater chance of developing discontinuity.
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    Patterns of Benzodiazepine Underdosing in the Established Status Epilepticus Treatment Trial
    (Wiley, 2021) Sathe, Abhishek G.; Underwood, Ellen; Coles, Lisa D.; Elm, Jordan J.; Silbergleit, Robert; Chamberlain, James M.; Kapur, Jaideep; Cock, Hannah R.; Fountain, Nathan B.; Shinnar, Shlomo; Lowenstein, Daniel H.; Rosenthal, Eric S.; Conwit, Robin A.; Bleck, Thomas P.; Cloyd, James C.; Neurology, School of Medicine
    Objective: This study was undertaken to describe patterns of benzodiazepine use as first-line treatment of status epilepticus (SE) and test the association of benzodiazepine doses with response to second-line agents in patients enrolled in the Established Status Epilepticus Treatment Trial (ESETT). Methods: Patients refractory to an adequate dose of benzodiazepines for the treatment of SE were enrolled in ESETT. Choice of benzodiazepine, doses given prior to administration of second-line agent, route of administration, setting, and patient weight were characterized. These were compared with guideline-recommended dosing. Logistic regression was used to determine the association of the first dose of benzodiazepine and the cumulative benzodiazepine dose with the response to second-line agent. Results: Four hundred sixty patients were administered 1170 doses of benzodiazepines (669 lorazepam, 398 midazolam, 103 diazepam). Lorazepam was most frequently administered intravenously in the emergency department, midazolam intramuscularly or intravenously by the emergency medical services personnel, and diazepam rectally prior to ambulance arrival. The first dose of the first benzodiazepine (N = 460) was lower than guideline recommendations in 76% of midazolam administrations and 81% of lorazepam administrations. Among all administrations, >85% of midazolam and >76% of lorazepam administrations were lower than recommended. Higher first or cumulative benzodiazepine doses were not associated with better outcomes or clinical seizure cessation in response to second-line medications in these benzodiazepine-refractory seizures. Significance: Benzodiazepines as first-line treatment of SE, particularly midazolam and lorazepam, are frequently underdosed throughout the United States. This broad and generalizable cohort confirms prior single site reports that underdosing is both pervasive and difficult to remediate.