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The human eye is the organ which gives us the sense of sight,

allowing us to observe and learn more about the surrounding


world than we do with any of the other four senses. We use our
eyes in almost every activity we perform, whether reading,
working, watching television, writing a letter, driving a car, and
in countless other ways. Most people probably would agree that
sight is the sense they value more than all the rest.
The eye allows us to see and interpret the shapes, colors, and
dimensions of objects in the world by processing the light they
reflect or emit. The eye is able to detect bright light or dim
light, but it cannot sense objects when light is absent.
process of vision
Light waves from an object (such as a tree)
enter the eye first through the cornea,
which is the clear dome at the front of the
eye. The light then progresses through the pupil, the circular
opening in the center of the colored iris.
Fluctuations in incoming light change the size of the eye’s
pupil. When the light entering the eye is bright enough, the
pupil will constrict (get smaller), due to the pupillary light
response.
Initially, the light waves are bent or converged first by the
cornea, and then further by thecrystalline lens (located
immediately behind the iris and the pupil), to a nodal point (N)
located immediately behind the back surface of the lens. At that
point, the image becomes reversed (turned backwards) and
inverted (turned upside-down).
The light continues through the vitreous humor, the clear gel
that makes up about 80% of the eye’s volume, and then, ideally,
back to a clear focus on the retina, behind the vitreous. The
small central area of the retina is the macula, which provides the
best vision of any location in the retina. If the eye is considered
to be a type of camera, the retina is equivalent to the film inside
of the camera, registering the tiny photons of light interacting
with it.
Within the layers of the retina, light impulses are changed into
electrical signals. Then they are sent through the optic nerve,
along the visual pathway, to the occipital cortex at the posterior
(back) of the brain. Here, the electrical signals are interpreted or
“seen” by the brain as a visual image.
Actually, then, we do not “see” with our eyes but, rather, with
our brains. Our eyes merely are the beginnings of the visual
process.
myopia, hyperopia, astigmatism
If the incoming light from a far away object focuses before it
gets to the back of the eye, that eye’s refractive error is called
“myopia” (nearsightedness). If incoming light from something
far away has not focused by the time it reaches the back of the
eye, that eye’s refractive error is “hyperopia” (farsightedness).
In the case of “astigmatism,” one or more surfaces of the cornea
or lens (the eye structures which focus incoming light) are not
spherical (shaped like the side of a basketball) but, instead, are
cylindrical or toric (shaped a bit like the side of a football). As a
result, there is no distinct point of focus inside the eye but,
rather, a smeared or spread-out focus. Astigmatism is the most
common refractive error.
presbyopia (“after 40” vision)
After age 40, and most noticeably after age 45, the human eye is
affected by presbyopia. This natural condition results in greater
difficulty maintaining a clear focus at a near distance with an
eye which sees clearly far away.
Presbyopia is caused by a lessening of flexibility of
the crystalline lens, as well as to a weakening of the ciliary
muscles which control lens focusing. Both are attributable to
the aging process.
An eye can see clearly at a far distance naturally, or it can be
made to see clearly artificially, such as with the aid
of eyeglasses or contact lenses, or else following a
photorefractive procedure such as LASIK (laser-assisted in situ
keratomileusis). Nevertheless, presbyopia eventually will affect
the near focusing of every human eye.
eye growth
The average newborn’s eyeball is about 18 millimeters in
diameter, from front to back (axial length). In an infant, the eye
grows slightly to a length of approximately 19½ millimeters.
The eye continues to grow, gradually, to a length of about 24-25
millimeters, or about 1 inch, in adulthood. A ping-pong ball is
about 1½ inch in diameter, which makes the average adult
eyeball about 2/3 the size of a ping-pong ball.
The eyeball is set in a protective cone-shaped cavity in the skull
called the “orbit” or “socket.” This bony orbit also enlarges as
the eye grows.
extraocular muscles
The orbit is surrounded by layers of soft, fatty tissue. These
layers protect the eye and enable it to turn easily.
Traversing the fatty tissue are three pairs of extraocular
muscles, which regulate the motion of each eye: the medial &
lateral rectus muscles, the superior & inferior rectus muscles,
and thesuperior & inferior oblique muscles.
eye structures
Several structures compose the human eye. Among the most
important anatomical components are
the cornea, conjunctiva, iris, crystalline lens, vitreous
humor, retina, macula, optic nerve, and extraocular muscles.
You can click on the names of each of these 9 ocular structures
on the left (either in the upper picture or in the lower frame of
links) to learn more about them. Then take the three short
quizzes at the end, if you wish.
Anatomy, Physiology Ted M. Montgomery,
and Optometric
Pathology of the Human Physician
The Cornea Eye

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One-sixth of the outer layer of the eye (called the tunic fibrosa or fibrous tunic)
bulges forward as the cornea, the transparent dome which serves as the outer window
of the eye. The cornea is the primary (most powerful) structure focusing light
entering the eye (along with the secondary focusing structure, the crystalline lens).

The cornea is composed, for the most part, of connective tissue with a thin layer
of epithelium on the surface. Epithelium is the type of tissue that covers all free body
surfaces.

The cornea is composed of 5 layers, from the front to the back:

1. epithelium,
2. Bowman’s (anterior limiting) membrane,
3. stroma (substantia propria),
4. Descemet’s (posterior limiting) membrane, and
5. endothelium (posterior epithelium).

The transparency of the cornea is due to the fact that it contains hardly any cells and
no blood vessels. However, blood vessels can creep in from around it, if it is
constantly irritated or infected, which can interfere with vision.

On the other hand, the cornea contains the highest concentration of nerve fibers of any
body structure, making it extremely sensitive to pain. The nerve fibers enter on the
margins of the cornea and radiate toward the center. These fibers are associated with
numerous pain receptors that have a very low threshold. Cold receptors also are
abundant in the cornea, although heat and touch receptors seem to be lacking.

sclera
Along its circumference, the cornea is continuous with the sclera: the white, opaque
portion of the eye. The sclera makes up the back five-sixths of the eye’s outer layer.
It provides protection and serves as an attachment for the extraocular muscles, which
move the eye.

tears and tear glands


Coating the outer surface of the cornea is a “pre-corneal tear film.” People normally
blink the eyelids of their eyes about every six seconds to replenish the tear film. Tears
have four main functions on the eye:

• wetting the corneal epithelium, thereby preventing it from


being damaged due to dryness,
• creating a smooth optical surface on the front of the
microscopically irregular corneal surface,
• acting as the main supplier of oxygen and other nutrients to
the cornea,
• containing an enzyme called “lysozyme,” which destroys
bacteria and prevents the growth of microcysts on the cornea,
and
• flushing harmful bacteria and other microbes away from the
eye, into the lacrimal canals and then out through the nose.

The tear film resting on the corneal surface has three layers, from front to back:

• lipid or oil layer,


• lacrimal or aqueous layer, and
• mucoid or mucin layer

The most external layer of the tear film is the lipid or oil layer. This layer prevents
the lacrimal layer beneath it from evaporating. It also prevents the tears from flowing
over the edge of the lower eyelid (“epiphora”).

The lipid component of the tear film is produced by sebaceous glands known as
“Meibomian” glands (located in the tarsal plates along the eyelid margins) and the
glands of “Zeis” (which open into the hair follicles of the eyelashes). An enlargement
of a Meibomian gland is known as a “chalazion,” while an infection of a Zeis gland is
known as a “hordeolum” or “sty(e).”

