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More is becoming known about the importance of sleep to health, with inadequate sleep recognised as a significant public health issue. Sleep clinics have reported disproportionate numbers of Māori and Pacific peoples with more severe obstructive sleep apnoea syndrome (OSAS), raising concerns about accessibility of services and possible differences in prevalence between ethnic groups. Prevalence information on sleep disorders in Aotearoa is needed to assess its public health impact and plan for population health care needs. This thesis presents a national study examining the prevalence of OSAS symptoms and risk factors among Maori and non-Maori adults in Aotearoa. This project is also situated within the wider scope of ethnic inequalities in health between Maori and non-Maori and is concerned with making a positive contribution to Maori health and the elimination of disparities. Kaupapa Maori Research (KMR) is the underlying methodology that drives this study. As such, it assumes a Maori norm, and prioritises Maori needs. A Maori/non-Maori analytical framework is used that distinguishes Maori as tangata whenua, addresses Maori health needs as well as non-Maori, and enables the monitoring of guarantees as outlined by the Treaty of Waitangi. The goals of this thesis were to estimate the prevalence of OSAS symptoms and risk factors among Maori and non-Maori adults in New Zealand, and to examine independent predictive variables for specific OSAS symptoms. An objective was also to contribute to KMR through designing and undertaking a KMR project using a quantitative method, with the development of concepts for use in other areas of research. In April 1999, a short questionnaire was sent to a sample of 10000 New Zealands (5500 of Maori descent and 4500 non-Maori participants to enable research questions to be examined with equal statistical power for both groups. The results demonstrate that the prevalence of OSAS symptoms and risk factors, particularly among non-Maori, are comparable to other international studies, indicating that OSAS is likely to be a common problem among adults in Aotearoa. Furthermore, the results suggest that Maori are significantly more likely to suffer from OSAS than non-Maori, with higher rates of symptoms and risk factors of OSAS among both men and women. As an area of medicine that is under-serviced in Aotearoa, the results provide important information with which to plan for population needs. There are a number of health implications from this study, relating specifically to the diagnosis and management of OSAS in Aotearoa, and to Maori health and the elimination of disparities. These are multi-levelled and include health service implications across the continuum of care, from specialist sleep services to primary care; public health implications that involve preventive measures and broader determinants of health; and KMR principles that can be applied to interventions and health research in general. As a KMR project the implications and recommendations focus on Maori health research in general. As a KMR project the implications and recommendations focus on Maori health gain and addressing disparities in health. This is consistent with Maori health rights, and a population approach that considers health inequalities and the role of wider determinants of health and health services.

