Pigmentary Glaucoma and Pigment Dispersion Syndrome

From EyeWiki

Pigmentary Glaucoma and Pigment Dispersion Syndrome
Pigment is deposited on the endothelium in a vertical spindle shape


Pigment dispersion syndrome (PDS) and pigmentary glaucoma (PG) represent a spectrum of the same disease characterized by excessive pigment liberation throughout the anterior segment of the eye. The classic triad consists of dense trabecular meshwork pigmentation, mid-peripheral iris transillumination defects, and pigment deposition on the posterior surface of the central cornea. Pigment accumulation in the trabecular meshwork reduces aqueous outflow facility and may result in elevation of intraocular pressure (IOP), as seen in pigment dispersion syndrome, or in optic nerve damage associated with visual field loss, as seen in pigmentary glaucoma. Pigmentary glaucoma and PDS occur when pigment is released from the iris pigment epithelium due to rubbing of the posterior iris against the anterior lens zonules. The disease is more prevalent in males, and typically presents in the 3rd-4th decade of life.

Treatment options for Pigmentary Glaucoma are similar to Primary Open Angle Glaucoma and include medical therapy, laser trabeculoplasty, and incisional surgery with either trabeculectomy or glaucoma drainage implant. The efficacy of laser iridotomy in the prevention of PDS and subsequent Pigmentary Glaucoma is not firmly established.

Disease Entity

Pigmentary glaucoma (PG) and pigment dispersion syndrome (PDS).


Pigmentary glaucoma is a type of secondary open-angle glaucoma characterized by heavy homogenous pigmentation of the trabecular meshwork, iris transillumination defects, and pigment along the corneal endothelium (Krukenberg spindle). Individuals with these same findings who do not demonstrate optic nerve damage and/or visual field loss are classified as having PDS, even if the IOP is elevated. The prevalence of PDS and PG in the general population is poorly defined. After a period of about 15 years, approximately 15% of the patients with PDS will manifest raised IOP or develop glaucoma. It is an autosomal dominant condition with variable penetrance having a wide variety of genetic loci. Screening of New York City employees reported that 2.5% had at least one slit lamp finding consistent with PDS,[1] while a retrospective review of charts from a glaucoma practice demonstrated that roughly 1 in 25 patients (4%) was followed for either PDS or PG.[2] In Olmstead County, Minnesota, the annual incidence of diagnosed PDS and PG was 4.8/100,000 and 1.4/100,000, respectively.[3] True incidences are likely substantially higher, as many people with PDS and PG may have had the undiagnosed disease.


The underlying mechanism responsible for PDS and PG is the presence of a concave iris contour which causes rubbing of the posterior iris surface against the anterior lens zonules bundles during physiological pupil movement, leading to disruption of the iris pigment epithelial cell membrane and release of pigment granules.[4][5] Pigment granules can produce temporary elevation of IOP by overwhelming the trabecular meshwork and reducing outflow.[6][7][8] Over time, pathological changes in the trabecular endothelial cells and collagen beams can lead to increased resistance to aqueous outflow with chronic elevation of IOP and secondary glaucoma.[5][9] Patients with PDS or PG have a 15-fold higher concentration of aqueous pigment granules in their anterior chamber compared to normal controls.[7]

Pigment release requires irido-zonular contact and pupillary movement. Risk factors for irido-zonular contact based on ocular anatomy are discussed below. Irido-zonular contact has been demonstrated to increase with blinking in eyes with PDS or PG.[10][11] Blinking has been hypothesized to burp fluid from the posterior chamber to the anterior chamber in these eyes, resulting in a higher pressure in the anterior chamber as compared to the posterior chamber.[12] The resulting pressure gradient results in a posterior-bowing (concave) iris with greater than normal iridolenticular contact (also referred to as reverse pupillary block) which has been shown to be reduced with suppression of blinking.[10][11] The similar sounding Inverse Pupillary Block refers to blocking of pupil by crystalline lens with large anteroposterior diameter in Microspherophakia. Such inverse pupillary block in microspherophakia aggravates with the use of pilocarpine.

