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What Causes Glaucoma?
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The cause of glaucoma is
generally a failure of the
eye to maintain an
appropriate balance between
the amount of internal
(intraocular) fluids
produced and the amount that
drains away. Underlying
reasons for this imbalance
usually relate to the type
of glaucoma you have.
Just as a basketball or
football requires air
pressure to maintain its
shape, the eyeball needs
internal fluid pressure to
retain its globe-like shape
and ability to see. But when
glaucoma damages the ability
of internal eye structures
to regulate intraocular
pressure (IOP), eye pressure
can rise to dangerously high
levels.
Unlike a ball or balloon,
the eye can't relieve
pressure by springing a leak
and "deflating" when
pressure is too high.
Instead, high IOP just keeps
building and pushing against
the optic nerve until nerve
fibers are permanently
damaged and vision is lost.
Glaucoma and Eye Anatomy
To understand what causes
glaucoma, you first must
know something about the
eye's anatomy and how fluids
move through the eye:
-
Internal eye fluids are
produced by the ciliary
body, which is a small,
circular structure found
behind the iris or
colored portion of the
eye.
-
This fluid, known as the
aqueous humor, flows
behind the iris and
through the pupil or
central opening in the
middle of the iris.
Fluid then fills the
anterior chamber, a
space between the back
of the clear cornea and
the front of the iris.
-
The aqueous humor
escapes from the eye
through a structure
known as the filtration
angle, which is the
angle formed inside the
anterior chamber between
the iris and the
peripheral cornea.
-
The aqueous filters
through this angle and
through the sclera or
white part of the eye
and then joins with the
network of veins outside
the eye.
-
Any disruption of this
outflow of aqueous can
result in an increase in
IOP.
Anatomically, the eye's
filtration angle is referred
to as being either "open" or
"closed" (narrow). The
narrower the angle, the more
difficult it is for the
aqueous to flow through it.
An open angle also can
hinder the outflow of
aqueous, if structural
damage exists within the
ocular tissues of the angle
itself.
Glaucoma, Blood Flow and
Optic Nerve Damage
While high IOP often is
associated with glaucoma,
this eye disease also can
occur when internal eye
pressure is normal
(normal-tension glaucoma).
People with this condition
have highly
pressure-sensitive optic
nerves that are susceptible
to irreversible damage from
what ordinarily would be
considered "normal" IOP.
Conversely, certain
individuals with elevated
pressures known as ocular
hypertension may never
develop glaucoma.
Most conventional methods of
screening for glaucoma
involve testing eyes for the
presence of high IOP. But
because glaucoma can occur
even without high IOP,
direct examination of the
optic nerve with visual
field testing or other means
is essential in making (or
ruling out) the diagnosis of
glaucoma.
In normal-tension glaucoma,
some theories suggest that
decreased blood flow to the
optic nerve might be a
factor. Inadequate blood
flow also may help create
high IOP contributing to
optic nerve damage. Some
studies also indicate that
poor blood flow within the
eye can be directly
correlated with blind spots
(scotomas) that develop
within the visual field, as
occurs with glaucoma.*
An intriguing study reported
in August 2007 indicates a
potential common cause of
both glaucoma and
Alzheimer's, which creates
brain lesions and
accompanying memory loss.
London researchers who
conducted the study found
that buildup of a protein
known as beta-amyloid in the
eye's retina and brain
tissue appears related to
development of both glaucoma
and Alzheimer's.
However, abnormal
accumulation of beta-amyloid
proteins does not mean that
someone with Alzheimer's
will have glaucoma or vice
versa. Researchers said
similarities between certain
eye and brain tissue could
explain why the buildup of
beta-amyloid proteins can
affect both the eye and the
brain.
Increasingly, glaucoma
treatments now are being
investigated for their
ability to protect nerve
cells in the eye from
damage.
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