Biofidelity Assessment of the WIAMan Thorax by a Comparative Study With Hybrid III, THOR, and PMHS in Frontal Sled Testing.

The Warrior Injury Assessment Manikin (WIAMan) anthropomorphic test device (ATD) has been originally developed to predict and prevent injuries for occupants in military vehicles, in an underbody blast environment. However, its crash performance and biofidelity of the thoracic region have not been explored. The aim of this study was to determine and evaluate the WIAMan thoracic responses in a typical frontal sled test. The 40 kph frontal sled tests were conducted to quantify the WIAMan thoracic kinematics, chest deflection, and belt loads. Comparative biofidelities of the WIAMan thorax and other surrogates, including postmortem human surrogates (PMHSs), Hybrid III, and test device for human occupant restraint (THOR) ATDs, were assessed under comparable testing conditions. The similarities and differences between WIAMan and the other surrogates were compared and analyzed, including the motion of bilateral shoulders and T1, time histories of chest deflections, and belt loads. The CORrelation and Analysis (CORA) ratings were used to evaluate the correlations of thoracic responses between the ATDs and PMHS. Compared to the PMHS and THOR, the WIAMan experienced a similar level of left shoulder forward excursions. Larger chest deflection was exhibited in WIAMan throughout the whole duration of belt compression. Differences were found in belt loads between subject types. Overall, WIAMan had slightly lower CORA scores but showed comparable overall performance. The overall thoracic responses of WIAMan under the frontal sled test were more compliant than HIII, but still reasonable compared with PMHS and THOR. Comprehensive systematic studies on comparative biofidelity of WIAMan and other surrogates under different impact conditions are expected in future research.

The Effect of Muscle Activation on Head Kinematics During Non-injurious Head Impacts in Human Subjects.

In this study, twenty volunteers were subjected to three, non-injurious lateral head impacts delivered by a 3.7 kg padded impactor at 2 m/s at varying levels of muscle activation (passive, co-contraction, and unilateral contraction). Electromyography was used to quantify muscle activation conditions, and resulting head kinematics were recorded using a custom-fit instrumented mouthpiece. A multi-modal battery of diagnostic tests (evaluated using neurocognitive, balance, symptomatic, and neuroimaging based assessments) was performed on each subject pre- and post-impact. The passive muscle condition resulted in the largest resultant head linear acceleration (12.1 ± 1.8 g) and angular velocity (7.3 ± 0.5 rad/s). Compared to the passive activation, increasing muscle activation decreased both peak resultant linear acceleration and angular velocity in the co-contracted (12.1 ± 1.5 g, 6.8 ± 0.7 rad/s) case and significantly decreased in the unilateral contraction (10.7 ± 1.7 g, 6.5 ± 0.7 rad/s) case. The duration of angular velocity was decreased with an increase in neck muscle activation. No diagnostic metric showed a statistically or clinically significant alteration between baseline and post-impact assessments, confirming these impacts were non-injurious. This study demonstrated that isometric neck muscle activation prior to impact can reduce resulting head kinematics. This study also provides the data necessary to validate computational models of head impact.

Biomechanics of the Human Brain during Dynamic Rotation of the Head.

Traumatic brain injuries (TBI) are a substantial societal burden. The development of better technologies and systems to prevent and/or mitigate the severity of brain injury requires an improved understanding of the mechanisms of brain injury, and more specifically, how head impact exposure relates to brain deformation. Biomechanical investigations have used computational models to identify these relations, but more experimental brain deformation data are needed to validate these models and support their conclusions. The objective of this study was to generate a dataset describing in situ human brain motion under rotational loading at impact conditions considered injurious. Six head-neck human post-mortem specimens, unembalmed and never frozen, were instrumented with 24 sonomicrometry crystals embedded throughout the parenchyma that can directly measure dynamic brain motion. Dynamic brain displacement, relative to the skull, was measured for each specimen with four loading severities in the three directions of controlled rotation, for a total of 12 tests per specimen. All testing was completed 42-72 h post-mortem for each specimen. The final dataset contains approximately 5,000 individual point displacement time-histories that can be used to validate computational brain models. Brain motion was direction-dependent, with axial rotation resulting in the largest magnitude of displacement. Displacements were largest in the mid-cerebrum, and the inferior regions of the brain-the cerebellum and brainstem-experienced relatively lower peak displacements. Brain motion was also found to be positively correlated to peak angular velocity, and negatively correlated with angular velocity duration, a finding that has implications related to brain injury risk-assessment methods. This dataset of dynamic human brain motion will form the foundation for the continued development and refinement of computational models of the human brain for predicting TBI.

An Analytical Review of the Numerical Methods used for Finite Element Modeling of Traumatic Brain Injury.

Dozens of finite element models of the human brain have been developed for providing insight into the mechanical response of the brain during impact. Many models used in traumatic brain injury research are based on different computational techniques and approaches. In this study, a comprehensive review of the numerical methods implemented in 16 brain models was performed. Differences in element type, mesh size, element formulation, hourglass control, and solver were found. A parametric study using the SIMon FE brain model was performed to quantify the sensitivity of model outputs to differences in numerical implementation. Model outputs investigated in this study included nodal displacement (commonly used for validation) and maximum principal strain (commonly used for injury assessment), and these results were demonstrated using the loading characteristics of a reconstructed football concussion event. Order-of-magnitude differences in brain response were found when only changing the characteristics of the numerical method. Mesh type and mesh size had the largest effect on model response. These differences have important implications on the interpretation of results among different models simulating the same impacts, and of the results between model and in vitro experiments. Additionally, future studies need to better report the numerical methods used in the models.

Long Term Temporal Changes in Structure and Function of Rat Visual System After Blast Exposure.

Purpose: We identify long-term ocular sequelae subsequent to experimental blast exposure. Methods: Male Long-Evans rats were exposed to 230 kPa side-on primary blast overpressure using a compressed air driven shock tube. Visual system function and structure were assessed for 8 weeks after exposure using optokinetic nystagmus and optical coherence tomography. Vitreous protein expression and histology (TUNEL, H&E) were performed at 1 day and 1, 4, and 8 weeks. IOP was recorded bilaterally during blast in a subset of animals. Results: Blast pressure profiles resembled the Friedlander waveform indicative of an open field blast. Peak IOP in directly-exposed eyes (240 kPa) was similar to peak blast overpressure, but IOP in indirectly-exposed eyes was 30% lower. Contrast sensitivity of blast-exposed animals decreased significantly by 20% 1 day after blast and did not recover by 8 weeks. Significant swelling and structural damage to the corneal epithelial and stromal layers were observed 2 weeks after blast exposure. Swollen corneas increased 254 ± 143 µm from baseline by 6 weeks, and scarring developed by 8 weeks. Histology revealed additional lens pathology 1 week after blast, suggestive of cataract development. Endothelial cell density increased significantly in blast-exposed animals between 1 and 4 weeks. Neurofilament heavy chain significantly increased after blast and returned to near baseline values by 8 weeks. Inflammatory cytokine changes corroborated ocular pathology findings. Conclusions: These data demonstrate immediate visual dysfunction and biochemical responses, but delayed structural pathology, in response to single primary blast exposure. The delayed pathology time course may provide a window to implement treatment strategies for improved visual outcome.