eMedicine Specialties > Ophthalmology > Intraocular Pressure

Glaucoma, Pseudoexfoliation

Author: Mauricio E Pons, MD, Associate Physician, Charles A Garcia, MD, PA
Coauthor(s): Babak Eliassi-Rad, MD, Assistant Professor, Department of Ophthalmology, Boston University School of Medicine
Contributor Information and Disclosures

Updated: Feb 25, 2008

Introduction

Background

In 1917, a Finnish ophthalmologist named Lindberg first described pseudoexfoliation syndrome. This entity is characterized by flakes of granular material at the pupillary margin of the iris and throughout the inner surface of the anterior chamber. It is also associated with secondary open-angle glaucoma, known as pseudoexfoliation glaucoma, which is the most common identifiable form of secondary open-angle glaucoma worldwide. Dvorak-Thebold suggested the term pseudoexfoliation to differentiate it from true exfoliation or lamellar delamination of the lens capsule found in glassblowers. True exfoliation syndrome is due to heat or infrared-related changes in the anterior lens capsule.

Pathophysiology

Pseudoexfoliation syndrome is a common ocular manifestation of a systemic disease, known to cause disease primarily in the eye. Exact etiology of this condition remains unknown.

Pseudoexfoliation material is associated with abnormalities of the basement membrane in epithelial cells and has a wide distribution throughout the body. Pseudoexfoliative material has been found in the walls of the vortex veins and the central retinal artery. Extraocular tissues involved include lung, skin, liver, heart, kidney, gallbladder, blood vessels, extraocular muscle, connective tissue in the orbit, and meninges. In the anterior segment of the eye, it is characterized by deposition of pseudoexfoliative amyloidlike material on the anterior lens capsule, ciliary body, zonules, pupillary margin of the iris, corneal endothelium, anterior vitreous, and trabecular meshwork.

Some investigators believe that the iris pigment epithelium, the ciliary epithelium, and the peripheral anterior lens epithelium produce this pseudoexfoliative amyloidlike material, which moves into the aqueous humor and is carried to the trabecular meshwork, following the normal flow. Obstruction of the trabecular meshwork by this fibrillar material and pigment associated with degenerative changes in the Schlemm canal and the juxtacanalicular area causes elevation of the intraocular pressure (IOP) with associated glaucoma.

Zenkel et al have studied genes differentially expressed in anterior segment tissues and have postulated that pseudoexfoliation syndrome is a stress-induced elastic microfibrillopathy.1

Frequency

United States

Roth and Epstein reported that pseudoexfoliation glaucoma was present in 12% of patients with glaucoma.2 Kozart and Yanoff reported that glaucoma was present in 7% of 100 consecutive patients with pseudoexfoliation syndrome in Philadelphia.3 In the Framingham study, prevalence of pseudoexfoliation syndrome was 1.8%. In a prospective study, Cashwell and Shields found that the prevalence of pseudoexfoliation syndrome in the southeastern United States was 1.6% of the total population and in 6% of an open-angle glaucoma subpopulation.4 Prevalence of pseudoexfoliation syndrome in the glaucoma population of south Louisiana was found to be 2.7% in white patients and 0.4% in African American patients. Karger et al determined that the incidence of newly diagnosed pseudoexfoliation syndrome in residents of Olmsted County, Minnesota, was 25.9 cases per 100,000 population.5

Because of the increased mean age of populations, pseudoexfoliation syndrome may become more prevalent in the future.

International

Prevalence of pseudoexfoliation syndrome in Europe was found to be 4.7% in England, 6.3% in Norway, 4% in Germany, 1.1% in Greece, and 5.5% in France.

Bartholomew reported an 8.2% prevalence of pseudoexfoliation syndrome in the Bantu tribes of South Africa.6 In Asia, the prevalence in a Japanese population was 3.4%. Hospital-based studies showed a prevalence of 6.45% in Pakistan and 7.4% in India. A prevalence rate of 0.4% in patients aged 60 years or older was identified in China.

