Monash Trauma group
Traumatic brain injury (TBI), concussion, mild traumatic brain injury, post-traumatic stress disorder (PTSD), epilepsy, polytrauma, fracture, muscle injury, heterotopic ossification, pain
The Monash Trauma Group consists of a team of Principal Investigators, each of whom are leading scientists within their respective fields. Our collective goal is to study the effects, underlying pathophysiological mechanisms, biomarkers, and treatments of trauma related conditions including TBI, concussion, PTSD, epilepsy, polytrauma, fracture, muscle injury, heterotopic ossification, and pain.
TBI is a major focus of the group. TBI is a leading cause of death and morbidity worldwide, and there is no intervention to improve long-term outcomes. The Monash Trauma Group aims to improve the understanding and treatment of TBI by utilizing a translational research approach that incorporates both animal model and patient studies. The groups also investigates the relationship between TBI and other neurodegenerative conditions (e.g., epilepsy and ALS), and how these effects can be prevented.
Another key focus of the group is mild TBI (mTBI), often referred to as concussion. Evidence suggests that mTBIs are associated with long-term neurological consequences and neurodegenerative disease. Unfortunately, it is not known why these effects occur or how they can be prevented. We are currently conducting studies in amateur and professional athletes, as well as in animal models, to provide insight into questions related to mTBI.
We are also one of the few research teams in the world investigating how concomitant peripheral insults (e.g., infection, aging, extracranial traumas) affect TBI pathobiology and outcomes. Related to this, we are studying neurological heterotopic ossification (NHO) - a common and debilitating consequence of TBI that involves the formation of bone in soft tissue.
Chronic pain is a debilitating consequence of many of the traumatic events studied by the group. Our research aims to examine this transition from acute to chronic pain in an attempt to pinpoint where and why the shift occurs in order to better manage it. We also aim to determine why some people recover without incident, and others go on to suffer persistently.
A/Prof Sandy Shultz
A/Prof Richelle Mychasiuk
Dr Stuart McDonald
Dr Mujun Sun
Dr Rhys Brady
Current project funding
- 2018-2022: NHMRC; Project grant; 1141643; Sandy Shultz (Chief Investigator); Mild traumatic brain injuries and neurodegenerative disease
- 2017-2022; CIHR; Project grant; 3164568; Sandy Shultz (Co-Chief Investigator); Modulation of adolescent traumatic brain injury via the orexin system, sleep, and glymphatic function
- 2017-2022; NIH-NINDS; Centers without walls; EpiBios 4Rx; Sandy Shultz (Investigator)
- 2017-2022: Alfred Health; Establishment grant; Sandy Shultz (Chief Investigator); Translational traumatology laboratory
- 2015-2019; NHMRC; Career development fellowship;1087172; Sandy Shultz (Chief Investigator); Treatments and biomarkers for traumatic brain injury
Selected recent publications
For recent publications, visit Pubmed.
- Clough M, Mutimer S, Wright DK, Tsang A, Costello DM, Gardner AJ, Stanwell P, Mychasiuk R, Sun M, Brady RD, McDonald SJ, Webster KM, Johnstone MR, Semple BD, Agoston DV, White OB, Frayne R, Fielding J, O'Brien TJ, Shultz SR. Ocularmotor cognitive control abnormalities in Australian rules football players with a history of concussion. J Neurotrauma 2018, 35, 730-738.
- Sun M, McDonald SJ, Brady RD, O'Brien TJ, Shultz SR. The influence of immunological stressors on traumatic brain injury. Brain Behav Immun 2018, 69, 618-628.
- Shultz SR, McDonald SJ, Vonder Haar C, Meconi A, Vink R, van Donkelaar P, Taneja C, Iverson GL, Christie BR. The potential for animal models to provide insight into mild traumatic brain injury: Translational challenges and strategies. Neurosci Biobehav Rev 2017, 76, 396-414.
- Wright DK, Liu S, van der Poel C, McDonald SJ, Brady RD, Taylor L, Yang L, Gardner AJ, Ordidge R, O'Brien TJ, Johnston LA, Shultz SR. Traumatic brain injury results in cellular, structural and functional changes resembling motor neuron disease. Cereb Cortex 2017, 27, 4503-4515.
- Shultz SR, Wright DK, Zheng P, Stuchbery R, Liu SJ, Sashindranath M, Medcalf RL, Johnston LA, Hovens CM, Jones NC, O'Brien TJ. Sodium selenate reduces hyperphosphorylated tau and improves outcomes after traumatic brain injury. Brain 2015, 138, 1297-1313.