Greater iridolenticular contact also occurs with accommodation, in which the anterior lens surface moves anteriorly with contraction of the ciliary ring.[10] [13][14] Increase in iris concavity secondary to accommodation has also been reported in myopic eyes without PDS and normal eyes. This suggests that irides in eyes with PDS and PG may have inherent susceptibility to pigment liberation and factors other than iris shape and size may be at play.[15] Pupillary movement produced by pharmacologic dilation has been observed to produce pigment release and increased IOP in some patients with PG or PDS.[6][7][16] Likewise, physiological changes in pupil size resulting from lighting changes or accommodation, as previously mentioned, may also produce pigment release in individuals with iridozonular contact.[17] In some patients with PG or PDS, significant pigment release accompanied by IOP elevation has been observed after strenuous exercise.[17][18] However, systematic observation of IOP in patients with PDS or PG suggests that most patients do not have pigment release or IOP elevation after exercise.[7][17] Pigment release producing elevated IOP and glaucoma has also been observed with sulcus placement of certain intraocular lens designs after cataract surgery.[19][20][21] The terms PDS and PG are not applied to this secondary form of glaucoma, despite some underlying mechanistic similarities.

Risk Factors

  1. Male gender- Pigmentary glaucoma has a strong male predominance, with all case series showing a male to female ratio of between 2:1 and 5:1. Much less of a male predominance is noted for PDS, with case series describing male to female ratios between 1:1 and 2:1.[2][3][16][22][23]
  2. Age- Male patients with PG and PDS most often present in their 30s, whereas female patients typically present roughly a decade later in life.[3][16][22][24][25] Cases of PDS have been identified in patients as young as 12-15 years of age.[26][27][28] Disease may be more frequent in middle age when the lens has enlarged and the iris is flexible enough to form a concave position.[4]
  3. Myopia- The most common refractive error noted in eyes  with PDS and PG is moderate myopia, with mean spherical equivalents typically in the range of -3 to -4 D. A broad range of refractive errors is typically found, though hyperopia is relatively rare, usually accounting for only 5-10% of patients in most case series.[2][16][22][29]
  4. Race- Both pigment dispersion syndrome and PG occur infrequently (<5% of patients identified in case series) in persons of African ancestry.[2][16] However, the actual prevalence may be higher than reported as persons of African ancestry have thick brown irides making detection of iris transillumination defects more difficult.[30]
  5. Concave iris and posterior iris insertion- Patients with PDS and PG have greater iridolenticular contact than individuals without the disease. Increased iridolenticular contact results from a combination of a concave iris and a more posterior iris insertion, both of which are more common in patients with PDS or PG.[11][13][31]
  6. Flat corneas- Patients with PDS and PG have significantly flatter corneas than control subjects of similar age and refractive error.[29][32] A flat cornea might be more likely to result in burping of aqueous humor from the posterior chamber to the anterior chamber with blinking, resulting in increased iridozonular contact.[32]
  7. Family history- Direct examination of a small set of family members of PDS patients showed that disease was present in 2/19 (12%).[33] A second examination of family members reported signs of PDS in 36% of subjects’ parents and 50% of siblings, but no children, suggesting a possible autosomal dominant inheritance pattern with incomplete penetrance.[34]Families with PG have also been described across multiple generations.[35][36] Roughly 50% of family members in the described families had PDS or PG, reinforcing the idea of an autosomal dominant inheritance pattern.

Risk factors for progression of stage of disease or disease progression include:

  1. Intraocular pressure- A retrospective study from Olmstead County Minnesota found IOP > 21 to be the only risk factor for progression from PDS to PG. Age, refractive error and family history were not associated with conversion to PG.[3]
  2. Degree of iridolenticular contact in patients with asymmetric disease- The more affected eye was noted to have more iris-lens contact than the less affected eye. Features associated with greater iridolenticular contact (greater iris concavity, more posterior iris insertion) were also more common in patients with PDS or PG.[31]
  3. Greater trabecular meshwork pigmentation- In eyes with bilateral PDS, worse disease is typically found in the eye with more severe trabecular meshwork pigmentation.[2]

General Pathology

Autopsy specimens of eyes with PG demonstrate disruption of the iris pigment epithelium cell membrane with extrusion of pigment granules.[5] The trabecular meshwork in these eyes reveals collapse of trabecular sheets, free pigment granules and cellular debris clogging the intertrabecular spaces, and macrophages and degenerated trabecular endothelial cells filled with pigment.[5][9][37]


