Glaucoma is a disease of the optic nerve

It is always a sad day for the eye doctor when a new patient arrives, eyeglasses in hand, complaining she cannot see as clearly as before. The eye doctor assesses the eye health and discovers that the eyeglasses are not the problem at all. Rather the patient has glaucoma. Treatments will be recommended, but the damage has been done. The vision loss is permanent.

Most people think that glaucoma is a problem with high eye pressure. And while about 70% of glaucoma patients do have high pressure (>21 mm Hg) inside the eyes , about one-third do not. Similarly, many patients with pressure above the normal range do not have glaucoma.

So what is glaucoma?

Glaucoma is a name incorporating many different diseases that share common features:

  1. There is damage or risk of damage to the optic nerve that may be due to elevated eye pressure, weakening of the collagen supporting tissue, poor circulation, and other factors.
  2. The damage can cause loss of the thousands of fiber bundles comprising the nerve, known as the nerve fiber layer (NFL).
  3. The loss of nerve tissue, in later stages of the disease, can cause loss of peripheral and central vision that frequently causes no symptoms but is discovered upon testing within the eye doctor's office.

While prescription eyedrops, laser therapy and surgeries are all available for the treatment of glaucoma, the optic nerve damage - and vision loss if it has already occurred -  is permanent. Therefore the goal in glaucoma treatment in not reversal of optic nerve damage, but rather prevention of further damage.


While people frequently fool themselves into thinking their eyes are healthy because they don't wear eyeglasses or they haven't had a change in eyeglass prescription, the tests for glaucoma have nothing to do with an eyeglass prescription.

There are several tests that help an ophthalmologist or optometrist make a diagnosis of glaucoma. These include:

Eye Pressure - Measurement of eye pressure is one test, but not the only test for glaucoma. Ninety-five percent of people have eye pressures ranging from 10-21 mm Hg. Pressure measurement may be done with Goldmann applanation tonometry (most accurate), iCare tonometry, Tonopen, air puff non-contact tonometry or Schiotz tonometry.

Corneal Thickness (pachymetry) - Thin corneas that are less than 555 microns in depth have been associated with a higher chance of progression of ocular hypertension (high pressures without damage) to glaucoma (high pressures with damage), when the eye pressure is above 21 mm Hg.

Ocular Coherence Tomography (OCT) - An optical scan of the fibers that make up the optic nerve, this test is essential to accurately assess for both subtle and significant defects. These defects are frequently seen prior to any vision loss.

Visual Field Perimetry - Because glaucoma begins with unnoticed loss to small areas in the side or peripheral vision, it is not enough to read letters on an eye chart to rule out glaucoma damage. People frequently assume since they have 20/20 vision that they cannot have glaucoma. This is false.

Types of Glaucoma

There are two basic types of glaucoma, open angle and closed/narrow angle. The "angle" refers to the space of the anterior chamber angle and requires a special examination method known as gonioscopy.


Open Angle Glaucomas

Primary Open Angle Glaucoma

This is the most common of all the open angle glaucomas, in which filtration through the trabecular meshwork is diminished, but is not due to any trauma, inflammation, pigment or congenital deformity.

Pigmentary Glaucoma

This is a common but often missed form of open angle glaucoma in which the colored iris is bowed slightly backward, chafing against other ocular structures called zonules. Regardless of the color of the iris, there is brown pigment on the unseen side, which then disperses throughout the front of the eye. This floating pigment then clogs the trabecular meshwork, which is the drainage channel of the eye. Many people have pigmentary dispersion syndrome but not yet elevated pressures, but have to be monitored for the future development of glaucoma.

Pseudoexfoliative Glaucoma

This is a common form of open angle glaucoma that is also frequently missed. For unknown reasons, the eye forms a white material called a glycoprotein that circulates throughout the front of the eye and can clog the trabecular meshwork drainage channel. In addition, the white material can damage the zonules or springs that support the lens in the middle of the eye, making cataract surgery more difficult. 

Traumatic Glaucoma

Significant blunt force trauma to the eye can not only cause bleeding, inflammation or retinal detachments, but also damage to the trabecular meshwork drain that empties fluid each minute. This is often recognized as "angle recession" by the eye doctor during an exam with a gonioscopic mirror. This damage is often permanent, resulting in slower fluid outflow from the eye with resultant elevation in eye pressure and damage to the optic nerve.

Uveitic Glaucoma

Inflammation inside the eye is called uveitis. Uveitis can occur spontaneously, or due to viruses such as Herpes zoster and Herpes simplex, parasites such as Toxoplasmosis, or due to autoimmune diseases such as sarcoidosis, ankylosing spondylitis, presence of an HLA-B27 antigen in the blood. During uveitis, white blood cells and other blood materials associated with inflammation leak from the capillaries into the eye and can cause internal scarring and elevation in eye pressure. Treatment requires controlling the inflammation and eye pressure.

Congenital Glaucoma

While strictly categorized as a form of open angle glaucoma, the trabecular meshwork filtering structure inside the eye is malformed, and these diseases act as if the filtering structures are blocked. Congenital glaucoma may present as early as birth or as late as the late teens. They include, Primary Congenital Glaucoma, Axenfeld-Rieger Syndrome, Peter's Anomaly, and others.

