Principal Research Scientist, NeuRA
Associate Professor, UNSW
R.D. Wright Fellow, NHMRC
+612 9399 1814
Associate Professor Danny Eckert has been actively involved in human sleep and respiratory physiology research since 2001. In 2006, he completed his PhD at the University of Adelaide, based at the Adelaide Institute for Sleep Health. He was awarded the Thoracic Society of Australia and New Zealand Allen and Hanburys Respiratory Research Fellowship, followed by an NHMRC CJ Martin Fellowship to pursue postdoctoral studies.
After three years of postdoctoral training at the Brigham and Women’s Hospital, Harvard Medical School, he was promoted to Faculty as Assistant Professor. In late 2011 Assoc Prof Eckert returned to Australia to establish a comprehensive sleep and respiratory physiology research program at NeuRA. His dedicated team continues to advance knowledge into the causes of sleep apnoea and develop new treatments. He currently serves on the board of the Australasian Sleep Association, the peak profession boady and is Chair of the Research Committee.
Breathing is a complex motor task that needs to be coordinated at all times while we eat, speak, exercise and even during sleep. The breathing muscles are controlled automatically from the brainstem during normal breathing but can also be controlled voluntarily from the motor cortex. The way these two drives to the breathing muscles interact is still not well understood. While there is some evidence that there are at least two independent pathways, and that integration of the pathways occurs at the spinal cord, there is some uncertainty about whether these pathways may have some interaction in the brainstem. Our current experiments are looking at voluntary and involuntary drive to the breathing muscles to try to answer this fundamental question about the neural control of breathing. In addition we are looking at the potential cortical contributions to retsing breathing in respiratory disorders.
Obstructive sleep apnoea is a sleep disorder that affects more than 4% of the population and can lead to symptoms from daytime drowsiness to high blood pressure. People with sleep apnoea are often not breathing normally during sleep and may experience periods where the airway closes and they are unable to breathe. In severe sleep apnoea this can occur 50-60 times each hour. That is once each minute. The closure of the upper airway is thought to be due to a number of factors, one of which is that the neural drive to the airway muscles is insufficient in people with sleep apnoea. In our lab, we have made the first extensive recordings from the major muscle of the upper airway, genioglossus. We have shown that the neural drive to this muscle is very complex, more so than any limb muscle. At NeuRA, we have also pioneered new methods to image this muscle using fMRI and ultrasound. We are now planning to look at how changes in muscle architecture and mechanics relate to the neural drive to the muscle and whether that relationship is maintained in people with sleep apnoea.
After cervical spinal cord injury (SCI), the respiratory muscles are partly or completely paralysed. This has two major clinical consequences: a decreased ability to get air into the lungs and a decreased ability to cough and remove secretions. This results in a lifetime of recurrent respiratory tract infections (2/year/person) that often progress to pneumonia with frequent and extended hospital admissions. People with cervical SCI are 150 times more likely to die from respiratory complications than the general population, as many as 28% die within the first year after injury. For those that survive the first year, a cervical SCI has a lifetime cost of $9.5million, a large proportion of which is attributed to respiratory-related complications. A recent longitudinal study of people with cervical SCI showed that respiratory muscle weakness is associated with incidental pneumonia. Respiratory muscle weakness also causes dyspnoea (breathlessness) and sleep-disordered breathing, which is 4-10 times more prevalent in people with SCI than the able-bodied population. Therefore, there is an urgent need to identify a simple and cost-effective treatment for respiratory muscles weakness to prevent respiratory complications after SCI, improve quality of life and reduce the burden on the healthcare system.
Our primary aim is to determine definitively the effectiveness of training on respiratory muscle strength, respiratory physiology and health outcomes. To do this we will conduct a randomised controlled trial 2 times bigger than the largest previous study, of respiratory muscle resistive load training in individuals with acute and chronic cervical SCI. The project will provide critical new knowledge about the efficacy of a simple and inexpensive respiratory muscle training regime, which can be applied immediately in the hospital and community, to minimise respiratory morbidity in people with SCI. This project also provides a unique opportunity to investigate other consequential effects of long-term respiratory muscle training that have never been studied in people with SCI. These include effects on cough efficacy, sleep-disordered breathing, breathlessness, respiratory morbidity, respiratory health and neural drive to the diaphragm, as well as quality of life.
