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Pupil :
The iris acts like
the shutter of a camera. The pupil—the (normally)
circular hole in the middle of the iris, comparable to the
apperture of a camera—regulates the amount of light passing
through to the retina at the back of the eye.
As the
amount of light entering the eye diminishes (such as in the
dark or at night), the iris dilator muscle (which runs
radially through the iris like spokes on a wheel) pulls away
from the center, causing the pupil to “dilate” and allowing
more light to reach the retina. When too much light is
entering the eye, the iris sphincter muscle (which encircles
the pupil) pulls toward the center, causing the pupil to
“constrict” and allowing less light to reach the
retina.
Constriction of the pupil also occurs when the
crystalline lens accommodates (changes focus) to a near
distance; this reaction is known as the “near reflex.” A
representation of parasympathic pathways in the pupillary
light reflex can be seen here: parasympathic
response.
Watching television in a dark room gives some
people eye aches or headaches. This is because as the
brightness of the television screen varies considerably every
few seconds, the dilator and sphincter iris muscles
controlling the pupil have to work overtime, constantly
adjusting the ever-changing levels of light entering the eye.
With a uniform background light present in the room,
causing the pupils to slightly constricted, there is less
variance in the size of the pupil as the television
illumination changes, and the muscles controlling the pupil
size become less tired.
Uvea:
The iris is the most
anterior portion of the uvea or uveal tract (also known as the
tunica vasculosa or vascular tunic). Anatomical
structures posterior to the iris, which also are part of the
uvea, are the ciliary body (within which is the ciliary muscle
which controls the shape of the crystalline lens) and the
choroid (located underneath the retina and which contains the
retina’s blood
supply).
iritis/uveitis/chorioretinitis :
It is not
uncommon for the iris, uvea, and/or the choroid/retina complex
to become inflammed. If the iris alone experiences
inflammation, this is called an “iritis.” If the ciliary
body is involved as well, it is an “iridocyclitis” (or alone,
a “cyclitis”). If the entire uveal tract is inflammed,
this is considered a “uveitis”; whereas, if only the choroid
and retina are involved, it is a “chorioretinitis.”
(Even though the retina is not part of the uveal tract,
it frequently becomes inflammed when the choroid does;
however, an inflammation of the choroid alone is a
“choroiditis.”)
Although the exact cause of an iritis
or uveitis often is unknown, in many cases the inflammation is
related to a disease or infection in another part of the body.
Sometimes diseases such as arthritis, tuberculosis,
syphilis, ankylosing spondylitis, Reiter’s syndrome,
toxoplasmosis, histoplasmosis, cytomegalovirus (CMV),
sarcoidosis, and toxocariasis and others can cause a uveal
inflammation. Infection of some parts of the body
(tonsils, sinus, kidney, gallbladder, and teeth) also can
cause inflammation of the iris or of the entire uveal
tract.
The symptoms of iritis usually appear suddenly
and develop rapidly over a few hours or days. Iritis
commonly causes pain, tearing, light sensitivity, and blurred
vision. A red eye, usually with inflammed blood vessels
occurring around the limbus (the junction of the cornea and
sclera), often is present when there is an iritis. Some
people may experience floaters, which appear as small specks
or dots moving in the field of vision. In addition, the
pupil may become smaller in the eye affected by
iritis.
Caught in the early stages, an iritis or
uveitis usually is readily treated with corticosteroids and/or
antibiotics. However, without treatment, or with chronic
occurrences of the inflammation, there can be a permanent
decrease in vision or, in rare cases, even blindness. A
case of iritis usually lasts 6 to 8 weeks. During this
time, a person should be observed carefully (by an optometrist
or ophthalmologist) to monitor potential side effects from
medications and any complications which may occur.
Cataracts, glaucoma, corneal changes, and secondary
inflammation of the retina may occur as a result of iritis
and/or the medications used to treat the
disorder.
RETINA:
The
retina is the innermost layer of the eye (the tunica intima or
internal tunic) and is comparable to the film inside of a
camera. It is composed of nerve tissue which senses the
light entering the eye. This complex system of nerves
sends impulses through the optic nerve back to the brain,
which translates these messages into images that we see.
(We “see” with our brains; our eyes merely collect the
information to do so.)
