What is glaucoma?

Causes and Symptoms

Glaucoma is a group of eye diseases characterized by damage to the
optic
nerve, most often due to higher-than-normal pressure inside
the eye. Damage to the optic nerve can lead to visual impairments or complete
blindness. Of all the causes of blindness, glaucoma is among
the most common, but it is also the most preventable. If diagnosed early, it can
be controlled and the loss of vision avoided.
What complicates the problem is that the most common form of glaucoma, primary
open-angle glaucoma, shows no symptoms until extensive, irreversible damage has
occurred. There is no pain and elevated intraocular pressure may not be present at
the time of a physical examination; the first sign that something is amiss may be
that peripheral vision and seeing out of the corner of the eye is diminished,
while frontal vision remains clear. The second most common form of primary
glaucomas, angle-closure glaucoma, occurs there is an increased resistance to
aqueous humor outflow from the inner eye. Glaucomas may be considered primary,
when the cause is unknown, or secondary, when the cause is known. Causes of
secondary glaucoma include inflammation, trauma, neovascularization, or
tumors.

To understand glaucoma, it is helpful to understand the structure of the
eye. The outer layer of the eye is called the
cornea. The inner surface of the cornea is nourished by the
aqueous humor, which is also called the aqueous fluid. This secretion from the
ciliary body flows into the space behind the iris and then through the pupil into
the space in front of the iris. Where the front of the iris joins the back of the
cornea is a point called the venous sinus, at the anterior drainage angle. Here
the aqueous humor is reabsorbed and transported to the bloodstream. In a normal
eye, this drainage process works correctly and the balance between the amount
secreted and the amount reabsorbed maintains a constant intraocular pressure. In
most forms of glaucoma, the drainage part of the process works inefficiently. For
a variety of reasons, some of which are not fully understood, the drainage
mechanism can become defective. The upset balance in secretion drainage causes the
unwanted increase in intraocular pressure in one eye or both eyes. The iris is
pushed forward, further inhibiting drainage of the aqueous fluid. However, not all
forms of glaucoma are caused by increased intraocular pressure; normal-tension
glaucoma is characterized by damage to the optic nerve while eye pressure remains
normal. Normal-tension glaucoma may be caused by reduced blood supply to the optic
nerve.

Even a very small elevation in intraocular pressure will affect the eye adversely,
causing damage to its most delicate parts. Although the eye as a whole is quite
tough, the optic nerve is vulnerable to increased pressure or deterioration due to
lack of blood supply. This vital connection between the eye and the brain can be
damaged by the higher pressure within the eyeball. The delicate nerve fibers and
blood vessels of the optic disc, as the beginning of the optic nerve is called,
then die. Once they die, they can never be regenerated or replaced, and vision
loss is the result.

The damage that glaucoma inflicts is progressive. In many cases, the defect in
drainage does not necessarily worsen, and the pressure, once elevated, does not
necessarily continue to increase. Once begun, however, the damage to the optic
nerve cells continues until the resulting loss of vision progresses to total
blindness. The first nerve fibers to die are the ones near the outer edge of the
optic disc, which originates near the periphery of the retina. The first decrease
in vision, therefore, is in one’s peripheral vision. Then, as each layer of nerve
fibers dies, the visual field progressively narrows.

This slow, progressive route to blindness is typical of open-angle glaucoma, which
accounts for two-thirds of primary glaucoma cases. The rise in intraocular
pressure does not result from any known underlying reason. Although individuals
with a family history of glaucoma are more prone to the disease, it is not
directly hereditary. Moreover, not everyone with a family history of glaucoma will
develop the disease. For reasons that are not well understood, people of African
ancestry suffer from glaucoma at greater rates than those of European
ancestry.

