Practice Essentials
Pigment dispersion syndrome (PDS) and pigmentary glaucoma (PG) are characterized by loss of pigment from the posterior surface of the iris and excessive pigment release throughout the anterior segment of the eye. [1] The essential diagnostic signs include a unique pattern of mid-peripheral iris transillumination defects and pigment deposits on the corneal endothelium, the trabecular meshwork (TM), the iris, and the lens. [2] Individuals with PDS may have normal or elevated intraocular pressure (IOP) without glaucomatous optic nerve damage. Patients with these same findings who demonstrate optic nerve damage and/or visual field defect are classified as having PG.
Pigment dispersion syndrome and PG are more prevalent in males, and the mean age of diagnosis is typically in the fourth or fifth decade of life. [3, 4] The age of onset for PDS and PG likely is earlier than this, but is missed due to lack of patient symptoms or screening at this age. Contact of the posterior iris against the lens is thought to produce excessive pigment release into the anterior segment. Pigment accumulation in the trabecular meshwork impairs aqueous outflow, elevating IOP, and may subsequently cause chronic outflow dysfunction, optic nerve damage, and visual loss.
Treatment options are similar to those for primary open-angle glaucoma and include medical therapy, laser iridotomy, laser trabeculoplasty, and invasive surgical interventions.
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Radial, mid-peripheral iris transillumination defects.
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Hyperpigmentation of the trabecular meshwork.
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Krukenberg spindle.
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Pigment on posterior surface of cornea.
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Characteristic iris transillumination defects.
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Trabecular meshwork hyperpigmentation.
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Pigment accumulation on anterior surface of iris.
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Pigment deposits on anterior lens surface.
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Pigment accumulation on posterior lens zonules.
