Dr Jason Amatoury


Postdoctoral Fellow 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 computer and biomedical engineering foundation (UNSW) with a PhD from the University of Sydney (Ludwig Engel Centre for Respiratory Research) in upper airway physiology and modelling.

Dr Amatoury’s research is focused on utilising both physiology and engineering to better understand the causes of sleep-related breathing disorders (such as obstructive sleep apnoea) and develop new & improved methods for their diagnosis and treatment. He has a particular interest in upper airway physiology & biomechanics, and the role of the hyoid bone in keeping the upper airway open during sleep. He is also interested in the measurement and quantification of snoring-associated neck tissue vibrations and their potential pathological impact on the carotid artery and surrounding pharyngeal tissues. Dr Amatoury utilises a broad range of approaches in his research, including physiological experiments (animal and human studies), biomedical imaging, biological signal processing, physical bench modelling and computational finite element modelling.

Dr Amatoury’s current research activities involve: 1) developing simplified/automated methods for overnight physiological phenotyping of sleep-disordered breathing and sleep disruption; 2) utilising dynamic magnetic resonance imaging methods to study the movement of the hyoid bone and other upper airway structures; 3) investigating the mechanisms of respiratory-related cortical arousals and their physiological consequences during sleep in humans; and 4) computational modelling of the upper airway.

Projects Dr Jason Amatoury is currently involved with


Obstructive Sleep Apnoea Imaging

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


Obstructive Sleep Apnoea Imaging

NeuroSleep: A NHMRC Centre for Research Excellence

This project aims to understand the bidirectional relationship between sleep and the brain to test and develop new approaches to treatment for sleep disruption across a range of medical disorders.  


NeuroSleep: A NHMRC Centre for Research Excellence

Determining new targets and approaches for treating sleep apnoea

We are running a range of projects to determine how existing treatments for sleep apnoea work so that we can optimise therapy and improve treatment success.


Determining new targets and approaches for treating sleep apnoea



DR PETER BURKE Postdoctoral fellow

RICHARD LIM Honours student


DR CHINH NGUYEN NeuroSleep NHMRC CRE Postdoctoral Fellow


AMAL OSMAN PhD student

Ben Tong

BENJAMIN TONG Sleep Lab Manager : 9399 1886
: sleeplab@neura.edu.au

DR NIRU WIJESURIYA Postdoctoral Fellow

Jayne Carberry

DR JAYNE CARBERRY NeuroSleep NHMRC CRE Postdoctoral Fellow

Katie Pelland

KATIE PELLAND Visiting PhD student

Rob Lloyd

ROB LLOYD PhD student

Lauriane Juge

DR LAURIANE JUGE Postdoctoral fellow

Elizabeth Clarke

DR ELIZABETH CLARKE Visiting postdoctoral fellow

DR ELIZABETH BROWN Postdoctoral fellow

ALICE HATT Research assistant

ALICE PONG PhD student

FIONA KNAPMAN Research assistant


Snoring-related energy transmission to the carotid artery in rabbits.

Amatoury J, Howitt L, Wheatley JR, Avolio AP, Amis TC

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.

Onset of airflow limitation in a collapsible tube model: impact of surrounding pressure, longitudinal strain, and wall folding geometry.

Amatoury J, Kairaitis K, Wheatley JR, Bilston LE, Amis TC

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.

A threshold lung volume for optimal mechanical effects on upper airway airflow dynamics: studies in an anesthetized rabbit model.

Kairaitis K, Verma M, Amatoury J, Wheatley JR, White DP, Amis TC

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.

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