Uveal pigment has been demonstrated to increase resistance to aqueous outflow in experimental studies,[38][39] and to result in increased IOP in vivo.[6]

Primary prevention

No methods have been established for prevention of PDS or PG. In young patients with iris concavity and active release of pigment, a laser iridotomy has been suggested to be of benefit by equalizing pressures in the anterior and posterior chambers and pulling the iris away from the zonules, although no definitive benefit has been demonstrated. Older patients with glaucoma are less likely to benefit from iridotomy due to permanent changes in the trabecular meshwork architecture. One large study reported that the risk of conversion from PDS to PG is approximately 10% at 5 years and 15% at 15 years.[3] This suggests that treatment of all patients with iridotomy is not advisable. The decision to perform a laser should be individualized depending on the patient’s IOP and amount of pigment liberation.


Pigment dispersion syndrome is diagnosed clinically based on the presence of iris transillumination defects in the mid-peripheral iris, pigment on the corneal endothelium (Krukenberg spindle, vertically oriented due to convection currents), and heavy pigmentation of the trabecular meshwork. The presence of all three of these findings in the absence of another cause (i.e. history of trauma or posterior chamber IOL) suggests definite disease. No formal criteria have been set forth in defining whether disease exists in eyes with 1 or 2 of the above findings. Disease is likely present when 2 of the above 3 findings are present, particularly if other exam findings consistent with PDS or PG (i.e. elevated IOP, zonular pigment, posterior capsular pigment) are present. Pigmentary glaucoma is present when the criteria for PDS are accompanied by optic nerve cupping and/or visual field loss.[40] PDS can occur with normal or elevated IOP.


Patients should be asked about a history of previous trauma, surgery, or eye disease. The presence of family members with glaucoma (and the type of glaucoma) should be queried. Visual symptoms are unusual except in patients with visual field loss. Some patients may describe episodes of haloes and blurry vision resulting from intermittent IOP elevation. Patients with such symptoms should be asked if they are brought about by exercise or dark exposure, which have been previously described in patients with PDS or PG.

Physical examination

Careful slit lamp examination is critical to identification of PDS. Findings are typically bilateral, but can be markedly asymmetric on occasion.

  1. The posterior surface of the central cornea should be carefully examined for the presence of pigment.
    Krukenberg Spindle (Photo Courtesy of Sarwat Salim, MD, University of Tennessee)
    Pigment is often arranged in a the shape of a Krukenberg spindle, narrow or rounded oval of brown pigment, usually 0.5 to 2.5 mm wide, and 2-6 mm in length. Pigment is typically densest at the center, thinning out at the edges in the shape of a spindle.[41] Krukenberg spindles are present in roughly 90% of patients with PDS or PG. Whether a dense Krukenberg spindle or very fine granules of pigment are present, visual acuity is not reported to be affected. Corneas of patients with PDS or PG have not been demonstrated to be thicker or to have decreased endothelial cell counts.[42]
  2. The anterior chamber should be examined for the presence of pigment granules and depth. On slit-lamp, pigments are brown and are smaller than anterior chamber cells as seen in uveitis. Examination should be performed prior to and after pupillary dilation.
  3. The iris should be examined with retroillumination to look for iris transillumination defects.
    Iris transillumination defects in Pigmentary Glaucoma (Photo Courtesy of Sarwat Salim, MD, University of Tennessee)
    Transillumination defects are most common in the mid-peripheral iris, where contact between iris pigment epithelium and anterior lens zonules is maximal. Transillumination defects appear in a spoke-like configuration, and are most common or most prominent inferiorly or inferonasally.[12][26] Roughly 90% of PDS/PG patients demonstrate iris transillumination defects in at least 1 eye,[16] though transillumination defects may be absent in patients with thick, dark irides.[23][30] In asymmetric cases, frank iris heterochromia with increased iris pigmentation in the eye with greater pigmentation can be noted in the more affected eye.[16][23] The eye with greater pigment loss can also have a larger pupil resulting in clinical anisocoria, possibly secondary to iris dilator hypertrophy.[43][44][45]
  4. The lens should be examined for the presence of pigment on the anterior surface, along the zonules, and along the posterior surface. Zonular pigment is best noted after pupillary dilation with the patient gazing upwards to bring the inferior zonules into view.[46] Rarely, pigment can migrate posteriorly, where it can be found trapped between the posterior lens capsule and anterior hyaloid.[47][48]
    Densely pigmented TM in Pigmentary Glaucoma (Photo Courtesy of Sarwat Salim, MD, University of Tennessee)
  5. Gonioscopy should be completed prior to dilation to evaluate the extent of trabecular pigmentation. The angle is typically widely open and the trabecular meshwork typically shows dense, homogenous pigmentation.[23]Pigment deposition may be noted on Schwalbe’s line. The peripheral concavity of the iris may be more prominently appreciated on gonioscopy. Pigment deposition along the zonular attachment at the posterior capsule of lens may be noted (Schie line or Zentmayer line). This can give rise to a pigmented round line at the posterior capsule just internal to the equator of the lens.
  6. Intraocular pressure should be measured. In a community based retrospective study, IOP at time of diagnosis for a population of patients with PG and PDS was 29 mm Hg and 24 mm Hg, respectively.[3] Other studies confirm that patients presenting with PG typically have higher pressures.[22][49]


