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Daniele Prada, Giovanna Guidoboni, Samuele Terragni, Riccardo Sacco, Paola Causin, Brent A Siesky, Alon Harris; Effect of scleral anchorage on the perfusion of the lamina cribrosa. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4255.
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The circulation with the lamina cribrosa (LC) nourishes the axons of the retinal ganglion cells (RGC). Alterations in LC perfusion may contribute to RGC damage. Several factors influence LC perfusion, including intraocular pressure (IOP) and scleral anchorage. Current imaging techniques do not allow visualizing and assessing LC perfusion in vivo in humans. Here, we use a mathematical model to theoretically investigate the influence of scleral anchorage on LC perfusion for various IOP levels.
The LC is modeled as a two-dimensional poroelastic material, where blood vessels are viewed as pores in a solid matrix, LC porosity (N) (ratio between blood volume and LC total volume) changes with the local state of stress and strain, LC permeability (ability of the porous material to allow fluid passing through it) is assumed to be proportional to the square of N; the solid matrix is assumed to behave as linear elastic material. Blood flow is driven by the difference between the arterial pressure (Pa) in the short posterior ciliary arteries and the venous pressure (Pv) in the central retinal vein. The LC deforms under the difference between IOP and retrolaminar tissue pressure (RLTp). At the scleral junction (x=0), scleral anchorage is modeled either by enforcing zero displacement (case 1) or by imposing a normal tension, calculated via Laplace’s law, while allowing rotations (case 2). At the LC central axis (x=0.075) displacement symmetry is imposed.
N and blood velocity (V) are simulated and compared for IOP = 15, 25 and 35 mmHg. Control values are N=0.1, V=0.02cm/s, Pa = 30mmHg, Pv = 20mmH, RLTp = 7mmHg. The model predicts that, for a given IOP level, values and distributions of N and V in cases 1 and 2 are noticeably different. As IOP increases from 15 to 35 mmHg, N undergoes a maximum percent reduction from baseline of 12.2% in case 1 and 7.7% in case 2. In case 1, the minimum values of N and V are attained at the scleral junction, whereas in case 2 they are attained at the LC central axis.
This exploratory two-dimensional analysis suggests that scleral anchorage has a strong influence on LC perfusion. Several studies suggested that changes in scleral anchorage are associated to ocular pathologies, including glaucoma. Our study suggests that changes in scleral anchorage might contribute to RGC damage via induced alterations in LC porosity and perfusion.
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