Beneath the lipid layer is located the lacrimal or aqueous layer of the tear film. This
middle layer is the thickest of the three tear layers, and it is formed primarily by the
glands of “Krause” and “Wolfring” and secondarily by the “lacrimal” gland, all of
which are located in the eyelids. The lacrimal gland is the major producer of tears
when one is crying or due to foreign body irritation.

Lacrimal fluid, containing salts, proteins, and lysozyme, has several functions:

• taking the main nutrients (such as oxygen) to the cornea,


• carrying waste products away from the cornea,
• helping to prevent corneal infection, and
• maintaining the tonicity of the tear film.

If the eye’s tears are “isotonic,” there will be no change in water volume in the cornea
and vision will remain normal. (Tears normally have a tonicity equal to .9% saline.)
If the tears are “hypotonic,” water will flow into the cornea (such as when crying or
swimming in a pool) and it will swell, causing it to become more myopic. If the tears
are “hypertonic,” water will flow out of the cornea (such as when swimming in the
ocean) and it will shrink, causing it to become more hyperopic.

The epithelial surface of the cornea is naturally “hydrophobic” (water-repelling).


Therefore, for a tear layer to be able to remain on the corneal surface without rolling
off, the “hydrophilic” (water-attracting) mucoid or mucin layer of the tear film is laid
down onto the surface of the cornea by “goblet cells,” which are present in the
bulbar conjunctiva. In turn, the lacrimal layer of the tear film, located above the
mucoid layer, can defy gravity and remain on the front of the eye.

dry eye
A deficiency of any of the three layers of the tear film can lead to a “dry eye”
condition, causing anything from mild eye irritation to severe pain. Interestingly, in
some cases, excessive tearing or watering of the eyes can be a symptom of a dry eye
condition. This is because when, for whatever reason, there is an inadequate normal
tear layer on the eye, irritation results; this causes an overproduction of the lacrimal
gland and a flooding of lacrimal fluid into the eye (“reflex tearing”).

Besides excessive tearing, symptoms associated with dry eyes can include the
following:

• eye irritation, scratchiness, grittiness, or pain;


• redness of the eye(s);
• a burning sensation in the eye(s);
• a feeling of something in the eye(s);
• eyes that feel “glued shut” after sleeping;
• blurred vision; and
• eye discomfort with contact lens wear.

There can be multiple causes of a dry eye condition, and these are some of the
possibilities:

• lid or blinking problems (for instance, an injury or stroke


affecting one of the nerves which helps us blink);
• reading or working at a computer screen for long periods of
time;
• medications like antihistamines, oral contraceptives, beta
blockers, diuretics, tranquilizers, pain relievers, or
antidepressants;
• a dry climate (including heating and air conditioning in a home,
airplane, or motel room), wind, UV radiation, tobacco smoke,
and dust;
• diseases such as rheumatoid arthritis, Sjogren’s syndrome,
keratoconjunctivitis sicca, xerophthalmia, lupus
erythematosus, Grave’s disease, diabetes, or scleroderma;
• hormonal changes accompanying menopause;
• chemical, radiation, or thermal burns to the eye;
• vitamin A deficiency;
• aging, since the tear glands produce fewer tears as we age;
and
• idiopathic (unknown) causes.

A dry eye problem often can be relieved with the use of over-the-counter eyedrops
which behave as “artificial tears” on the eyes. These types of drops can soothe the
eyes, moisturize dry spots, supplement tears, and protect eyes from further irritation.
Some drops are formulated to match the pH of human tears for added comfort.
Special ocular lubricant ointments, applied to the eyes for overnight use, also are
available.

Artificial tears may be preserved or unpreserved. Bottle contamination is less likely


with preserved drops; however, an allergic reaction to the preservatives can occur. If
unpreserved eyedrops are used, care must be taken not to contaminate the bottle by
touching the tip to any surface, including the eyeball.

Some eyedrops contain “vasoconstrictors” (chemicals such as tetrahydrozaline or


naphazoline), which constrict the conjunctival blood vessels, thereby reducing the
amount of redness on the surface of the eyes. These drops may or may not contain a
tear substitute component for red eyes. Overuse of such drops can cause eyes to
become even more red (“rebound hyperemia”), due to a weakening of the muscles
persistently constricting the blood vessels.

In certain cases, artificial tear drops do not relieve the discomfort due to dry eyes. In
such cases, if the discomfort is severe enough, other options are available. The most
common of these involves closing the tear ducts (which act as “drains” for the tears).
Using either a silicone plug or scarring the tear duct closed by cauterization (with a
“hot poker”) decreases or stops the passage of the tears into the tear ducts. That way,
any tears naturally produced, or artificially placed into eyes, will remain longer (until
they evaporate). It can be a very successful way to make irritated eyes with a chronic
dry eye syndrome feel more comfortable.
keratoconus
“Keratoconus”—which is a combination of two Greek words: karato, meaning
cornea, and konos, meaning cone—is a non-inflammatory condition in which there is
progressive central thinning of the cornea, changing it from dome-shaped to cone-
shaped. An asymmetrical, cone-like bulge develops, eventually resulting in
significant distortion and visual impairment.

As keratoconus progresses, the corneal tissue continues to thin and to bulge forward
and downward, becoming very irregular. In advanced stages, there can be a
precipitous drop in vision due to sudden clouding of the cornea, referred to as “acute
hydrops,” where there is a sudden infusion of fluid into the stretched cornea. This
usually resolves over weeks to months but often is followed by central corneal
scarring, further impairing vision.

An uncommon disorder, keratoconus affects about 1 out of every 2,000 people. It


almost always is bilateral (affecting both eyes) and typically takes years or decades to
progress, usually beginning at puberty or later in the teens. Its progression can halt at
any stage, from mild to severe.

Although keratoconus does not cause complete blindness, it often causes a dramatic
increase in myopia (nearsightedness) and irregular astigmatism, significantly blurring
and distorting vision, as well as causing significant photophobia (light sensitivity) and
glare.

The cause of keratoconus most likely is genetic; about 7-8% of people with the
condition also have other family members with it. Severe rubbing of the eyes also
may exacerbate the problem. In its early stages, keratoconus can be diagnosed only
by using detailed computer maps of the corneal surface, detecting subtle changes in
corneal shape.

Initially, stronger eyeglasses are successful in correcting the progressive myopia and
astigmatism; however, as the disease advances, rigid gas permeable (RGP) contact
lenses are necessary to flatten the anterior corneal surfaces and obtain optimal visual
acuity. Contact lens fitting can be difficult in patients with keratoconus, usually
requiring frequent doctor visits and lens changes.

Ultimately, if good vision no longer can be attained with contact lenses, or if


intolerance to the contact lenses develops, corneal transplantation is recommended.
This procedure is necessary in only about 10% of people with keratoconus and is
successful in greater than 90% of cases, one of the highest success rates for corneal
transplantation. Although this procedure replaces the thinned central portion of the
cornea (with a section of donor cornea), contact lenses and/or eyeglasses often
continue to be required for maximum visual acuity.

Anatomy, Physiology Ted M. Montgomery,


and Optometric
The Extraocular Pathology of the Human
Eye
Physician

Muscles
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The extraocular muscles, considering their relatively small size, are incredibly strong
and efficient. There are the six extraocular muscles, which act to turn or rotate an eye
about its vertical, horizontal, and antero-posterior axes:

1. medial rectus (MR),


2. lateral rectus (LR),
3. superior rectus (SR),
4. inferior rectus (IR),
5. superior oblique (SO), and
6. inferior oblique (IO).