In persons of all races, open-angle glaucoma usually begins after the age of
forty; however, the aging process does not seem to be a direct cause of glaucoma.
Unlike the formation of age-related cataracts, which
result from eye changes as one grows older, glaucoma’s development is not
explained by the aging process. It can safely be said that glaucoma seems to occur
in persons who have a tendency toward inadequate aqueous fluid drainage or who
have highly sensitive optic nerves. As persons grow older and their bodies lose
their resiliency in general, the drainage problem can reach a point where it
begins to raise the intraocular pressure beyond the normal range. Those with
untreated open-angle glaucoma are seldom aware of the disease before considerable
damage has been done. The progressive destruction of nerve fibers is ordinarily
very slow because the elevation of pressure is slight and causes no pain or
blurriness of sight. In persons with normal-tension glaucoma, atherosclerosis can potentially reduce blood supply to the
optic nerve, causing irreversible damage.

In secondary glaucoma, the drainage defect is caused by some complication of a
different condition. The causes of chronic secondary glaucoma include inflammation
from an eye infection, an allergic reaction, trauma to the eye, a tumor, or even
the presence of a cataract. Medications such as corticosteroids can sometimes cause this type of glaucoma to
develop. Whatever the cause, secondary glaucomas exhibit increased pressure, slow
nerve destruction, and ultimate loss of vision.

Acute glaucoma is both rare and dramatic in its onset. The increase in intraocular
pressure is many times higher than that in open-angle glaucoma. It also occurs
very rapidly, sometimes within hours. The anterior drainage angle where drainage
is accomplished is almost totally blocked. The eyeball becomes so hard that the
elevated pressure can often be felt simply by touching the front of the eye. The
great pressure causes terrible pain and immediate damage to the eye. When nausea,
vomiting, and severe headaches accompany eye pressure, acute glaucoma should be
suspected. Immediate treatment is required to prevent blindness. Acute glaucoma
can be either primary or secondary. It is termed primary when a drainage area that
has always been abnormally narrow suddenly becomes totally blocked. It is called
secondary when it is precipitated by some other eye condition.

The rarest type of glaucoma, congenital glaucoma, is present at birth or develops
during early infancy. It results from the incorrect formation of drainage canals
while the eye is developing. Because a baby’s eyeball is much smaller and softer
than an adult’s, this glaucoma is often recognized by the bulging of the eyes.

Treatment and Therapy

The treatments available for glaucoma include eye drops, ointments, pills, and
surgery using both incisions and lasers. In both acute and congenital glaucoma,
there is often little time for long-term medication management; patients typically
need to be admitted to the hospital and operated on immediately if their eyesight
is to be saved. For open-angle glaucoma, medications may be topical—eye drops or
ointments, or inserts, thin medicated strips put in to the corner of the eye—or
oral (pills and tablets). Prostaglandin analogs and beta-adrenergic antagonists
are the most frequent first-line choices to reduce intraocular pressure. If
diagnosed early, cases of both chronic primary and chronic secondary glaucomas can
often be effectively treated by medications.

If drops or gels do not produce the desired reduction in pressure, pills can be
used, not to replace the drops but to supplement them. Beta blockers, carbonic
anhydrase inhibitors, or alpha-2-adrenergic agonists in addition to prostaglandin
analogs may help to further reduce intraocular pressure.

Although surgery cannot reverse the optic nerve damage that has already occurred,
it is often effective in preventing further destruction by alleviating elevated
intraocular pressure. One of the most common of these surgical procedures was
developed in the mid-nineteenth century. Called an iridotomy, it attempts to
provide a better access to the patient’s drainage angle by removing part of the
iris. Today, an iridotomy may be completed with incisions or lasers, although
laser iridotomy is preferred. The most common forms of laser iridotomy are
bilateral laser iridotomy and laser peripheral iridotomy. In laser peripheral
iridotomy, which is often used in the treatment of angle-closure glaucoma, a laser
makes a small hole in the iris to allow fluid to move more freely within the eye
and drain from the fluid channel more easily.

