Optic disk

The posterior segment of the eye contains vitreous humor (a clear "jellylike" substance), the retina, retinal vasculature, and the optic nerve head. The retina transforms light energy into neural signals, which are transmitted out of the eye by the retinal ganglion cells. The axons of the retinal ganglion cells converge and exit at the optic nerve head (optic disc) to form the optic nerve (Fig. 61-3). The optic nerve contains 1 million nerve fibers and synapses at the lateral geniculate nucleus of the brain. The optic nerve head is the portion of the optic nerve that is susceptible to elevations in

IOP and is visible on fundoscopic examination. The optic nerve head is vertically oval and pale yellow with a depression in the center of the optic nerve, called a physiologic cup which is formed by convergence of the axons. The area surrounding the optic nerve head is the nerve fiber layer which consists of converging retinal ganglion cell axons. Retinal nutrition is dependent upon the transport of trophic factors from the retinal cell ganglion axon to their cell bodies.

Glaucomatous changes to the optic nerve head precede visual field loss, making optic nerve head evaluation a useful screening and prognostic tool. The optic nerve head should be assessed for cupping, nerve fiber layer changes, and presence of splinter hemorrhages using a slit-lamp biomicroscope. Cupping refers to an increase in the size of the physiologic cup. The cup increases with the loss of retinal ganglion cell axons and the collapse of lamina cribrosa. The cup size is expressed as the ratio of the size of the cup to the size of the optic nerve head. A cup-to-disc ratio greater than 0.55 is associated with an increased risk of developing visual field loss. Other

findings include atrophy and notching of the nerve fiber layer. ' ' ' Pathophysiology of Open-Angle Glaucoma

The pathophysiology of glaucomatous neurodegeneration has not been completely elucidated. It is unclear whether the optic neuropathy is caused by increased IOP, decreased retinal blood flow, or a combination of these factors.5,7 Several theories, including autoimmune reactions, excess nitric oxide, and glutamate toxicity have been p^ as ,o ^ « causes the retinal — cells » undergo apoptos-

The level of IOP is related to the death of retinal ganglion cell and optic nerve fibers. As optic neurodegeneration progresses over time, the optic nerve becomes more susceptible to high IOP. Increased IOP causes the retinal ganglion cell axons to undergo mechanical stress, alters axonal protein transport, and decreases blood sup-


ply to the retina and the optic nerve leading to tissue ischemia. ' ' Glaucomatous optic neuropathy may also occur independent of increased IOP. Pressure independent causes of optic neuropathy include abnormal blood flow, systemic hypotension, and abnormal blood coagulability.19 Current glaucoma therapies fail to target IOP-in-dependent glaucoma pathophysiologic factors. However, IOP reduction may still be beneficial as the rate of visual field progression is decreased in some patients who re-


ceive IOP reduction via medical or surgical modalities.

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