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

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

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Title: Changes in the Propofol-Induced Frontal Electroencephalogram in Children With Autism Spectrum Disorder
Author: Walsh, Elisa Claire
Citation: Walsh, Elisa Claire. 2017. Changes in the Propofol-Induced Frontal Electroencephalogram in Children With Autism Spectrum Disorder. Doctoral dissertation, Harvard Medical School.
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Abstract: General anesthetic drugs induce characteristic oscillations within brain circuits that can be readily assessed using the electroencephalogram (EEG), allowing a controlled and noninvasive way to study the circuitry of the human brain. During propofol-induced unconsciousness, frontal EEG demonstrates large-amplitude slow-delta oscillations (0.1-4 Hz) and frontally coherent alpha oscillations (8-13 Hz), the latter of which are thought to reflect propofol’s actions within frontal thalamocortical circuits. Previous studies from our laboratory show significant age-related changes in the propofol-induced frontal EEG that are thought to reflect the development of underlying circuits mediated by GABAergic interneurons. Interestingly, autism spectrum disorder (ASD) is increasingly seen in the clinical setting and is thought to arise from deficits in GABAergic signaling leading to abnormal neurodevelopment and neuromodulation. To investigate differences in how ASD patients respond to the GABAergic agent propofol, we recorded continuous 4-channel frontal EEG during the routine care of ASD patients who received propofol as a primary anesthetic for endoscopy and compared the data to a similar cohort of neurotypical (NT) patients. We found that the trajectory of age-dependent alpha (8-13 Hz) and slow (0.1-1 Hz) power showed notable differences in ASD vs. NT patients. Additionally, we found that the incidence of burst suppression or prolonged suppression was significantly higher in ASD vs. NT patients (28.57% vs. 12.30%, p<0.01) despite lower propofol doses. These results suggest that ASD patients respond differently to the GABAergic drug propofol and may have lowered anesthesia requirements for GABAergic agents compared to NT patients. These differences and their age-dependence may reflect underlying differences in GABAergic circuit function and development in ASD. As a similar pattern of decreased alpha power and increased sensitivity to burst suppression develops progressively with age in NT adults, our results may signify a form of accelerated neuronal aging in adolescent ASD patients. Taken together, our results suggest that measuring the propofol-induced EEG in ASD patients may enable insights into the underlying differences in neural circuitry of ASD and yield safer practices for managing anesthesia for ASD patients.
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Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:32676116
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