Prof Danny Eckert

RESEARCHER PROFILE

Principal Research Scientist, NeuRA Associate Professor, UNSW
R.D. Wright Fellow, NHMRC


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 body and is Chair of the Research Committee.

DANNY ECKERT ON ABC NEWS TALKING ABOUT THE DREAMING “HOT ZONE”

NEW APPROACHES TO TREATING SLEEP APNOEA

EFFECTS OF LOW DOSE MORPHINE ON PERCEIVED SLEEP QUALITY IN PEOPLE WITH REFRACTORY BREATHLESSNESS

FACEBOOK

AUSTRALASIAN SLEEP ASSOCIATION

SLEEP HEALTH FOUNDATION

RESEARCH TEAM

PUBLICATIONS

Zopiclone Increases the Arousal Threshold without Impairing Genioglossus Activity in Obstructive Sleep Apnea.

Carter SG, Berger MS, Carberry JC, Bilston LE, Butler JE, Tong BK, Martins RT, Fisher LP, McKenzie DK, Grunstein RR, Eckert DJ

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.

Mechanisms contributing to the response of upper-airway muscles to changes in airway pressure.

Carberry JC, Hensen H, Fisher LP, Saboisky JP, Butler JE, Gandevia SC, Eckert DJ

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.

Defining phenotypic causes of obstructive sleep apnea. Identification of novel therapeutic targets.

Eckert DJ, White DP, Jordan AS, Malhotra A, Wellman A

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.

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