STRUCTURAL MULTI-MECHANISM MODEL Model FOR CEREBRAL ARTERIAL TISSUE with Damage

Intracranial arteries (ICA) are abnormal saccular dilations of cerebral arteries, commonly found at apices of arterial bifurcations and curved segments of arteries at the base of the brain. If untreated, an ICA can continue to expand until rupture, resulting in hemorrhage which is followed by death or severe disability in the majority of patients. Screening and preventative treatment strategies are notably absent in the clinical handling of this disease. This is in stark contrast to other diseases such as atherosclerosis, in which detailed knowledge of the pathobiology is instrumental in establishing screening procedures and developing effective pharmaceutical treatments such as statins.

This talk will focus on research directed at modeling the development of ICA from a segment of arterial tissue. Early stage cerebral aneurysms are characterized by the disruption of the internal elastic lamina (IEL). The cause of this breakdown is still not understood, but it has been conjectured to be caused by fatigue failure or alternatively 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 builds on a previously introduced nonlinear, inelastic multi-mechanism model for cerebral arteries (Wulandana, Robertson, 2005), as well as a recent generalization to include the wall anisotropy (Li, Robertson, 2009). In the multi-mechanism model, elastin and collagen fibers are treated as separate components (mechanisms) of the artery. The aniostropic material response of the wall is introduced through the collagen mechanism which is composed of helically distributed families of fibers.
The orientation of these families is described using either a finite number of fiber orientations or using a fiber distribution function. The current model includes subfailure damage of elastin, represented by changes in tissue mechanical properties and unloaded reference length. A structural model is used to characterize 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. Inelastic experimental data for cerebral arteries are used to evaluate the constitutive model.