A reduced outflow facility is the fundamental abnormality of aqueous humor dynamics in POAG.273 As glaucoma progresses, outflow facility declines progressively. Measurements of outflow facility by tonography are not part of the routine clinical assessment of glaucoma today. Single measurements of outflow facility do not help much in the diagnosis of POAG or in the assessment of the efficacy of treatment.

An afferent pupillary defect can be seen in patients with asymmetric or unilateral glaucoma.This finding, which is also referred to as Marcus Gunn’s sign, is elicited by the swinging flashlight test. It has even been noted in patients with asymmetric cupping and normal kinetic visual fields.274

The angles are open in patients with POAG. The angles can be narrow, but there can be no peripheral anterior synechiae (unless caused by prior laser treatment or surgery), no apposition between the iris and the trabecular meshwork, and no developmental abnormalities of the angle. Moderate pigmentation of the meshwork is often present in proportion to the patient’s age and race. Heavy pigmentation is suggestive of other disorders, including pigmentary glaucoma, exfoliative syndrome, trauma, and uveitis.

The crucial clinical findings in POAG are those that occur in the optic disc and visual field. Defects in the nerve fiber layer are also seen in most patients. These matters are presented in detail in Chapters 10 and 13 and are not discussed further here. Other findings include impairment of contrast sensitivity, temporal contrast sensitivity, loss of color perception, and other psychophysical impairments as outlined in Chapter 11.

Differential diagnosis

The differential diagnosis of POAG includes conditions that can mimic any of the cardinal features of the disease, such as elevated IOP, cupping and atrophy of the optic disc, and visual field loss. Primary open-angle glaucoma must be distinguished from a variety of secondary and developmental glaucomas.These include exfoliative syndrome, pigmentary dispersion, trauma, anterior segment inflammation, subacute or chronic angle closure, elevated episcleral venous pressure, Axenfeld’s and Rieger’s syndromes, and corticosteroid administration. These conditions are usually distinguished from POAG by a careful history and clinical examination.

Optic disc cupping is typical but not pathognomonic of glaucoma. Cupping has been reported in association with arteritic and non-arteritic anterior ischemic optic neuropathy,275 as well as with

compressive optic nerve lesions.276 At times, pits or colobomas of the optic nerve can be mistaken for enlarged cups,277,278

although the glaucomatous process can produce a pit-like appearance of the optic nerve.279,280 As a general rule, glaucoma causes

more optic disc cupping than pallor, whereas the opposite occurs for most neurologic or ischemic diseases.281–283

Many conditions can cause visual field loss that has an arcuate or nerve fiber bundle appearance.284–285 Box 17-1 lists some of these

conditions.

Treatment

Indications

Generally the ophthalmologist institutes treatment when the patient either has the classic glaucoma triad of visual field loss,

Box 17-1  Differential diagnosis of arcuate scotoma

Chorioretinal lesions

Myopic degeneration

Atypical retinitis pigmentosa286,287

Photoreceptor degeneration288,289

Branch vein occlusion

Branch artery occlusion

Juxtapapillary chorioretinitis290

Optic disc lesions

Drusen291

Pits

Colobomas

Papillitis

Chronic papilledema292

Optic nerve lesions

Arteritic and non-arteritic ischemic optic neuropathy

Retrobulbar neuritis

Exophthalmos

Pituitary tumors

Meningiomas

Aneurysms

Chiasmatic arachnoiditis

optic nerve cupping, and elevated IOP, or is at high risk of developing them. Other indications for treatment include progressive cupping without detectable visual field loss, the development of visual field loss, episodes of corneal edema caused by elevated IOP, and a vascular occlusion associated with increased IOP. In patients with asymmetric POAG (i.e., bilateral elevated IOP with unilateral optic nerve cupping and unilateral visual field loss), the other eye usually is treated aggressively because it has at least a 40% chance of developing visual field loss over a 5-year period.293

Goals

The major goal of glaucoma treatment is to preserve good visual function for the patient’s lifetime and prevent interference, in so far as is possible, with the quality of life. This is accomplished by lowering the IOP (until a better treatment comes along) to a level that will stop, or at least slow, the progression of optic nerve damage and its consequent vision loss.The treatment should maximize good visual function and comfort, as well as preserve a reasonable quality of life for the patient by minimizing the side effects from the treatment itself, the risk of vision loss and, in many cases, the costs associated with treatment.

For some years, doubt existed regarding the efficacy of pressure lowering for glaucoma. However, a spate of randomized, prospective clinical trials over the past decade have left no doubt that pressure lowering is effective both in slowing or stopping the progression of actual glaucoma and in reducing the risk of conversion from ocular hypertension to frank glaucoma.294 While at this point in history, we have many choices of pressure-lowering therapy, including medications, laser surgery and incisional surgery, no curative therapy exists for POAG, so one can only aim at controlling the disease.We can lower the IOP but as yet cannot directly protect the optic nerve or enable regeneration of damaged or dead ganglion cells. Although some improvement in optic nerve parameters can be expected in a minority of patients treated for glaucoma,