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.

Sulcal Cavitation in Linear Head Acceleration: Possible Correlation With Chronic Traumatic Encephalopathy

“…To the authors knowledge, this is the first experimental data localizing intra-sulcal cavitation and capturing the resultant response of model gyri / sulci during head trauma. Previous studies ( 29 , 30 , 34 , 35 ) also observed cavitation as a result of loading and recent computational results also suggest intrasulcal cavitation could occur during blast exposure ( 46 ). However, the previously reported experiments supporting the cavitation mechanism either incorporated a neck-model directly, or observed the cavitation after the onset of rotational or angular acceleration.…”

“…Arterial vasculature resides in the same subarachnoid space where cavitation is hypothesized to exist and thus could be directly injured from a cavitation event. The presence of vascular structures within the CSF space further confines fluid and this confinement could increase likelihood of cavitation—as has been suggested in computational simulations of blast injury ( 46 ). However, the mechanisms of cavitation within confined fluid spaces remain complex and will require dedicated studies.…”

Measuring vibrations on a biofidelic brain using ferroelectret nanogenerator

“…1 b and c. This model demonstrates the overall size characteristics of the human brain with the interactions of the sulci and gyri (folds and grooves). This phantom was reviewed and verified by a board-certified neurologist who confirmed the phenomenology similarity with a real brain 18 . The computational model was able to show higher strains within the brain interfaces and folds, supporting the hypothesis that blast TBI causes more damage in sulci and gyri 18 .…”

“…This phantom was reviewed and verified by a board-certified neurologist who confirmed the phenomenology similarity with a real brain 18 . The computational model was able to show higher strains within the brain interfaces and folds, supporting the hypothesis that blast TBI causes more damage in sulci and gyri 18 . To build a brain phantom suitable for experiments, Wermer et al studied different materials to determine the best biofidelic representative of the brain matter.…”

Long-Term Effects of Repeated Blast Exposure in United States Special Operations Forces Personnel: A Pilot Study Protocol

“… 7 , 14 , 15 The potential injury to neurons, glia, and cerebrovasculature may be heterogeneous with respect to anatomic distribution, cell type, and severity. 16 This pathophysiological heterogeneity may explain the broad range of mutually exacerbating symptoms experienced by highly exposed military personnel. 17–21 …”