This report contains a summary of our efforts to correlate head injury simulations predicting intracranial fluid cavitation with clinical assessments of brain injury from blunt impact to the head. Magnetic resonance imaging (MRI) data, collected on traumatic brain injury (TBI) subjects by researchers at the MIND Institute of New Mexico, was acquired for the current work. Specific blunt impact TBI case histories were selected from the TBI data for further study and possible correlation with simulation. Both group and single-subject case histories were examined. We found one single-subject case that was particularly suited for correlation with simulation. Diffusion tensor image (DTI) analysis of the TBI subject identified white matter regions within the brain displaying reductions in fractional anisotropy (FA), an indicator of local damage to the white matter axonal structures. Analysis of functional magnetic resonance image (fMRI) data collected on this individual identified localized regions of the brain displaying hypoactivity, another indicator of brain injury. We conducted high fidelity simulations of head impact experienced by the TBI subject using the Sandia head-neck-torso model and the shock physics computer code CTH. Intracranial fluid cavitation predictions were compared with maps of DTI fractional anisotropy and fMRI hypoactivity to assess whether a possible correlation exists. The ultimate goal of this work is to assess whether one can correlate simulation predictions of intracranial fluid cavitation with the brain injured sites identified by the fMRI and DTI analyses. The outcome of this effort is described in this report.
We conducted computational macroscale simulations predicting blast-induced intracranial fluid cavitation possibly leading to brain injury. To further understanding of this problem, we developed microscale models investigating the effects of blast-induced cavitation bubble collapse within white matter axonal fiber bundles of the brain. We model fiber tracks of myelinated axons whose diameters are statistically representative of white matter. Nodes of Ranvier are modeled as unmyelinated sections of axon. Extracellular matrix envelops the axon fiber bundle, and gray matter is placed adjacent to the bundle. Cavitation bubbles are initially placed assuming an intracranial wave has already produced them. Pressure pulses, of varied strengths, are applied to the upper boundary of the gray matter and propagate through the model, inducing bubble collapse. Simulations, conducted using the shock wave physics code CTH, predict an increase in pressure and von Mises stress in axons downstream of the bubbles after collapse. This appears to be the result of hydrodynamic jetting produced during bubble collapse. Interestingly, results predict axon cores suffer significantly lower shear stresses from proximal bubble collapse than does their myelin sheathing. Simulations also predict damage to myelin sheathing, which, if true, degrades axonal electrical transmissibility and general health of the white matter structures in the brain.
Willis, Adam M.; Cooper, Candice F.; Miller, Scott T.; Mejia-Alvarez, Ricardo M.; Tartis, Michaelann S.; Welsh, Kelsea W.; Wermer, Ann W.; Hovey, Chad B.; Massomi, Faezeh M.; Vidhate, Suhas V.; Ferguson, Kyle F.; Fuller, Ian F.; Morgan, Robert M.; Perl, Daniel P.; Taylor, Paul A.
Light body armor development for the warfighter is based on trial-and-error testing of prototype designs against ballistic projectiles. Torso armor testing against blast is nonexistent but necessary to protect the heart and lungs. In tests against ballistic projectiles, protective apparel is placed over ballistic clay and the projectiles are fired into the armor/clay target. The clay represents the human torso and its behind-armor, permanent deflection is the principal metric used to assess armor protection. Although this approach provides relative merit assessment of protection, it does not examine the behind-armor blunt trauma to crucial torso organs. We propose a modeling and simulation (M&S) capability for wound injury scenarios to the head, neck, and torso of the warfighter. We will use this toolset to investigate the consequences of, and mitigation against, blast exposure, blunt force impact, and ballistic projectile penetration leading to damage of critical organs comprising the central nervous, cardiovascular, and respiratory systems. We will leverage Sandia codes and our M&S expertise on traumatic brain injury to develop virtual anatomical models of the head, neck, and torso and the simulation methodology to capture the physics of wound mechanics. Specifically, we will investigate virtual wound injuries to the head, neck, and torso without and with protective armor to demonstrate the advantages of performing injury simulations for the development of body armor. The proposed toolset constitutes a significant advance over current methods by providing a virtual simulation capability to investigate wound injury and optimize armor design without the need for extensive field testing.
Light body armor development for the warfighter is based on trial-and-error testing of prototype designs against ballistic projectiles. Torso armor testing against blast is virtually nonexistent but necessary to ensure adequate protection against injury to the heart and lungs. In this report, we discuss the development of a high-fidelity human torso model, it's merging with the existing Sandia Human Head-Neck Model, and development of the modeling & simulation (M&S) capabilities necessary to simulate wound injury scenarios. Using the new Sandia Human Torso Model, we demonstrate the advantage of virtual simulation in the investigation of wound injury as it relates to the warfighter experience. We present the results of virtual simulations of blast loading and ballistic projectile impact to the tors o with and without notional protective armor. In this manner, we demonstrate the ad vantages of applying a modeling and simulation approach to the investigation of wound injury and relative merit assessments of protective body armor without the need for trial-and-error testing.
Light body armor development for the war fighter is based on trial-and-error testing of prototype designs against ballistic projectiles. Torso armor testing against blast is virtually nonexistent but necessary to ensure adequate mitigation against injury to the heart and lungs. In this paper, we discuss the development of a high-fidelity human torso model and the associated modeling & simulation (M&S) capabilities. Using this torso model, we demonstrate the advantage of virtual simulation in the investigation of wound injury as it relates to the war fighter experience. Here, we present the results of virtual simulations of blast loading and ballistic projectile impact to the torso with and without notional protective armor. Our intent here is to demonstrate the advantages of applying a modeling and simulation approach to the investigation of wound injury and relative merit assessments of protective body armor.
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 mm{sup 3} voxels), 5 material model of the human head was created by segmentation of color cryosections from the Visible Human Female dataset. 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 (shear) stress within the first 2 milliseconds 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 msec 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.