Table 4. Indications to perform neuroimaging evaluation in normal-tension glaucoma

General

Young age (less than 50 years)

New onset or increased severity of headaches

Localizing neurologic symptoms other than migraine

Neurologic visual abnormalities

Ocular

Color vision abnormalities

Pallor of the remaining neuroretinal rim

Highly asymmetric cupping

Unilateral or highly asymmetric abnormalities

Lack of disc and visual field correlation

Visual field defect respecting vertical midline

evaluation is not performed in NTG diagnosis. Studies have shown that anterior visual pathway compression is a rare finding in neuroimaging of patients with a presumptive diagnosis of NTG (Greenfield et al., 1998). Relative indications to perform neuroimaging include younger age, decreased visual acuity, vertically aligned visual field defects that respect the midline, significant asymmetry, and neuroretinal rim pallor that exceeds the amount of cupping (Table 4).

Therapy

IOP reduction

The mainstay of treatment for glaucoma remains IOP reduction. The CNTGS recommendation is to reduce IOP by at least 30% to reduce the incidence of visual field progression. The modalities for IOP reduction include glaucoma medications, laser trabeculopasty, and glaucoma surgery. Glaucoma medications are the usual initial therapy for treatment. Glaucoma filtering surgery with antifibrotic agents (5-fluorouracil or mitomycin C) is the preferred surgery for NTG as it can achieve a very low postoperative IOP. The rate of cataract formation is higher after glaucoma surgery as shown in the CNTGS and other studies (AGIS Investigators, 2001). In fact, the protective effect of IOP reduction on visual field was masked by the progression of cataract in the treated group. Only by removing the data affected by cataract, the protective effect of IOP lowering on preservation of

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visual field was made evident (CNTGS, 1998a, b). It is important to point out that cataracts are reversible through a highly successful surgical procedure whereas visual field loss from glaucoma is not. Consequently, both the stage of glaucoma and the longevity of the patient need to be considered before embarking on surgical treatment that may accelerate cataract formation.

Systemic medications

New glaucoma therapies target IOP-independent mechanisms. Calcium channel blockers may protect visual field by increasing the capillary perfusion of the optic nerve head by relieving the effect of vasospasm in susceptible individuals, although results are conflicting and nonpersuasive. Various studies have suggested some benefits of nifedipine, verapamil, and nimodipine in protecting against glaucoma progression (Kitazawa et al., 1989; Bose et al., 1995; Netland et al., 1995), while other studies have shown no beneficial effect. Experts in the field of glaucoma do not commonly use calcium channel blockers because of a lack of clear evidence of efficacy and potential harmful side effects such as postural hypotension. If ophthalmologists wish to use calcium channel blocker therapy, they should coordinate treatment with a primary care physician because of potentially dangerous side effects such as systemic hypotension (Lumme et al., 1991). Another new but still experimental treatment is the use of angiotensin-converting enzyme (ACE) inhibitors. One small retrospective study found ACE inhibitors may have a favorable effect on visual field in NTG (Hirooka et al., 2006). The clinical significance of this study remains uncertain. A randomized controlled study is needed to evaluate the effect of ACE inhibitors in the prevention of visual field progression in NTG. Existing cardiovascular abnormalities (i.e., anemia, congestive heart failure, transient ischemic attack, arrhythmias) should be treated to ensure maximum perfusion of the optic nerve head.

Neuroprotection

IOP-independent mechanisms of glaucomatous optic nerve damage may play an important role in