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Age-Dependent Changes in the Propofol-Induced Electroencephalogram in Children With Autism Spectrum Disorder

Authors :
Institute for Medical Engineering and Science
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Brown, Emery Neal
Walsh, Elisa C.
Lee, Johanna M.
Terzakis, Kristina
Zhou, David W.
Burns, Sara
Buie, Timothy M.
Firth, Paul G.
Shank, Erik S.
Houle, Timothy T.
Purdon, Patrick L.
Institute for Medical Engineering and Science
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Brown, Emery Neal
Walsh, Elisa C.
Lee, Johanna M.
Terzakis, Kristina
Zhou, David W.
Burns, Sara
Buie, Timothy M.
Firth, Paul G.
Shank, Erik S.
Houle, Timothy T.
Purdon, Patrick L.
Source :
Frontiers
Publication Year :
2018

Abstract

Patients with autism spectrum disorder (ASD) often require sedation or general anesthesia. ASD is thought to arise from deficits in GABAergic signaling leading to abnormal neurodevelopment. We sought to investigate differences in how ASD patients respond to the GABAergic drug propofol by comparing the propofol-induced electroencephalogram (EEG) of ASD and neurotypical (NT) patients. This investigation was a prospective observational study. Continuous 4-channel frontal EEG was recorded during routine anesthetic care of patients undergoing endoscopic procedures between July 1, 2014 and May 1, 2016. Study patients were defined as those with previously diagnosed ASD by DSM-V criteria, aged 2–30 years old. NT patients were defined as those lacking neurological or psychiatric abnormalities, aged 2–30 years old. The primary outcome was changes in propofol-induced alpha (8–13 Hz) and slow (0.1–1 Hz) oscillation power by age. A post hoc analysis was performed to characterize incidence of burst suppression during propofol anesthesia. The primary risk factor of interest was a prior diagnosis of ASD. Outcomes were compared between ASD and NT patients using Bayesian methods. Compared to NT patients, slow oscillation power was initially higher in ASD patients (17.05 vs. 14.20 dB at 2.33 years), but progressively declined with age (11.56 vs. 13.95 dB at 22.5 years). Frontal alpha power was initially lower in ASD patients (17.65 vs. 18.86 dB at 5.42 years) and continued to decline with age (6.37 vs. 11.89 dB at 22.5 years). The incidence of burst suppression was significantly higher in ASD vs. NT patients (23.0% vs. 12.2%, p < 0.01) despite reduced total propofol dosing in ASD patients. Ultimately, we found that ASD patients respond differently to propofol compared to NT patients. A similar pattern of decreased alpha power and increased sensitivity to burst suppression develops in older NT adults; one interpretation of our data could be that ASD patients undergo a form of accelerat

Details

Database :
OAIster
Journal :
Frontiers
Notes :
application/pdf
Publication Type :
Electronic Resource
Accession number :
edsoai.on1141894050
Document Type :
Electronic Resource