Early stage cerebral aneurysms are characterized by the disruption of the internal elastic lamina. The cause of this breakdown is still not understood, but it has been conjectured to be due to fatigue failure and/or by a breakdown in homeostatic mechanisms in the wall arising from some aspect of the local hemodynamics and wall tension. We propose to model this disruption using a structural damage model. It is built on a previously introduced nonlinear, inelastic multi-mechanism model for cerebral arteries (2005, “An Inelastic Multi-Mechanism Constitutive Equation for Cerebral Arterial Tissue,” Biomech. Model. Mechanobiol., 4(4), pp. 235–248), as well as a recent generalization to include the wall anisotropy (2009, “A Structural Multi-Mechanism Constitutive Equation for Cerebral Arterial Tissue,” Int. J. Solids Struct., 46(14–15), pp. 2920–2928). The current model includes subfailure damage of the elastin, represented by changes in the tissue mechanical properties and unloaded reference length. A structural model is used to characterize the gradual degradation, failure of elastin, and recruitment of anisotropic collagen fibers. The collagen fibers are arranged in two helically oriented families with dispersion in their orientation. Available inelastic experimental data for cerebral arteries are used to evaluate the constitutive model. It is then implemented in a commercial finite element analysis package and validated using analytical solutions with representative values for cerebral arterial tissue.

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