Mydriatic provocative testing has limited utility in diagnosing or predicting the course of PDS or PG. In one case series, roughly 1/3 of patients demonstrated extensive anterior chamber pigment after phenylephrine administration, and only a fraction of these (20%) had an associated IOP rise.[17]


See discussion above in history section.

Clinical diagnosis

See diagnosis section above.

Diagnostic procedures

Patients with suspected PDS or PG should undergo gonioscopy to document the extent of trabecular pigmentation. In older patients, the only sign of PDS may be the “pigment reversal sign,” where the trabecular meshwork is found to be darker in the superior quadrant when compared with the inferior quadrant. This finding helps to differentiate patients with “burned out” PG from other types of glaucomas. Iris concavity and the extent of iridolenticular contact can also be examined using ultrasound biomicroscopy (UBM) or anterior segment optical coherence tomography (AS-OCT). However, neither test is necessary for diagnosis.

Laboratory test

No laboratory testing is recommended.

Differential diagnosis

Krukenberg spindles have been described in conditions other than PDS and PG, including uveitis and trauma. Trauma, previous ocular surgery, and pseudoexfoliation can also produce heavy trabecular pigmentation. Exfoliation syndrome presents in older age group and clinical signs include peri-pupillary transillumination defects, exfoliative material on the anterior lens capsule, and more uneven pigment distribution in the angle. However, it is important to remember that the exfoliation syndrome is more common in PDS/PG than in the general population. Some patients may have both, an entity described as “overlap syndrome”. Sulcus intraocular lens placement and iris melanoma can also produce a PG.


General treatment

Treatment for PG and PDS is similar to the treatment of primary open angle glaucoma, though laser iridotomy may be considered as a prophylactic treatment. Men and persons of African descent often present with advanced disease, and may require more aggressive therapy.[49] In one case series, patients with PDS or PG were more likely to require surgery than a control group with POAG.

Medical therapy

Pilocarpine has been demonstrated to reduce iris concavity and has been shown to block the exercise-induced elevation of IOP found in some patients.[18][27][50] However, pilocarpine treatment can induce additional myopia and accommodative spasms. Peripheral retina should be carefully examined before the initiation of miotics since lattice degeneration is present in up to 20% of these eyes, and the incidence of retinal detachment in patients with PDS and PG is higher than in general population.[12]Therefore, treatment with pilocarpine has largely been replaced by newer medical agents including topical prostaglandins, beta-blockers, carbonic anhydrase inhibitors, and alpha-adrenergic agonists. Prostaglandin analogues may be preferred over aqueous suppressants as treatment with aqueous suppressants slows down the clearance of pigment from the trabecular meshwork.

Medical follow up

Patients treated medically should be followed up periodically every 3-6 months to ensure adequate control of intraocular pressure and to confirm that the glaucoma has not progressed through examination, visual field testing, and/or imaging of the optic nerve head and nerve fiber layer.


