Neurocognitive disturbance in obstructive sleep apnoea: mechanisms of harm

Research output: ThesisDoctoral Thesis

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[Truncated] The overarching aim addressed by this thesis was the investigation of the relationship between cognitive dysfunction and mechanisms of harm (sleep fragmentation and hypoxia) in Obstructive Sleep Apnoea (OSA). It begins with a general introduction to the nocturnal features and cognitive profile of OSA (Chapter 1), continues with three research studies (reported over Chapters 2, 4 and 5, Chapter 3 details methods and recruitment), and concludes with a general discussion (Chapter 6).
Study 1 (Chapter 2) considered the profile of executive dysfunction in individuals with OSA. OSA is a frequent and often under-diagnosed condition that is associated with upper airway collapse, oxygen desaturation, and sleep fragmentation leading to cognitive dysfunction. There is good meta-analytic evidence that sub-domains of attention and memory are affected by OSA. However, a thorough investigation of the impact of OSA on different sub-domains of executive function had yet to be conducted. Study 1 (Chapter 2) investigated the impact of untreated and treated OSA, in adult patients, on five, theorised, sub-domains of executive function. An extensive literature search was conducted of published and unpublished materials, returning 35 studies that matched selection criteria. Meta-analysis was used to synthesise the results from studies examining the impact of OSA on executive functioning compared to controls (21 studies) and before and after treatment (19 studies); 5 studies met inclusion in both categories. All domains of executive function (Shifting, Updating, Inhibition, Generativity and Fluid Reasoning) demonstrated medium to very large impairments in OSA independent of age, and disease severity. All domains improved (small to medium effects) with CPAP treatment, and this improvement was not moderated by age or disease severity. Further studies are needed to explore the extent of primary (neural damage in a region, with corresponding behavioural dysfunction, e.g., damage to areas responsible for memory, and demonstrated memory difficulties) or secondary nature (neural damage resulting in secondary dysfunction, e.g., damage in areas responsible for attention control, impacting on memory capacity) of these deficits, and the impact of age and pre-morbid ability (cognitive reserve).
Chapter 3 reports the recruitment procedures, participants and methods used in this thesis.
Original languageEnglish
QualificationDoctor of Philosophy
Publication statusUnpublished - Apr 2014


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