Conjoint Lecturer, School of Medical Sciences, University of New South Wales
Honorary Research Fellow, Sydney Medical School, University of Sydney
+61 2 9399 1834
Dr Jason Amatoury is a NeuroSleep NHMRC CRE Postdoctoral Fellow working with the NeuRA Sleep and Breathing research team. He has a background in computer & biomedical engineering (UNSW) with a PhD in upper airway physiology and modelling (USYD).
Dr Amatoury’s overall research agenda is focussed on utilising both physiology and engineering to better understand the causes of sleep-related breathing disorders such as obstructive sleep apnoea (OSA), and developing new & improved methods for their diagnosis and treatment. He has a particular interest in the physiology and biomechanics of the upper airway (or throat region), which repeatedly collapses and limits breathing during sleep to cause OSA.
Dr Amatoury incorporates a broad range of approaches and models in his research, including: acute/overnight physiological and clinical experimentation, biomedical imaging (MRI and CT), advanced signal processing, physical bench modelling and computational finite element modelling. Current research activities (with projects available for Honours, Masters and PhD students), include:
Jason is also passionate about science communication and raising awareness about the importance of sleep health, the disorders that can affect it and the current lifestyle and medical treatments available to improve it. Part of this he fulfils as a media spokesperson for the Sleep Health Foundation, in addition to serving on several other international and national professional committees in his field.
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 PETER BURKE Postdoctoral fellow
RICHARD LIM Honours student
DR AHMAD BAMAGOOS PhD student
DR CHINH NGUYEN NeuroSleep NHMRC CRE Postdoctoral Fellow
AMAL OSMAN PhD student
Sleep Lab Manager
: 9399 1886
DR NIRU WIJESURIYA Postdoctoral Fellow
DR JAYNE CARBERRY NeuroSleep NHMRC CRE Postdoctoral Fellow
KATIE PELLAND Visiting PhD student
ROB LLOYD PhD student
DR ELIZABETH CLARKE Visiting postdoctoral fellow
DR ELIZABETH BROWN Postdoctoral fellow
ALICE HATT Research assistant
ALICE PONG PhD student
FIONA KNAPMAN Research assistant
Epidemiological studies link habitual snoring and stroke, but mechanisms involved are poorly understood. One previously advanced hypothesis is that transmitted snoring vibration energy may promote carotid atheromatous plaque formation or rupture. To test whether vibration energy is present in carotid artery walls during snoring we developed an animal model in which we examined induced snoring (IS)-associated tissue energy levels. In six male, supine, anesthetized, spontaneously breathing New Zealand White rabbits, we surgically inserted pressure transducer-tipped catheters (Millar) to monitor tissue pressure at the carotid artery bifurcation (PCT) and within the carotid sinus lumen (PCS; artery ligated). Snoring was induced via external compression (sandbag) over the pharyngeal region. Data were analyzed using power spectral analysis for frequency bands above and below 50 Hz. For frequencies below 50 Hz, PCT energy was 2.2 (1.1-12.3) cmH2O2 [median (interquartile range)] during tidal breathing (TB) increasing to 39.0 (2.5-95.0) cmH2O2 during IS (P = 0.05, Wilcoxon's signed-rank test). For frequencies > 50 Hz, PCT energy increased from 9.2 (8.3-10.4) x 10(-4) cmH2O2 during TB to 172.0 (118.0-569.0) x 10(-4) cmH2O2 during IS (P = 0.03). Concurrently, PCS energy was 13.4 (8.5-18.0) x 10(-4) cmH2O2 during TB and 151.0 (78.2-278.8) x 10(-4) cmH2O2 during IS (P < 0.03). The PCS energy was greater than PCT energy for the 100-275 Hz bandwidth. In conclusion, during IS there is increased energy around and within the carotid artery, including lower frequency amplification for PCS. These findings may have implications for carotid atherogenesis and/or plaque rupture.
We studied the impact of wall strain and surrounding pressure on the onset of airflow limitation in a thin-walled "floppy" tube model. A vacuum source-generated steady-state (baseline) airflow (0-350 ml/s) through a thin-walled latex tube (length 80 mm, wall thickness 0.23 mm) enclosed within a rigid, sealed, air-filled, cylindrical chamber while upstream minus downstream pressure, chamber pressure (Pc), and lumen geometry [in-line digital camera; segmentation (Amira 5.2.2) and analysis (Rhinoceros 4) software] were monitored. Longitudinal strain (S; 0-62.5%) and Pc (0-20 cmH(2)O) combinations were imposed, and Pc associated with onset of 1) reduced airflow and 2) fully developed airflow limitation recorded. At any strain, increasing Pc resulted in a decrease in airflow. Across all baseline airflow, threshold pressure was 1-7 cmH(2)O for S < 25%, 6-8 cmH(2)O at S = 25% and 37.5%, and 5-7 cmH(2)O at S = 50% and 62.5%. Pc associated with fully developed airflow limitation was 4-6 cmH(2)O for S < 25%, >20 cmH(2)O at S = 25% (i.e., no flow limitation), 18 cmH(2)O at S = 37.5%, and 8-12 cmH(2)O at S = 50% and 62.5%. Lumen area decreased with increasing Pc but was 1) larger at S = 25% and 2) characterized by bifold narrowing at S < 25% and trifold narrowing at S ≥ 25%. In conclusion, tube function was modulated by Pc vs. S interactions, with S = 25% producing trifold lumen narrowing, maximal patency, and no airflow limitation. Findings may have implications for understanding peripharyngeal tissue pressure and pharyngeal wall strain effects on passive pharyngeal airway function in humans.
Increasing lung volume improves upper airway airflow dynamics via passive mechanisms such as reducing upper airway extraluminal tissue pressures (ETP) and increasing longitudinal tension via tracheal displacement. We hypothesized a threshold lung volume for optimal mechanical effects on upper airway airflow dynamics. Seven supine, anesthetized, spontaneously breathing New Zealand White rabbits were studied. Extrathoracic pressure was altered, and lung volume change, airflow, pharyngeal pressure, ETP laterally (ETPlat) and anteriorly (ETPant), tracheal displacement, and sternohyoid muscle activity (EMG%max) monitored. Airflow dynamics were quantified via peak inspiratory airflow, flow limitation upper airway resistance, and conductance. Every 10-ml lung volume increase resulted in caudal tracheal displacement of 2.1 ± 0.4 mm (mean ± SE), decreased ETPlat by 0.7 ± 0.3 cmH(2)O, increased peak inspiratory airflow of 22.8 ± 2.6% baseline (all P < 0.02), and no significant change in ETPant or EMG%max. Flow limitation was present in most rabbits at baseline, and abolished 15.7 ± 10.5 ml above baseline. Every 10-ml lung volume decrease resulted in cranial tracheal displacement of 2.6 ± 0.4 mm, increased ETPant by 0.9 ± 0.2 cmH(2)O, ETPlat was unchanged, increased EMG%max of 11.1 ± 0.3%, and a reduction in peak inspiratory airflow of 10.8 ± 1.0%baseline (all P < 0.01). Lung volume, resistance, and conductance relationships were described by exponential functions. In conclusion, increasing lung volume displaced the trachea caudally, reduced ETP, abolished flow limitation, but had little effect on resistance or conductance, whereas decreasing lung volume resulted in cranial tracheal displacement, increased ETP and increased resistance, and reduced conductance, and flow limitation persisted despite increased muscle activity. We conclude that there is a threshold for lung volume influences on upper airway airflow dynamics.