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Traumatic Brain Injury

It is estimated that between 15-20% of US Veterans who were deployed in either Iraq, Afghanistan, or both returned with mild traumatic brain injury (Hoge, McGurk et al. 2008, Evans, St Andre et al. 2013, Iverson, Pogoda et al. 2013). It is also estimated that a significant cause of most of this mild traumatic brain injury (mTBI) resulted from so called “blast injury” (Elder, Dorr et al. 2012). This kind of head trauma occurs when soldiers are exposed to blast-wave pressure from explosions and can present with no outward physical indicators of head injury. In Iraq and Afghanistan, the repeated exposure to low levels of blast overpressure from improvised explosive devices is believed to account for the majority of mild traumatic brain injury. Because most of the troops exposed to blast-waves remain conscious, they were often redeployed quickly and as a result were often exposed multiple times to blast-wave pressure from explosions, which may have aggravated their undiagnosed (and untreated) traumatic brain injury from their initial exposures.

The medical problems resulting from mild traumatic brain injury in returning veterans have been described in detail in the medical literature (Evans, St Andre et al. 2013). These include a greater frequency of substance abuse and addiction, a much higher incidence of suicide, the persistence of past-trauma stress disorder, and a whole host of cognitive deficiencies. What is missing is an understanding of the biochemical, physiological, and structural changes that occur as a result of single or repeated exposure to blast-wave pressure from explosions. Achieving this understanding could lead to earlier, and more precise diagnosis, better treatment options and perhaps a path to developing effective prevention of mild traumatic brain injury resulted from blast injury.

In order to begin to study these issues, we would like to establish a UTSW program in neuroimaging of traumatic injury that would be directed at addressing the clinical and scientific issues described above. This program would include the following:


  1. Developing biomechanical models of traumatic brain injury specifically addressing ballast-injury.
  2. Establishing animal models for the systematic study of the biochemical, physiological, and histopathological alterations that occur as a result of single or repeated exposure to blast-wave pressure from explosions.
  3. Developing non-invasive neuroimaging methods to both diagnosis mTBI in humans as well as provide a basis for mechanistic studies in animal models.
  4. Develop biomarkers for assessing the effects of treatment on patients who have symptoms related to mTBI.
  5. Explore biomechanical and mechanistically based approaches for prevention of blast-injury.



Elder, G. A., et al. (2012). “Blast Exposure Induces Post-Traumatic Stress Disorder-Related Traits in a Rat Model of Mild Traumatic Brain Injury.” Journal of Neurotrauma 29(16): 2564-2575.

Evans, C. T., et al. (2013). “An Evaluation of the Veterans Affairs Traumatic Brain Injury Screening Process Among Operation Enduring Freedom and/or Operation Iraqi Freedom Veterans.” Pm&R 5(3): 210-220.

Hoge, C. W., et al. (2008). “Mild traumatic brain injury in US Soldiers returning from Iraq.” New England Journal of Medicine 358(5): 453-463.

Iverson, K. M., et al. (2013). “Deployment-Related Traumatic Brain Injury Among Operation Enduring Freedom/Operation Iraqi Freedom Veterans: Associations with Mental and Physical Health by Gender.” Journal of Womens Health 22(3): 267-275.

Publications on Head Injury

  1. Rango M, Lenkinski RE, Alves WM, Gennarelli TA. Brain pH in Head-Injury – an Image-Guided P-31 Magnetic-Resonance Spectroscopy Study. Annals of Neurology 1990;28(5):661-667.
  2. Rango M, Lenkinski RE, Alves WM, Cruz J, Gennarelli TA. Brain pH in acute head injury. Minerva Anestesiol 1993;59(12):835-836.
  3. Smith DH, Meaney DF, Lenkinski RE, Alsop DC, Grossman R, Kimura H, McIntosh TK, Gennarelli TA. New Magnetic-Resonance-Imaging Techniques for the Evaluation of Traumatic Brain Injury. Journal of Neurotrauma 1995;12(4):573-577.
  4. Yamakami I, Vink R, Faden AI, Gennarelli TA, Lenkinski RE, McIntosh TK. Effects of Acute Ethanol Intoxication on Experimental Brain Injury in the Rat – Neurobehavioral and P-31 Nuclear-Magnetic-Resonance Spectroscopy Studies. Journal of Neurosurgery 1995;82(5):813-821.
  5. Kimura H, Meaney DF, McGowan JC, Grossman RI, Lenkinski RE, Ross DT, McIntosh TK, Gennarelli TA, Smith DH. Magnetization transfer imaging of diffuse axonal injury following experimental brain injury in the pig: Characterization by magnetization transfer ratio with histopathologic correlation. Journal of Computer Assisted Tomography 1996;20(4):540-546.
  6. Rubin Y, Cecil K, Wehrli S, McIntosh TK, Lenkinski RE, Smith DH. High-resolution H-1 NMR spectroscopy following experimental brain trauma. Journal of Neurotrauma 1997;14(7):441-449.
  7. Cecil KM, Hills EC, Sandel E, Smith DH, McIntosh TK, Mannon LJ, Sinson GP, Bagley LJ, Grossman RI, Lenkinski RE. Proton magnetic resonance spectroscopy for detection of axonal injury in the splenium of the corpus callosum of brain-injured patients. Journal of Neurosurgery 1998;88(5):795-801.
  8. Cecil KM, Lenkinski RE, Meaney DF, McIntosh TK, Smith DH. High-field proton magnetic resonance spectroscopy of a swine model for axonal injury. Journal of Neurochemistry 1998;70(5):2038-2044.
  9. Smith DH, Cecil KM, Meaney DF, Chen XH, McIntosh TK, Gennarelli TA, Lenkinski RE. Magnetic resonance spectroscopy of diffuse brain trauma in the pig. Journal of Neurotrauma 1998;15(9):665-674.
  10. Sinson G, Bagley LJ, Cecil KM, Torchia M, McGowan JC, Lenkinski RE, McIntosh TK, Grossman RI. Magnetization transfer imaging and proton MR spectroscopy in the evaluation of axonal injury: Correlation with clinical outcome after traumatic brain injury. American Journal of Neuroradiology 2001;22(1):143-151.