A Member of the University of Maryland Medical System   |   In Partnership with the University of Maryland School of Medicine

Share

Email PageEmail Print PagePrint

Home > Medical Reference > Patient Education

Glaucoma - Introduction

Description

An in-depth report on the causes, diagnosis, treatment, and prevention of glaucoma.

Introduction:

Glaucoma is a disease of the optic nerve, in which the nerve cells in the front of the optic nerve (the ganglion cells) die. The process is irreversible. Previously, it was believed that glaucoma was almost always due to increased intraocular pressure. However, glaucoma can occur in patients with normal and even low eye pressure, so damage to the optic nerve is now key for diagnosis.

The Aqueous Humor. To understand glaucoma, it is important to first consider aqueous humor, the clear, watery fluid that circulates continuously through the front (anterior) chamber of the healthy eye and is a primary focus of glaucoma research. (This fluid is not related to tears, nor is it the dense jelly-like substance called vitreous humor that is contained in the rear chamber.)

Aqueous humor serves two important functions in the eye:

  • Nourishing the area around the colored iris and behind the cornea
  • Exerting pressure to help maintain the eyeâ ' s shape

Draining the Fluid and Intraocular Pressure. The aqueous fluid is continuously produced within the front of the eye, causing pressure known as intraocular pressure (IOP). To offset the in-flowing fluid and to maintain normal IOP, the fluid drains out between the iris and cornea (an area known as the drainage angle). It does so through two channels within this angle:

  • The trabecular meshwork, a sponge-like, porous network, and its connecting passageways are referred to as the "conventional" outflow pathway. Most of the eye fluid outflow occurs in this region and flows from the trabecular meshwork to a group of vessels encircling the anterior chamber, called Schlemm's canal. From here, the fluid enters collection chambers and then flows out into the general blood circulatory system of the body.
  • The uveoscleral pathway is located behind the trabecular meshwork and is called the "unconventional" pathway. Up to 30% of the fluid flows out through this channel.

Intraocular Eye Pressure. Increased IOP is, indeed, present in most cases of glaucoma, but some patients have normal IOP, which is usually maintained at measurements of 10 - 20 mmHg. Higher IOP measurements increase the risk of glaucoma, but do not necessarily mean that the patient has glaucoma.

Glaucoma is a term used to describe several types of eye conditions that affect the optic nerve. In most cases, damage to the optic nerve is caused by increased pressure in the eye, also known as intraocular pressure (IOP). Glaucoma can cause partial vision loss, with blindness as a possible eventual outcome.
Glaucoma

Primary Open-Angle Glaucoma

Most people with glaucoma have the form called primary-open-angle glaucoma (also called chronic open-angle glaucoma). Open-angle glaucoma is essentially a plumbing problem.

The disease process may occur as follows:

  • The drainage angle remains open, but tiny drainage channels in the trabecular meshwork pathway become clogged. This pathway is responsible for most aqueous humor fluid outflow. An imbalance then occurs as fluid continues to be produced but does not drain out efficiently.
  • The fluid in the eyeâ ' s anterior chamber builds up and increases pressure within the eye (intraocular pressure).
  • The intraocular pressure exerts force on the optic nerve at the back of the eye.
  • Over time, the persistent pressure or other factors irreversibly damages the delicate long fibers of the optic nerve, called axons, which convey images to the brain.
  • As these axons die, the small cup-like head of the optic nerve may eventually collapse into an enlarged irregular shape.

Optic nerve damage is the basic glaucoma condition. If it is untreated, eventually the nerve deteriorates until a person loses sight, first in the peripheral vision (the vision in the "corner of the eyes"). If it becomes severe, the person loses central vision (in the middle of the eyes), and may eventually become blind. (Blindness is fortunately nearly always preventable with early treatment.)

Primary open-angle glaucoma tends to start in one eye but eventually involves both. About half of patients have generalized (spread out) nerve damage. In the other half the disease is localized, causing wedge-shaped abnormalities in the nerve fiber layers of the retina.

Normal Tension Glaucoma

Intraocular eye pressure is normal (12 - 22 mmHg) in about 25 - 30% of U.S. glaucoma cases, a condition known as normal-tension glaucoma. Other factors are present that cause optic nerve damage but do not affect IOP.

Closed-Angle Glaucoma

Closed-angle glaucoma (also called angle-closure glaucoma) is responsible for 15% of all cases. It is less common than open-angle glaucoma in the U.S., but it constitutes about half of the world's glaucoma cases because of its higher prevalence among Asians. The iris is pushed against the lens, sometimes sticking to it, closing off the drainage angle. This can occur very suddenly, resulting in an immediate rise in pressure. It often occurs in genetically susceptible people when the pupil shrinks suddenly. Closed-angle glaucoma can also be chronic and gradual, a less common condition.

Congenital Glaucoma

Congenital glaucoma, in which the eye's drainage canals fail to develop correctly, is present from birth. It is very rare, occurring in about 1 in 10,000 newborns. This may be an inherited condition and often can be corrected with microsurgery.

The Eye

The Light-Processing Parts. To understand sight, one begins with light and its passage through the eye's sensitive camera-like structures:

  • Light first passes through the cornea, a clear tissue at the front of the eye.
  • Behind the cornea, the iris (the colored tissues of the eye) opens and closes like a camera shutter to regulate the passage of light.
  • The lens, located behind the iris, focuses the light, which then hits the retina.
  • The retina is an electric fragile membrane of nerve cells called photoreceptors that receive light and translate it into signals.
  • A layer of cells, called the retinal ganglia, receive signals from the retina. These nerve cells are the front ends of the optic nerve cable, which, in turn, receive the signals.
  • The optic nerve is actually a cable of about 1.2 million nerve fibers called axons. It carries the signals to the brain, which interprets them as images.
  • They exit the eye through the optic disc, located in the back of the eye.