Here is a schematic of a left eye, showing how its extraocular muscles insert into the
eye:

muscle movements
A given extraocular muscle moves the pupil, at the front of the eye, in a specific
direction or directions, as follows:
• medial rectus (MR)—
o moves the eye inward, toward the nose (adduction)
• lateral rectus (LR)—
o moves the eye outward, away from the nose (abduction)
• superior rectus (SR)—
o primarily moves the eye upward (elevation)
o secondarily rotates the top of the eye toward the nose
(intorsion)
o tertiarily moves the eye inward (adduction)
• inferior rectus (IR)—
o primarily moves the eye downward (depression)
o secondarily rotates the top of the eye away from the nose
(extorsion)
o tertiarily moves the eye inward (adduction)
• superior oblique (SO)—
o primarily rotates the top of the eye toward the nose
(intorsion)
o secondarily moves the eye downward (depression)
o tertiarily moves the eye outward (abduction)
• inferior oblique (IO)—
o primarily rotates the top of the eye away from the nose
(extorsion)
o secondarily moves the eye upward (elevation)
o tertiarily moves the eye outward (abduction)

The primary muscle that moves an eye in a given direction is known as the “agonist.”
A muscle in the same eye that moves the eye in the same direction as the agonist is
known as a “synergist,” while the muscle in the same eye that moves the eye in the
opposite direction of the agonist is the “antagonist.” According to “Sherrington’s
Law,” increased innervation to any agonist muscle is accompanied by a corresponding
decrease in innervation to its antagonist muscle(s).

cardinal positions of gaze


The “cardinal positions” are six positions of gaze which allow comparisons of the
horizontal, vertical, and diagonal ocular movements produced by the six extraocular
muscles. These are the six cardinal positions:

• up/right
• up/left
• right
• left
• down/right
• down/left

In each position of gaze, one muscle of each eye is the primary


mover of that eye and is yoked to the primary mover of the other
eye. Below, each of the six cardinal positions of gaze is shown,
along with upward gaze, downward gaze, and convergence:

MR = Medial LR = Lateral
Rectus Rectus

SR = Superior IR = Inferior
Rectus Rectus

SO = Superior IO = Inferior
Oblique Oblique

muscle innervations
Each extraocular muscle is innervated by a specific cranial nerve (C.N.):
• medial rectus (MR)—cranial nerve III (Oculomotor)
• lateral rectus (LR)—cranial nerve VI (Abducens)
• superior rectus (SR)—cranial nerve III (Oculomotor)
• inferior rectus (IR)—cranial nerve III (Oculomotor)
• superior oblique (SO)—cranial nerve IV (Trochlear)
• inferior oblique (IO)—cranial nerve III (Oculomotor)

The following can be used to remember the cranial nerve


innervations of the six extraocular muscles:

LR6(SO4)3.

That is, the lateral rectus (LR) is innervated by C.N. 6, the superior
oblique (SO) is innervated by C.N. 4, and the four remaining muscles
(MR, SR, IR, and IO) are innervated by C.N. 3.

anatomical arrangement
All of the extraocular muscles, with the exception of the inferior oblique, form a
“cone” within the bony orbit. The apex of this cone is located in the posterior aspect
of the orbit, while the base of the cone is the attachment of the muscles around the
midline of the eye.

The apex of the conic structure is a tendonous ring called the “annulus of Zinn.”
Through the annulus, and along the middle of the cone of muscles, runs the optic
nerve (cranial nerve II). Within the optic nerve are contained the ophthalmic artery
and the ophthalmic vein.

The superior oblique, although part of the cone of muscles, differs from the other
muscles in a significant way. Before it attaches to the eye, it passes through a ring-
like tendon, the “trochlea,” in the nasal portion of the orbit. The trochlea acts as a
pulley for the superior oblique muscle.

The inferior oblique, which is not a member of the cone of muscles originating from
annulus of Zinn, arises from the lacrimal fossa in the nasal portion of the bony orbit.
This muscle attaches to the inferior portion of the eye.

ductions
When considering each eye separately, any movement is called a “duction.”
Describing movement around a vertical axis, “abduction” is a horizontal movement
away from the nose, caused by a contraction of the LR muscle, with an equal
relaxation of the MR muscle. Conversely, “adduction” is a horizontal movement
toward the nose, caused by a contraction of the MR muscle, with an equal relaxation
of the LR muscle.

Describing movement around a horizontal axis, “supraduction” (elevation) is a


vertical movement upward, caused by the contraction of the SR and IO muscles, with
an equal relaxation of the of the IR and SO muscles. Conversely, “infraduction”
(depression) is a vertical movement downward, caused by the contraction of the IR
and SO muscles, with an equal relaxation of the SR and IO muscles.

Describing movement around an antero-posterior axis, “incycloduction” (intorsion) is


a nasal or inward rotation (of the top of the eye), caused by the contraction of the SR
and SO muscles, with an equal relaxation of the IR and IO muscles. Conversely,
“excycloduction” (extorsion) is a temporal or outward rotation (of the top of the eye),
caused by the contraction of the IR and IO muscles, with an equal relaxation of the SR
and SO muscles.

versions
When considering how the eyes work together, a “version” or “conjugate” movement
involves simultaneous movement of both eyes in the same direction. Agonist muscles
in both eyes, which work together to move the eyes in the same direction, are said to
be “yoked” together. According to “Hering’s Law,” yoked muscles receive equal and
simultaneous innervation.

There are six principle versional movements, where both eyes look or move together
in the same direction, simultaneously:

• dextroversion (looking right)—


o right lateral rectus
o left medial rectus
• levoversion (looking left)—
o left lateral rectus
o right medial rectus
• supraversion or sursumversion (looking straight up)—
o right & left superior recti
o right & left inferior obliques
• infraversion or deorsumversion (looking straight down)—
o right & left inferior recti
o right & left superior obliques
• dextroelevation (looking right and up)—
o right superior rectus
o left inferior oblique
• dextrodepression (looking right and down)—
o right inferior rectus
o left superior oblique
• levoelevation (looking left and up)—
o right inferior oblique
o left superior rectus
• levodepression (looking left and down)—
o right superior oblique
o left inferior rectus
• dextrocycloversion (rotation to the right)—
o right inferior rectus & inferior oblique
o left superior rectus & superior oblique
• levocycloversion (rotation to the left)—
o left inferior rectus & inferior oblique
o right superior rectus & superior oblique

vergences
A “vergence,” or “disconjugate” movement, involves simultaneous movement of both
eyes in opposite directions. There are two principle vergence movements:

• convergence—both eyes moving nasally or inward


• divergence—both eyes moving temporally or outward

If one eye constantly is turned inward (“crossed-eye”), outward (“wall-eye”), upward,


or downward, this is referred as a “strabismus” or “heterotropia,” discussed later.

Usually, a vergence is performed relative to a point of fixation. For instance,


someone could be looking at TV across the room (at a far distance). Then, when a
commercial comes on, that person could converge both eyes to read a book (at a near
distance). Then, after the commercial is over, both eyes would diverge to look at the
TV again.