Given that PDS or PG results from a pressure differential across the iris (from the anterior to posterior chambers), it has been suggested that the underlying mechanism of disease might be eliminated by treatment with laser iridotomy. Indeed, reports have demonstrated that laser iridotomy can eliminate iris concavity and reduce iridolenticular contact in eyes with PDS.[51][52][53][54] However, some eyes may retain a concave iris configuration even after laser treatment,[55] and this intervention may not always prevent exercise-induced pigment release and IOP elevation.[50][56] Limited data is available regarding whether laser iridotomy is effective in controlling IOP in patients with PDS or PG. A small randomized controlled trial of 21 patients demonstrated a lower rate of IOP elevation over 2 years of follow up in eyes treated with laser as compared to eyes not receiving laser (52% vs. 5%),[57] while a retrospective study of 60 patients did not suggest any benefit for laser iridotomy with regards to the future IOP course.[58] Given the heavy trabecular pigmentation in PDS and PG, argon laser trabeculoplasty (ALT) may be an effective treatment option.[59][60][61][62][63] However, long-term control of IOP is unlikely, and 1/3 of eyes or more may require trabeculectomy.[63] Younger patients are more likely to have long-term IOP lowering after ALT.[63]The effects of Selective Laser Trabeculoplasty (SLT) as a treatment in PDS and PG has not been well studied. With either ALT or SLT, lower energy settings should be used to avoid release of pigment and IOP spikes.

Patients demonstrating disease progression despite treatment with medicines and/or trabeculoplasty should be considered for trabeculectomy or other incisional surgery. Long term results of trabeculectomy for PG have not been reported. The use of newer surgical modalities in the treatment of PG has not been well described.

Surgical follow up

Follow-up after laser iridotomy is similar to the follow-up for iridotomy performed for angle closure. Follow-up after ALT and SLT is similar for the follow-up schedule used for ALT/SLT with primary open angle glaucoma.


Rise in intraocular pressure after iridotomy is greater in PDS and PG patients than in patients with occludable angles. To avoid this, lower energy levels should be used, alpha adrenergic agonists should be administered before and after the laser treatment, and argon laser should be used, as it is less disruptive than a YAG laser in terms of pigment liberation and inflammation.[64]


Blindness from PG is rare. In a community based study of 113 PDS and PG patients followed for a median of 6 years, 1 patient went unilaterally blind while a second went bilaterally blind.[3] In the same study, 10% of PDS patients progressed to PG at 5 years, while 15% progressed at 10 years, though 23% of patients were noted to have PG at diagnosis.[3] Forty-four percent of patients with PG had worsening of visual fields over a mean follow-up period of 6 years. Similar rates of blindness were found in a group of patients followed in a glaucoma clinic, but higher rates of progression from PDS to PG were observed (35% over a median follow-up at 15 years) and roughly 40% of PG patients were observed to have worsening of optic nerve damage.[25]No risk factor for progression has been identified other than elevated intraocular pressure.[3][25] In some cases, PG may regress over time. Both TM pigmentation and iris transillumination defects have been observed to normalize over time.[8][23][28] Even elevated IOP has been observed to normalize, suggesting return of normal TM function.[65] Additionally, older patients with diagnosis of normal tension glaucoma have been identified with iris transillumination defects and dense TM pigmentation suggesting they may have had PG with subsequent normalization of IOP due to cessation of pigment release.[66] In such patients, presence of “pigment reversal sign” helps to distinguish between different types of glaucomas.