The retina is composed of 10
layers, from the outside (nearest the blood vessel enriched
choroid) to the inside (nearest the gelatinous vitreous
humor):
1. pigmented epithelium
2. photoreceptors; bacillary layer (outer and inner
segments of cone and rod photoreceptors)
3.
external (outer) limiting membrane
4.
outer nuclear (cell bodies of cones and rods)
5. outer plexiform (cone and rod axons, horizontal cell
dendrites, bipolar dendrites)
6. inner nuclear
(nuclei of horizontal cells, bipolar cells, amacrine cells,
and Müller cells)
7. inner plexiform (axons of
bipolar cells and amacrine cells, dendrites of ganglion
cells)
8. ganglion cells (nuclei of ganglion
cells and displaced amacrine cells)
9. axons
(nerve fibers from ganglion cells traversing the retina to
leave the eye at the optic disk)
10. internal
limiting membrane (separates the retina from the
vitreous)
Beneath the pigmented epithelium of the
retina are these 4 layers, from the outside (furthest from the
retina) to the inside (closest to the retina):
1. sclera (white part of the eye)
2.
large choroidal blood vessels
3.
choriocapilaris
4. Bruch’s membrane
(separates the pigmented epithelium of the retina from the
choroid)
Light entering the eye is converged first by
the cornea, then by the crystalline lens. This focusing
system is so powerful that the light rays intersect at a point
just behind the lens (inside the vitreous humor) and diverge
from that point back to the retina. The diverging light
passes through 9 (clear) layers of the retina and, ideally, is
brought into focus in an upside-down image on the first
(outermost) retinal layer (pigmented epithelium). The
image is reflected back onto the adjacent second layer, where
the rods and cones are located.
photoreceptors (cones
and rods)
Rods and cones actually face away from incoming
light, which passes by these photoreceptors before being
reflected back onto them. Light causes a chemical
reaction with “iodopsin” in cones and with “rhodopsin” in
rods, beginning the visual process. Activated
photoreceptors stimulate bipolar cells, which in turn
stimulate
ganglion cells. The impulses continue into
the axons of the ganglion
cells, through the optic
nerve, and to the visual center at the back of the brain,
where the image is perceived as right-side up. (See more
on the visual pathway for greater detail.) The brain
actually can detect one photon of light (the smallest unit of
energy) being absorbed by a photoreceptor.
There are
about 6.5 to 7 million cones in each eye, and they are
sensitive to bright light and to color. The highest
concentration of cones is in the macula. The fovea
centralis, at the center of the macula, contains only cones
and no rods. There are 3 types of cone pigments, each
most sensitive to a certain wavelength of light: short
(430-440 nm), medium (535-540 nm) and long (560-565 nm).
The wavelength of light perceived as brightest to the
human eye is 555 nm, a greenish-yellow. (A
“nanometer”—nm—is one billionth of a meter, which is one
millionth of a millimeter.) Once a cone pigment is
bleached by light, it takes about 6 minutes to
regenerate.
There are about 120 to 130 million rods in
each eye, and they are sensitive to dim light, to movement,
and to shapes. The highest concentration of rods is in
the peripheral retina, decreasing in density up to the macula.
Rods do not detect color, which is the main reason it is
difficult to tell the color of an object at night or in the
dark. The rod pigment is most sensitive to the light
wavelength of 500 nm. Once a rod pigment is bleached by
light, it takes about 30 minutes to regenerate.
Defective or damaged cones results in color deficiency;
whereas, defective or damaged rods results in problems seeing
in the dark and at night.
retinal detachment
(RD)
Normally, with age, the vitreous gell collapses and
detaches from the retina—an event known as a posterior
vitreous detachment. Occasionally, however, the vitreous
membrane pulls on and creates a tear in the retina.
Vitreous fluid can seep into or underneath the retina,
detaching it from the pigmented epithelium
underneath.
When a retinal detachment occurs, a shower
of floaters may be observed by the person experiencing the
detachment. These are thousands of blood cells being
liberated from a tiny blood vessel which has been broken due
to the retinal tear or detachment. Sometime the floaters
are described as a “shower of pepper” before the
eyes.
Sudden flashes of light, as well as a “web” or
“veil” in front of the eye or in the periphery, also may
appear in conjunction with the onset of floaters. If the
retinal tear and subsequent detachment are not repaired as
soon as possible (by sealing it using an argon laser, or
freezing it in a procedure known as “cryotherapy,” or securing
it with a tiny belt or “scleral buckle” around the equator of
the eye), permanent vision loss can result.
retinitis
pigmentosa (RP)
One of the most devastating conditions
affecting the rods is “retinitis pigmentosa,” an inherited
disorder in which the rods gradually degenerate. With
time, night vision is severely affected. Eventually, all
peripheral vision will continue to be destroyed to the point
where only central or “tunnel” vision remains. There is
no known treatment; however, since blue and ultraviolet light
may make aggravate the condition, amber-colored glasses with
an ultraviolet absorption coating, worn during the day, may
slow down the disease process. Studies have shown that
retinitis pigmentosa is caused by mutations in the rhodopsin
gene, the peripherin gene, and possibly in other genes within
the rod. Mutations in the peripherin gene also may be
the cause of another devastating retinal disorder: “macular
dystrophy.”