One cannot actually voluntarily diverge both eyes outward, at the same time, from
looking straight ahead. That is, the two lateral recti muscles cannot pull the eyes
outward, simultaneously and voluntarily, while one is viewing something far away.
However, if one is falling asleep with one’s eyes still open, it is possible for the eyes
to diverge, momentarily and involuntarily, causing temporary diplopia (double
vision).

strabismus (heterotropia)
Normally, when viewing an object, the “lines of sight” of both eyes intersect at the
object; that is, both eyes point directly at the object being viewed. An image of the
object is focused upon the macula of each eye, and the brain merges the two retinal
images into one.

Sometimes, however, due to some type of extraocular muscle imbalance, one eye is
not aligned with the other eye, resulting in a “strabismus,” also called a “heterotropia”
or simply a “tropia.” Occasionally, this ocular deviation is referred to as a “squint,”
although this term is not very descriptive and no longer is commonly used.

With strabismus, while one eye is fixating upon a particular object, the other eye is
turned in another direction, relative to the first eye, whether inward (“cross-eyed”),
outward (“wall-eyed”), upward, or downward. As a result, the person may experience
“diplopia” (double vision), since two different objects are imaged onto the maculas of
both eyes. However, if the person’s brain has learned to “suppress” (turn off) the
image of the strabismic (turning) eye, the brain will perceive only the single image
from the other eye.

If the strabismus occurs sometimes, but not all of the time, it is said to be
“intermittent.” If the strabismus occurs all of the time, it is said to be “constant.”

Occasionally, whether the strabismus is intermittent or constant, one eye will be the
deviating eye at certain times, while the opposite eye will be the deviating eye at other
times. That is, one eye will turn sometimes, but at other times the alternate eye will
turn. This is referred to as “alternating” strabismus.

The misalignment of a strabismic eye occurs in about 2% of children. The deviant


eye may be in any direction: inward (“esotropia” or “crossed-eye”), outward
(“exotropia” or “wall-eye”), upward (“hypertropia”), downward (“hypotropia”), or
any combination of these.

Strabismus also can occur due to a nerve paralysis or paresis, injury, or even due to a
retinal disease. Sometimes a strabismus will result when there is a very different
refractive error (usually much higher) in the strabismic eye compared to the other eye.
The angle of deviation of the strabismus is measured in “prism diopters.” If the angle
of deviation remains the same in all cardinal positions of gaze, the strabismus is
classified as “concomitant” (or “nonparalytic”). If the angle of deviation is not the
same in all cardinal positions of gaze, the strabismus is classified as
“nonconcomitant” (or “paralytic”).

Below, views of the two most common types of strabismus—esotropia and exotropia
—are displayed:

OD (Right Eye) OD (Right Eye)


Esotropia Exotropia

Esotropia can be congenital (a muscle imbalance present from birth), and usually the
angle of deviation is large. Management involves surgical correction, typically at age
six months or earlier.

Some cases of low-angle esotropia do not require surgery but, instead, respond
successfully to visual therapy. This is true especially in a child or an adult for which
the esotropia is of recent onset and for which there is no macular damage (that is,
when the strabismic eye is capable of good visual acuity).

The esotropia also can be accommodative, usually due to a high amount of


uncorrected hyperopia (farsightedness). This causes a great deal of accommodation to
be required to focus retinal images, resulting in a subsequent over-convergence (by
the medial rectus muscles) and a subsequent esotropia. The usual treatment for
accommodative esotropia is eyeglasses or contact lenses, which compensate for the
hyperopia, allowing the deviating eye to straighten.

Exotropia also can be congenital, although this is very unusual. More commonly,
exotropia develops in infancy or in early childhood, often beginning as an intermittant
(occasional) strabismus and sometimes leading to a constant strabismus.

A carefully planned regimen of visual therapy often can be used to treat exotropia,
especially in cases where complete suppression of the strabismic eye has not yet
occurred and the eye is capable of good visual acuity.

However, in cases where visual therapy is not successful, surgical correction should
be used to provide a cosmetically improved appearance of the deviating eye. This
does not necessarily ensure that binocular vision will result.
amblyopia and eccentric fixation
If the vision in a strabismic (deviating or turning) eye is suppressed (turned off) for
too long, that eye very well may develop “amblyopia” or a “lazy eye” condition. This
means that the visual acuity in that eye no longer is as good as the visual acuity in the
other eye, which is used all the time.

In this case, when the normal eye is covered, thus forcing the strabismic eye to take
over, the strabismic eye usually does not point exactly straight at the object being
fixated. Therefore, the image of the object being viewed does not fall directly upon
the macula, as it should. Rather, the image falls upon some eccentric point, away
from the macula, where the acuity is not as good. Thus, this is referred to as
“eccentric fixation.”

An eye is not a “lazy eye” simply because it turns and does not align with the other
eye. Amblyopia (“lazy eye”) simply refers to decreased visual acuity in one eye,
compared to the other eye. That is, an eye is referred to as “lazy” because it does not
see as clearly as the other eye. The most common reason for amblyopia is the
presence of eccentric fixation in a strabismic eye.

acquired muscle palsy


Damage to cranial nerve III, IV, or VI often will cause a “palsy” (paralysis or paresis)
of the extraocular muscle(s) innervated by that nerve. The cause of the palsy usually
is acquired (due to a lesion, a stroke, or other trauma), although occasionally it can be
congenital (at birth).

An extraocular palsy may cause the eyes to be misaligned, which is a strabismus.


The most common symptom of a muscle palsy is diplopia (double vision)—that is,
seeing two images either side-by-side, one on top of the other, or displaced
diagonally.

When the oculomotor nerve (cranial nerve III) is damaged, a palsy in the medial
rectus, superior rectus, inferior rectus, and/or inferior oblique muscle(s) may occur. If
all of these muscles are affected, the effected eye will be turned outward and
downward (due to unopposed action of the lateral rectus and superior oblique
muscles). The affected eye cannot turn inward past the midline, nor can it turn
upward past the midline.

In a complete cranial nerve III paralysis, the upper eyelid also will be nearly closed
from a ptosis. The pupil might be dilated and unreactive as well.
When the trochlear nerve (cranial nerve IV) is damaged, a palsy of the superior
oblique muscle may occur, resulting in a hypertropia of the affected eye. People with
this condition will experience both a vertical and a torsional diplopia, and they will
compensate for this by tilting the head toward the shoulder of the unaffected eye.

When utilizing the Bielschowsky head-tilt test, the person is told to tilt his/her head
toward the shoulder of the affected eye. An overaction of the inferior oblique, and an
elevation of the affected eye (and marked diplopia), will result.

When the abducens nerve (cranial nerve VI) is damaged, a palsy of the lateral rectus
(LR) muscle may occur, resulting in an esotropia of the affected eye. That eye
generally will not be able to look outward past the midline, and it will be somewhat
turned inward when the other eye is fixating straight ahead. Diplopia will be observed
by the person when he/she gazes to the side with the palsied muscle, and the person
will compensate for this by turning his/her face toward the side of the palsied eye.

An extraocular muscle palsy may resolve on its own with time; however, this may not
occur. If the palsy and resultant diplopia are permanent, a prismatic correction may
be incorporated into spectacle lenses to merge the double images into a single image.
Some people prefer simply to keep one eye patched to take away their double vision.

In some cases, muscle surgery is another option. However, it should not be performed
for at least six months after the onset of diplopia, since the effects of the palsy may
resolve spontaneously over a few weeks or months. If a ptosis (drooping upper
eyelid) is involved, such as in a cranial nerve III paralysis, probably the best option is
surgical elevation of the eyelid.