Additional Resources


  1. Ritch R, Steinberger D, Liebmann JM. Prevalence of pigment dispersion syndrome in a population undergoing glaucoma screening. Am J Ophthalmol. 1993;115(6):707-710.
  2. 2.0 2.1 2.2 2.3 2.4 Scheie HG, Cameron JD. Pigment dispersion syndrome: a clinical study. Br J Ophthalmol. 1981;65(4):264-269.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 Siddiqui Y, Ten Hulzen RD, Cameron JD, Hodge DO, Johnson DH. What is the risk of developing pigmentary glaucoma from pigment dispersion syndrome? Am J Ophthalmol. 2003;135(6):794-799.
  4. 4.0 4.1 Campbell DG. Pigmentary dispersion and glaucoma. A new theory. Arch Ophthalmol. 1979;97(9):1667-1672.
  5. 5.0 5.1 5.2 5.3 Kampik A, Green WR, Quigley HA, Pierce LH. Scanning and transmission electron microscopic studies of two cases of pigment dispersion syndrome. Am J Ophthalmol. 1981;91(5):573-587.
  6. 6.0 6.1 6.2 Jewelewicz DA, Radcliffe NM, Liebmann J, Ritch R. Temporal evolution of intraocular pressure elevation after pupillary dilation in pigment dispersion syndrome.J Glaucoma. 2009;18(3):184-185.
  7. 7.0 7.1 7.2 7.3 Mardin CY, Kuchle M, Nguyen NX, Martus P, Naumann GO. Quantification of aqueous melanin granules, intraocular pressure and glaucomatous damage in primary pigment dispersion syndrome. Ophthalmology. 2000;107(3):435-440.
  8. 8.0 8.1 Richter CU, Richardson TM, Grant WM. Pigmentary dispersion syndrome and pigmentary glaucoma. A prospective study of the natural history. Arch Ophthalmol. 1986;104(2):211-215.
  9. 9.0 9.1 Richardson TM, Hutchinson BT, Grant WM. The outflow tract in pigmentary glaucoma: a light and electron microscopic study. Arch Ophthalmol. 1977;95(6):1015-1025.
  10. 10.0 10.1 10.2 Liebmann JM, Tello C, Chew SJ, Cohen H, Ritch R. Prevention of blinking alters iris configuration in pigment dispersion syndrome and in normal eyes. Ophthalmology. 1995;102(3):446-455.
  11. 11.0 11.1 11.2 Doyle JW, Hansen JE, Smith MF, Hamed LM, McGorray S, Sherwood MB. Use of scheimpflug photography to study iris configuration in patients with pigment dispersion syndrome and pigmentary glaucoma. J Glaucoma. 1995;4(6):398-405.
  12. 12.0 12.1 12.2 Ritch R. A unification hypothesis of pigment dispersion syndrome. Trans Am Ophthalmol Soc. 1996;94:381-405; discussion 405-9.
  13. 13.0 13.1 Mora P, Sangermani C, Ghirardini S, Carta A, Ungaro N, Gandolfi S. Ultrasound biomicroscopy and iris pigment dispersion: a case--control study. Br J Ophthalmol. 2010;94(4):428-432.
  14. Pavlin CJ, Macken P, Trope GE, Harasiewicz K, Foster FS. Accommodation and iridotomy in the pigment dispersion syndrome. Ophthalmic Surg Lasers. 1996;27(2):113-120.
  15. Pavlin CJ, Macken P, Trope GE, Harasiewicz K, Foster FS. Accommodation and iridotomy in the pigment dispersion syndrome. Ophthalmic Surg Lasers. 1996;27(2):113-120.
  16. 16.0 16.1 16.2 16.3 16.4 16.5 16.6 Sugar HS. Pigmentary glaucoma. A 25-year review. Am J Ophthalmol. 1966;62(3):499-507.
  17. 17.0 17.1 17.2 17.3 Epstein DL, Boger WP,3rd, Grant WM. Phenylephrine provocative testing in the pigmentary dispersion syndrome. Am J Ophthalmol. 1978;85(1):43-50.
  18. 18.0 18.1 Schenker HI, Luntz MH, Kels B, Podos SM. Exercise-induced increase of intraocular pressure in the pigmentary dispersion syndrome. Am J Ophthalmol. 1980;89(4):598-600
  19. Samples JR, Van Buskirk EM. Pigmentary glaucoma associated with posterior chamber intraocular lenses. Am J Ophthalmol. 1985;100(3):385-388.
  20. Ballin N, Weiss DM. Pigment dispersion and intraocular pressure elevation in pseudophakia. Ann Ophthalmol. 1982;14(7):627-630.
  21. Caplan MB, Brown RH, Love LL. Pseudophakic pigmentary glaucoma. Am J Ophthalmol. 1988;105(3):320-321.
