Stresses and fluid flow in lamina cribrosa through anisotropic poroelasticty
Riccardo Cavuoto, Sofia Damian, Luca Deseri, Massimiliano Fraldi, Alon Harris, Brent Siesky, Alice Verticchio, Giovanna Guidoboni
TL;DR
The paper develops a transversely isotropic poroelastic model of the Lamina Cribrosa (LC) using Reissner–Mindlin plate theory to study how intraocular pressure (IOP) variations couple solid deformation with fluid transport. By formulating and solving the TI poroelastic equations with physiologic and pathologic boundary conditions, the authors quantify how stress measures (Von Mises) and shear strain peak in the LC periphery, while fluid content monotonically decreases with rising $IOP$. The work demonstrates that isotropic assumptions underestimate fluid content and overestimate shear, underscoring the importance of anisotropy in LC biomechanics and perfusion. It also shows that the central retinal vessels canal stiffness significantly affects stress distribution and displacements, suggesting avenues for inverse parameter estimation and personalized glaucoma assessment. Overall, the model provides a rigorous framework to explore the coupled mechanical and hemodynamic behavior of the LC under glaucomatous conditions and to infer otherwise inaccessible mechanical properties from observable data.
Abstract
To explore the possible mechanical correlations between intraocular pressure (IOP) variations and glaucoma, this study presents a transversely isotropic poroelastic model of the Lamina Cribrosa (LC) based on Reissner Mindlin plate theory, ultimately highlighting the interplay between solid matrix deformation and blood flow behavior under pathological conditions. Starting from poroelasticity theory, the equilibrium equations governing the LC were formulated and analytically solved by applying appropriate mechanical and hydraulic boundary conditions. The results indicate that both strain and stress measures (in the form of shear strain and von Mises stress) peak in the peripheral region of the LC, which is currently suspected to be the initial site of glaucomatous damage. These quantities increase with IOP, suggesting a pressure-dependent mechanical insult to the retinal ganglion cell (RGC) axons. In parallel, the model predicts a monotonic reduction in fluid content as IOP rises, which may contribute to ischemic phenomena and disc haemorrhages. The influence of material anisotropy was also examined, revealing that isotropic assumptions tend to underestimate the fluid content while overestimating shear strain. Given the current experimental challenges in measuring blood flow within the LC, the proposed model provides a valuable framework for exploring the coupled mechanical hemodynamic behavior of the tissue and for inverse estimation of its mechanical parameters, such as the stiffness of the opening for the central retinal vessels.
