Abstract
Exposure to blast waves is suspected to cause primary traumatic brain injury. However, existing finite-element (FE) models of the rat head lack the necessary fidelity to characterize the biomechanical responses in the brain due to blast exposure. They neglect to represent the cerebral vasculature, which increases brain stiffness, and lack the appropriate brain material properties characteristic of high strain rates observed in blast exposures. To address these limitations, we developed a high-fidelity three-dimensional FE model of a rat head. We explicitly represented the rat’s cerebral vasculature and used high-strain-rate material properties of the rat brain. For a range of blast overpressures (100 to 230 kPa) the brain-pressure predictions matched experimental results and largely overlapped with and tracked the incident pressure–time profile. Incorporating the vasculature decreased the average peak strain in the cerebrum, cerebellum, and brainstem by 17, 33, and 18%, respectively. When compared with our model based on rat-brain properties, the use of human-brain properties in the FE model led to a three-fold reduction in the strain predictions. For simulations of blast exposure in rats, our findings suggest that representing cerebral vasculature and species-specific brain properties has a considerable influence in the resulting brain strain but not the pressure predictions.
Highlights
Exposure to explosive devices is the leading cause of traumatic brain injury (TBI) in U.S Soldiers deployed to Iraq and Afghanistan.[23]
From the simulations of the rat head with cerebral vasculature (RHwCV) model, we determined the biomechanical responses of the rat head when exposed to blast overpressure (BOP) in a shock tube
For a mesh size that was double that of the current model for the shock tube, pressure at the center of the brain changed by 2.6%
Summary
Exposure to explosive devices is the leading cause of traumatic brain injury (TBI) in U.S Soldiers deployed to Iraq and Afghanistan.[23]. Multiple studies provide evidence that such blast-induced TBI is caused primarily by penetrating and blunt trauma.[2,18] In contrast, other studies postulate that the mere exposure to a blast wave can cause brain injury, the so-called non-impact primary TBI.[6,21] In the absence of humanexposure data, these studies invariably entail the use of animal models, rats in particular, with blast exposure induced by a shock tube.[3,17] In this context, laboratory experiments allow us to detect and quantify potential injuries in the rat brain and computational finite-element (FE) models allow us to characterize the biomechanical responses of the brain and the possible mechanisms of injury.[17,19,25] current FE models for blast-induced TBI in rats lack the necessary fidelity,[19,25] as they do not consider the influence of cerebral vasculature and lack high-strain-rate material properties characteristic of blast exposures of the rat brain
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