Study on the deformations of the lamina cribrosa during glaucoma

Abstract

The lamina cribrosa is the primary site of the optic nerve injury induced by elevated intraocular pressure during glaucoma. Under high intraocular pressure, the optic nerve channel near to the periphery of the lamina cribrosa (Channel A) is deformed to become into a tortuous elliptical horn from a straight cylinder, while the optic nerve channel near to the center of the lamina cribrosa (Channel B) is deformed to become into a straight horn from a straight cylinder. These deformations cause both the axoplasm flow obstacle in the axon fibers and the blocked blood flow in the capillaries which pass through the channels, and trigger the visual field defect during glaucoma.

An in vitro pressure model towards studying the response of primary retinal ganglion cells to elevated hydrostatic pressures

“…8. Trench-shaped PDMS devices were produced by laser ablation 63 and imprinting 64 . The building blocks of the poly(methyl methacrylate) (PMMA) mold were designed by a computer-aided design software (AutoCAD 2014, Autodesk, San Rafael, CA, USA) and engraved by a laser ablation machine (Model VLS 2.30, Universal Laser Systems, Scottsdale, AZ, USA) (Fig.…”

Problems in CSF and Ophthalmic Disease Research

“…Another potential confounding variable is the thickness of the lamina cribrosa and the transmission and action of pressure across this tissue. The lamina is known to be thinner in patients with glaucoma, possibly increasing the transmissibility of pressures (34). Studying the role of CSFP and IOP counterbalance factoring lamina cribrosa thickness and biomechanics is very difficult, and an area in need of further study.…”

Biomechanical research into lamina cribrosa in glaucoma

“…Mechanically, the LC is a thin, clamped, circular plate with small deflections and is subjected to three loads: IOP and intracranial pressure (ICP), which act perpendicularly to the anterior and posterior surfaces of the LC, respectively; and in-plane pretension due to scleral expansion, which is parallel to the surface of the LC. Because ICP is constant under high IOP, the other two loads play the leading role in determining the state of the LC [ 10 ]. In response to these loads, the LC undergoes thickening/thinning, excavation, migration and scarring, accompanied by remodeling, synthesis and degradation of collagen fibrils.…”

“…Because the thin film model ignored the thickness and flexural resistance, it resulted in severe overestimation of deformation. Soon afterwards, many models were proposed, employing Kirchhoff's thin plate theory [ 12 ] and finite element method (FEM), to further study the deformation of the LC, but none of the results were in good agreement with relevant experiments [ 10 ]. This is because Kirchhoff's thin plate theory inherently ignores the shear effects in the LC, while FEM can hardly obtain the accurate deformation of the LC as the optic nerve channels and the laminar sheets in the LC both have very small dimensions and tangled structures.…”

“…Recently, a new mechanical model of the LC was developed based on Reissner's thin plate theory [ 10 ]. Because the model abandons Kirchhoff's hypothesis of straight normals, it provides all the stresses and deformations present in the LC under elevated IOP, which have proven to be in good agreement with the existing experiments.…”