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Thesis

English

ID: <

10670/1.bcjjn2

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Sleep apnoea and the brain : a bidirectional relationship

Abstract

The human brain is a perfect example of our dependence on oxygen. Brain physiological constraints render it vulnerable to hypoxia, such as encountered in environmental conditions (high altitude exposure) or pathological hypoxemic conditions. Among those pathological conditions, and due to its high prevalence in general population and the various levels of hypoxia resulting of the different degrees of severity of the pathology, obstructive sleep apnoea syndrome (OSAS) is a pathophysiological model of choice to investigate the detrimental effects of hypoxia on the brain. The cyclical, repeated episodes of apnoea and hypopnea during sleep that characterize OSAS result in intermittent hypoxia, sleep fragmentation and fluctuations in intrathoracic pressure, which are stressors that triggers mechanisms contributing to the initiation and progression of life-threatening cardiometabolic diseases, as well as several brain repercussions, such as cognitive impairment and stroke. This Thesis work explores the bidirectional relationship between sleep apnoea syndromes (SAS) and the brain. The first axis is focused on the neurocognitive consequences of OSAS through the lens of gait control. The neurocognitive signature of OSAS has been thoroughly investigated but recently, gait impairments have been highlighted in severe OSAS, with dose-response relationship between OSAS severity and the magnitude of gait impairments. As gait control relies at least partly on frontal lobe functions, it has been suggested that gait could represent a marker of OSAS brain repercussions. We investigated the effects of continuous positive airway pressure (CPAP) treatment on gait control, with contrasting results. In a first prospective controlled study, eight weeks of CPAP improved gait control in severe OSAS patients (Baillieul et al., 2018, Plos One). In order to validate those results and investigate the neurophysiological correlates of the link between gait control and OSAS, we conducted a randomized controlled trial which investigated the impact of an 8-week CPAP treatment compared to sham-CPAP on gait control in severe OSAS patients (Baillieul et al., 2020, Submitted). Contrary to our hypothesis, we found no improvement in gait control in the CPAP group and this result is substantiated by the absence of impact of CPAP on the determinants of gait control, further illustrating the complexity of the OSAS-neurocognitive relationship. The second axis is focused on the cerebrovascular repercussions of SAS. SAS and stroke are both severe intertwined conditions, SAS being both cause and potentially consequence of stroke. The present work is focused on the identification of phenotypic traits of SAS in post-stroke patients, to improve diagnosis of SAS following stroke (Baillieul et al., in preparation). Screening stroke patients for SAS is crucial due to the high risk of morbimortality and functional consequences associated to SAS following stroke but cannot be achieved without a more accurate identification of patients at risk to develop SAS following stroke. The third axis has been conceived as a perspective that will serve the development of the second axis. In this last axis, the potential of brain imagery and in particular magnetic resonance imagery to develop markers of stroke recovery as well as investigate the pathophysiological mechanisms underlying stroke-related deficiencies are presented, with a specific focus on gait and walking activity. The neural correlates of walking activity following stroke are highlighted, using a voxel-based lesion-symptom mapping approach (Baillieul et al., 2019, Hum. Mov. Sci.). Imagery markers of walking recovery following stroke using diffusion tensor imaging are also presented (Soulard et al. 2019, Neurology). This work on brain imagery markers of stroke recovery will further serve the development of investigations focused on the neural correlates of SAS following stroke.

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