Narrow (Closed) Angle Glaucomas

Pupil Block/Primary Narrow Angle Glaucoma

Primary Narrow Angle Glaucoma is the most common form of narrow angle glaucoma. It occurs when the space between the colored iris and internal lens of the eye is so small that fluid cannot follow its natural flow path into the front eye the iris. The high pressure behind the iris then pushes the iris forward, causing the iris to then block the trabecular meshwork outflow channel. Treatment is often curative, and involves equalizing the pressure behind and in front of the iris by making a small communication hole in the iris with a laser. This procedure is called a laser iridotomy, and is usually performed as a brief procedure in the eye doctor's office.

Plateau Iris Narrow Angle Glaucoma

In this form of glaucoma, the peripheral iris bunches up against the trabecular meshwork outflow channel. These patients always require laser iridotomy to rule out the more common pupil block of primary narrow angle glaucoma.

Neovascular Glaucoma

New, fragile, contractile blood vessels that serve no healthy purpose can form in response to severe diabetes of the retina or central retinal vein occlusions of the retina. A chemical signal can get sent to the front of the eye from the retina, and these "neovascular" blood vessels can begin to grown on the peripheral iris, causing rapid scarring of the of the trabecular meshwork fluid outflow structure. These eyes are very ill, requiring multiple treatments, including injection of anti-VEGF medications into the vitreous gel in the back of the eye to stop the chemical signal, medications to attempt to gain control of the eye pressures, and frequently complex glaucoma surgeries to lower eye pressure in the presence of aggressive scarring.

Uveitic closed angle glaucoma

Uveitis (inflammation inside the eye) can cause high pressure simply from the white blood cells and inflammatory debris. But resultant scarring can also cause peripheral anterior synechiae (scarring between the iris and cornea) that causes blockage of the fluid filtering structure of the eye, or scarring between the iris and lens that causes pupil block narrow angle glaucoma.

Treatment of Glaucoma

Treatment of glaucoma primarily involves lowering of eye pressure, because this is the only proven method of slowing or stopping the progression of this disease. But there is no absolute level of eye pressure that makes an eye safe. If starting pressure is 30 with little or no optic nerve damage, pressure of 19 is often safe, whereas is pressure is 17 with severe optic nerve damage and vision loss, then pressure of 10 might be required to safeguard against further vision loss.

The three methods of lowering eye pressure are:

  1. Medications
  2. Laser
  3. Surgery


Most glaucoma medications are in the form of eyedrops, and they include:

Beta blockers - These reduce the rate of fluid formation by the ciliary body inside the eye. Examples are timolol and levobunalol.

Alpha agonists - Dual mechanism of action, reducing fluid formation by the ciliary body and increasing fluid exit ability through a vague mechanism known as uveal-scleral outflow.

Carbonic anhydrase inhibitors - Reduce aqueous humor fluid formation by the ciliary body. Eyedrop examples: brinzolamide, dorzolamide. Oral examples: methazolamide, acetazolamide.

Prostoglandin inhibitors - Increase fluid exit ability through a vague mechanism known as uveal-scleral outflow. Examples: latanoprost, travoprost, bimatoprost and latanoprostene (Vyzulta - also increases trabecular meshwork outflow by formation of nitric oxide).

Rho-Kinase Inhibitors - Increase trabecular meshwork outflow. May also lower episcleral venous pressure. Example: netasudil (Rhopressa).

Acetyl choline agonists - Increase trabecular meshwork outflow, but also contract pupil and ciliary body as side effects. Examples: pilocarpine, carbamylcholine

Laser Treatment of Glaucoma

Treatment depends on whether the glaucoma is primary an open or closed angle type.

Open angle glaucomas are treated with selective laser trabeculoplasty (SLT) in the office or endolaser cyclophotocoagulation (ECP) or trans-scleral cyclophotocoagulation (TSCPC) in the operating room. SLT is applied to the trabecular meshwork to improve its function of fluid outflow, whereas ECP and TSCPC are applied to the ciliary body to decrease its function of fluid formation.


Surgical Treatment of Glaucoma

Surgical treatment of glaucoma always attempts to improve the ease of fluid getting out of the eye.

Trabeculectomy - Creation of a surgical trap door, using only the eye's natural tissues, so that fluid inside the eye drains below the thin covering conjunctival layer and is ultimately absorbed by the small blood vessels.

Glaucoma Shunts - Insertion of a silicone tube inside the eye that leads to a large drainage plate beneath the thin covering conjunctival layer and is ultimately absorbed by the small blood vessels. Examples: Ahmed Baerveldt

Trabecular Meshwork Stents - Small devices that insert into the trabecular meshwork drain and are designed to bypass the restrictive flow into Schlemm's canal. Examples: iStent, Hydrus

Canaloplasty - Dilation of Schlemm's canal to improve its outflow. Examples Omni

Goniotomy - Removal or tearing of the trabecular meshwork to create direct access to Schlemm's canal.