Finite Element Modeling Predicts Neural Tissue Shear in the Neuroretinal Rim Caused by Pulsatile Blood Pressure

Abstract

Purpose : (1) To use finite element (FE) analysis to model the origin of the ocular pulse; (2) To study and rank the biomechanical factors affecting the resulting optic nerve head (ONH) deformations during the cardiac cycle (diastole-to-systole).

Methods : A FE model of a healthy eye was reconstructed. The choroid was biphasic and consisted of a solid phase (connective tissues) and a fluid phase (blood). We applied arterial pressure at 18 entry sites (posterior ciliary arteries) and venous pressure at 4 exit sites (vortex veins). For 1 cardiac cycle, we reported the ocular pulse amplitude (OPA), and diastole-to-systole ONH deformations. Sensitivity studies were performed to study how pressure variations (IOP, ophthalmic artery pressure, and cerebrospinal fluid pressure [CSFP]), and tissue stiffness (sclera, choroid, border tissues of Elschnig & Jacoby) could influence ONH deformations (diastole-to-systole).

Results : During the cardiac cycle, a change in arterial pressure resulted in choroidal thickening, which in turn induced a change in IOP (the OPA) and ONH deformations. Both choroidal thickening and the OPA contributed to shear neural tissues within the neuroretinal rim (Figure 1). Among all pressures, the systolic ophthalmic artery pressure influenced the most diastole-to-systole shear in the neuroretinal rim (high pressure = high shear; Figure 2). A stiff choroid reduced shear, but a stiff sclera increased it.

Conclusions : Our models indicate that, during the cardiac cycle, the OPA and choroidal thickening can deform the ONH with a net shearing of neural tissues within the neuroretinal rim. The systolic ophthalmic artery pressure and choroidal stiffness influenced the most that shear.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.