THE OPTIC
NERVE:
The optic nerve (also known as cranial nerve
II) is a continuation of the axons of the ganglion cells in
the retina. There are approximately 1.1 million nerve
cells in each optic nerve. The optic nerve, which acts
like a cable connecting the eye with the brain, actually is
more like brain tissue than it is nerve tissue.
visual
pathway
As the optic nerve leaves the back of the eye, it
travels to the optic chiasm, located just below and in front
of the pituitary gland (which is why a tumor on the pituitary
gland, pressing on the optic chiasm, can cause vision
problems). In the optic chiasm, the optic nerve fibers
emanating from the nasal half of each retina cross over to the
other side; but the nerve fibers originating in the temporal
retina do not cross over.
From there, the nerve fibers
become the optic tract, passing through the thalamus and
turning into the optic radiation until they reach the visual
cortex in the occipital lobe at the back of the brain.
This is where the visual center of the brain is located.
The visual cortex ultimately interprets the electrical
signals produced by light stimulation of the retina, via the
optic nerve, as visual images. A representation of
parasympathic pathways in the pupillary light reflex can be
seen here: parasympathic response.
blind spot
The
beginning of the optic nerve in the retina is called the optic
nerve head or optic disk. Since there are no
photoreceptors (cones and rods) in the optic nerve head, this
area of the retina cannot respond to light stimulation.
As a result, it is known as the “blind spot,” and
everybody has one in each eye. The reason we normally do
not notice our blind spots is because, when both eyes are
open, the blind spot of one eye corresponds to seeing retina
in the other eye. Here is a way for you to see just how
absolutely blind your blind spot is. Below, you will
observe a dot and a plus.
Follow these viewing instructions:
-
Sit about arm’s length away from your computer
monitor/screen.
-
Completely cover your left eye (without
closing or pressing on it), using your hand or other flat
object.
-
With your right eye, stare directly at the
above. In your periphery, you will notice the
to the right.
-
Slowly move closer to the screen,
continuing to stare at the .
-
At about 16-18 inches from
the screen, the should disappear completely, because it
has been imaged onto the blind spot of your right eye.
(Resist the temptation to move your right eye while the
is gone, or else it will reappear. Keep staring at
the .)
-
As you continue to look at the , keep moving
forward a few more inches, and the will come back into
view.
-
There will be an interval where you will be able to
move a few inches backward and forward, and the will be
gone. This will demonstrate to you the extent of your
blind spot.
-
You can try the same thing again, except this
time with your right eye covered stare at the with your
left eye, move in closer, and the will disappear.
If you really want to be amazed at the total
sightlessness of your blind spot, do a similar test outside at
night when there is a full moon. Cover your left eye,
looking at the full moon with your right eye. Gradually
move your right eye to the left (and maybe slightly up or
down). Before long, all you will be able to see is the
large halo around the full moon; the entire moon itself will
seem to have disappeared.
Like any other ocular
structure, certain pathologies can have an adverse affect on
the optic disk and optic nerve. Although there are too
many to list completely, a few will be included
here.
optic atrophy
“Optic atrophy” of the optic
disk (visible to an eye doctor looking inside the eye) is the
result of degeneration of the nerve fibers of the optic nerve
and optic tract. It can be congenital (usually
hereditary) or acquired. If acquired, it can be due to
vascular disturbances (occlusions of the central retinal vein
or artery or arteriosclerotic changes within the optic nerve
itself), may be secondary to degenerative retinal disease
(e.g., optic neuritis or papilledema), may be a result of
pressure against the optic nerve, or may be related to
metabolic diseases (e.g., diabetes), trauma, glaucoma, or
toxicity (to alcohol, tobacco, or other poisons). Loss
of vision is the only symptom. A pale optic disk and
loss of pupillary reaction are usually proportional to the
visual loss. Degeneration and atrophy of optic nerve
fibers is irreversible.
optic neuritis
“Optic
neuritis” is an inflammation of the optic nerve. It may
affect the part of the nerve and disk within the eyeball
(papillitis) or the portion behind the eyeball (retrobulbar
optic neuritis, causing pain with eye movement). It also
includes degeneration or demyelinization of the optic nerve.
There will be no visible changes in the optic nerve head
(disk) unless some optic atrophy has occurred.
