• Accomplishments
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• Research
• Spinal Cord Injury Projects
• Traumatic Brain Injury Projects
  • Assessment & Intervention for Mild TBI
  • Can Eye Movements Predict Persistent Problems in Paediatric Mild TBI?
  • Cognitive and Neural Substrates of Socially Maladaptive Behaviours in Adolescents with Traumatic Brain Injury
  • DECRA Trial (DECompressive CRAniectomy Trial)
  • Enhancing Neurogenesis Post -TBI
  • Fluid Resuscitation in TBI
  • Headstart: Multi-family Groups for Traumatic Brain Injury
  • Hypothermia in Childhood TBI (HiTBIC)
  • Improving the functional communication ability of adults with TBI
  • Long term consequences of childhood head injury - 15 year follow-up
  • Longitudinal Hippocampal Study
  • Measuring the Impact of TBI on People's Lives
  • Mobility Following Childhood TBI
  • New Treatments for Brain and Spinal Cord Injuries
  • Neural Basis of Communication Disorder in Children
  • Neurotrauma Tissue/Fluid Bank
  • Normoglycaemia in Intensive Care Traumatic Brain Injury Study (NICE-TBI)
  • Preventing Neuronal Cell Death Following Brain Trauma
  • Prevention and Treatment of Social Problems Following TBI
  • Rehabilitation of Attention Following TBI
  • Role of Tissue Type Plasminogen Activator
  • TBI in Older Adults
  • Transcranial Magnetic Stimulation (TMS) Treatment in Depression After Traumatic Brain Injury
  • Traumatic Hypoxia and Cerebral Inflammation
  • Virtual Reality and Upper Limb Function Following TBI in Children
• Targeted Initiatives
• Completed TBI and SCI Projects
• Program Grants

Traumatic Hypoxia and Cerebral Inflammation

Role of Post-Traumatic Hypoxia in the Exacerbation of Cerebral Inflammation Elicited by Brain Injury

Chief Investigator: Associate Professor Cristina Morganti-Kossmann
Associate Investigators: Professor Thomas Kossmann, Professor Jamie Cooper, Professor Jeffrey Rosenfeld
Lead Organisation: Bayside Health
VNI Funding: $232,794
Project Start Date: 01-Mar-07

Project Summary:
There is clinical evidence showing that 45% of patients with severe Traumatic Brain Injury (TBI) are subjected to respiratory distress leading to reduced oxygen delivery to the brain or hypoxia. Although brain hypoxia is thought to aggravate tissue damage caused by trauma, its impact on secondary pathological pathways has not been thoroughly investigated. Based on previous evidence showing that hypoxia itself induces brain inflammation, we hypothesize that the combination of TBI and post-traumatic hypoxia will exacerbate the production of inflammatory mediators in the injured brain, thus aggravating tissue and neurological damage. This hypothesis will be tested in a model of diffuse traumatic axonal injury (TAI) in which rats will be subjected to trauma with or without post-traumatic hypoxia. Clinical relevance of the results obtained in the animal models will be characterised on patients with severe TBI. Candidate injury marker proteins with potential prognostic and diagnostic value from animal data will also be validated in the human samples to determine clinical suitability.