Pathophysiology of pigment dispersion syndrome and pigmentary glaucoma.
Pigmentary glaucoma results from zonular-pigment dispersion, primarily in young, myopic, white individuals. The concavity of the midperipheral iris allows iridozonular contact. Released pigment is carried to the trabecular meshwork where it resides: (1) benignly, not affecting the intraocular pressure, as in pigment dispersion syndrome; or (2) malignantly, elevating the intraocular pressure, as in pigmentary glaucoma. Small amounts of pigment are quickly phagocytized. If the particulate load is heavy, the cells migrate further along the outflow pathway. The flattening of the iris in pigmentary glaucoma patients receiving iridotomies, along with the backward flow of pigment observed during treatment, demonstrates a greater pressure in the anterior than the posterior chamber. This reverse pupillary block may be due to temporary ocular deformations caused by blinking, as small aqueous aliquots are forced into the anterior chamber. Flattening of the concave iris is the key to current and future management of these patients.
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D002924:Ciliary Body / Q000648:ultrastructure; D017889:Exfoliation Syndrome / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery; D005902:Glaucoma, Open-Angle / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery; D006801:Humans; D007429:Intraocular Pressure; D007498:Iris / Q000601:surgery / Q000648:ultrastructure; D008022:Ligaments / Q000648:ultrastructure; D010857:Pigment Epithelium of Eye / Q000473:pathology; D014129:Trabecular Meshwork / Q000473:pathology