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A. Doshi, D. van der Heide, K. Singh, P. Pinsky; A Mechanical Model For Non–Progressive Optic Neuropathy Mimicking Glaucoma . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1232.
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To derive a mechanical model of the optic nerve head which explains a novel form of optic neuropathy with visual field changes suggestive of glaucoma but non–progressive.
A retrospective, non–case control review was performed on 10 young, myopic patients with non–progressive visual field defects suggestive of glaucoma over 7 years. In order to explain these findings, four digital, three–dimensional models of the optic nerve head were created to approximate both normal anatomy and myopic degenerative changes using finite element analysis. Three models used an untilted, circular optic nerve head insertion with a varying thickness of peripapillary choroid and retina. The fourth model employed an optic nerve head tilted by 15 degrees with temporal choroidal and retinal atrophy. Scleral, choroidal, and sensory retina material properties were calculated through serial sections of fresh porcine eyes using a tensometer. Finite element analyses were performed at IOPs of 0 mm Hg, 15 mm Hg (2000 Pa), and 30 mm Hg.
Moduli of elasticity for load–bearing and non–load bearing tissues follow an exponential curve. 1% and 50 % tissue strain for sclera yield moduli of elasticity of 600 kPa and 5 MPa; for choroid 500 kPa and 3.1 Mpa; sclera and choroid 1.5 kPa and 6.7. Finite element analysis using these values indicates that thinning of the peripapillary choroid and sensory retina increases the IOP related strain on prelaminar optic nerve head tissue. Tilting of the optic nerve increases IOP related strain for normal ranges of IOP. Patients with non–progressive visual field defects suggestive of glaucoma all had normal IOPs with variable tilting of the optic nerve head and peripapillary atrophy.
Peripapillary atrophy and optic nerve head tilt increase strain related deformation on prelaminar optic nerve head tissue even at normal levels of IOP. This increase in strain may lead to axonal deformation at the level of the lamina cribrosa. Non–progressive visual field loss may result from suprathreshold strain to susceptible axons with relative sparing of axons undergoing subthreshold strain. These findings may help explain visual field loss in patients with progressive myopia and normal tension glaucoma.
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