Prospective Students

Broad Research Area: Mechanisms and Consequences of Sleep Disordered Breathing

The Adelaide Institute for Sleep Health provides a clinical service for patients with sleep related problems, such as obstructive sleep apnoea (repeated obstructive breathing events in sleep in otherwise healthy people), insomnia and sleep hypoventilation in patients with known respiratory muscle weakness or lung disease. Breathing disturbance and sleep fragmentation have important daytime consequences including pathological daytime sleepiness, neurocognitive impairments and a substantially increased risk of traffic and other accidents. Sleep apnoea is also associated with cardiovascular disease (eg hypertension and heart disease).

Our group is one of the leading clinical research laboratories in Australia investigating cardiorespiratory sleep physiology, with a particular focus on mechanisms and consequences of sleep breathing disorders. In 2011 there are opportunities for up to 2 Honours projects in the research areas listed below.

Supervisors

Prof Doug McEvoy
T: 8275 1187 F: 8277 6890
E: doug.mcevoy@health.sa.gov.au

 

A/Prof Peter Catcheside
T: 8275 1309 F: 8277 6890
E: peter.catcheside@health.sa.gov.au

 

Institutions

Honours and PhD studies can be undertaken at AISH through the following institutions:

  • Adelaide University - Discipline of Physiology, School of Molecular and Biomedical Sciences
  • Flinders University - Sleep Research Laboratory / School of Psychology
  • UniSA - Centre for Sleep Research / School of Psychology / School of Health Sciences 

Scholarships & Employment:

A $3000 stipend is available from AISH. Many of our students also obtain employment in the Sleep Lab as clinical sleep technicians.
To apply: Contact one of the supervisors, and your institution's honours program coordinator for further details of how to apply.

Potential Honours Projects for 2011

  1. Patterns of morning salivary cortisol secretion in untreated versus treated obstructive sleep apnoea. Read More..
  2. Treatment effectiveness and compliance with a new supine-avoidance therapy for posture dependent obstructive sleep apnoea and snoring. Read more..
  3. The effect of mild carbon-dioxide inhalation on breathing and upper airway function in patients with obstructive sleep apnoea. Read more..
  4. Does the auditory-arousal system suppress snoring-induced arousal during inspiration? Read more..
  5. Sensory mechanisms involved in respiratory load perception. Read more..

1. Patterns of morning salivary cortisol secretion in untreated versus treated obstructive sleep apnoea

Obstructive sleep apnoea OSA is a common condition, affecting ~10% of adults, that causes frequent nighttime awakenings due to problems with breathing. OSA is strongly associated with obesity, which is a leading risk factor for cardiovascular and metabolic diseases in its own right. However, in addition to severely disrupted sleep and associated daytime problems, OSA patients are at greater risk of early death and disability from cardiovascular disease and type 2 diabetes than would be expected due to obesity alone. A key problem in OSA may be that repeated nighttime awakenings negatively impact "body clock" regulated patterns of release of powerful hormones that coordinate all body tissue function around the 24-hour circadian rhythm. Consequently, disorganised secretion of these hormones, especially cortisol (a major regulatory hormone in humans), is almost certainly involved in cardiovascular and metabolic problems in OSA. Although there is evidence to support this idea, few studies have combined sleep laboratory measurements with those of cortisol release due to the challenges and expense of overnight blood sampling in a sleep laboratory setting. However, salivary measures of cortisol have now been perfected within the psychobiology research community, and strong associations with a broad range of health outcomes have already been shown. However, these methods have yet to be adopted in sleep medicine, such that there is a major paucity of reliable data on salivary cortisol in OSA.

For 3 months in early 2011, Prof Angela Clow, a leading international expert on salivary measures of cortisol will be visiting Adelaide, creating a unique opportunity for a collaborative project combining normally disparate areas of expertise with strong reciprocal relevance.

The aims of this project is to determine if salivary cortisol secretion is aberrant in untreated versus treated OSA patients.