Mortality/Morbidity

In a retrospective study, Shrum et al found no association between ocular pseudoexfoliation and cardiovascular or cerebrovascular mortality.7 However, other authors have found that pseudoexfoliation is linked with Alzheimer disease, senile dementia, cerebral atrophy, chronic cerebral ischemia, stroke, transient ischemic attacks, heart disease, and hearing loss. Vessani et al found that homocysteine levels were higher among patients with pseudoexfoliation syndrome and pseudoexfoliative glaucoma compared with controls.8 Roedl et al reported increased homocysteine concentrations in tear fluid and plasma of patients with pseudoexfoliation glaucoma.9 Elevated plasma homocysteine levels have been described as a risk factor for cardiovascular disease.

Race

Although it occurs in virtually every area of the world, a considerable racial variation exists in the incidence of pseudoexfoliation glaucoma.

  • In Scandinavian countries, more than 50% of cases of open-angle glaucoma are caused by pseudoexfoliation syndrome.
  • Pseudoexfoliation syndrome is relatively rare among African Americans and Eskimos. It was not observed at all in the Inuit who live throughout the Canadian Arctic.
  • Prevalence is high in the Sami people who are indigenous of northern Europe.
  • Among the Bantu tribes of South Africa, exfoliation was found in 19% of patients in a glaucoma clinic.
  • In Saudi Arabia, Summanen and Tonjum reported a prevalence of pseudoexfoliation syndrome of 13%.10
  • Prevalence of pseudoexfoliation syndrome in Spanish Americans in New Mexico was estimated to be 3-6%.

Sex

Pseudoexfoliation syndrome is more common in females than in males. In a series by Kozart and Yanoff, pseudoexfoliation syndrome was 3 times more common in women than in men.3

Age

Pseudoexfoliation syndrome is rarely seen before age 50 years, and its incidence increases steadily with age.

  • In Norway, Aasved reported that the prevalence of pseudoexfoliation was 0.4% in individuals aged 50-59 years and 7.9% in individuals aged 80-89 years.11 The reported mean age of pseudoexfoliation syndrome ranges from 69-75 years.
  • Jonasson et al reported a 10% annual increase for both open-angle glaucoma and pseudoexfoliation in persons aged 50 years and older in Iceland.12

Clinical

History

Patient may be asymptomatic, or they may complain of decreased visual acuity secondary to cataract or glaucomatous visual field changes.

Physical

  • Pseudoexfoliation syndrome is diagnosed clinically by slit lamp examination with an 85% sensitivity rate and a 100% specificity rate.  
    • Pseudoexfoliative material can be seen on the pupillary border of the iris without dilation.
    • The most commonly recognized feature is the 3-ring sign on the anterior lens capsule, formed by a central disk, a peripheral ring, and a clear zone, which separates the two. The clear zone varies in diameter and may exhibit curled edges.
    • The central disc measures 1-2.5 mm in diameter and has well-demarcated borders.
    • The peripheral ring typically is seen after pupillary dilation. Its size is variable, and its inner border has many radial striations.
    • The translucent zone most likely is created by the physiologic rubbing of the posterior surface of the iris against the lens. It scrapes the pseudoexfoliative material from the surface of the lens. This scraping results in a secondary pigmentary dispersion syndrome, with a loss of melanin from the iris pigment epithelium at the pupillary margin and an accumulation of melanin granules in the trabecular meshwork. Peripupillary iris atrophy is a common finding.
    • Gonioscopy shows a discontinuous pigmentation of the trabecular meshwork, usually less dense than seen in pigmentary glaucoma. Also, pigment characteristically is deposited on the Schwalbe line or anterior to the Schwalbe line (the Sampaolesi line). A high incidence of narrow, or occludable, angles in eyes with pseudoexfoliation has been reported.
    • Elevated IOP leads to glaucoma development in about 50% of patients. Puska et al reported that the conversion rate from pseudoexfoliation syndrome to pseudoexfoliation glaucoma was 3.2% per year.13 Jeng et al found that, in patients with pseudoexfoliation, the probability of developing glaucoma was 44% after 15 years, and, in a study by Grodum et al, 55.1% of patients developed glaucoma after a mean of 8.7 years.14,15
    • When glaucoma develops, it is frequently referred to as capsular glaucoma. Patients with pseudoexfoliation syndrome have higher IOP than patients with primary open-angle glaucoma. Because of these higher IOPs, visual field loss and optic nerve damage are more pronounced.
    • Other signs of pseudoexfoliation syndrome are insufficient mydriasis, posterior synechiae, pigment deposition on the iris surface, deposition of pigment and pseudoexfoliation material on the corneal endothelium, pigment liberation after pupillary dilation, and pseudoexfoliation material covering the ciliary processes and the zonules. Phacodonesis, lens subluxation, and corneal endothelial decompensation can be present. An associated nuclear cataract is a common finding.
    • Pseudoexfoliation syndrome typically presents unilaterally. Why this occurs remains unknown. The fellow eye develops signs of pseudoexfoliation in more than 40% of cases, but pseudoexfoliation material can almost always be demonstrated in fellow eyes on electron microscopy.
    • Pseudoexfoliation syndrome is associated with reduced ocular blood flow, iris hypoperfusion, and anterior chamber hypoxia.