Anatomy, Physiology Ted M. Montgomery,


and Optometric
Pathology of the Human Physician
The Optic Nerve Eye

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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
parasympathetic pathways in the pupillary light reflex can be seen
here: parasympathetic response.

blind spot
The beginning of the optic nerve in the retina is called the optic nerve head or optic
disc. Since there are no photoreceptors (cones androds) 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 retina that is seeing properly 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:

1. Sit about arm’s length away from your computer


monitor/screen.
2. Completely cover your left eye (without closing or pressing on
it), using your hand or other flat object.
3. With your right eye, stare directly at the above. In your
periphery, you will notice the to the right.
4. Slowly move closer to the screen, continuing to stare at
the .
5. 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 .)
6. As you continue to look at the , keep moving forward a few
more inches, and the will come back into view.
7. 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.
8. 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 disc and optic nerve. Although there are too many to list completely, a few will
be included here.

optic atrophy
“Optic atrophy” of the optic disc (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 disc and loss of pupillary reaction
are usually proportional to the visual loss. Degeneration and atrophy of optic nerve
fibers is irreversible, although in some cases, intravenous steroid injections have been
seen to slow down the process.

optic neuritis
“Optic neuritis” is an inflammation of the optic nerve. It may affect the part of the
nerve and disc 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 (disc) unless some optic atrophy has occurred.

This condition can be caused by any of the following:

• 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 disc, and posterior, in which the optic disc 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. 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. Thus, less visual impulses are able to reach the brain.

In advanced glaucoma, the visual field in the peripheral retina is decreased or lost,
leaving vision in the central retina (macular area) intact. This results in “tunnel
vision.” Elevated eye pressure occurs when too much aqueous fluid enters the eye
and not enough of the aqueous fluid is leaving the eye. Eye pressure can be measured
by performing a “tonometry” test.

Normally, fluid enters the eye by seeping out of the blood vessels in the ciliary body.
This fluid eventually makes its way past thecrystalline 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 thecanal of Schlemm.

If the rate of aqueous fluid is entering the eye is too great, or if the trabecular
meshwork “drain” gets clogged (for instance, with debris or cells) so that the fluid is
not leaving the eye quickly enough, the pressure builds up in what is known as “open
angle glaucoma.” It is more common with increasing age.
Open angle glaucoma, which tends to be a chronic and painless condition, 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”). This can prevent
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 because it cannot flow out of the eye properly.
This causes an increased intraocular pressure in what is known as “closed angle
glaucoma.” Typically, there is an acute (sudden), painful onset. It can be
accompanied by the appearance of rainbow-colored rings around white lights.

An internal pressure more than that which the eye can tolerate can deform the lamina
cribrosa, the small cartilaginous section of thesclera at the back of the eye through
which the optic nerve passes. A deformed 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 to be “ocular hypertensive” and are 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 actually 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. Conversely, many people with IOP’s which would
be considered high have no evidence of glaucomatous damage.

Glaucomatous changes in the optic disk (optic nerve head) usually can be detected
over time. If the optic cup within the optic disk increases in size over a period of
months or years, if notching is observed anywhere around the nerve head rim, and/or
if an asymmetry is observed between the optic cups of the two eyes, then that person
may be considered to be a “glaucoma suspect.” In glaucoma, optic nerve rim atrophy
and/or notching, with a corresponding visual field decrease, usually will occur in this
order:
Optic Nerve Visual Field
Quadrant Loss

1. Inferior Superior
Quadrant Field

2. Superior
Inferior Field
Quadrant

3. Temporal
Nasal Field
Quadrant

Temporal
4. Nasal Quadrant
Field

Visual field loss, caused by optic nerve damage, is measured by using a “visual field
analyzer” or “perimeter,” especially by measuring and comparing changes over time.
The procedure is known as “perimetry.” Most 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 than a standard
perimeter in detecting early glaucomatous visual field losses.

Typically, the elevated pressure in open angle glaucoma can be controlled


using glaucoma medications, which either decrease the production of aqueous fluid
or else increase its outflow from the eye. However, closed angle glaucoma often
requires surgical intervention to be controlled.

Anatomy, Physiology Ted M. Montgomery,


and Optometric
The Crystalline Pathology of the Human
Eye
Physician

Lens
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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:

1. capsule,
2. subcapsular epithelium,
3. cortex, and
4. 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 or zonules of
Zinn, 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. These thin
ligaments or zonules hold the lens in place.

accommodation
The ciliary body is circular, and the ciliary muscle within it is a sphincter muscle,
shaped like a tiny doughnut. The inside diameter of the muscle gets smaller when it
contracts and larger when it relaxes.

When the eye is viewing an object at a far distance (such that parallel rays of light are
entering the eye), the ciliary muscle within the ciliary body relaxes. The ciliary
processes pull on the suspensory ligaments (or zonules), 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 the far-away object.

Conversely, when the eye views an object at a near


distance, an “accommodative demand” is created. As a
result, the ciliary muscle works or contracts, causing
tension to be released on the suspensory ligaments and, subsequently, on the lens
capsule. This causes both (front and back) lens surfaces to become more convex and
the eye to be able to focus at near. (View another Accommodation of the
Crystalline Lens graphic.)

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 (decrease in size) of the pupil. The animated diagram above
illustrates the change in stance of the ciliary body, crystalline lens, and pupil as the
eye looks back and forth between far and near.

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 a person is 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—
no hyperopia, myopia, norastigmatism—or it can refer to the optical system of an
eye corrected to “plano” [0.00 diopters of refractive error] with glasses, contact
lenses, or refractive surgery.)

Ranges of Accommodation by Age


Nearpoint of Accommodation
Age Amplitude 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

nearpoint stress
Normally, the accommodative process, or accommodation, of the crystalline lens is
smooth and effortless. When one changes one’s focus from far to near, the ciliary
muscle quickly contracts, causing the crystalline lens to accommodate (become
thicker) and the object at a near distance to become clear. Then, when looking back
again at a far distance, the ciliary muscle immediately relaxes, causing the crystalline
lens to revert to a thin shape and one’s far-distance vision to become clear again.

Sometimes, though, this process can undergo significant stress after having done
several weeks or months of prolonged near work. Often, someone who always has
had good far distance vision gradually, or even suddenly, notices that his/her far
vision is beginning to blur. Often, one eye will experience a change first; then, with
time, the other eye will follow. A person in this situation most likely is a victim of
“nearpoint stress,” which eventually can manifest itself in myopia (nearsightedness)
or blurred distance vision.

Although nearpoint stress is more common in students, from elementary school


through college, it can occur at any age in the eyes of somebody performing extended
periods of near work. This especially can be the case when there are not proper
breaks to rest the eyes.

Besides eyelid twitching, eyestrain, and headaches, one of the first symptoms of
nearpoint stress is noticed when looking up from a long period of close work,
discovering that things are a little blurry across the room. In the initial stages of
nearpoint stress, far away objects will clear up gradually (as the ciliary muscles slowly
relax).

However, with maintained nearpoint stress over time, far distance vision will remain
blurry (because the ciliary muscles are unable to relax completely). Myopia will have
begun to become “embedded” within the accommodative system of the eye(s), and far
away vision will be compromised when trying to read such things as words written on
the blackboard at school, food section signs down the aisles of supermarkets, or street
and freeway signs at night.