  22. 22.0 22.1 22.2 22.3 Gillies WE, Brooks AM. Clinical features at presentation of anterior segment pigment dispersion syndrome. Clin Experiment Ophthalmol. 2001;29(3):125-127.
  23. 23.0 23.1 23.2 23.3 23.4 Lichter PR, Shaffer RN. Diagnostic and prognostic signs in pigmentary glaucoma. Trans Am Acad Ophthalmol Otolaryngol. 1970;74(5):984-998.
  24. Bick MW. Sex differences in pigmentary glaucoma. Am J Ophthalmol. 1962;54:831-837.
  25. 25.0 25.1 25.2 Migliazzo CV, Shaffer RN, Nykin R, Magee S. Long-term analysis of pigmentary dispersion syndrome and pigmentary glaucoma. Ophthalmology. 1986;93(12):1528-1536.
  26. 26.0 26.1 SCHEIE HG, FLEISCHHAUER HW. Idiopathic atrophy of the epithelial layers of the iris and ciliary body; a clinical study. Arch Ophthalmol. 1958;59(2):216-228.
  27. 27.0 27.1 Kaiser-Kupfer MI, Kupfer C, McCain L. Asymmetric pigment dispersion syndrome. Trans Am Ophthalmol Soc. 1983;81:310-324.
  28. 28.0 28.1 Rodrigues MM, Spaeth GL, Weinreb S, Sivalingam E. Spectrum of trabecular pigmentation in open-angle glaucoma: a clinicopathologic study. Trans Sect Ophthalmol Am Acad Ophthalmol Otolaryngol. 1976;81(2):258-276.
  29. 29.0 29.1 Lord FD, Pathanapitoon K, Mikelberg FS. Keratometry and axial length in pigment dispersion syndrome: a descriptive case-control study. J Glaucoma. 2001;10(5):383-385.
  30. 30.0 30.1 Roberts DK, Chaglasian MA, Meetz RE. Clinical signs of the pigment dispersion syndrome in blacks. Optom Vis Sci. 1997;74(12):993-1006.
  31. 31.0 31.1 Kanadani FN, Dorairaj S, Langlieb AM, et al. Ultrasound biomicroscopy in asymmetric pigment dispersion syndrome and pigmentary glaucoma. Arch Ophthalmol. 2006;124(11):1573-1576.
  32. 32.0 32.1 Yip LW, Sothornwit N, Berkowitz J, Mikelberg FS. A comparison of interocular differences in patients with pigment dispersion syndrome. J Glaucoma. 2009;18(1):1-5.
  33. Roberts DK, Meetz RE, Chaglasian MA. The inheritance of the pigment dispersion syndrome in blacks. J Glaucoma. 1999;8(4):250-256.
  34. McDermott JA, Ritch R, McDermott J. Familial occurrence of pigmentary dispersion syndrome. Invest Ophthalmolol Vis Sci. 1987;28(suppl):136.
  35. STANKOVIC I. A contribution to the knowledge of the heredity of pigment glaucoma. Klin Monbl Augenheilkd Augenarztl Fortbild. 1961;139:165-174.
  36. Andersen JS, Pralea AM, DelBono EA, et al. A gene responsible for the pigment dispersion syndrome maps to chromosome 7q35-q36.Arch Ophthalmol. 1997;115(3):384-388.
  37. Gottanka J, Johnson DH, Grehn F, Lutjen-Drecoll E. Histologic findings in pigment dispersion syndrome and pigmentary glaucoma. J Glaucoma. 2006;15(2):142-151.
  38. Grant WM. Experimental aqueous perfusion in enucleated human eyes. Arch Ophthalmol. 1963;69:783-801.
  39. Petersen HP. Can pigmentary deposits on the trabecular meshwork increase the resistance of the aqueous outflow? Acta Ophthalmol (Copenh). 1969;47(3):743-749.
  40. Foster PJ, Buhrmann R, Quigley HA, Johnson GJ. The definition and classification of glaucoma in prevalence surveys. Br J Ophthalmol. 2002;86(2):238-42.
  41. Evans WH, Odom RE, Wenaas EJ. Krukenberg's spindle; A study of two hundred and two collected cases. Arch Ophthal. 1941:1023.
  42. Murrell WJ, Shihab Z, Lamberts DW, Avera B. The corneal endothelium and central corneal thickness in pigmentary dispersion syndrome. Arch Ophthalmol. 1986;104(6):845-846.
  43. Haynes WL, Thompson HS, Kardon RH, Alward WL. Asymmetric pigmentary dispersion syndrome mimicking Horner's syndrome. Am J Ophthalmol. 1991;112(4):463-464.
  44. Feibel RM. Anisocoria in the pigmentary dispersion syndrome: further cases. J Glaucoma. 1993;2(1):37-38.