Another common form of glaucoma surgery is called trabeculectomy, which can be
performed in several different ways. Argon laser trabeculoplasty is often used to
treat open-angle glaucoma. This procedure aims a laser at a special contact lens
that is placed in front of the eye, opening the fluid channels of the eye and
relieving the intraocular pressure. The passageway created permits the aqueous
humor to drain properly from the inner eye.

A different approach to glaucoma control, called laser cyclophotocoagulation,
attempts to help the patient by destroying part of the source of the excess fluid,
the oversecreting ciliary body. This procedure is usually performed only on older
patients who already have severe damage from glaucoma or for whom other surgeries
were not successful.

All the above treatments for glaucoma, whether pharmaceutical or surgical, have
the potential for serious side effects and complications. Consequently, research
continues to seek therapies with better rates of success and fewer complications.
Some of the possible complications of surgery include infection, sensitivity to
light, bleeding, long-term irritation or inflammation, loss of vision, and the
need for more surgery. Risk factors for complications from surgery include
obesity, smoking, diabetes, high blood pressure, and bleeding disorders.
Nevertheless, glaucoma surgery is a common procedure with a relatively high
success rate.

Perspective and Prospects

In 1851, the German doctor Hermann von
Helmholtz invented the ophthalmoscope, which enables one to
study the interior of the eye. His instrument focused a beam of light into the
patient’s eye and then magnified its reflection. If this test revealed early signs
of cupping of the optic disc, glaucoma could be diagnosed long before other
symptoms have appeared. Today, it is recommended that patients have regular eye
exams to detect elevated intraocular pressure so that it be alleviated before loss
of vision occurs. An eye exam is recommended every two to four years for patients
under the age of forty, one to three years for patients between forty and
fifty-four, one to two years for patients between fifty-five and sixty-five, and
every six to twelve months for patients over the age of sixty-five.

Intraocular pressure can be measured with an instrument called a tonometer. The
two basic varieties are called Schiötz tonometry and applanation tonometry. Both
became possible only after biochemists developed anesthetic drops to put in the
eye so that the patient would not feel the device touching the very sensitive
cornea. The earlier of the two devices, developed in 1905 by the Norwegian
physician Hjalmar Schiötz, is a very simple device that is still the most widely
used tonometer in the world. With the patient lying down and looking upward, the
physician places the hand-sized instrument directly on the cornea. A simple lever
is moved by the pressure within the eye to indicate whether that pressure is
within the normal range or dangerously high. The Goldman applanation tonometer is
considered even more accurate and is often used to confirm the results of the
simpler Schiötz device. An orange dye called fluorescein is added to the
anesthetic. The patient, in a sitting position, rests the head against a bar to
steady it. The doctor uses a tonometer to touch the cornea while simultaneously
peering into it with a well-illuminated microscope.

More specialized glaucoma examination may include ophthalmoscopy, gonioscopy, or
perimetry. An ophthalmoscopy involves the dilation of the pupil and an examination
of the optic nerve with a microscope to detect damage to the nerve. If damage is
suspected, the doctor may then recommend other diagnostic exams, such as perimetry
and gonioscopy. Perimetry involves visual field tests, which can give a map of the
central area where vision is sharp and more acute versus the peripheral area where
it is weaker. Since damage to the optic nerve causes a narrowing of the visual
field, this mapping is very important. The ability to measure the field has grown
from oculokinetic perimetry—using an inexpensive test chart, pencil, record sheet,
and human examiner—to the sophisticated automated perimetry, which generates a
computer analysis. Gonioscopy involves the placement of a contact lens on the eye.
This specialized contact lens has mirrors and facets to provide an illuminated
view of the drainage angle, a normally dark corner at a 90 degree angle from the
examiner. Excessive narrowing of the angle is an indication of glaucoma.

All these tests, developed through years of ophthalmic research, have given
medical science invaluable tools to diagnose glaucoma in its early stages and
prevent blindness. Glaucoma is estimated to affect one out of every forty adults
over the age of forty years.

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