Obstructive sleep apnoea (OSA) is a common respiratory disorder characterised by repetitive periods of upper airway (UA) collapse during sleep. OSA is more common in males and the obese but the reasons why remain poorly understood. Abdominal obesity, particularly common in males, is likely to indirectly modulate the amount of tension (tracheal traction) exerted on the UA by the trachea and other intrathoracic structures, potentially leading to increased UA collapsibility. Other factors such as lung volume changes with obesity, altered drive to UA muscles and exaggerated arousal responses are also likely to contribute to UA instability. An investigation of these potential contributing factors forms the basis of this thesis. In the first study, the effect of external abdominal compression on UA collapsibility during sleep was investigated in a group of obese male OSA patients. A large pneumatic cuff wrapped around the abdomen was inflated to increase intra-abdominal pressure, aiming to produce an upward force on the diaphragm, designed to reduce axial tension on the UA. Abdominal compression increased end-expiratory gastric (PGA) and end-expiratory transdiaphragmatic (PDI) pressure by ~50% and produced a significant rise in UA collapsibility compared to the cuff deflated condition. These data support that increased intra-abdominal pressure has a negative effect on UA function during sleep. This effect may help explain why obesity is the leading risk factor for OSA and why OSA affects men more than women, given that abdominal obesity is particularly common in obese males. In the second study, differences in minimum expiratory (tonic) diaphragm activity during wakefulness were compared between 8 obese OSA patients and 8 healthyweight controls. Changes in tonic diaphragm activity and lung volume following sleep onset were also compared between the two groups. There was no evidence of increased tonic diaphragmatic activity during wakefulness in obese OSA patients to support significant diaphragmatic compensation for abdominal compressive effects of obesity. There were small decrements in lung volume following sleep onset in both groups (<70 ml), with significantly greater lung volume and diaphragmatic EMG decrements when sleep onsets were immediately followed by respiratory events. While lung volume decrements at sleep onset were relatively small, this does not discount that UA function is not more sensitive to effects of reduced lung volume in obese OSA patients. To more closely investigate the potential interactive effects of obesity on physiological variables likely influencing UA function, the third study investigated the temporal relationships between a comprehensive range of relevant physiological variables leading into and following the termination of obstructive apnoeas during sleep in 6 obese OSA patients. Prior to UA obstruction, diaphragm and genioglossus muscle activity decreased, while UA resistance increased. Lung volume and end-expiratory PGA and end-expiratory PDI also fell during this period, consistent with diaphragm ascent. There was a substantial increase in ventilation, muscle activity and lung volume immediately following the termination of obstructive events. Respiratory events and arousals occurred in close temporal proximity prior to and following obstructive apnoeas, supporting that cyclical respiratory events and arousals may both help to perpetuate further events. The results from this study support that there is a ‘global’ loss in respiratory drive to UA dilator and pump muscles precipitating obstructive respiratory events. The associated decreases in UA dilator muscle activity and lung volume may therefore both contribute to the propensity for the UA to obstruct. In summary, increased intra-abdominal pressure was shown to negatively impact UA airway collapsibility during sleep. A decrease in lung volume at sleep onset and prior to UA obstruction further support that lung volume decrement, coincident with a decline in overall respiratory drive, potentially contributes to the propensity for airway obstruction. Further studies are needed to elucidate the relative contribution of relatively small changes in lung volume versus changes in respiratory and UA muscle activity per se on UA patency in OSA patients. / Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2010

Obstructive Sleep Apnoea (OSA) is a disease characterised by repetitive upper airway obstructions which are manifest by desaturation and arousal from sleep. It has been known for many years that this interruption to the normal architecture of sleep may present to the clinician as excessive daytime somnolence often with a complaint of difficulties with concentration and short term memory. Previous work had demonstrated a relationship between variables of cognitive dysfunction in patients with obstructive sleep apnoea, however, little was known about which components of the syndrome contributed to this outcome and whether specific clinical thresholds of sleep disordered breathing could be defined for the development of cognitive dysfunction. In the context of this body of work cognitive dysfunction is defined as: a level of cognitive performance below normal derived values for a given cognitive test, when the subjects performance is controlled for age, sex and level of education.

Obstructive Sleep Apnoea (OSA) is a disease characterised by repetitive upper airway obstructions which are manifest by desaturation and arousal from sleep. It has been known for many years that this interruption to the normal architecture of sleep may present to the clinician as excessive daytime somnolence often with a complaint of difficulties with concentration and short term memory. Previous work had demonstrated a relationship between variables of cognitive dysfunction in patients with obstructive sleep apnoea, however, little was known about which components of the syndrome contributed to this outcome and whether specific clinical thresholds of sleep disordered breathing could be defined for the development of cognitive dysfunction. In the context of this body of work cognitive dysfunction is defined as: a level of cognitive performance below normal derived values for a given cognitive test, when the subjects performance is controlled for age, sex and level of education.

