Abstract

Cupping of the optic nerve head associated with normal intraocular pressure (IOP) is a common clinical presentation for which clearly defined management guidelines have not been established. The clinical approach represents a diagnostic challenge because the mechanism of optic nerve injury is often difficult to objectively establish. Of paramount importance is the primary distinction between physiologic cupping and pathologic cupping, and the accurate subclassification of eyes with pathologic cupping. Therefore, it is essential for clinicians to differentiate glaucomatous from nonglaucomatous disc damage. This article reviews the clinical differentiation of eyes with glaucomatous and nonglaucomatous optic disc cupping.An effective, albeit imperfect, rule of thumb dictates that eyes with retention of central acuity, absence of dyschromatopsia, and vertical cupping that corresponds to a nerve fiber bundle visual field defect are generally glaucomatous. Compressive lesions of the anterior visual pathway are an uncommon finding in the evaluation of glaucoma patients with visual field loss associated with normal levels of IOP. Clinically silent lesions, unassociated with visual pathway compression, may be found in less than 10% of patients.The most specific signs of glaucomatous cupping are splinter optic disc hemorrhages, family history of glaucoma, and nerve fiber bundle visual field defects. The most specific signs of nonglaucomatous cupping are age under 50 years, optic disc pallor in excess of cupping, and field defects that border the vertical meridian. Attention to these clinical variables may help provide high quality yet cost-effective health care to patients with visual field loss associated with optic nerve cupping at normal levels of IOP.

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