Serum Autoantibodies to Optic Nerve Head Glycosaminoglycans in Patients With Glaucoma

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Abstract
THE LAMINA cribrosa provides mechanical and functional support for optic nerve fiber bundles as they exit the eye. Structural changes of the optic nerve head secondary to elevated intraocular pressure are thought to influence the susceptibility of optic nerve fibers to injury in glaucomatous eyes.1,2 However, in some eyes, glaucomatous damage can be seen with normal intraocular pressure. In these eyes, changes of the optic nerve head and lamina cribrosa are similar to those described in patients with primary open-angle glaucoma, namely, mechanical compression, strangulation, and overstretching of nerve fibers accompanied by the disarrangement and backward bowing of the lamina cribrosa.1-5 These observations suggest that weakness of the laminar beams and deformation of the lamina cribrosa that accompany optic nerve damage in glaucomatous eyes may depend on factors other than elevated intraocular pressure.