历史至关重要：反复头部撞击下损伤介导的脑变形与损伤风险放大效应
History Matters: Damage-Mediated Amplification of Brain Deformation and Injury Risk under Repeated Head Impacts
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中文总结 AI 辅助
该研究在高保真有限元头部模型中引入Ogden-Roxburgh Mullins损伤公式，发现反复头部撞击下，损伤介导的软化会显著放大脑变形与损伤风险，提示需完善相关模型以更准确评估反复载荷下的脑损伤风险。
中文摘要 AI 辅助
计算头部模型通常仅应用于孤立撞击场景，而反复头部载荷的作用在很大程度上未被探索。本研究在高保真有限元头部模型中引入Ogden-Roxburgh Mullins损伤公式，以表征循环脑组织变形中依赖载荷历史的软化效应。研究采用混合武术头部撞击数据得到的反复载荷历史，与无损伤的超弹性（HE）及线性粘超弹性（LVHE）模型变体进行对比。在五次相同的单轴循环载荷下，与HE模型相比，Mullins型软化逐渐增大了应变及应变率指标；基于Mullins模型的损伤概率逐渐超过基于应变的HE模型预测值，且与基于运动学的不变预测值出现偏离，表明忽略前期软化可能低估损伤风险。在随机二十次多轴循环序列中，相同运动学强度的循环因前期软化程度不同，产生不同的变形与损伤风险估计值：HE和LVHE模型初始预测的损伤概率更高，而Mullins模型在后续循环中产生最大估计值，且序列中至少发生一次损伤的概率最高。区域放大效应取决于载荷方向与前期软化程度，脑亚结构间无方向独立的趋势；脑回单元的累积最大主应变高于脑沟单元，脑沟单元相对于初始响应的放大程度更大。这些发现表明，在相同载荷历史下，短期损伤介导的软化可使组织变形与损伤风险估计值较无损伤头部模型显著放大；需进一步开展循环脑组织软化的实验表征，以完善反复头部载荷与创伤性脑损伤模型。
英文摘要
Computational head models are typically applied to isolated impacts, leaving repeated head loading largely unexplored. An Ogden-Roxburgh Mullins damage formulation was implemented in a high-fidelity finite element head model to represent loading-history-dependent softening during cyclic brain-tissue deformation. Repeated-loading histories derived from mixed martial arts head-impact data were applied and compared with damage-free hyperelastic (HE) and linear visco-hyperelastic (LVHE) model variants. Under five identical single-axis cycles, Mullins-type softening progressively increased strain and strain rate metrics relative to the HE model. Mullins-based injury probabilities progressively exceeded strain-based HE predictions and diverged from unchanged kinematics-based predictions, indicating that neglecting prior softening may underestimate injury risk. In a randomized twenty-cycle multiaxial sequence, cycles of similar kinematic intensity produced different deformation and injury-risk estimates depending on prior softening. HE and LVHE models predicted higher injury probabilities initially, whereas the Mullins-based model produced the largest later-cycle estimates and highest probability of at least one injury over the sequence. Regional amplification depended on loading direction and prior softening, with no direction-independent trend among brain substructures. Gyral elements exhibited higher cumulative maximum principal strain than sulcal elements, which showed greater amplification relative to initial responses. These findings demonstrate that short-term damage-mediated softening can substantially amplify tissue deformation and injury-risk estimates beyond damage-free head models under the same loading histories. Further experimental characterization of cyclic brain-tissue softening is needed to improve models of repeated head loading and traumatic brain injury.
