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A Transition Model for Finite Element Simulation of Kinematics of Central Nervous System White Matter

机译:中枢神经系统白质运动学有限元模拟的过渡模型

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摘要

Mechanical damage to axons is a proximal cause of deficits following traumatic brain injury and spinal cord injury. Axons are injured predominantly by tensile strain, and identifying the strain experienced by axons is a critical step toward injury prevention. White matter demonstrates complex nonlinear mechanical behavior at the continuum level that evolves from even more complex, dynamic, and composite behavior between axons and the “glial matrix” at the microlevel. In situ, axons maintain an undulated state that depends on the location of the white matter and the stage of neurodevelopment. When exposed to tissue strain, axons do not demonstrate pure affine or non-affine behavior, but instead transition from non-affine-dominated kinematics at low stretch levels to affine kinematics at high stretch levels. This transitional and predominant kinematic behavior has been linked to the natural coupling of axons to each other via the glial matrix. In this paper, a transitional kinematic model is applied to a micromechanics finite element model to simulate the axonal behavior within a white matter tissue subjected to uniaxial tensile stretch. The effects of the transition parameters and the volume fraction of axons on axonal behavior is evaluated and compared to previous experimental data and numerical simulations.
机译:轴突的机械损伤是外伤性脑损伤和脊髓损伤后缺陷的近端原因。轴突主要受到拉伸应变的伤害,识别轴突承受的应变是预防伤害的关键步骤。白质在连续水平上表现出复杂的非线性力学行为,这种微观力学行为是从轴突和“胶质基质”在微观水平上更为复杂,动态和复合的行为演变而来的。原位,轴突维持起伏的状态,这取决于白质的位置和神经发育的阶段。当暴露于组织应变时,轴突不表现出纯仿射或非仿射行为,而是从低拉伸水平的非仿射为主的运动学转变为高拉伸水平的仿射运动学。这种过渡性的和主要的运动学行为已经通过神经胶质基质与轴突彼此之间的自然偶联联系在一起。在本文中,将过渡运动学模型应用于微力学有限元模型,以模拟白质组织在单轴拉伸下的轴突行为。过渡参数和轴突的体积分数对轴突行为的影响进行了评估,并与以前的实验数据和数值模拟进行了比较。

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