The etiology of this condition is not known. Hypotheses include developmental abnormalities of the iris dilator muscle or mechanical rubbing of zonules against the iris, resulting in pigment dispersion in the anterior chamber and pressure elevation. PDS is then viewed as a variant of primary open-angle glaucoma or may be secondary to pigment deposited in the angle structures with secondary damage to the trabecular meshwork. A hereditary component does appear to play a role in the PDS syndrome and may also predispose to the development of glaucoma.