Citation

Panzer MB, Myers BS, Capehart BP, Bass CR. Ann. Biomed. Eng. 2012; 40(7): 1530-1544.

Affiliation

Department of Biomedical Engineering, Duke University, 136 Hudson Hall, Box 90281, Durham, NC, 27708, USA, matthew.panzer@duke.edu.

Copyright

(Copyright © 2012, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s10439-012-0519-2

PMID

22298329

Abstract

Blast-related traumatic brain injury is the most prevalent injury for combat personnel seen in the current conflicts in Iraq and Afghanistan, yet as a research community, we still do not fully understand the detailed etiology and pathology of this injury. Finite element (FE) modeling is well suited for studying the mechanical response of the head and brain to blast loading. This paper details the development of a FE head and brain model for blast simulation by examining both the dilatational and deviatoric response of the brain as potential injury mechanisms. The levels of blast exposure simulated ranged from 50 to 1000 kPa peak incident overpressure and 1-8 ms in positive-phase duration, and were comparable to real-world blast events. The frontal portion of the brain had the highest pressures corresponding to the location of initial impact, and peak pressure attenuated by 40-60% as the wave propagated from the frontal to the occipital lobe. Predicted brain pressures were primarily dependent on the peak overpressure of the impinging blast wave, and the highest predicted brain pressures were 30% less than the reflected pressure at the surface of blast impact. Predicted shear strain was highest at the interface between the brain and the CSF. Strain magnitude was largely dependent on the impulse of the blast, and primarily caused by the radial coupling between the brain and deforming skull. The largest predicted strains were generally less than 10%, and occurred after the shock wave passed through the head. For blasts with high impulses, CSF cavitation had a large role in increasing strain levels in the cerebral cortex and periventricular tissues by decoupling the brain from the skull. Relating the results of this study with recent experimental blast testing suggest that a rate-dependent strain-based tissue injury mechanism is the source primary blast TBI.

Language: en