Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 41, Issue 10, Pages 2712-2724Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X211012109
Keywords
Obstructive sleep apnea; cerebral hypoperfusion; intermittent hypoxemia; sleep fragmentation; cognition
Categories
Funding
- National Institutes of Health [P41EB015922, U54EB020406, U19AG024904, U01NS086090]
- BrightFocus Research Grant award [A2019052S]
- Samsung Biomedical Research Institute [OTC1190671]
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Altered cerebral perfusion patterns were observed in OSA patients compared to healthy reference subjects. This impaired perfusion, mainly affecting the parietal and prefrontal cortices, may contribute to neurocognitive deficits in OSA. Correlation analysis showed distinctive associations between regional hypoperfusion and parameters of intermittent hypoxia and sleep fragmentation, suggesting a potential pathomechanism for neurocognitive deficits in OSA.
Altered cerebral perfusion has been reported in obstructive sleep apnea (OSA). Using dynamic susceptibility contrast MRI, we compared cerebral perfusion between male OSA patients and male healthy reference subjects and assessed correlations of perfusion abnormalities of OSA patients with sleep parameters and neuropsychological deficits at 3 T MRI, polysomnography and neuropsychological tests in 68 patients with OSA and 21 reference subjects. We found lower global and regional cerebral blood flow and cerebral blood volume, localized mainly in bilateral parietal and prefrontal cortices, as well as multiple focal cortical and deep structures related to the default mode network and attention network. In the correlation analysis between regional hypoperfusion and parameters of polysomnography, different patterns of regional hypoperfusion were distinctively associated with parameters of intermittent hypoxia and sleep fragmentation, which involved mainly parietal and orbitofrontal cortices, respectively. There was no association between brain perfusion and cognition in OSA patients in areas where significant association was observed in reference subjects, largely overlapping with nodes of the default mode network and attention network. Our results suggest that impaired cerebral perfusion in important areas of functional networks could be an important pathomechanism of neurocognitive deficits in OSA.
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