We have developed novel imaging methods to measure the stiffness and movement of the upper airway muscles, and are using these together with measures of pharyngeal sensation, and electromyography to determine the patient-specific causes of obstructive sleep apnoea. We aim to use this information to tailor treatments for patients. One such treatment is a mandibular advancement splint, but currently it’s not possible to predict who will benefit from use a splint. We have a major project that aims to predict splint treatment outcome, based on our novel imaging methods.• Honours and PhD projects are available to study the neural, biomechanical and physiological aspects of obstructive sleep apnoea, including computational modelling
RICHARD LIM Honours student
AHMAD BAMAGOOS PhD student
PETER BURKE Postdoctoral Fellow
CHINH NGUYEN NeuroSleep NHMRC CRE Postdoctoral Fellow
SOPHIE CARTER PhD student
AMAL OSMAN PhD student
DR JASON AMATOURY NeuroSleep NHMRC CRE Postdoctoral Fellow
RODRIGO TOMAZINI MARTINS PhD student
BEN TONG Sleep Lab Manager
DR NIRU WIJESURIYA Postdoctoral Fellow
DR JAYNE CARBERRY NeuroSleep NHMRC CRE Postdoctoral Fellow
Numerous studies have demonstrated upper-airway neuromuscular abnormalities during wakefulness in snorers and obstructive sleep apnea (OSA) patients. However, the functional role of sensorimotor impairment in OSA pathogenesis/disease progression and its potential effects on protective upper-airway reflexes, measures of respiratory sensory processing, and force characteristics remain unclear. This study aimed to gain physiological insight into the potential role of sensorimotor impairment in OSA pathogenesis/disease progression by comparing sensory processing properties (respiratory-related evoked potentials; RREP), functionally important protective reflexes (genioglossus and tensor palatini) across a range of negative pressures (brief pulses and entrained iron lung ventilation), and tongue force and time to task failure characteristics between 12 untreated OSA patients and 13 controls. We hypothesized that abnormalities in these measures would be present in OSA patients. Upper-airway reflexes (e.g., genioglossus onset latency, 20 ± 1 vs. 19 ± 2 ms, P = 0.82), early RREP components (e.g., P1 latency 25 ± 2 vs. 25 ± 1 ms, P = 0.78), and the slope of epiglottic pressure vs. genioglossus activity during iron lung ventilation (-0.68 ± 1.0 vs. -0.80 ± 2.0 cmH(2)O/%max, P = 0.59) were not different between patients and controls. Maximal tongue protrusion force was greater in OSA patients vs. controls (35 ± 2 vs. 27 ± 2 N, P < 0.01), but task failure occurred more rapidly (149 ± 24 vs. 254 ± 23 s, P < 0.01). Upper-airway protective reflexes across a range of negative pressures as measured by electromyography and the early P1 component of the RREP are preserved in OSA patients during wakefulness. Consistent with an adaptive training effect, tongue protrusion force is increased, not decreased, in untreated OSA patients. However, OSA patients may be vulnerable to fatigue of upper-airway dilator muscles, which could contribute to disease progression.
The causes of obstructive sleep apnea (OSA) are multifactorial. Neural injury affecting the upper airway muscles due to repetitive exposure to intermittent hypoxia and/or mechanical strain resulting from snoring and recurrent upper airway closure have been proposed to contribute to OSA disease progression. Multiple studies have demonstrated altered sensory and motor function in patients with OSA using a variety of neurophysiological and histological approaches. However, the extent to which the alterations contribute to impairments in upper airway muscle function, and thus OSA disease progression, remains uncertain. This brief review, primarily focused on data in humans, summarizes: (1) the evidence for upper airway sensorimotor injury in OSA and (2) current understanding of how these changes affect upper airway function and their potential to change OSA progression. Some unresolved questions including possible treatment targets are noted.
Understanding the inter-relationship between pharmacological agents, ventilatory control, upper airway physiology and their consequent effects on sleep-disordered breathing may provide new directions for targeted drug therapy. Where available, this review focuses on human studies that contain both drug effects on sleep-disordered breathing and measures of ventilatory control or upper airway physiology. Many of the existing studies are limited in sample size or comprehensive methodology. At times, the presence of paradoxical findings highlights the complexity of drug therapy for OSA. The existing studies also highlight the importance of considering inter-individual pharmacokinetics and underlying causes of sleep apnea in interpreting drug effects on sleep-disordered breathing. Practical ways to assess an individual's ventilatory control and how it interacts with upper airway physiology is required for future targeted pharmacotherapy in sleep apnea.