Relevant Publications

  1. Schmoller A, et al. Continuous positive airway pressure therapy decreases evening cortisol concentrations in patients with severe obstructive sleep apnea. Metabolism 2009;58:848-53.
  2. Vgontzas AN, et al. Hypothalamic-pituitary-adrenal axis activity in obese men with and without sleep apnea: effects of continuous positive airway pressure therapy. J Clin Endocrinol Metab 2007;92:4199-207.
  3. Clow A, et al. The cortisol awakening response: more than a measure of HPA axis axis function. Neuroscience and Biobehavioural Reviews 2010;(In Press).

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2. Treatment effectiveness and compliance with a new supine-avoidance therapy for posture dependent obstructive sleep apnoea and snoring

Around one third of OSA patients and many heavy snorers could be effectively treated by simply avoiding sleeping on their back. Classic supine-discomfort based treatments are remarkably effective, but most patients cease treatment within a few months due to the inherent discomfort of this approach. Our group has developed and tested a simple vibration alarm device to monitor and record sleep posture and discourage supine sleep, without discomfort and with minimal sleep disturbance to the bed partner. We have already shown the device accurately and reliably records body position, almost completely abolishes supine sleep and appears to be highly effective in treating supine OSA. However, long-term acceptance and use of this therapy and the effectiveness in snorers remains to be established. This project would investigate the effectiveness and longer-term patient usage of the supine-avoidance device for treating OSA and/or snoring.

Relevant Publications

1. Bignold JJ, Deans-Costi G, Goldsworthy MR, Robertson CA, McEvoy RD, Catcheside PG, Mercer JD. Poor long-term patient compliance with the tennis ball technique for treating positional obstructive sleep apnea. J Clin Sleep Med 2009;5(5):428-30.

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3. The effect of mild carbon-dioxide inhalation on breathing and upper airway function in patients with obstructive sleep apnoea

Reduced ventilatory drive and upper airway muscle activity is a major factor contributing to frequent complete (obstructive apnoea) and partial upper airway collapse (snoring) during sleep. Most airway obstruction events in sleep begin with "passive" partial or complete airway collapse late in expiration. Even the most severely affected patients maintain an open airway during wakefulness, but then frequently develop airway obstruction within the first 5-10 seconds after sleep onset when upper airway and other muscle activity is abruptly diminished. Most obstructive sleep apnoea (OSA) patients show markedly improved OSA in deep sleep, indicating that respiratory control and arousal factors can generally overcome any underlying anatomical problem to stabilize upper airway function and breathing in deep sleep. We believe that mild CO2 accumulation naturally develops during deepening sleep and can sufficiently stimulate breathing and upper airway muscle activity to achieve improved upper airway function and more stable breathing in sleep. The aim of this study is to investigate the effects of mild CO2 stimulation on breathing and upper airway function during sleep in OSA patients.

Relevant Publications

  1. Ratnavadivel R, Chau N, Stadler D, Yeo A, McEvoy RD, Catcheside PG. Marked reduction in obstructive sleep apnea severity in slow wave sleep. J Clin Sleep Med 2009;5(6):519-24.
  2. Stadler D, McEvoy RD, Bradley J, Paul D, Catcheside PG. Changes in lung volume and diaphragm muscle activity at sleep onset in obese obstructive sleep apnea patients versus healthy-weight controls. J. Appl. Physiol. (In press 2010).
  3. Ratnavadivel R, Stadler D, Windler S, Bradley J, Paul D, McEvoy RD, Catcheside PG. Upper airway function and arousability to ventilatory challenge in slow wave versus stage 2 sleep in obstructive sleep apnoea. Thorax 65(2): 107-112, 2010.

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4. Does the auditory-arousal system suppress snoring-induced arousal during inspiration?