This
condition can be caused by demyelinating diseases (e.g.,
multiple sclerosis, postinfectious encephalomyelitis),
systemic infections (viral or bacterial), nutritional and
metabolic diseases (e.g., diabetes, pernicious anemia,
hyperthyroidism), Leber’s Hereditary Optic Neuropathy (a rare
form of inherited optic neuropathy which mainly affects young
men, causing them to lose central vision), secondary
complications of inflammatory diseases (e.g., sinusitis,
meningitis, tuberculosis, syphilis, chorioretinitis, orbital
inflammation), toxic reactions (to tobacco, methanol, quinine,
arsenic, salicylates, lead), and trauma.
The condition
is unilateral rather than bilateral. If the nerve head
is involved, it is slightly elevated, and pupillary response
in that eye is sluggish. There usually is a marked but
temporary decrease in vision for several days or weeks, and
there is pain in the eye when it is moved. Single
episodes generally do not result in optic atrophy nor in
permanent vision loss; however, multiple episodes can result
in both.
papilledema
“Papilledema” is edema or
swelling of the optic disc (papilla), most commonly due to an
increase in intracranial pressure (often from a tumor),
malignant hypertension, or thrombosis of the central retinal
vein. The condition usually is bilateral, the nerve head
is very elevated and swollen, and pupil response typically is
normal. Vision is not affected initially (although there
is an enlargement of the blind spot), and there is no pain
upon eye movement. Secondary optic atrophy and permanent
vision loss can occur if the primary cause of the papilledema
is left untreated.
ischemic optic
neuropathy
“Ischemic optic neuropathy” is a severely
blinding disease resulting from loss of the arterial blood
supply to the optic nerve (usually in one eye), as a result of
occlusive disorders of the nutrient arteries. Optic
neuropathy is divided into anterior, which causes a pale edema
of the optic disk, and posterior, in which the optic disk is
not swollen and the abnormality occurs between the eyeball and
the optic chiasm. Ischemic anterior optic neuropathy
usually causes a loss of vision that may be sudden or occur
over several days; whereas, ischemic posterior optic
neuropathy is uncommon, and the diagnosis depends largely upon
exclusion of other causes, chiefly stroke and brain
tumor.
glaucoma
“Glaucoma” is an insidious disease
which damages the optic nerve, typically because the
“intraocular pressure” (IOP) is higher than the retinal
ganglion cells can tolerate. This eventually results in
the death of the ganglion cells and their axons which comprise
the optic nerve, thereby causing less and less visual impulses
from the eye to reach the brain. In advanced glaucoma,
the peripheral retina is decreased or lost, leaving only the
central retina (macular area) intact, resulting in “tunnel
vision.” Elevated IOP—which can be measured by a
“tonometry” test—is a result of too much fluid entering the
eye and not enough fluid leaving the eye.
Normally, fluid enters the eye by seeping out of
the blood vessels in the ciliary body. This fluid
eventually makes its way past the crystalline lens, through
the pupil (the central opening in the iris), and into the
irido-corneal angle, the anatomical angle formed where the
iris and the cornea come together. Then the fluid passes
through the trabecular meshwork in the angle and leaves the
eye via the canal of Schlemm.
If too much fluid is
entering the eye, or if the trabecular meshwork “drain” gets
clogged up (for instance, with debris or cells) so that not
enough fluid is leaving the eye, the pressure builds up in
what is known as “open angle glaucoma.” Open angle
glaucoma also can be caused when the posterior portion of the
iris, surrounding the pupil, somehow adheres to the anterior
surface of the lens (creating a “pupillary block”), preventing
intraocular fluid from passing through the pupil into the
anterior chamber. On the other hand, if the angle
between and iris and the cornea is too narrow or is even
closed, then the fluid backs up, causing increased pressure in
what is known as “closed angle glaucoma.”
An internal
pressure more than that which the eye can tolerate can deform
the lamina cribrosa, the small cartilaginous section of the
sclera at the back of the eye through which the optic nerve
passes. Deformation of the lamina cribrosa seems to
“pinch” nerve fibers passing though it, eventually causing
axon death. Untreated glaucoma eventually leads to optic
atrophy and blindness.
Eye pressure is measured by
using a “tonometer” (with the test being called “tonometry”),
and the standard tonometer generally is considered to be the
“Goldmann tonometer.” The normal range of intraocular
pressure (IOP) is 10 mm Hg to 21 mm Hg, with an average of
about 16 mm Hg. Typically, eyes with intraocular
pressure measurements of 21 mm Hg or higher, using a Goldmann
tonometer, are considered suspect for glaucoma. However,
although glaucoma typically is associated with elevated IOP,
the amount of pressure which will cause glaucoma varies from
eye to eye and person to person. Many people with
glaucoma have IOP’s in the normal range (“low tension”
glaucoma), possibly indicating that their lamina cribrosas are
too weak to withstand even normal amounts of pressure;
whereas, many people with IOP’s which would be considered high
have no evidence of glaucomatous damage.
