Biomechanism of traumatic brain injury induced by acceleration based on animal models
- 1Key Laboratory of Biomechanics and Mechanobiology (Beihang University), Ministry of Education, Beijing Advanced Innovation Center for Biomedical Engineering, School of Biological Science and Medical Engineering, Beihang University, Beijing, 100191, China
- 2China Automotive Technology and Research Center Co. Ltd, Tianjin, 300300, China
Abstract
Acceleration-induced traumatic brain injury (TBI) arises from rapid motion generated by external mechanical loading. Its major biomechanical responses include intracranial pressure changes and brain tissue deformation. These responses are strongly influenced by the type and characteristics of acceleration. We summarize biomechanical studies of acceleration-induced TBI based on animal models, with emphasis on linear, rotational, and combined acceleration. Evidence from these models is integrated across brain tissue responses, injury patterns, model validation, and imaging assessment. Linear acceleration mainly induces intracranial pressure gradients and local tissue compression. Rotational acceleration more commonly causes shear deformation and multiaxial strain in white matter fibers and is closely associated with axonal injury. In real-world head impacts, linear and rotational motions usually occur together. Their interaction may induce both focal and diffuse injuries and complicates the identification of individual injury mechanisms. Animal models differ in brain anatomy, loading methods, and kinematic characteristics. Model validation should be based on actual head motion and include intracranial pressure, brain deformation, and neuropathological outcomes. Neuroimaging provides important complementary information for detecting microstructural injury. Diffusion tensor imaging, magnetization transfer imaging, quantitative susceptibility mapping, and multiparametric magnetic resonance imaging can reveal abnormalities that may not be visible on conventional structural imaging. However, heterogeneity in kinematic control, head–neck constraints, brain anatomy, and injury assessment limits cross-study comparison and cross-species translation. Future studies should integrate finite element modeling, multimodal imaging, histopathology, and functional assessment to establish quantitative relationships among external loading, local tissue deformation, and injury outcomes.
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BibTeX
@article{liang2026biomechanism,
title = {{Biomechanism of traumatic brain injury induced by acceleration based on animal models}},
author = {Xin Liang and Weidong Liu and Zhixin Liu and Lizhen Wang and Yubo Fan},
journal = {Medicine in Novel Technology and Devices},
year = {2026},
month = oct,
doi = {10.1016/j.medntd.2026.100467},
url = {https://doi.org/10.1016/j.medntd.2026.100467},
note = {CC BY},
}
RIS
TY - JOUR
TI - Biomechanism of traumatic brain injury induced by acceleration based on animal models
AU - Xin Liang
AU - Weidong Liu
AU - Zhixin Liu
AU - Lizhen Wang
AU - Yubo Fan
PY - 2026
DA - 2026/10/30
JO - Medicine in Novel Technology and Devices
DO - 10.1016/j.medntd.2026.100467
UR - https://doi.org/10.1016/j.medntd.2026.100467
AB - Acceleration-induced traumatic brain injury (TBI) arises from rapid motion generated by external mechanical loading. Its major biomechanical responses include intracranial pressure changes and brain tissue deformation. These responses are strongly influenced by the type and characteristics of acceleration. We summarize biomechanical studies of acceleration-induced TBI based on animal models, with emphasis on linear, rotational, and combined acceleration. Evidence from these models is integrated across brain tissue responses, injury patterns, model validation, and imaging assessment. Linear acceleration mainly induces intracranial pressure gradients and local tissue compression. Rotational acceleration more commonly causes shear deformation and multiaxial strain in white matter fibers and is closely associated with axonal injury. In real-world head impacts, linear and rotational motions usually occur together. Their interaction may induce both focal and diffuse injuries and complicates the identification of individual injury mechanisms. Animal models differ in brain anatomy, loading methods, and kinematic characteristics. Model validation should be based on actual head motion and include intracranial pressure, brain deformation, and neuropathological outcomes. Neuroimaging provides important complementary information for detecting microstructural injury. Diffusion tensor imaging, magnetization transfer imaging, quantitative susceptibility mapping, and multiparametric magnetic resonance imaging can reveal abnormalities that may not be visible on conventional structural imaging. However, heterogeneity in kinematic control, head–neck constraints, brain anatomy, and injury assessment limits cross-study comparison and cross-species translation. Future studies should integrate finite element modeling, multimodal imaging, histopathology, and functional assessment to establish quantitative relationships among external loading, local tissue deformation, and injury outcomes.
SN - 2590-0935
ER -