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This comprehensive review evaluates the neurophysiological effects of sedative agents on EEG in pediatrics, suggesting improved decision-making for safer outcomes.
The utility of pediatric electroencephalography (EEG) is frequently compromised by motion artifacts and limited patient cooperation, necessitating pharmacological sedation to ensure signal quality. However, sedative agents produce distinct neurophysiological signatures that can obscure diagnostic landmarks or interfere with modern automated analysis pipelines. This review evaluates a five-agent framework comprising dexmedetomidine, chloral hydrate, midazolam, ketamine, and melatonin, with emphasis on their molecular mechanisms, developmental effects, and spectral influences on the EEG background. We highlight that biomimetic agents such as melatonin and dexmedetomidine preserve natural sleep architecture and interictal epileptiform discharges, whereas gamma-aminobutyric acid (GABA)-ergic (GABAergic) modulators such as midazolam and N-methyl-D-aspartate antagonists such as ketamine induce disruptive beta crowding and gamma bursts, respectively. The review also addresses age-dependent responses, including the neonatal GABAergic polarity shift, which may lead to paradoxical excitation. By integrating clinical safety profiles with signal-integrity requirements, we propose a tiered clinical decision-making framework that prioritizes diagnostic yield. Ultimately, a mechanism-based approach to sedative selection may help neurophysiologists optimize both patient safety and the precision of visual and digital EEG interpretation in the evolving landscape of pediatric neurology.
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Yune et al. (2026) studied this question.
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