Deputy Director and Foundation Scientist, NeuRA
Senior Principal Research Fellow, NHMRC
Conjoint Prof, UNSW
Honorary Prof, USyd and UQld
+612 9399 1617
Simon Gandevia (MD PhD DSc FAA FRACP) trained at the University of New South Wales and the Prince Henry Hospital. He has broad research interests in human movement control and he has used a wide range of techniques to examine fundamental aspects of pathophysiology in human neuroscience and clinical medicine. His work often sits at the interface between medicine and basic human neurophysiology.
Professor Gandevia is one of the four Founding Scientists of the Prince of Wales Medical Research Institute (in 1992), which was later renamed NeuRA. He was also a founder of the 3T Clinical Research Imaging Centre and is a Clinical Neurophysiologist at the Prince of Wales Hospital. He has served on many editorial boards, including the Journal of Physiology (1993-2000; 2011-) and is currently a Senior Editor. He is currently Associate Editor for the Journal of Applied Physiology (since 2005). His clinical work includes patients with neuromuscular disorders and those with spinal cord injury.
Not only are the breathing muscles controlled automatically from the brainstem and motor cortex, but they can be activated in response to emotion, e.g. during laughing and crying. We plan to investigate the neural pathways involved in emotional breathing in healthy volunteers.
This basic science project aims to examine the behaviour of human motoneurones during sustained activation to reveal their mechanisms of recovery after activation. We will take the fundamental findings from this study and compare the behaviour of motoneurones innervating muscles affected by neurological injury such as spinal cord injury and stroke.
Respiratory complications are the major cause of death for people with spinal cord injuries. People with a high level spinal cord injury are 150 times more likely to die from pneumonia than the general population. This is because after high level spinal cord injury, people have a reduced ability to cough and to clear secretions from the lungs. The major group of muscles that produce a cough are the abdominal muscles. If the abdominal muscles are paralysed after spinal cord injury then the strength of the cough will be severely reduced. In our lab, we are looking at ways to improve cough in people with spinal cord injury by using surface functional electrical stimulation of the abdominal muscles. We have shown that this type of stimulation can improve cough significantly. We are now looking for ways to further improve cough through muscle training as well as ways to develop a portable stimulator that would allow independent activation of a cough.
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.
Our recent studies of the control of breathing muscles have shown a strong link between neural drive and mechanical action of the muscle. We showed that for a number of breathing muscles, the neural drive is directed to the muscles with the best mechanical effect for breathing. We termed this link between mechanics and neural drive ‘neuromechanical matching’. It is a new principle of muscle activation that allows for metabolically efficient activation of the muscles. This basic research finding is now leading to further studies in patients with respiratory disorders where muscle mechanics have changed. Chronic obstructive pulmonary disease is one such disease, where muscle mechanics are known to change. Our new studies will look at whether these patients have “adapted” to the changed muscle mechanics or whether their muscles may be activated inefficiently.
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 PHU HOANG
NeuRA Post-Doctoral Fellow, MS Senior Physiotherapist
: +612 9399 1832
DR MARTIN HÉROUX Research officer
DR PETER NICKOLLS
Honorary Senior Research Officer
: +612 9399 1013
DR ANNE BUTLER Research Officer
DR CHAMINDA LEWIS PhD student
Four weeks of isometric strength training of the elbow flexors increased muscle strength and voluntary activation, without a change in the muscle. The improvement in activation suggests that voluntary output from the cortex was better able to recruit motoneurons and/or increase their firing rates. The lack of change in CMEPs indicates that neither corticospinal transmission nor motoneuron excitability was affected by training.
In vivo measurements of muscle architecture provide insight into inter-individual differences in muscle function and could be used to personalise musculoskeletal models. When muscle architecture is measured from ultrasound images, as is frequently done, it is assumed that fascicles are oriented in the image plane and, for some measurements, that the image plane is perpendicular to the aponeurosis at the intersection of fascicle and aponeurosis. This study presents an in vivo validation of these assumptions by comparing ultrasound image plane orientation to three-dimensional reconstructions of muscle fascicles and aponeuroses obtained with diffusion tensor imaging (DTI) and high-resolution anatomical MRI scans. It was found that muscle fascicles were oriented on average at 5.5±4.1° to the ultrasound image plane. On average, ultrasound yielded similar measurements of fascicle lengths to DTI (difference <3mm), suggesting that the measurements were unbiased. The absolute difference in length between any pair of measurements made with ultrasound and DTI was substantial (10mm or 20% of the mean), indicating that the measurements were imprecise. Pennation angles measured with ultrasound were significantly smaller than those measured with DTI (mean difference 6°). This difference was apparent only at the superficial insertion of the muscle fascicles so it was probably due to pressure on the skin applied by the ultrasound probes. It is concluded that ultrasound measurements of deep pennation angles and fascicle lengths in the medial gastrocnemius are unbiased but have a low precision and that superficial pennation angles are underestimated by approximately 10°. The low precision limits the use of ultrasound to personalise fascicle length in musculoskeletal models.
Obstructive sleep apnoea (OSA) is linked to local neural injury that evokes airway muscle remodelling. The upper airway muscles of patients with OSA are exposed to intermittent hypoxia as well as vibration induced by snoring. A range of electrophysiological and other studies have established altered motor and sensory function of the airway in OSA. The extent to which these changes impair upper airway muscle function and their relationship to the progression of OSA remains undefined. This review will collate the evidence for upper airway remodelling in OSA, particularly the electromyographic changes in upper airway muscles of patients with OSA.