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Finite Element Analysis of Traumatic Subdural Hematoma

机译:创伤性硬膜体血肿的有限元分析

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A two-dimensional finite element model of the head of a rhesus monkey was built to simulate the head acceleration experiments done by Gennarelli and his colleagues. The purposes of the study were to better understand the mechanisms of traumatic subdural hematoma and to estimate its threshold of occurrence. The brain was treated as an isotropic homogeneous elastic material with and without structural damping and the skull was treated as a rigid shell. To simulate Abel et al.'s (1) experiments, the head was subjected to an enforced forward rotation around the neck. The loading had an initial acceleration phase followed by deceleration. During both acceleration and deceleration phases, high shear stress (and thus strain) occurred at the vertex, where the parasagittal bridging veins are located. The deformation of the bridging vein depended on its orientation relative to the direction of impact. Bridging veins that drain forward into the superior sagittal sinus would be stretched during the acceleration phase and would be compressed during deceleration. Therefore, subdural hematoma may have occurred during the acceleration phase in the primate experiments, in contrast to Gennarelli and Thibault's (2) belief that this phase could be neglected in analyzing the subdural hematoma data. The head motion could be reduced to equivalent rotational and translational components at the head center of mass. With a brain Poisson's ratio of 0.475, both components contributed equally to bridging vein deformation. At a Poisson's ratio of 0.49, rotational acceleration was the dominant factor. Translational acceleration, although less important, did influence deformations and should not be neglected in analyzing the tolerance data of subdural hematoma. The primate subdural hematoma data were replotted in terms of peak angular vs. peak tangential accelerations. The combined effects of tangential and angular accelerations on bridging vein deformation, as determined at the lower levels of test severity from the finite element analysis, were used to estimate tolerance thresholds for subdural hematoma in the experiments.
机译:建立了恒河猴头部的二维有限元模型,以模拟Gennarelli和他的同事所做的头部加速实验。该研究的目的是更好地理解创伤性硬膜体血肿的机制,并估计其发生阈值。将脑被视为具有并且没有结构阻尼的各向同性均匀弹性材料,并且颅骨被处理为刚性壳。为了模拟abel等人。(1)实验,头部围绕颈部的强制前进旋转。装载具有初始加速阶段,然后进行减速。在加速度和减速相期间,在顶点发生高剪切应力(和因此应变),其中放气桥静脉位于顶点。桥接静脉的变形相对于撞击方向取决于其取向。在加速相期间延伸进入卓越的矢状窦中的桥接静脉将在减速期间被拉伸。因此,在灵长类动物实验中的加速阶段期间可能发生了硬膜镜血肿,与Gennarelli和Thibault(2)相比,这种相对于分析软骨血肿数据可以忽略该阶段。头部运动可以在头部头部中心的等效旋转和平移组件。随着脑泊松的比例为0.475,两种部件同样贡献到桥接静脉变形。在泊松比例为0.49,旋转加速度是显性因素。平移加速度虽然不太重要,但在分析软骨血肿的耐受性数据时不容忽视变形。在峰角与峰值切向加速度方面,重新激发灵长类的硬膜体血肿数据。与有限元分析中的测试严重程度下降的桥接和角度加速度对桥接静脉变形的联系和角度加速的组合效应用于估计实验中的软骨血肿的耐受性阈值。

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