Spinal Injury is a devastating condition, usually resulting in paralysis, loss of sensation and disruption of body functions. Our research ranges from development of preventative strategies to studies of treatments that improve the health and capacity of spinal patients
The Spinal Injuries Research Centre (SIRC) incorporates work on spinal cord injury by more than ten laboratories in NeuRA. The research ranges from experimental studies of the effects of spinal transection on the responsiveness of blood vessels and on inflammation (possibly leading to spinal hyperexcitability and neurone death) to better understanding of how spinal cysts develop in the long term after spinal injuries and even the design of improved child restraints in motor cars. Projects on people with spinal cord injury included measurements of the excitability of motor and sensory axons, the evaluation of nerve-muscle units in atrophied muscles and the development of stimulation techniques for generating more effective muscle force to assist coughing and coordinated walking during rehabilitation.
SIRC members were particularly successful in the second round of the NSW Ministry of Health and Medical Research Program for Spinal Cord Injury and Related Neurological Conditions. A Program Grant worth $1.5 million was awarded to Professors Elspeth McLachlan and Vaughan Macefield and Assoc Professors James Brock and Matthew Kiernan for studies of the changes in nerve and muscle excitability below a spinal cord injury. Project grants were also awarded to Assoc Professor Kiernan for a study of motor neurone disease and Professor George Paxinos to prepare a spinal cord atlas.
Contact: +61 2 9399 1031; e.mclachlan@neura.edu.au
Contact: +61 2 9399 1017; s.gandevia@neura.edu.au
Professor McLachlan and her collaborators have been investigating what happens within the lumbosacral spinal cord distal to a mid-thoracic spinal transection. They postulated that degeneration of descending and ascending pathways would lead to inflammatory responses within the cord below the damage site. The debris of degenerated pathways is cleared over several weeks as the spinal cord atrophies. Activated and reactive microglia express an immune recognition protein and inflammatory cells, including T-lymphocytes, invade both grey and white matter.
Phagocytic cells become densest superficially around the cord. However, neither inflammation nor tissue loss is restricted to the white matter, suggesting that nerve cells previously projecting to the brain also degenerate. This idea is now being tested directly. The aim is to find out whether the activated immune cells release growth factors that might play a role in the remodelling of spinal cord pathways. Alternatively the immune cells may release cytotoxic substances that could account for progressive death of nerve cells at sites far beyond the initial damage. If this happens, it will threaten the success of attempts to improve regeneration of descending pathways from the brain.