Visual field
loss, caused by optic nerve damage, is measured by using a
“visual field analyzer” or “perimeter.” The procedure is
known as “perimetry.” Field loss due to glaucoma usually
is not even measurable until 25% to 40% of the optic nerve’s
axons have been destroyed. Studies seem to show that the
first fibers to die are the larger fibers, which primarily
carry form and motion information, rather than the smaller
fibers, which primarily detect light. Therefore, pattern
discrimination perimetry (PDP), which requires detection of
both form and motion, may be a better test for early glaucoma
than conventional perimetry, which requires detection of spots
of light.
In PDP, various locations of the retina are
stimulated with a checkerboard pattern on a background of
randomly moving dots. The more random the dot movements,
the more difficult it is to continue to perceive the
checkerboard pattern. (Even a normal eye eventually will
not be able to see the checkerboard when the dot movement is
random enough.) The more advanced the stage of
glaucomatous nerve damage, the less “noisy” the dots need to
be for the checkerboard pattern to be indistinguishable from
the background of moving dots. In effect, the PDP seems
to be more sensitive in detecting early glaucomatous visual
field losses than a standard
perimeter.
THE CRYSTALLINE
LENS
The transparent crystalline lens of the eye is located
immediately behind the iris. It is composed of fibers
that come from epithelial (hormone-producing) cells. In
fact, the cytoplasm of these cells makes up the transparent
substance of the lens.
The crystalline lens is composed
of 4 layers, from the surface to the center:
-
Capsule
-
subcapsular epithelium
-
cortex
-
nucleus
The
lens capsule is a clear, membrane-like structure that is quite
elastic, a quality that keeps it under constant tension.
As a result, the lens naturally tends towards a rounder
or more globular configuration, a shape it must assume for the
eye to focus at a near distance. Slender but very strong
suspensory ligaments (also known as zonules), which attach at
one end to the lens capsule and at the other end to the
ciliary processes of the circular ciliary body around the
inside of the eye, hold the lens in
place.
accommodation
When the ciliary muscle in the
ciliary body relaxes, the ciliary processes pull on the
suspensory ligaments, which in turn pull on the lens capsule
around its equator. This causes the entire lens to
flatten or to become less convex, enabling the lens to focus
light from objects at a far away distance. Likewise,
when the ciliary muscle works or contracts, tension is
released on the suspensory ligaments, and subsequently on the
lens capsule, causing both lens surfaces to become more convex
again and the eye to be able to refocus at near. This
adjustment in lens shape, to focus at various distances, is
referred to as “accommodation” or the “accommodative process”
and is associated with a concurrent constriction of the
pupil.
The “amplitude of accommodation” of an eye is
the maximum amount that the eye’s crystalline lens can
accommodate (change shape), in diopters (D). This amount
is very high when young and decreases with age. The
amplitude of accommodation is equivalent to the inverse
(reciprocal) of the distance (“nearpoint of accommodation”) at
which the emmetropic eye can focus clearly.
(“Emmetropia” refers to an eye having no refractive
error, whether hyperopia, myopia, or astigmatism, or it can
refer to the optical system of an eye corrected with glasses
or contact lenses.)
Ranges of Accommodation by
Age Age Amplitude of Accommodation Nearpoint of
Accommodation
(in an Emmetropic Eye)
5 16.00 diopters
6.3 cm (2.5 in)
10 14.00 diopters 7.1 cm (2.8 in)
15
12.00 diopters 8.3 cm (3.3 in)
20 10.00 diopters 10.0 cm
(3.9 in)
25 8.50 diopters 11.8 cm (4.6 in)
30 7.00
diopters 14.3 cm (5.6 in)
35 5.50 diopters 18.2 cm (7.2
in)
40 4.50 diopters 22.2 cm (8.7 in)
45 3.50 diopters
28.6 cm (11.2 in)
50 2.50 diopters 40.0 cm (15.7 in)
55 1.75 diopters 57.0 cm (22.5 in)
60 1.00 diopter
100.0 cm (39.4 in)
65 0.50 diopter 200.0 cm
(78.8 in)
70 0.25 diopter 400.0 cm (157.5 in)
75
0.12 diopter optical infinity
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