0739 Cerebrovascular Response to Intermittent Hypoxia During Sleep in OSA Patients

Abstract

Abstract Introduction Obstructive sleep apnea (OSA) is associated with increased risks of cerebrovascular accidents, but it remains unclear how OSA impacts the cerebral vasculature. Intermittent hypoxia is a hallmark feature of OSA and recurs throughout sleep. In awake humans, the cerebrovascular response to intermittent hypoxia has been well characterized, as an increase of blood perfusion that begins at least a few seconds after the start of hypoxia. Functional magnetic resonance imaging (fMRI) that measures the blood oxygen level dependent (BOLD) signal has revealed significant differences between the cerebrovascular responses in awake humans with and without OSA. However, intermittent hypoxia occurs primarily during sleep in OSA, yet the cerebrovascular response to intermittent hypoxia has not been studied during sleep. Methods Eight adult patients with severe OSA were recruited to this study. Each subject first underwent an acclimatization session in which they tried to sleep in the MRI scanner while listening to sound recordings of the fMRI. Each acclimatized subject then underwent an overnight study in which T2*-weighed BOLD fMRI of the whole brain was conducted for 1.5-3 hours in total (TE: 35 ms, TR: 2.0 s, 35 sagittal slices, 3.5 mm isotropic). Oxygen saturation (SaO2), chest movement, end-tidal carbon dioxide and scalp encephalography (EEG) were simultaneously recorded with the fMRI. After rigid-body motion correction and removal of artifacts, the temporal correlation between BOLD signal and the SaO2 signal was analyzed on a voxel-by-voxel basis. Results Four subjects (50%) were acclimatized to sleep in the MRI scanner and completed this study. In all subjects, the BOLD fMRI signal showed an initial decrease corresponding to the decrease of SaO2, followed by a delayed increase corresponding to the hyperperfusion, throughout the gray matter of cerebral cortex. The time course of BOLD fMRI signal was significantly advanced in time, by 2-4 seconds, in the visual cortex compared to the rest of cerebral cortex in all subjects. This phenomenon was also observed in some other brain regions, but not consistently across subjects. Conclusion This study is, to our knowledge, the first study of the cerebrovascular response to intermittent hypoxia during sleep in humans. In patients with OSA, we observed spatiotemporal heterogeneity of the cerebrovascular response, such that the response in the visual cortex was significantly advanced in time than other brain regions. This phenomenon has not been reported before, and future studies are needed to understand how this heterogeneity is associated with OSA. Support (If Any) AASM Foundation