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Contempo 1999 |

New Perspectives on Glaucoma

Evan Benjamin Dreyer, MD, PhD; Stuart A. Lipton, MD, PhD
JAMA. 1999;281(4):306-308. doi:10.1001/jama.281.4.306.
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Extract

Conventional wisdom defines glaucoma as "a collection of ophthalmic disorders in which the intraocular pressure [IOP] is sufficiently elevated to cause excavation and degeneration of the optic disc" (Figure 1).1 The glaucomas are a leading cause of irreversible blindness both worldwide and in the United States.2 Although early physicians could not differentiate between visual loss from glaucoma and cataract, our understanding of glaucoma really dates to 1622. Richard Banister, a British oculist, wrote, "if one feele the eye by rubbing upon the eie-lids that the eye be growne more solid and hard than naturally it should be . . . the humour settled in the hollow nerves be growne to any solid or hard substance, it is not possible to be cured."3 Although his examination retains some currency, we have made some therapeutic progress in the ensuing 377 years. Nonetheless, much about this disease is still enigmatic.

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Figure 1. Optic Nerves.
Grahic Jump Location
Left, Normal optic nerve with healthy neural tissue. Right, Glaucomatous optic nerve from a different patient shows a greatly enlarged cup as a result of loss of neural tissue, and the blood vessels are displaced nasally.
Figure 2. Normal Eye.
Grahic Jump Location
The retina of the normal eye is a multilayered structure; its innermost layer contains both ganglion cell bodies and their axons. These axons course toward the back of the eye and exit at the lamina cribrosa, where they form the optic nerve. A single axon and cell body are depicted here. The first synapse for the ganglion cell axon is at the lateral geniculate nucleus. In this illustration, a small cup is illustrated. Glaucomatous damage leads to a loss of neural tissue and consequent enlargement of the cup.

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