Localizing Clinical Patterns of Blast Traumatic Brain Injury Through Computational Modeling and Simulation

Abstract

Blast traumatic brain injury is ubiquitous in modern military conflict with significant morbidity and mortality. Yet the mechanism by which blast overpressure waves cause specific intracranial injury in humans remains unclear. Reviewing of both the clinical experience of neurointensivists and neurosurgeons who treated service members exposed to blast have revealed a pattern of injury to cerebral blood vessels, manifested as subarachnoid hemorrhage, pseudoaneurysm, and early diffuse cerebral edema. Additionally, a seminal neuropathologic case series of victims of blast traumatic brain injury (TBI) showed unique astroglial scarring patterns at the following tissue interfaces: subpial glial plate, perivascular, periventricular, and cerebral gray-white interface. The uniting feature of both the clinical and neuropathologic findings in blast TBI is the co-location of injury to material interfaces, be it solid-fluid or solid-solid interface. This motivates the hypothesis that blast TBI is an injury at the intracranial mechanical interfaces. In order to investigate the intracranial interface dynamics, we performed a novel set of computational simulations using a model human head simplified but containing models of gyri, sulci, cerebrospinal fluid (CSF), ventricles, and vasculature with high spatial resolution of the mechanical interfaces. Simulations were performed within a hybrid Eulerian-Lagrangian simulation suite (CTH coupled via Zapotec to Sierra Mechanics). Because of the large computational meshes, simulations required high performance computing resources. Twenty simulations were performed across multiple exposure scenarios-overpressures of 150, 250, and 500 kPa with 1 ms overpressure durations-for multiple blast exposures (front blast, side blast, and wall blast) across large variations in material model parameters (brain shear properties, skull elastic moduli). All simulations predict fluid cavitation within CSF (where intracerebral vasculature reside) with cavitation occurring deep and diffusely into cerebral sulci. These cavitation events are adjacent to high interface strain rates at the subpial glial plate. Larger overpressure simulations (250 and 500kPa) demonstrated intraventricular cavitation-also associated with adjacent high periventricular strain rates. Additionally, models of embedded intraparenchymal vascular structures-with diameters as small as 0.6 mm-predicted intravascular cavitation with adjacent high perivascular strain rates. The co-location of local maxima of strain rates near several of the regions that appear to be preferentially damaged in blast TBI (vascular structures, subpial glial plate, perivascular regions, and periventricular regions) suggest that intracranial interface dynamics may be important in understanding how blast overpressures leads to intracranial injury.

Keywords: blast; cavitation; computation; interfacial injury; simulation; traumatic brain injury.

Figure 1

Construction of test object from principle investigators brain magnetic resonance imaging (MRI): (A) Axial section of principal investigators brain with measurements of length scales of width, length, gyral thickness, gray matter thickness, sulci width, sulci depth, average skull thickness. (Not shown is coronal section to determine height length scale). Using obtained length scales from axial section, CAD developed canonical axial brain slice. (B) This axial brain slice was visually compared to original axial slice to ensure gross representation of dominant length scales, then slice was extruded to match the height of human brain. (C) This extruded axial prism was meshed to create three dimensional test object. (D) Results presented are two dimensional projections of the element values from the mid-plane of test object.

Figure 2

Surrogate head model and embedding finite element solver into gas dynamics solver.

Figure 3

Simulation scenarios of front, side, and wall blast. Later time simulation of wall shown to highlight complexity of reflected waves between skull and head.

Figure 4

Canonical Blast Results: (a) Cavitation events are highlighted in red. This simulation highlights both parenchymal cavitation events (smaller box) and sulcal cavitation events (larger box). (b) Zoomed shear strain around three gyri of interest, label “1,” “2,” and “3.” (c) Dilatational strain. (d) Shear strain rate. (e) Dilatational strain rate. (f) Shear strain region of parenchymal cavitation. (g) dilatational strain in region of parenchymal cavitation. (h) Shear strain rate in region of parenchymal cavitation (i) dilatational strain rate in region of parenchymal cavitation.

Figure 5

Vascular simulation results at 2.5 ms. (A) Cross-section of vascular model. Highlighted are the vessel models of diameters of 0.6, 0.8, 1.2, and 1.6 mm. Vessels are numbered from lateral to medial position. (B) Shear strain maximum in early time simulation. (C) Shear strain rate in early time simulation. (D) Intravascular cavitation events of 0.6 mm vessel –position 6 (top). Focal strain rates within vessel wall (bottom). (E) Total vessel cavitation volume as function of position and diameter. (F) Percent of vessel volume cavitation as a function of position and diameter.

Figure 6

Cumulative cavitation events as a function of blast exposure over entire 6 ms simulation.

Figure 7

Parameter study. Simulation results (cavitation, shear strain, and shear strain rate) in Normal simulations, shear “softened” simulations, and 8.0 GPa skull.