Snoring is a very common problem in sleep and is one of the primary complaints leading to patients (or their partners) seeking treatment. There is also some evidence that transmission of snoring related vibration and sheer stress to the carotid arteries could contribute to carotid arterial plaque formation and rupture; a mechanism that could potential help explain increased adverse cardiovascular event risk in snorers and patients with obstructive sleep apnoea. While complaints around snoring are frequent and significant, existing treatments are limited and often unsatisfactory. These generally focus on strategies to open and stiffen upper airway structures that vibrate in snoring (e.g. constant positive airway pressure, mandibular advancement splits and surgery). Another useful strategy is to discourage supine sleep, since upper airway function is generally most compromised in the supine compared to lateral and prone postures. Some posture avoidance therapies, and potentially snoring alarm-based treatments, inherently rely on an alarm (e.g. auditory and/or vibration) to sufficiently alert the patient to change to a more favourable posture. However, snorers appear to be surprisingly resistant to being woken by their own snoring, a phenomenon likely influenced by sleep depth and habituation, and potentially respiratory modulation of arousal mechanisms. This project would investigate if sensory process underpinning auditory and/or non-auditory arousal are "gated" during inspiration.

Relevant Publications

  1. Kato T, Montplaisir1 JY, Lavigne GJ. Experimentally induced arousals during sleep: a cross-modality matching paradigm. J. Sleep Res. 2004; 13, 229-238
  2. Herzog M, Schieb E, Bremert T, Herzog B, Hosemann W, Kaftan H, Kühnel T. Frequency analysis of snoring sounds during simulated and nocturnal snoring. Eur Arch Otorhinolaryngol. 2008; 265(12):1553-62.
  3. McDonald, D. G. and Carpenter, F. A. Habituation of the orienting response in sleep. Psychophysiology, 1975, 12: 618-623.

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5. Sensory mechanisms involved in respiratory load perception

Humans can detect the presence of impediments to breathing with considerable acuity, and sensations arising from the airways, lungs and/or chest wall are an important component of several key protective reflex and behavioural responses while awake and asleep (e.g. cough, seeking asthma treatment, ventilatory compensation to increased breathing load and arousal from sleep). Our group has shown that hypoxia, which frequently accompanies compromised breathing awake and asleep (e.g. acute asthma, chronic lung disease, sleep hypoventilation and sleep apnoea) appears to suppress awake load sensations and the cough reflex and delay arousal in sleep. However, key questions remain concerning the main mechanisms through which respiratory signals (changes pressure vs flow) contribute to respiratory load perception awake and arousal responses to respiratory load during sleep. This project would explore relationships between the timing (first detection) and perceived magnitude of different types of respiratory load delivered during wakefulness compared to the stimulus timing and magnitude of disturbances in pressure and flow induced by each load.

Relevant Publications

  1. Hlavac MC, Catcheside PG, McDonald R, Eckert DJ, Windler S, McEvoy RD. Hypoxia impairs the arousal response to external resistive loading and airway occlusion during sleep. Sleep 29(5): 624-631, 2006.
  2. Eckert DJ, Catcheside PG, McDonald R, Adams AM, Webster KE, Hlavac MC, McEvoy RD. Sustained hypoxia depresses sensory processing of respiratory resistive loads. Am J Respir Crit Care Med. 172(8):1047-54, 2005. 
  3. Eckert DJ, Catcheside PG, Smith JH, Frith PA, McEvoy RD. Hypoxia suppresses symptom perception in asthma. Am. J. Resp. Crit. Care Med. 169(11): 1224-1230, 2004. 
  4. Eckert D.J., Catcheside P.G., Stadler D.L., McDonald R., Hlavac M.C., McEvoy R.D. Acute sustained hypoxia suppresses the cough reflex in healthy subjects. Am J Respir Crit Care Med 2006; 173(5):506-11.
  5. Orr RS, Jordan AS, Catcheside P, Saunders NA, McEvoy RD. Sustained isocapnic hypoxia suppresses the perception of the magnitude of inspiratory resistive loads. J Appl Physiol 2000; 89: 47-55.

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