• M C LaPlaca, C M Simon, G R Prado, and D K Cullen.
• Neural Injury Biomechanics and Repair Laboratory, Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 313 Ferst Dr., Atlanta, GA 30332-0535, USA. michelle.laplaca@bme.gatech.edu
• Prog. Brain Res. 2007 Jan 1; 161: 13-26.

AbstractTraumatic brain injury (TBI) and traumatic spinal cord injury (SCI) are acquired when an external physical insult causes damage to the central nervous system (CNS). Functional disabilities resulting from CNS trauma are dependent upon the mode, severity, and anatomical location of the mechanical impact as well as the mechanical properties of the tissue. Although the biomechanical insult is the initiating factor in the pathophysiology of CNS trauma, the anatomical loading distribution and the resulting cellular responses are currently not well understood. For example, the primary response phase includes events such as increased membrane permeability to ions and other molecules, which may initiate complex signaling cascades that account for the prolonged damage and dysfunction. Correlation of insult parameters with cellular changes and subsequent deficits may lead to refined tolerance criteria and facilitate the development of improved protective gear. In addition, advancements in the understanding of injury biomechanics are essential for the development and interpretation of experimental studies at both the in vitro and in vivo levels and may lead to the development of new treatment approaches by determining injury mechanisms across the temporal spectrum of the injury response. Here we discuss basic concepts relevant to the biomechanics of CNS trauma, injury models used to experimentally simulate TBI and SCI, and novel multilevel approaches for improving the current understanding of primary damage mechanisms.

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