The mechanics of nearpoint-stress-induced myopia vary from person to person. In


most cases, though, the intraocular ciliary muscle controlling the eye’s crystalline lens
goes into a spasm (known as “ciliary spasm”). At first, this can be temporary. With
time, if the stress is not relieved, this can become more permanent. This can cause the
crystalline lens of the eye to take on and lock into a fatter, thicker shape (from front to
back), resulting in myopia. This is not equated with a deterioration of the ciliary
muscle but, rather, is due to a continual overaction of this muscle.

Too much near work, without giving the eyes frequent and sufficient breaks to view
things across the room or further away, may result in an “over-heating” of the ciliary
muscle of the eye. This excess heat can be transmitted into the vitreous humor and,
over time, may cause pockets of this gel-like substance to soften. Immobile organic
debris (known as “floaters”), located in some areas of the vitreous, then may begin to
move around.

If these particles migrate toward the center of the vitreous, they can cast shadows on
the retina, resulting in the impression of “spots” or “dots” before the eyes. Floaters
tend to be more prevalent in people with high myopia.

Another consequence of prolonged near work can be a spasming of the ciliary muscle,
which in turn can cause a constant overly convex shaping of the crystalline lens,
which in turn will cause images to focus in front of the retina when viewing distant
objects: myopia. This is the most common cause of nearpoint-stress-induced myopia.

Often, rather than both eyes being overworked an equal amount, the person’s
dominant eye will tend to perform a disproportionate amount of the near work,
resulting in the onset or progression of myopia only or mostly in that eye. To some
extent, this difference in the eyes, if great enough, also can hinder one’s depth
perception.

A thorough ocular examination by a qualified, knowledgeable eye doctor usually can


detect even the slightest degree of nearpoint stress in an eye. The doctor may suspect
nearpoint stress when a comparison with previous (especially within the past year or
so) measurements of the eye’s refractive error indicates a change toward myopia.

The primary means of preventing nearpoint stress should be to attempt to reduce or


eliminate the strain on the ciliary muscles of the eyes during long periods of close
work. First and foremost, it is extremely important to keep near objects as far away as
possible from the eyes when viewing them for more than a few minutes at a time.
Good lighting on a page and proper brightness on a computer monitor can be an
essential key in creating good contrast, thus making text clear enough to help motivate
a person to maintain the proper viewing distance.

The closer an object is to the eyes, the more effort the ciliary muscles must exert for
the eyes to focus clearly on that object, accordingly producing more strain on the
intraocular muscles and, often, headaches. Thus, it is imperative to do these things:

• sit up straight (rather than hunched over) when writing;


• keep paper away from the eyes (that is, do not bring it close to
the face) when reading; and
• maintain at least an arm’s-length distance between the eyes
and a computer monitor (rather than leaning forward) when
typing or reading; a further distance is even better.

Reading and writing material should be kept at least 20 inches away from the eyes,
and a computer monitor should be no closer than 25 inches away—the further, the
better. Occasionally, a glare-free screen can be helpful in reducing ocular discomfort;
but viewing a regular screen at a comfortable distance is more beneficial than
decreasing screen glare when trying to minimize nearpoint stress.

Usually, simply looking up across the room or out of a window frequently (for a few
seconds every few minutes) should relax the ciliary muscles sufficiently to prevent
nearpoint stress. When looking up and away, if distant objects are blurry, this is a
sign that nearpoint stress has been occurring.

One should not resume a near task at least until one’s far vision has become clear.
Sometimes looking alternately from far to near and then to far again, back and forth a
few times, will enhance the flexibility of the ciliary muscles and decrease the chance
of a cilary spasm.

Commonly, minus lenses are prescribed for a person with myopia, even in the initial
stages, enabling him/her to see clearly far away. However, when these glasses are
worn to do near work, it increases the amount of nearpoint stress, since the eyes
already have attempted to adapt to a near distance without the glasses. Thus, if the
person wears the new glasses (which focus the eyes at a far distance) while doing all
near work, it actually can accelerate the progression of the myopia.

If eyestrain, eyelid twitching, headaches, and/or temporary distance blur frequently is


noticed after near work, it may be that a pair of “reading” glasses, prescribed by a
qualified eye doctor, even prior to the onset of presbyopia, will be helpful in
preventing or reversing myopia induced by nearpoint stress. Another option is
bifocals, where the top portion of the lenses contains the far prescription and the
bottom portion the near prescription. The idea behind a reading prescription is that
these convex (plus) lenses, while performing near visual tasks, will refocus the
entering light, thus doing some of the focusing for the person’s crystalline lenses and
reducing some, or even all, of the ongoing stress on the ciliary muscles.

In most cases, the relief of tension on the focusing system, via the use of the proper
plus lens prescription for near work, is enough to prevent over-contraction of these
intraocular muscles and, thus, avert a nearpoint-stress event. Sometimes, a regimen of
certain vision therapy techniques can be done to reverse the effects (including low
myopia) of the nearpoint stress. Prevention or reversing of nearpoint-stress-induced
myopia, though, is much more likely to occur very soon after the onset of the
condition, rather than at a later point. If the myopia has been embedded too deeply
into the eyes’ focusing system, it can be very difficult, or impossible, to reverse.

It has been theorized that in some cases of nearpoint stress, the cornea of the eye
takes on a “steeper” (more convex) shape, due to prolonged pressure behind it. If so,
the pressure may be due to frequent anterior-to-posterior expanding of the eye’s
crystalline lens from focusing too much at near, inducing a compression of the
aqueous fluid anterior to the lens and, thus, resulting in pressure on the posterior
cornea.

That a change in corneal shape may be a factor in some types of nearpoint stress may
be evidenced by the fact that, in many cases, rigid contact lenses can retard or stop the
progression of myopia. Apparently, in such cases, the rigid lens prevents the anterior
cornea from becoming more convex, thus arresting the advancement of myopia in the
eye.

If the latter pressure on the cornea can occur from nearpoint stress, similar pressure,
theoretically, could occur behind the crystalline lens of the eye, being transmitted
through the vitreous gel and then to the retina. If so, it may be, in some cases, that
the retina and the back of the eye (the sclera) gradually are pushed posteriorly,
eventually resulting in a lengthening of the eyeball and in the onset or increase of
myopia.
presbyopia
After age 40 in most people, and by age 45 in virtually all, a clear, comfortable focus
at a near distance becomes more difficult with eyes which see clearly (whether with or
without glasses) at a far distance. This normal condition is known as “presbyopia,”
and it is due both to a lessening of flexibility of the crystalline lens and to a
generalized weakening of the ciliary muscle which causes the lens to accommodate
(change focus).

By the time one reaches age 65 or so, the crystalline lens is virtually incapable of
changing shape. Unless one is nearsighted, it is not possible to focus objects (such as
print on a page) clearly at even an arm’s length distance.

Interestingly, the first symptom of presbyopia often is not blurred print or eyestrain
while reading. Rather, one may observe that objects across the room appear
momentarily blurry after looking away from a near distance (that is, after reading,
writing, or viewing a computer screen for awhile). This is because the crystalline
lenses within the eyes have become less flexible than they used to be, resulting in their
being less able to accommodate (change focus) from near to far.

With time, it will take longer and longer to refocus objects far away after having done
close work. Nearpoint stress can intensify and accentuate this process.

