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Localizing Clinical Patterns of Blast Traumatic Brain Injury Through Computational Modeling and Simulation.
Scott T Miller1, Candice F Cooper2, Paul Elsbernd3
1Computational Solid Mechanics & Structural Dynamics, Sandia National Laboratories, Albuquerque, NM, United States.
Frontiers in Neurology
|June 7, 2021
Summary
Blast traumatic brain injury (TBI) causes intracranial injury at mechanical interfaces. Computational simulations reveal cavitation and high strain rates in vulnerable brain regions, suggesting a new injury mechanism.
Area of Science:
- Neuroscience
- Biomechanics
- Computational Modeling
Background:
- Blast traumatic brain injury (TBI) is a prevalent injury in modern military conflicts, with unclear mechanisms of intracranial damage.
- Clinical and neuropathologic findings in blast TBI reveal injury patterns at material interfaces within the brain, such as blood vessels and glial layers.
- A hypothesis suggests blast TBI results from mechanical stresses at intracranial interfaces.
Purpose of the Study:
- To investigate the hypothesis that blast TBI is caused by mechanical forces acting on intracranial interfaces.
- To explore the dynamics of intracranial mechanical interfaces under blast overpressure conditions using computational simulations.
Main Methods:
- Developed a high-resolution computational model of the human head, including gyri, sulci, cerebrospinal fluid (CSF), ventricles, and vasculature.
- Utilized a hybrid Eulerian-Lagrangian simulation suite (CTH coupled via Zapotec to Sierra Mechanics) on high-performance computing resources.
- Performed twenty simulations across various blast overpressures (150-500 kPa), durations (1 ms), exposure directions (front, side, wall), and material property variations.
Main Results:
- Simulations predicted fluid cavitation within the CSF, particularly in cerebral sulci, adjacent to high interface strain rates at the subpial glial plate.
- Higher overpressure simulations (250-500 kPa) showed intraventricular cavitation associated with high periventricular strain rates.
- Intravascular cavitation was predicted in simulated vascular structures (0.6 mm diameter) with adjacent high perivascular strain rates.
Conclusions:
- The study suggests that blast TBI may be an injury mechanism occurring at intracranial mechanical interfaces.
- Co-location of predicted high strain rates and cavitation near vulnerable brain regions (vasculature, glial plate, perivascular, periventricular areas) supports this hypothesis.
- Computational modeling provides insights into the biomechanics of blast TBI, highlighting the role of interface dynamics in injury causation.
