The pathophysiology of pigment dispersion syndrome and pigmentary glaucoma (PG) was described first in 1979 by Campbell.1 Posterior bowing of the iris produces iridozonular friction, resulting in pigment liberation and characteristic midperipheral iris transillumination defects. Dispersed pigment may deposit on the corneal endothelium (Krukenberg spindle) and the posterior capsule at Weigert’s ligament (Scheie stripe). Accumulation of pigment within the trabecular meshwork can cause irreversible trabecular damage with associated intraocular pressure (IOP) elevation.
