The Effects of Glaucoma on the Pressure-Induced Strain Response of the Human Lamina Cribrosa

Purpose To measure the ex vivo pressure-induced strain response of the human optic nerve head and analyze for variations with glaucoma diagnosis and optic nerve axon damage. Methods The posterior sclera of 16 eyes from 8 diagnosed glaucoma donors and 10 eyes from 6 donors with no history of glaucoma were inflation tested between 5 and 45 mm Hg. The optic nerve from each donor was examined for degree of axon loss. The posterior volume of the lamina cribrosa (LC) was imaged with second harmonic generation and analyzed using volume correlation to calculate LC strains between 5 and 10 and 5 and 45 mm Hg. Results Eye length and LC area were larger in eyes diagnosed with glaucoma ( P ≤ 0 . 03). Nasal-temporal E XX and circumferential E θθ strains were lower in the LC of diagnosed glaucoma eyes at 10 mm Hg ( P ≤ 0 . 05) and 45 mm Hg ( P ≤ 0 . 07). E XX was smaller in the LC of glaucoma eyes with <25% axon loss compared with undamaged normal eyes ( P = 0 . 01, 45 mm Hg). In general, the strains were larger in the peripheral than central LC. The ratio of the maximum principal strain E max in the peripheral to central LC was larger in glaucoma eyes with >25% axon loss than in glaucoma eyes with milder damage ( P = 0 . 004, 10 mm Hg). Conclusions The stiffness of the LC pressure-strain response was greater in diagnosed glaucoma eyes and varied with glaucomatous axon damage. Lower LC strains in glaucoma eyes with milder damage may represent baseline biomechanical behavior that contributes to axon loss, whereas greater LC strain and altered radial LC strain variation in glaucoma eyes with more severe damage may be caused by glaucoma-related remodeling.