The Supportive Chambers. To help support and protect these sensitive structures, the eye contains two fluid-filled chambers:

  • The posterior (rear) chamber is the large area behind the iris.
  • Fluid passes from the posterior into the anterior (forward) chamber located in the bulging area between the iris and the front of the eye.

Resources

References

Aptel F, Cucherat M, Denis P. Efficacy and tolerability of prostaglandin analogs: a meta-analysis of randomized controlled clinical trials. J Glaucoma. 2008 Dec;17(8):667-73.

Burr JM, Mowatt G, Hernández R, Siddiqui MA, Cook J, Lourenco T, et al. The clinical effectiveness and cost-effectiveness of screening for open angle glaucoma: a systematic review and economic evaluation. Health Technol Assess. 2007 Oct;11(41):iii-iv, ix-x, 1-190.

Chang R, Budenz DL. New developments in optical coherence tomography for glaucoma. Curr Opin Ophthalmol. 2008 Mar;19(2):127-35.

Cheng JW, Wei RL, Cai JP, Li Y. Efficacy and tolerability of nonpenetrating filtering surgery with and without implant in treatment of open angle glaucoma: a quantitative evaluation of the evidence. J Glaucoma. 2009 Mar;18(3):233-7.

Dueker DK, Singh K, Lin SC, Fechtner RD, Minckler DS, Samples JR, et al. Corneal thickness measurement in the management of primary open-angle glaucoma: a report by the American Academy of Ophthalmology. Ophthalmology. 2007 Sep;114(9):1779-87.

Gedde SJ, Schiffman JC, Feuer WJ, Herndon LW, Brandt JD, Budenz DL. Treatment outcomes in the tube versus trabeculectomy study after one year of follow-up. Am J Ophthalmol. 2007 Jan;143(1):9-22.

Hatt S, Wormald R, Burr J. Screening for prevention of optic nerve damage due to chronic open angle glaucoma. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD006129.

Hernández R, Rabindranath K, Fraser C, Vale L, Blanco AA, Burr JM; OAG Screening Project Group. Screening for open angle glaucoma: systematic review of cost-effectiveness studies. J Glaucoma. 2008 Apr-May;17(3):159-68.

Higginbotham EJ. Managing glaucoma during pregnancy. JAMA. 2006 Sep 13;296(10):1284-5.

Hodge WG, Lachaine J, Steffensen I, Murray C, Barnes D, Foerster V, et al. The efficacy and harm of prostaglandin analogues for IOP reduction in glaucoma patients compared to dorzolamide and brimonidine: a systematic review. Br J Ophthalmol. 2008 Jan;92(1):7-12.

Kwon YH, Fingert JH, Kuehn MH, Alward WL. Primary open-angle glaucoma. N Engl J Med. 2009 Mar 12;360(11):1113-24.

Lam DS, Tham CC, Lai JS, Leung DY. Current approaches to the management of acute primary angle closure. Curr Opin Ophthalmol. 2007 Mar;18(2):146-51.

Lemij HG, Reus NJ. New developments in scanning laser polarimetry for glaucoma. Curr Opin Ophthalmol. 2008 Mar;19(2):136-40.

Leske MC, Heijl A, Hyman L, Bengtsson B, Dong L, Yang Z; EMGT Group. Predictors of long-term progression in the early manifest glaucoma trial. Ophthalmology. 2007 Nov;114(11):1965-72. Epub 2007 Jul 12.

Rivera JL, Bell NP, Feldman RM. Risk factors for primary open angle glaucoma progression: what we know and what we need to know. Curr Opin Ophthalmol. 2008 Mar;19(2):102-6.

Rolim de Moura C, Paranhos A Jr, Wormald R. Laser trabeculoplasty for open angle glaucoma. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD003919.

Rosenberg EA, Sperazza LC. The visually impaired patient. Am Fam Physician. 2008 May 15;77(10):1431-6.

Stewart WC, Konstas AG, Nelson LA, Kruft B. Meta-analysis of 24-hour intraocular pressure studies evaluating the efficacy of glaucoma medicines. Ophthalmology. 2008 Jul;115(7):1117-1122.e1. Epub 2008 Feb 20.

Vass C, Hirn C, Sycha T, Findl O, Bauer P, Schmetterer L. Medical interventions for primary open angle glaucoma and ocular hypertension. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD003167.

Wishart MS, Dagres E. Seven-year follow-up of combined cataract extraction and viscocanalostomy. J Cataract Refract Surg. 2006 Dec;32(12):2043-9.

  • Reviewed last on: 6/23/2009
  • Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.
The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. © 1997- A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.
adam.com
Adam QualityA.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission (www.urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial policy, editorial process and privacy policy. A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation (www.hon.ch).

The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. © 1997- A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.
adam.com
Connect with UMMC
Facebook Twitter YouTube Blog iPhone

Please rate the quality of this article.

Do you find this article to be helpful / informative?
              
Poor                                       Excellent

Do you have any brief comments on this page: (up to 255 characters)

© 2011 University of Maryland Medical Center (UMMC). All rights reserved.
UMMC is a member of the University of Maryland Medical System,
22 S. Greene Street, Baltimore, MD 21201. TDD: 1-800-735-2258 or 1.866.408.6885