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 resting 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
DR HANNA HENSEN PhD student
DR PETER BURKE Postdoctoral fellow
RICHARD LIM Honours student
DR AHMAD BAMAGOOS PhD student
DR CHINH NGUYEN NeuroSleep NHMRC CRE Postdoctoral Fellow
SOPHIE CARTER PhD student
AMAL OSMAN PhD student
DR JASON AMATOURY NeuroSleep NHMRC CRE Postdoctoral Fellow
Sleep Lab Manager
: 9399 1886
DR NIRU WIJESURIYA Postdoctoral Fellow
DR JAYNE CARBERRY NeuroSleep NHMRC CRE Postdoctoral Fellow
To determine the effects of the nonbenzodiazepine sedative zopiclone on the threshold to arousal with increasing respiratory effort and genioglossus muscle activity and to examine potential physiological factors mediating disparate effects of zopiclone on obstructive sleep apnea (OSA) severity between patients. In a group of patients with predominantly severe OSA, zopiclone increased the arousal threshold without reducing genioglossus muscle activity or its responsiveness to negative pharyngeal pressure. These properties may be beneficial in some patients with OSA with certain pathophysiological characteristics but may worsen hypoxemia in others.
This study assessed the effects of inhaled lignocaine to reduce upper airway surface mechanoreceptor activity on 1) basal genioglossus and tensor palatini EMG, 2) genioglossus reflex responses to large pulses (∼10 cmH2O) of negative airway pressure, and 3) upper airway collapsibility in 15 awake individuals. Genioglossus and tensor palatini muscle EMG and airway pressures were recorded during quiet nasal breathing and during brief pulses (250 ms) of negative upper-airway pressure. Lignocaine reduced peak inspiratory (5.6 ± 1.5 vs. 3.8 ± 1.1% maximum; mean ± SE, P < 0.01) and tonic (2.8 ± 0.8 vs. 2.1 ± 0.7% maximum; P < 0.05) genioglossus EMG during quiet breathing but had no effect on tensor palatini EMG (5.0 ± 0.8 vs. 5.0 ± 0.5% maximum; P = 0.97). Genioglossus reflex excitation to negative pressure pulses decreased after anesthesia (60.9 ± 20.7 vs. 23.6 ± 5.2 μV; P < 0.05), but not when expressed as a percentage of the immediate prestimulus baseline. Reflex excitation was closely related to the change in baseline EMG following lignocaine (r(2) = 0.98). A short-latency genioglossus reflex to rapid increases from negative to atmospheric pressure was also observed. The upper airway collapsibility index (%difference) between nadir choanal and epiglottic pressure increased after lignocaine (17.8 ± 3.7 vs. 28.8 ± 7.5%; P < 0.05). These findings indicate that surface receptors modulate genioglossus but not tensor palatini activity during quiet breathing. However, removal of input from surface mechanoreceptors has minimal effect on genioglossus reflex responses to large (∼10 cmH2O), sudden changes in airway pressure. Changes in pressure rather than negative pressure per se can elicit genioglossus reflex responses. These findings challenge previous views and have important implications for upper airway muscle control.
To define carefully the proportion of key anatomic and nonanatomic contributions in a relatively large cohort of patients with OSA and control subjects to identify pathophysiologic targets for future novel therapies for OSA. This study confirms that OSA is a heterogeneous disorder. Although Pcrit-anatomy is an important determinant, abnormalities in nonanatomic traits are also present in most patients with OSA.