30

Simulate pigment dispersion syndrome (PDS) — a condition in which melanin granules are liberated from the posterior iris pigment epithelium (IPE) by mechanical rubbing of the posterior iris surface against anterior zonular packets of the crystalline lens. The freed melanin granules circulate in the aqueous humour and deposit on anterior chamber structures: vertically on the central corneal endothelium forming the pathognomonic Krukenberg spindle (a vertical fusiform deposit of brown-black melanin pigment on the posterior corneal surface, typically 1–3 mm wide × 4–6 mm tall, shaped by aqueous convection currents); densely within the trabecular meshwork (TM) causing progressive aqueous outflow obstruction — the basis of pigmentary glaucoma (PG), a form of secondary open-angle glaucoma; on the anterior lens capsule in a ring pattern (Zentmayer ring or Scheie stripe); and within the iridocorneal angle as homogeneous dense pigmentation on gonioscopy. The iris shows characteristic spoke-like mid-peripheral transillumination defects (TIDs) — radial slit-like defects visible on retroillumination, corresponding to the sites of iris pigment epithelium loss. PDS is strongly associated with myopia (axial length >25 mm), younger age (20–50 years), male sex (M:F ≈ 2–3:1), and Caucasian race. Approximately 35–50% of PDS patients develop pigmentary glaucoma over 15 years, with IOP spikes characteristically triggered by exercise, pupil dilation, or accommodation due to acute pigment liberation. Model PDS without glaucoma, pigmentary glaucoma with optic nerve damage, and advanced pigmentary glaucoma with severe visual field loss using ΔE colour shift, CIE xy chromaticity, and image simulation.

Pigment dispersion syndrome colour science simulation by Auric Artisan.

Base color
Clinical stage & settings
Glaucomatous damage severity 50%
Image simulation
Upload JPG/PNG (max 1200 × 1200). See how a scene appears through pigmentary glaucoma: PDS without glaucoma (minimal visual impact — Krukenberg spindle and iris TIDs present but visual function normal), pigmentary glaucoma (progressive retinal ganglion cell and RNFL loss causing arcuate visual field defects — nasal step, Bjerrum scotoma), or advanced pigmentary glaucoma (tunnel vision, severe contrast sensitivity loss).
Research notes
Pigment dispersion syndrome clinical key points: PDS is the most common identifiable cause of secondary open-angle glaucoma in young myopic adults. The hallmark clinical triad is (1) Krukenberg spindle, (2) spoke-like mid-peripheral iris transillumination defects, and (3) dense homogeneous trabecular meshwork pigmentation on gonioscopy (Scheie grade III–IV). Exercise-induced IOP spikes (5–10 mmHg acute rise from jogging, basketball, or accommodation) result from acute pigment liberation caused by pupillary excursion rubbing the posterior iris against zonular packets. The "pigment reversal sign" — gradual clearing of pigment from the TM and Krukenberg spindle over decades (age 50–70) as the lens enlarges and pushes the iris anteriorly — can paradoxically improve IOP control but NOT reverse established glaucomatous optic nerve damage.
Swatches
Normal
HEX: — • RGB: — • xy: —
PDS affected
HEX: — • RGB: — • xy: —
ΔE (CIE76)
—
ΔE (CIEDE2000)
—
Deep preview
Normal
PDS (deep)
Chromaticity (CIE xy)
Glaucomatous optic neuropathy chromaticity shift
D65 white point: 0.313, 0.329
Image simulation

Pigment dispersion syndrome simulations model the progressive glaucomatous optic neuropathy caused by trabecular meshwork melanin obstruction and elevated IOP. PDS without glaucoma: minimal visual impact — the Krukenberg spindle and iris transillumination defects are structural anterior segment findings that do not directly affect colour perception or visual function; the simulation reflects the normal visual state. Pigmentary glaucoma: models retinal ganglion cell and RNFL loss as progressive contrast sensitivity reduction and mild blue-yellow (tritan-like) colour axis weakening — consistent with the known preferential damage to large-diameter magnocellular RGCs and small bistratified (S-cone) RGCs in early glaucoma. Advanced PG: models severe generalised RGC loss as diffuse luminance and chroma reduction. ΔE2000 per Sharma et al. (2005). Not for clinical diagnosis — PDS/PG requires slit-lamp examination, gonioscopy, IOP measurement, visual field testing, and OCT RNFL analysis.

Multi-condition comparison
5
Compare PDS without glaucoma (normal visual function despite anterior segment pigment deposition), pigmentary glaucoma (early-moderate glaucomatous damage with arcuate defects and contrast loss), and advanced PG (severe diffuse RGC loss, tunnel vision). Observe the glaucoma-specific tritan-axis colour weakness and progressive luminance attenuation.