Eventually, if presbyopic eyes are forced to continue to focus unwillingly at near,


one’s far vision will become and remain noticeably blurry. For a person who never
had to wear glasses to see clearly far away, myopia (nearsightedness) and/or
astigmatism will have set in, requiring a far-distance prescription in glasses or contact
lenses to see clearly again. For a person who already is myopic, the degree of
nearsightedness will have increased, requiring a stronger lens prescription to regain
clear vision.

A myopic (nearsighted) person with presbyopia often can remove his/her glasses to
focus clearly at near. If this is too inconvenient, he/she can obtain multifocal or
progressive addition lenses to be able to focus clearly at far and near with the same
pair of glasses.

When a person wearing single-vision contact lenses develops presbyopia, it will be


necessary to wear some type of reading prescription (in glasses) over the contacts to
achieve and maintain a clear, unstrained focus at near. In many cases, bifocal or
aspheric contact lenses can provide adequate vision at far and near distances, without
the use of glasses.
For some people, one eye (usually the dominant eye) may be fit with a contact lens
focusing that eye for far away viewing and the other eye fit with a lens focusing that
eye for near viewing. This is called a “monovision” fit. However, with this
arrangement, one’s depth perception (which is important when driving) may be
compromised to some extent.

Note that “presbyopia” is not the same as “hyperopia” or farsightedness. Presbyopia


is an age-related condition, resulting in difficulty keeping a clear, comfortable focus
at a near distance, even with an eye which is not hyperopic (farsighted). On the other
hand, hyperopia is a refractive error which makes it more difficult than normal to
maintain a focus at a near distance than at a far away distance at any age (although, if
one has a moderate to high degree of hyperopia, even maintaining a clear focus far
away is difficult).

A hyperopic (farsighted) person with presbyopia generally must acquire reading


glasses for near work, or else multifocal or progressive addition lenses for full-time
wear. In some cases, a “monovision” contact lens arrangement also may be
appropriate for a hyperopic person with presbyopia.

For some people with presbyopia, store-bought (non-prescription) reading glasses


may be an option. However, store-bought glasses have equal strengths in the right
and left lenses. Since most people’s eyes have at least slightly unequal refractive
errors, the focusing between their two eyes will not be balanced when wearing non-
prescription readers. Thus, one or both eyes may experience eyestrain. Headaches
also may result.

The amount of presbyopia inevitably increases with age. Therefore, the additional
“plus power” of the lens strength required to maintain a clear, unstrained focus at near
will need to be increased every few years to compensate for the irreversible effect of
the presbyopia.

cataract
Normally, all the layers of the crystalline lens are clear, and light passes through it
unobstructed. However, with age or due to certain systemic diseases, as well as with a
cumulative absorption of ultraviolet radiation over many years, the lens material can
become cloudy, yellow, brown, and even opaque. Anything in the lens which
obstructs entering light is referred to as a “cataract.”

More than 50% of people over the age of 60 have some form of a cataract. It has been
said that if one lives long enough, he/she will develop a cataract. Even some infants
are born with a “congenital” cataract which, if left untreated, can cause permanent
visual impairment or blindness, even if the cataract is removed years later.

It is not possible to remove a primary cataract without irreparably damaging the


crystalline lens within which the cataract is contained. A laser cannot be used
successfully to remove a cataract, except as described later (in the case of
a secondary cataract). Therefore, cataract surgery involves removing most or all of
the lens of the eye and replacing it with an artificial “intraocular lens” or “lens
implant,” made of a hard plastic (polymethyl methacrylate or PMMA), silicone,
acrylic, or hydrogel material.

An “extracapsular” cataract extraction (ECCE) is the routine type of cataract


removal. In an ECCE procedure, an opening is made in the front of the lens capsule.
Through this opening, the lens nucleus is removed, either as a whole or by dissolving
it into tiny pieces and vacuuming out the pieces, a procedure called
“phacoemulsification.” Next, the lens cortex also is sucked out, leaving the lens
capsule in place, and into the lens capsule is inserted the artificial lens implant.

Prior to the 1980’s, the entire crystalline lens was removed in a cataract surgery,
called an “intracapsular” cataract extraction (ICCE). Usually, this was performed
using “cryoextraction,” where a cryoprobe froze the entire lens, permitting its
complete removal. Now, in the unusual case of an intracapsular lens extraction, or
ICCE, the implant lens is placed in front of the iris, rather than behind it, because
there is no lens capsule to hold the implant in place. Rarely is this procedure done
anymore.

Approximately 1-2% of post-cataract extraction patients develop swelling in the area


of the retina responsible for central vision (themacula). This swelling occurs in
cystoid spaces, and is referred to as cystoid macular edema. After an initial
improvement following surgery, these patients subsequently will describe blurred
vision. Cystoid macular edema can occur as early as days, or as late as several years,
following surgery. Treatment options include observation, topical therapy, periocular
injections, and surgery.

Naturally occuring carotenoids in the crystalline lens—


lutein and zeaxanthin (molecular cousins of beta carotene and vitamin A)—have been
shown to reduce the risk of cataracts. These pigments act as antioxidants within the
lens, inhibiting the formation of free radicals, which can damage lenticular material
and contribute to the development of cataracts.

Thus, it may be that the greater the amount of antioxidants such as lutein and
zeaxanthin in the system, the less the risk of cataract formation. These two
antioxidants are found particularly in yellow fruits and in green leafy vegetables
(especially xanthophyll-rich vegetables such as spinach, kale, collard greens, and
broccoli), in eggs, and as nutritional supplements.

secondary cataract
Not uncommonly, following an “extracapsular” cataract extraction (ECCE), a few
cells of the crystalline lens cortex remain adhered to the inner surface of the posterior
lens capsule. After a few weeks or months, these cells can become opaque, resulting
in a secondarycataract. Fortunately, the eye does not have to be reopened for this
simple cataract to be removed.

Rather, a YAG (yttrium aluminum garnet) laser is used, in a procedure taking only a
few minutes, to fire through the clear cornea andpupil and to obliterate the secondary
cataract (and a small portion of the capsule behind it). This enables light to pass into
the eye again, unobstructed. If this laser procedure is successful, a cataract never
again should pose a problem for that eye.
Anatomy, Physiology Ted M. Montgomery,
and Optometric
Pathology of the Human Physician
The Macula Eye

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The macula lutea is the small, yellowish central portion of the retina. It is the area
providing the clearest, most distinct vision. When one looks directly at something, the
light from that object forms an image on one’s macula. A healthy macula ordinarily is
capable of achieving at least 20/20 (“normal”) vision or visual acuity, even if this is
with a correction in glasses or contact lenses.

Not uncommonly, an eye’s best visual acuity is 20/15; in this case, that eye can
perceive the same detail at 20 feet that a 20/20 eye must move up to 15 feet to see as
distinctly. Some people are even capable of 20/10 acuity, which is twice as good as
20/20. Vision this sharp may be due to there being more cones per square millimeter
of the macula than in the average eye, enabling that eye to distinguish much greater
detail than normal.

fovea centralis
The center of the macula is called the fovea centralis, an area where all of the
photoreceptors are cones; there are no rods in the fovea. The fovea is the point of
sharpest, most acute visual acuity. The very center of the fovea is the “foveola.”

Because the fovea has no rods, small dim objects in the dark cannot be seen if one
looks directly at them. For instance, to detect faint stars in the sky, one must look just
to one side of them so that their light falls on a retinal area, containing numerous rods,
outside of the macular zone. Rods detect dim light, as well as movement.

