Simulation of Blast-Induced Early-Time Intracranial Wave Physics leading to Traumatic Brain Injury (original) (raw)
Research Papers
Department of Penetration Systems,
Sandia National Laboratories
, Albuquerque, NM 87185
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Department of Neurology,
University of New Mexico Health Sciences Center
, Albuquerque, NM 87131-0001
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Paul A. Taylor
Department of Penetration Systems,
Sandia National Laboratories
, Albuquerque, NM 87185
Corey C. Ford
Department of Neurology,
University of New Mexico Health Sciences Center
, Albuquerque, NM 87131-0001
J Biomech Eng. Jun 2009, 131(6): 061007 (11 pages)
Published Online: April 27, 2009
Received:
February 11, 2008
Revised:
February 26, 2009
Published:
April 27, 2009
The objective of this modeling and simulation study was to establish the role of stress wave interactions in the genesis of traumatic brain injury (TBI) from exposure to explosive blast. A high resolution (1 mm3 voxels) five material model of the human head was created by segmentation of color cryosections from the Visible Human Female data set. Tissue material properties were assigned from literature values. The model was inserted into the shock physics wave code, CTH, and subjected to a simulated blast wave of 1.3 MPa (13 bars) peak pressure from anterior, posterior, and lateral directions. Three-dimensional plots of maximum pressure, volumetric tension, and deviatoric (shear) stress demonstrated significant differences related to the incident blast geometry. In particular, the calculations revealed focal brain regions of elevated pressure and deviatoric stress within the first 2 ms of blast exposure. Calculated maximum levels of 15 KPa deviatoric, 3.3 MPa pressure, and 0.8 MPa volumetric tension were observed before the onset of significant head accelerations. Over a 2 ms time course, the head model moved only 1 mm in response to the blast loading. Doubling the blast strength changed the resulting intracranial stress magnitudes but not their distribution. We conclude that stress localization, due to early-time wave interactions, may contribute to the development of multifocal axonal injury underlying TBI. We propose that a contribution to traumatic brain injury from blast exposure, and most likely blunt impact, can occur on a time scale shorter than previous model predictions and before the onset of linear or rotational accelerations traditionally associated with the development of TBI.
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