Chinh D Nguyen1,2, Andrew Wellman3, Amy S Jordan4, Danny J Eckert1,5. 1. Neuroscience Research Australia (NeuRA), Randwick, New South Wales, Australia. 2. Woolcock Institute of Medical Research and Sydney Medical School, University of Sydney, Glebe, New South Wales, Australia. 3. Brigham and Women's Hospital and Harvard Medical School, Boston, MA. 4. University of Melbourne, Parkville VIC, Australia: Institute for Breathing and Sleep, Heidelberg VIC, Australia. 5. School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia.
Abstract
STUDY OBJECTIVES: To determine the effects of mild airflow limitation on K-complex frequency and morphology and electroencephalogram (EEG) spectral power. METHODS: Transient reductions in continuous positive airway pressure (CPAP) during stable N2 sleep were performed to induce mild airflow limitation in 20 patients with obstructive sleep apnea (OSA) and 10 healthy controls aged 44 ± 13 y. EEG at C3 and airflow were measured in 1-min windows to quantify K-complex properties and EEG spectral power immediately before and during transient reductions in CPAP. The frequency and morphology (amplitude and latency of P200, N550 and N900 components) of K-complexes and EEG spectral power were compared between conditions. RESULTS: During mild airflow limitation (18% reduction in peak inspiratory airflow from baseline, 0.38 ± 0.11 versus 0.31 ± 0.1 L/sec) insufficient to cause American Academy of Sleep Medicine-defined cortical arousal, K-complex frequency (9.5 ± 4.5 versus 13.7 ± 6.4 per min, P < 0.01), N550 amplitude (25 ± 3 versus 27 ± 3 μV, P < 0.01) and EEG spectral power (delta: 147 ± 48 versus 230 ± 99 μV(2), P < 0.01 and theta bands: 31 ± 14 versus 34 ± 13 μV(2), P < 0.01) significantly increased whereas beta band power decreased (14 ± 5 versus 11 ± 4 μV(2), P < 0.01) compared to the preceding non flow-limited period on CPAP. K-complex frequency, morphology, and timing did not differ between patients and controls. CONCLUSION: Mild airflow limitation increases K-complex frequency, N550 amplitude, and spectral power of delta and theta bands. In addition to providing mechanistic insight into the role of mild airflow limitation on K-complex characteristics and EEG activity, these findings may have important implications for respiratory conditions in which airflow limitation during sleep is common (e.g., snoring and OSA).
STUDY OBJECTIVES: To determine the effects of mild airflow limitation on K-complex frequency and morphology and electroencephalogram (EEG) spectral power. METHODS: Transient reductions in continuous positive airway pressure (CPAP) during stable N2 sleep were performed to induce mild airflow limitation in 20 patients with obstructive sleep apnea (OSA) and 10 healthy controls aged 44 ± 13 y. EEG at C3 and airflow were measured in 1-min windows to quantify K-complex properties and EEG spectral power immediately before and during transient reductions in CPAP. The frequency and morphology (amplitude and latency of P200, N550 and N900 components) of K-complexes and EEG spectral power were compared between conditions. RESULTS: During mild airflow limitation (18% reduction in peak inspiratory airflow from baseline, 0.38 ± 0.11 versus 0.31 ± 0.1 L/sec) insufficient to cause American Academy of Sleep Medicine-defined cortical arousal, K-complex frequency (9.5 ± 4.5 versus 13.7 ± 6.4 per min, P < 0.01), N550 amplitude (25 ± 3 versus 27 ± 3 μV, P < 0.01) and EEG spectral power (delta: 147 ± 48 versus 230 ± 99 μV(2), P < 0.01 and theta bands: 31 ± 14 versus 34 ± 13 μV(2), P < 0.01) significantly increased whereas beta band power decreased (14 ± 5 versus 11 ± 4 μV(2), P < 0.01) compared to the preceding non flow-limited period on CPAP. K-complex frequency, morphology, and timing did not differ between patients and controls. CONCLUSION: Mild airflow limitation increases K-complex frequency, N550 amplitude, and spectral power of delta and theta bands. In addition to providing mechanistic insight into the role of mild airflow limitation on K-complex characteristics and EEG activity, these findings may have important implications for respiratory conditions in which airflow limitation during sleep is common (e.g., snoring and OSA).
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