Computational modeling investigation of pulsed high peak power microwaves and the potential for traumatic brain injury.

When considering safety standards for human exposure to radiofrequency (RF) and microwave energy, the dominant concerns pertain to a thermal effect. However, in the case of high-power pulsed RF/microwave energy, a rapid thermal expansion can lead to stress waves within the body. In this study, a computational model is used to estimate the temperature profile in the human brain resulting from exposure to various RF/microwave incident field parameters. The temperatures are subsequently used to simulate the resulting mechanical response of the brain. Our simulations show that, for certain extremely high-power microwave exposures (permissible by current safety standards), very high stresses may occur within the brain that may have implications for neuropathological effects. Although the required power densities are orders of magnitude larger than most real-world exposure conditions, they can be achieved with devices meant to emit high-power electromagnetic pulses in military and research applications.

Nonlinearity of the coefficient of thermal expansion in brain tissue.

The coefficient of thermal expansion (CTE) in biological tissues is an integral parameter behind the application of electromagnetic energy to biomedical technologies; however, its behavior is far from being fully characterized. In this study, we apply digital image correlation (DIC) to non-invasively measure the microscale thermal expansions of recently excised embryonic E18 rodent brain tissue slices. Although the CTE has been measured previously in soft tissues, the literature surrounding the expansion of brain tissue remains sparse. Previous work in measuring the thermal expansion behavior of soft tissue often simplifies the results into a single measurement of a linear CTE parameter and fails to convey the temperature-dependent nonlinearity that exists. In this work, we demonstrate that: (1) the coefficient of brain tissue is more similar to fat than blood, and (2) there exists a significant nonlinear increase in CTE at physiologically-relevant temperatures. This suggests some limitations with the interpretation of previously reported values of the CTE, which are often measured at room temperature.

A computational investigation of strain concentration in the brain in response to a rapid temperature rise.

Following the mysterious health attacks on U.S. diplomats in Cuba in 2016, the cause of concussion-like symptoms concurrent with strange noises heard by the diplomats remains undetermined. A wide range of possible causes of the sensations have been proposed: pulsed microwave exposure, infrasound acoustic devices, pesticides/neurotoxins, and even mass hysteria (psychogenic illness). Here, we numerically examine the pulsed microwave exposure hypothesis and the simulated mechanical response of brain tissue. A computational model is used to examine the influence of various spatially varying temperature gradients and pulse durations on the mechanical response of brain tissue. We show that a stress-focusing effect due to a rapid temperature increase may result in brain tissue strains larger than the initially applied thermal strains.

Quantifying the Local Mechanical Properties of Cells in a Fibrous Three-Dimensional Microenvironment.

Measurements of the mechanical response of biological cells are critical for understanding injury and disease, for developing diagnostic tools, and for computational models in mechanobiology. Although it is well known that cells are sensitive to the topography of their microenvironment, the current paradigm in mechanical testing of adherent cells is mostly limited to specimens grown on flat two-dimensional substrates. In this study, we introduce a technique in which cellular indentation via optical trapping is performed on cells at a high spatial resolution to obtain their regional mechanical properties while they exist in a more favorable three-dimensional microenvironment. We combine our approach with nonlinear contact mechanics theory to consider the effects of a large deformation. This allows us to probe length scales that are relevant for obtaining overall cell stiffness values. The experimental results herein provide the hyperelastic material properties at both high (∼100 s-1) and low (∼1-10 s-1) strain rates of murine central nervous system glial cells. The limitations due to possible misalignment of the indenter in the three-dimensional space are examined using a computational model.

A mechanism for injury through cerebral arteriole inflation.

An increase in arterial pressure within the cerebral vasculature appears to coincide with ischemia and dysfunction of the neurovascular unit in some cases of traumatic brain injury. In this study, we examine a new mechanism of brain tissue damage that results from excessive cerebral arteriole pressurization. We begin by considering the morphological and material properties of normotensive and hypertensive arterioles and present a computational model that captures the interaction of neighboring pressurized arterioles and the surrounding brain tissue. Assuming an axonal strain-induced injury criterion, we find that the injury depends on vessel spacing, proximity to an unconfined free surface, and the relative difference in stiffness between the arterioles and the surrounding tissue. We find that a steeper heterogeneity (stiffer vessels surrounded by softer brain tissue) causes larger axial strains to develop at some distance from the arteriole wall, within the brain parenchyma. For a more gradual heterogeneity (softer vessels), we observe more larger strain fields close to the arteriole walls. Both deformation patterns are comparable to damage seen in previous pathology studies on postmortem TBI patients. Finally, we use an analytical model to approximate the interplay between internal pressure, arteriole thickness, and the variation in mechanical properties of arterioles.

Combining the finite element method with structural connectome-based analysis for modeling neurotrauma: connectome neurotrauma mechanics.

This article presents the integration of brain injury biomechanics and graph theoretical analysis of neuronal connections, or connectomics, to form a neurocomputational model that captures spatiotemporal characteristics of trauma. We relate localized mechanical brain damage predicted from biofidelic finite element simulations of the human head subjected to impact with degradation in the structural connectome for a single individual. The finite element model incorporates various length scales into the full head simulations by including anisotropic constitutive laws informed by diffusion tensor imaging. Coupling between the finite element analysis and network-based tools is established through experimentally-based cellular injury thresholds for white matter regions. Once edges are degraded, graph theoretical measures are computed on the "damaged" network. For a frontal impact, the simulations predict that the temporal and occipital regions undergo the most axonal strain and strain rate at short times (less than 24 hrs), which leads to cellular death initiation, which results in damage that shows dependence on angle of impact and underlying microstructure of brain tissue. The monotonic cellular death relationships predict a spatiotemporal change of structural damage. Interestingly, at 96 hrs post-impact, computations predict no network nodes were completely disconnected from the network, despite significant damage to network edges. At early times (t < 24 hrs) network measures of global and local efficiency were degraded little; however, as time increased to 96 hrs the network properties were significantly reduced. In the future, this computational framework could help inform functional networks from physics-based structural brain biomechanics to obtain not only a biomechanics-based understanding of injury, but also neurophysiological insight.