Article ID Journal Published Year Pages File Type
3043215 Clinical Neurophysiology 2015 7 Pages PDF
Abstract

•Hypoxia has been considered as the key mechanism in daytime drowsiness and neurocognitive impairment in sleep-disordered breathing.•We compared the effect of hypoxia and hypercapnia on EEG spectra during wakefulness using a rigorously controlled experimental method, and found that hypercapnia, but not hypoxia caused EEG slowing.•These data imply that hypercapnia may be more mechanistically important in neurobiological impairments in sleep-disordered breathing patients.

ObjectiveHypoxia has been postulated as a key mechanism for neurocognitive impairment in sleep-disordered breathing. However, the effect of hypoxia on the electroencephalogram (EEG) is not clear.MethodsWe examined quantitative EEG recordings from 20 normal volunteers under three 5-min ventilatory control protocols: progressive hypercapnia with iso-hyperoxia (pO2 = 150 mmHg) (Protocol 1), progressive hypercapnia with iso-hypoxia (pO2 = 50 mmHg) (Protocol 2), and progressive hypoxia with a CO2 scrubber in the circuit (Protocol 3). Each protocol started with a 5-min session of breathing room air as baseline.ResultsIn Protocol 1, compared to its baseline, iso-hyperoxia hypercapnia led to a lower Alpha% and higher Delta/Alpha (D/A) ratio. Similarly, in Protocol 2, the iso-hypoxia hypercapnia induced a higher Delta%, a lower Alpha% and higher D/A ratio. No difference was found in any EEG spectral band including the D/A ratio when Protocols 1 & 2 were compared. In Protocol 3, the Delta%, Alpha% and D/A ratio recorded during hypoxia were not significantly different from baseline.ConclusionsWe found that hypercapnia, but not hypoxia, may play a key role in slowing of the EEG in healthy humans.SignificanceHypercapnia may be a greater influence than hypoxia on brain neuroelectrical activities.

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