Obstructive sleep apnoea (OSA) is characterised by repetitive reductions or pauses in breathing during sleep due to upper airway narrowing or closure. Due to disruption to normal sleep patterns, many patients with OSA suffer from increased daytime sleepiness. Epidemiological studies have established a link between OSA and driver fatigue and accidents, generally showing a two to seven times increased risk of road traffic accidents in non-commercial drivers with OSA. There is emerging evidence that commercial drivers have a higher prevalence of OSA than the general population, being predominately male, middle-aged and overweight, three important risk factors for OSA. However, little is known about the relationship between OSA and driver sleepiness in commercial drivers, whether road accidents are increased in commercial drivers with OSA, and whether OSA interacts with other fatigue promoting factors, such as sleep deprivation, to further escalate road accident risk. One thousand randomly selected commercial drivers were surveyed in the field. In addition, 61 randomly selected NSW commercial drivers had in hospital sleep studies and daytime performance testing, including a PC based driving simulator task. The prevalence of OSA, defined as Respiratory Disturbance Index (RDI) < 10, was approximately 50% in NSW commercial drivers. Approximately one quarter of the drivers reported pathological daytime sleepiness, and 12-14% had both OSA and pathological daytime sleepiness. A diagnosis of OSA was the most important factor predicting excessive daytime sleepiness in these drivers: OSA was more important than 15 other work-related, lifestyle and medical factors that could be expected to promote, or be associated with, daytime sleepiness. Drivers with sleep apnoea syndrome (both OSA and pathological daytime sleepiness) had an increased driving accident risk, using driving simulator and daytime performance testing as proxy measures for accident risk. These results demonstrate the importance of OSA as a cause of driver fatigue in commercial drivers and suggest that all commercial drivers should be screened for the presence of sleep apnoea syndrome in order to potentially reduce road accident risk through treatment. A separate, but related body of work examined the combined effects of mild OSA and other fatigue promoting factors (sleep deprivation and circadian influences) on driving performance. Twenty nine subjects, consisting of a group with mild OSA and a group of non-OSA controls, were tested on several occasions throughout the night and day using an intensive performance battery, under both baseline conditions and after a period of 36 hours of total sleep deprivation. The results suggest that drivers with mild OSA are not different to the control group in their response to sleep deprivation or time of day influences. However, the subjects with mild OSA were less aware of their impairment due to sleep deprivation, which is of concern if drivers with OSA are relying on their subjective awareness of fatigue to make decisions about when to stop driving. A final perspective on OSA and driver fatigue is provided through a clinical case series of seven fall-asleep fatality associated MVA�s associated with unrecognised or under-treated sleep disorders. As well as demonstrating the day to day potential for devastating road accidents due, at least in part, to un-recognised or untreated sleep disorders, these cases also serve to highlight some of the current medico-legal controversies and difficulties in this area of driver fatigue. In conclusion, this body of work has provided novel information about the epidemiology and implications of OSA in commercial drivers, and about how OSA interacts with other fatigue promoting factors. Finally, it has explored some of the medico-legal issues that relate to sleep disorders and driver fatigue. As well as providing much needed information in the area of driver fatigue, at the same time this work raises many more questions and suggests areas of future research. For instance, such research should examine the relationship between objective accident rates and OSA/sleep apnoea syndrome in commercial drivers, the interaction between mild sleep apnoea syndrome and other fatigue risk factors, and driver perception of sleepiness prior to sleep onset in drivers with sleep disorders.

Clinical professionals in South Africa are generally unaware of the impact of obstructive sleep apnoea (OS A). The cost to the state of untreated apnoea may be extremely high. In primary health care encounters OSA often goes undiagnosed. The cascade of symptoms linked to OSA is profound, placing patients at risk for debilitating problems impacting on self and others. The aim of this study was to validate a questionnaire, which could be used at a primary health care level to identify patients with OSA thus cutting costs and improving efficient, effective and ethical service to patients. The Berlin Questionnaire (BQ) (Netzer et al. 1999) was administered to a clinical sample of consenting patients at a private sleep laboratory in Durban, South Africa (N = 119)(completed n = 110). Home-based sleep studies (n = 116) on a portable cardio-respiratory screening device were also obtained for objective comparison. From the results obtained in this South African sample, the BQ showed low validity and reliability (Cronbach a = 0.62 - 0.84) to individual items of the BQ. The total BQ score and high-risk symptom category analysis showed mildly significant correlations with internationally approved protocols. The BQ identified 60% of the high-risk group (AHI >5). Furthermore, risk categories were useful in predicting AHI ratings in 64% of moderate OSA cases and 25% of severe OSA cases. The BQ therefore has useful psychometric properties as an adjunct assessment tool to screen for high-risk OSA cases where resources are scant. Clinical health psychologists are in an ideal position to recognise the risk factors and symptoms of OSA. The clinical assessment and the value of the correct diagnosis will alleviate the treatment of psychological symptoms at a superficial level in primary health care facilities. / Thesis (M.Soc.Sc.)-University of KwaZulu-Natal, Pietermaritzburg, 2006.