  45. Feibel RM, Perlmutter JC. Anisocoria in the pigmentary dispersion syndrome. Am J Ophthalmol. 1990;110(6):657-660.
  46. Lichter PR. Pigmentary glaucoma--current concepts. Trans Am Acad Ophthalmol Otolaryngol. 1974;78(2):OP309-13.
  47. Zentmayer W. Association of an annular band of pigment on the posterior capsule of the lens with a Krukenberg spindle. Arch Ophthalmol. 1938;20:52.
  48. Lin DY, Volpicelli M, Singh K. Dense pigmentation of the posterior lens capsule associated with the pigment dispersion syndrome. J Glaucoma. 2003;12(6):491-493.
  49. 49.0 49.1 Farrar SM, Shields MB, Miller KN, Stoup CM. Risk factors for the development and severity of glaucoma in the pigment dispersion syndrome. Am J Ophthalmol. 1989;108(3):223-229.
  50. 50.0 50.1 Haynes WL, Johnson AT, Alward WL. Inhibition of exercise-induced pigment dispersion in a patient with the pigmentary dispersion syndrome. Am J Ophthalmol. 1990;109(5):601-602.
  51. Laemmer R, Mardin CY, Juenemann AG. Visualization of changes of the iris configuration after peripheral laser iridotomy in primary melanin dispersion syndrome using optical coherence tomography. J Glaucoma. 2008;17(7):569-570.
  52. Carassa RG, Bettin P, Fiori M, Brancato R. Nd:YAG laser iridotomy in pigment dispersion syndrome: an ultrasound biomicroscopic study. Br J Ophthalmol. 1998;82(2):150-153.
  53. Breingan PJ, Esaki K, Ishikawa H, Liebmann JM, Greenfield DS, Ritch R. Iridolenticular contact decreases following laser iridotomy for pigment dispersion syndrome. Arch Ophthalmol. 1999;117(3):325-328.
  54. Karickhoff JR. Pigmentary dispersion syndrome and pigmentary glaucoma: a new mechanism concept, a new treatment, and a new technique. Ophthalmic Surg. 1992;23(4):269-77.
  55. Jampel HD. Lack of effect of peripheral laser iridotomy in pigment dispersion syndrome. Arch Ophthalmol. 1993;111(12):1606.
  56. Haynes WL, Alward WL, Tello C, Liebmann JM, Ritch R. Incomplete elimination of exercise-induced pigment dispersion by laser iridotomy in pigment dispersion syndrome. Ophthalmic Surg Lasers. 1995;26(5):484-486.
  57. Gandolfi SA, Vecchi M. Effect of a YAG laser iridotomy on intraocular pressure in pigment dispersion syndrome. Ophthalmology. 1996;103(10):1693-5.
  58. Reistad CE, Shields MB, Campbell DG, Ritch R, Wang JC, Wand M. The influence of peripheral iridotomy on the intraocular pressure course in patients with pigmentary glaucoma. J Glaucoma. 2005;14(4):255-9.
  59. Robin AL, Pollack IP. Argon laser trabeculoplasty in secondary forms of open-angle glaucoma. Arch Ophthalmol. 1983;101(3):382-384.
  60. Lunde MW. Argon laser trabeculoplasty in pigmentary dispersion syndrome with glaucoma.Am J Ophthalmol. 1983;96(6):721-725.
  61. Horns DJ, Bellows AR, Hutchinson BT, Allen RC. Argon laser trabeculoplasty for open angle glaucoma. A retrospective study of 380 eyes. Trans Ophthalmol Soc U K. 1983;103 ( Pt 3)(Pt 3):288-296.
  62. Lehto I. Long-term follow up of argon laser trabeculoplasty in pigmentary glaucoma. Ophthalmic Surg. 1992;23(9):614-617.
  63. 63.0 63.1 63.2 Ritch R, Liebmann J, Robin A, et al. Argon laser trabeculoplasty in pigmentary glaucoma. Ophthalmology. 1993;100(6):909-913.
  64. Birt CM. Intraocular pressure spike after YAG iridotomy in patients with pigment dispersion. Can J Ophthalmol. 2004;39(3):234-9.
  65. Speakman JS. Pigmentary dispersion. Br J Ophthalmol. 1981;65(4):249-251.
  66. Ritch R. Nonprogressive low-tension glaucoma with pigmentary dispersion.Am J Ophthalmol. 1982;94(2):190-196.
The Academy uses cookies to analyze performance and provide relevant personalized content to users of our website.