OBJECTIVE: The aim of the present study was to investigate cerebral hemodynamics in patients with sleep-disordered breathing of variable severity using cerebral near-infrared spectroscopy. DESIGN: Prospective study. SETTING: Tertiary training and research hospital. METHODS: The study was performed in patients referred for daytime sleepiness, habitual nocturnal snoring, and witnessed apnea spells from October 2009 to March 2010. Full-night polysomnography was coupled with cerebral near-infrared spectroscopy recording. MAIN OUTCOME MEASURES: Cerebral O2 and peripheral capillary O2 saturation indexes were measured before sleep and during different stages of sleep. RESULTS: Thirty-one patients who fulfilled the inclusion criteria were recruited for the study. During wakefulness, mean peripheral capillary O2 saturation was 96.39 ± 1.54% (range 93-99%), whereas mean cerebral O2 saturation was 69.19 ± 6.96% (range 55-86%). Mean peripheral capillary O2 saturation decreased to 80.42 ± 9.73% (range 51-94%), whereas cerebral O2 saturation decreased to 61.91 ± 7.23% (range 45-79%) during sleep. Peripheral and cerebral hemodynamic status during sleep differed significantly in patients with different disease severity. Indeed, peripheral and cerebral O2 saturation levels were lower in patients with severe obstructive sleep apnea compared to those with mild and moderate apneas (p = .001 and p = .002, respectively). CONCLUSION: Our data suggest that acute cerebral hemodynamic consequences of sleep-disordered breathing are determined by the duration and type of the respiratory event and that the combination of the two determinants can lead to a failure of cerebral circulatory mechanisms and, eventually, brain tissue hypoxia.
OBJECTIVE: The aim of the present study was to investigate cerebral hemodynamics in patients with sleep-disordered breathing of variable severity using cerebral near-infrared spectroscopy. DESIGN: Prospective study. SETTING: Tertiary training and research hospital. METHODS: The study was performed in patients referred for daytime sleepiness, habitual nocturnal snoring, and witnessed apnea spells from October 2009 to March 2010. Full-night polysomnography was coupled with cerebral near-infrared spectroscopy recording. MAIN OUTCOME MEASURES: Cerebral O2 and peripheral capillary O2 saturation indexes were measured before sleep and during different stages of sleep. RESULTS: Thirty-one patients who fulfilled the inclusion criteria were recruited for the study. During wakefulness, mean peripheral capillary O2 saturation was 96.39 ± 1.54% (range 93-99%), whereas mean cerebral O2 saturation was 69.19 ± 6.96% (range 55-86%). Mean peripheral capillary O2 saturation decreased to 80.42 ± 9.73% (range 51-94%), whereas cerebral O2 saturation decreased to 61.91 ± 7.23% (range 45-79%) during sleep. Peripheral and cerebral hemodynamic status during sleep differed significantly in patients with different disease severity. Indeed, peripheral and cerebral O2 saturation levels were lower in patients with severe obstructive sleep apnea compared to those with mild and moderate apneas (p = .001 and p = .002, respectively). CONCLUSION: Our data suggest that acute cerebral hemodynamic consequences of sleep-disordered breathing are determined by the duration and type of the respiratory event and that the combination of the two determinants can lead to a failure of cerebral circulatory mechanisms and, eventually, brain tissue hypoxia.