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Biomed Sci Instrum ; 48: 126-33, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22846274

RESUMO

In the United States, traumatic brain injury (TBI) continues to be a leading source of death and disability, being responsible for 30.5% of all injury-related deaths [1]. Uncertainty still exists concerning the mechanisms and injury cascades involved. This study seeks to address many of the unknowns and criticisms of previous research. This study is focused on determining short term TBI development by finding a relationship between input accelerations and neuronal damage characterized by magnetic resonance spectroscopy (MRS) in an in vivo Göttingen minipig model. An injury device was designed and fabricated to impart rotational acceleration in the median plane of the animal using an articulated pendulum. Injury to the animal is caused by abrupt deceleration of the entire animal when the pendulum impacts brass tubes, which is repeatable. The animals (n=9) undergo baseline 7T MR scans prior to injury, immediately post-injury, and twenty-four hours post injury. MRS is performed on a voxel placed in the genu of the corpus callosum. Relevant metabolites include glutamate, N-acetylaspartate, myoInositol, creatine, and lactate. No clear trends were found for any of the metabolites for either time point. Further testing needs to be done in order to see the meaning of the metabolite differences in terms of underlying damage characterized by immunohistochemistry. This will give us insight into the meaning of using a noninvasive technique like MRS to look at TBI severity immediately post injury. Future work will include extending this study to define long term TBI development according to metabolite concentrations.

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