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Lucia Carichino, Giovanna Guidoboni, Yoel Arieli, Brent A. Siesky, Alon Harris; Effect of Lamina Cribrosa Deformation on the Hemodynamics of the Central Retinal Artery: a Mathematical Model. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2836.
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Several studies have shown that acute intraocular pressure (IOP) elevation alters flow velocity in the central retinal artery (CRA), one of the major vessels nourishing the retina. This study proposes a mathematical model to elucidate, estimate and quantify anatomical and mechanical factors contributing to IOP influence on CRA hemodynamics. In particular, we test the conjecture that the lamina cribrosa (LC) serves as a magnifier for the IOP effects on the CRA, which may increase the resistance of CRA flow.
The LC is modeled as a homogeneous linearly elastic circular plate of constant finite thickness, which deforms under the combined action of IOP, cerebrospinal fluid pressure (CSF), and scleral tension. The CRA is modeled as a fluid-structure interaction system: a stationary Stokes flow of an incompressible Newtonian viscous fluid filling a linearly elastic compliant tube. The walls of the CRA deform under the action of an external pressure which varies along the vessel length to include CSF, IOP and the compression induced by LC deformation.
The results show a significant increase of the LC compression due to acute IOP elevations and, accordingly, a decrease in lumen, blood velocity and flow in the CRA. The mathematical model predictions are in very good agreement with in vivo measurements of CRA blood velocity for different IOP levels, see Figure. Our results also show that individual variations in the optic nerve head anatomical structure give rise to significant differences in the CRA hemodynamics for the same IOP elevation.
The proposed mathematical model supports the conjecture that the mechanical factor behind flow and velocity reduction in the CRA after acute IOP elevation is the compression exerted by the LC on the CRA. This study also elucidates and quantifies a clear connection between anatomical, mechanical and vascular factors, which is thought to contribute to individual susceptibility to glaucomatous damage.
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