Central sympathetic nervous system reinforcement in obstructive sleep apnoea. (June 2018)

• Record Type: Journal Article
• Authors: Wszedybyl-Winklewska, Magdalena; Wolf, Jacek; Szarmach, Arkadiusz; Winklewski, Pawel J.; Szurowska, Edyta; Narkiewicz, Krzysztof
• Is Part Of: Sleep medicine reviews. Volume 39(2018)
• Page Start: 143
• Page End: 154
• Publication Date: 2018-06
• Subjects: Obstructive sleep apnoea -- Cerebral perfusion -- Functional neuroanatomy -- Central nervous system -- Autonomic regulation; Sleep disorders -- Periodicals; Sleep Disorders -- Periodicals; Sommeil, Troubles du -- Périodiques; Electronic journals; 616.8498
• DOI: 10.1016/j.smrv.2017.08.006
• Languages: English
• ISSNs: 1087-0792

Abstract

Summary: The available studies on cerebrovascular reactivity and cerebral oxygenation in obstructive sleep apnoea (OSA) patients brought conflicting results, yet the overall evidence suggests that resting state cerebral perfusion is diminished in these patients. Interestingly, in a group of healthy professional breath-hold divers who are exercising very long apnoeas – episodes corresponding to the ones observed in patients with OSA – demonstrated that cerebral oxygenation may remain stable at the expense of extreme sympathetic nervous system (SNS) activation. In the present review we address several mechanisms that could potentially explain these discrepancies. We focus in depth on mechanisms of central SNS reinforcement in OSA including dysfunctional baroreflex response, and inflammatory processes within the brain centres controlling the cardiovascular system. Additionally, novel insights into physiology of cerebral blood flow regulation are proposed, including the role of short-term blood pressure changes, heart rate fluctuations and baroreflex alterations. Finally, a potential role of increased blood flow pulsatility in cerebrospinal fluid circulation changes and its influence on SNS drive is highlighted. The presented review provides insights into how sympathetic nervous system reinforcement in OSA promotes maladaptive mechanisms that could alter cerebral perfusion regulation, and result in functional and structural cerebral changes.