Causes

  • Whether pseudoexfoliation syndrome occurs as part of a genetic process or in association with other diseases is not clear. Familial aggregation supports the notion that it may be inherited as an autosomal dominant trait with incomplete penetrance and late onset.
  • Its frequency increases with age; however, it is not part of normal aging. Possible predisposing factors include ultraviolet light, northern latitudes, and altitude. Climate factors may not play a definitive role in the pathogenesis of the disease.
  • The exact nature of pseudoexfoliation material remains unknown, although its close association with zonular fibers supports the idea of pseudoexfoliation syndrome as a type of elastosis, affecting elastic microfibrils. It seems to arise from abnormal aggregation of elastin microfibrillar components.
  • In a recent study, Thorleifsson et al showed that two nonsynonymous single-nucleotide polymorphisms in exon 1 of the LOXL1 gene on chromosome 15q24.1 confer risk for pseudoexfoliation glaucoma.16 According to the authors, the product of the LOXL1 gene modifies elastin fibers that are a major constituent of the intraocular lesions in pseudoexfoliation glaucoma.16 Approximately 25% of the general population is positive for these variants.
  • Glaucoma is a secondary event. Blockage of the trabecular spaces by pseudoexfoliation material promotes accumulation of pigment and cellular debris, which causes obstruction of the aqueous channels and limits access to the Schlemm canal. Accumulation of pseudoexfoliation material in the juxtacanicular tissue adjacent to the Schlemm canal leads to narrowing of the canal lumen, collapse of its walls, disruption of its endothelium, and partial obliteration. These changes appear to be the causative factors for chronic IOP elevation and pseudoexfoliation glaucoma.
  • Zonular laxity allows forward movement of the lens, causing decreased anterior chamber depth and pupillary or angle closure glaucoma.
  • Pseudoexfoliation syndrome itself does not produce optic nerve damage.

More on Glaucoma, Pseudoexfoliation

Overview: Glaucoma, Pseudoexfoliation
Differential Diagnoses & Workup: Glaucoma, Pseudoexfoliation
Treatment & Medication: Glaucoma, Pseudoexfoliation
Follow-up: Glaucoma, Pseudoexfoliation
Multimedia: Glaucoma, Pseudoexfoliation
References
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Further Reading

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Keywords

exfoliation glaucoma, pseudoexfoliation glaucoma, capsular glaucoma, glaucoma capsulare, exfoliative glaucoma, pseudoexfoliative glaucoma, pseudoexfoliation syndrome, fibrillopathia epitheliocapsularis, FEC, epithelio-capsular fibrillopathy

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Contributor Information and Disclosures

Author

Mauricio E Pons, MD, Associate Physician, Charles A Garcia, MD, PA
Mauricio E Pons, MD is a member of the following medical societies: American Academy of Ophthalmology and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Coauthor(s)

Babak Eliassi-Rad, MD, Assistant Professor, Department of Ophthalmology, Boston University School of Medicine
Babak Eliassi-Rad, MD is a member of the following medical societies: American Academy of Ophthalmology and American Glaucoma Society
Disclosure: Nothing to disclose.

Medical Editor

Bradford Shingleton, MD, Assistant Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary
Bradford Shingleton, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Ophthalmology
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

Martin B Wax, MD, Clinical Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Ophthalmology Research and Development, Head, Ophthalmology Discovery Research, Alcon Labs, Inc
Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Society for Neuroscience
Disclosure: Alcon Labs Salary Employment

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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