Abstract
Purpose :
<div>Decreased cerebrospinal fluid pressure (CSFP), parallel to an elevated intraocular pressure (IOP), is associated with the pathogenesis of glaucomatous optic neuropathy. An improved understanding of how pressure effect optic nerve head (ONH) biomechanical environment, is necessary to understand how pressure play a role in glaucomatous optic neuropathy.</div>
Methods :
A finite element model of optic nerve head tissues (pre- and postlaminar neural tissue, lamina cribrosa, central retinal vessel, sclera, and pia meter) was constructed. Stresses, strains and deformations were computered using finite elemnt modeling for a range of elevated IOP and reduced CSFP. Cup-disc ratio (C/D) were measured basic on the finite element model.
Results :
At an IOP of 20mmHg, C/D averaged from 0.38 to 0.48 with reduced CSFP from 10 mmHg to 2 mmHg. At an CSFP of 10 mmHg, C/D averaged from 0.38 to 0.43 with elevated IOP from 20 mmHg to 28 mmHg. By comparison, at a same trans-lamina cribrosa pressure of 16 mmHg, C/D is 0.45 caused by elevated IOP while C/D is 0.42 caused by reduced CSFP.
Conclusions :
<!--StartFragment --><!--StartFragment -->Finite element analysis of strain in the lamina cribrosa caused by acute elevated IOP are biologically significant and capable of contributing to the development of glaucomatous optic neuropathy. With mild elevated IOP and reduced CSFP, it is less biologically significant and may not result to direct mechanical damage. Moreover, according to C/D ratio, IOP- and CSFP-induced deformation of the lamina cribrosa at the same lamina cribrosa pressure is different. This finding implies that, there may be exists another mechanism of glaucomatous optic neuropathy with mild elevated IOP and reduced CSFP.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.