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Published on: December 6, 2016
Impaired cerebrovascular reactivity in obstructive sleep apnea: a case-control study
Laura B Ponsaing1, Ulrich Lindberg2, Egill Rostrup3
1Danish Center for Sleep Medicine, Department of Clinical Neurophysiology, Rigshospitalet, Glostrup, Denmark; Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark.
Obstructive sleep apnea (OSA) impairs the brain's blood flow response to carbon dioxide (CO2), especially with increased severity. This finding may explain the higher stroke risk in OSA patients.
Area of Science:
- Neurology
- Cardiovascular Science
- Sleep Medicine
Background:
- Obstructive sleep apnea (OSA) is a known stroke risk factor.
- Cerebrovascular hemodynamic changes during apnea are not well understood.
- Hypercapnia during apnea may compromise cerebral blood flow (CBF) due to reduced CO2 vasodilatory response.
Purpose of the Study:
- To investigate the effect of the apnea-hypopnea index (AHI) on cerebrovascular response to CO2.
- To evaluate if OSA severity influences the brain's ability to regulate blood flow during changes in CO2 levels.
Main Methods:
- Compared 11 OSA patients with 16 healthy controls.
- Utilized arterial spin labeling (ASL) and BOLD MRI to assess cerebrovascular responses.
- Included hypercapnia and breath-holding tasks to measure CO2 reactivity.
Main Results:
- CBF response to CO2 was significantly impaired with increasing AHI, indicating reduced reactivity in more severe OSA.
- OSA patients showed a significantly reduced CO2 response in white matter CBF compared to controls.
- No significant differences were found in BOLD response to CO2 or breath-holding tasks between groups.
Conclusions:
- Cerebrovascular CO2 reactivity, measured by CBF, is impaired with increasing OSA severity.
- These findings contribute to understanding the link between OSA and increased stroke risk.
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