There are about 110,000 to 115,000 cone cells in the fovea and only about 25,000
cones in the tiny foveola. The macular/foveal area is the main portion of the retina
used for color discrimination. Color vision deficiencies, which occur in less than 8%
of males and in less than 1% of females, are usually hereditary, although they also can
result from certain diseases, injury, or as a side effect of some medications or toxins.

The closer one’s cones are clustered together as a group, within the macula, the
sharper that person’s vision, potentially, will be. Some people’s cones are “spread
out” more (resulting in lesser acuity), while other people’s cones are more “clumped
together” (resulting in better acuity). It is quite possible, even common, for someone
to have a visual acuity better than 20/20, such as 20/15 or even 20/10 (see 20/20
compared with other acuities).

Basically, the denser the arrangement of cones is, the sharper the acuity. This is
because the incoming light is falling on more of the cones, so more information about
the object being viewed (and being projected as an image upon the retina) is
transmitted to the brain.

color vision
To see any color, the retinal cone cells first must be stimulated by light. “Red-
sensitive” cones are most stimulated by light in the red to yellow range, “green-
sensitive” cones are maximally stimulated by light in the yellow to green range, and
“blue-sensitive” cones are maximally stimulated by light in the blue to violet range.
Accordingly, due to their respective sensitivities to long (L), medium (M), and short
(S) wavelengths, they also are referred to as “L” cones, “M” cones, and “S” cones.

Collectively, the photoreceptors in the human eye are most sensitive to wavelengths
between 530 and 555 nanometers, which is bright green tending toward yellow. The
human visual system can detect the range of light in the visible spectrum from about
400 nanometers (violet) to about 700 nanometers (red).
“Red-sensitive” or “L” “Green-sensitive” or “M”
cones cones

“Blue-sensitive” or “S” cones

The brain must compare the input from the three different kinds of cone cells, as well
as make many other comparisons. This comparison begins in the retina (which
actually is an extension of the brain), where signals from “red” and “green” cones are
compared by specialized red-green “opponent” cells.

These opponent cells compute the balance between red and green light coming from a
particular part of the visual field. Other opponent cells then compare signals from
“blue” cones with the combined signals from “red” and “green” cones. When one
type of cone does not work properly, the proper color calculations, by the brain,
cannot take place.

color deficiency
If all of the cone receptors work, but one type does not work as well as the other two,
an “anomalous trichromatism” results, as follows:

• protoanomaly: a weakness in the long wavelength (“red” or


“L”) cones, where more long wavelength light is required in
order to perceive colors the same as a person with normal
color vision;
• deuteranomaly: a weakness in the medium wavelength
(“green” or “M”) cones, where more medium wavelength light
is required in order to perceive colors the same as a person
with normal color vision; and
• tritanomaly: a weakness in the short wavelength (“blue” or
“S”) cones, where more short wavelength light is required in
order to perceive colors the same as a person with normal
color vision.

When one type of cone receptor does not work at all, an “anomalous dichromatism”
results, as follows:

• protanopia: a lack of the receptors sensitive to long (reddish)


wavelengths of light; difficulty distinguishing between
blue/green and red/green;
• deuteranopia: a lack of the receptors sensitive to medium
(greenish) wavelengths of light; difficulty distinguishing
between red/purple and green/purple, and
• tritanopia: a lack of the receptors sensitive to short (bluish)
wavelengths of light; difficulty distinguishing between
yellow/green and blue/green.

When only one type of cone receptor functions, the color deficiency is
“monochromatism.” Very few people (about 3 in a million) have total “color
blindness” or “achromatopsia”; they see things only in shades of white, gray and
black.

Color deficiencies usually are genetic. However, sometimes such deficiencies are
acquired due to retinal diseases such as glaucoma or diabetes, or by retinal poisoning
by certain medications.

About 7% of males have a red-green deficiency, compared to about .4% of females.


The genes for the red and green receptors (cones) are carried on the X chromosome
(from the mother). As a result, a male with a defect in one of these genes does not
have another X chromosome to compensate (since his other sex chromosome is Y,
from his father) and, therefore, will be color deficient.

On the other hand, a female has two X chromosomes. If one X chromosome has a
defective gene, her other X chromosome, as a rule, will have a compensating normal
gene, enabling her to have normal color perception.
With a red-green deficiency, a person might have difficulty distinguishing between
things such as red and green traffic lights or electrical wiring. Red-green color
perception is altered in conditions such as optic neuritis. In some cases, a reddish “X-
chrome” contact lens, worn on the non-dominant eye, can help a red-green color
deficient person discern more easily between colors.

People with a less common type of deficiency cannot distinguish between blues or
yellows. The gene for the blue receptor (cone) is carried on Chromosome #7. Blue-
yellow color vision is diminished in many disorders, including glaucoma, diabetic
retinopathy, cataract, and retinal disease.

You might wish to screen your color vision. If so, go to Color Vision Testing.

macular degeneration
Certain conditions can affect the macula and, in turn, one’s central vision. Probably
the most common is “macular degeneration,” a hereditary ocular disease. Age-related
macular degeneration (ARMD) is the leading cause of irreversible blindness among
Americans 65 and older.

“Dry” macular degeneration generally is caused by a thinning of the macula’s layers,


and vision loss typically is gradual. However, tiny, fragile blood vessels can develop
underneath the macula.

“Wet” macular degeneration can result when these blood vessels hemorrhage, and
blood and other fluid further can destroy macular tissue, even causing scarring. In this
case, vision loss can be rapid—over months or even weeks—as well as very
devastating.

Macular tissue destroyed by either dry or wet macular degeneration cannot be


repaired. In the case of the wet form, a special laser can be used to seal the leaking
blood vessels in the retina. However, 1) the tiny spots where the laser burns the retina
will lose vision permanently, and 2) other blood vessels may leak in the future,
requiring further laser treatment.

The earliest symptom of macular degeneration usually is persistently blurred vision.


As more cells of the macula are destroyed, objects become distorted (for instance,
straight lines become crooked). Eventually, a small area of no vision, in the central
visual field, can develop and grow in size. This can progress to the point of
“doughnut” vision, where people’s faces are unrecognizable when looking directly at
them, yet peripheral vision remains unaffected.
Naturally occuring carotenoids in the macula, lutein and zeaxanthin (molecular
cousins of beta carotene and vitamin A), have been shown to be effective protectants
against degeneration of the macula. These pigments essentially act built-in macular
“sunglasses” by absorbing, and filtering out, near-to-blue ultraviolet radiation, which
potentially is the most damaging electromagnetic radiation reaching the macula.

Thus, the greater the amount of macular pigment there is, the less the risk is for
developing macular degeneration. Lutein and zeaxanthin are found particularly in
yellow fruits and in green leafy vegetables (especially xanthophyll-rich vegetables
such as spinach, kale, collard greens, and broccoli), in eggs, and as nutritional
supplements. ARMD vitamins may reduce the likelihood of progression of
intermediate and advanced degrees of macular degeneration.

It is suspected that VEGF (vascular endothelial growth factor) stimulates the


development and progression of neovascular ARMD. Lucentis and Avastin, both
injected medications, may halt or stop the progression of ARMD and seem to
be promising treatments for ARMD.

Amsler grid
A good way to detect early stages of macular degeneration (as well as some cases of
cystoid macular edema, central serous retinopathy, and macular pucker) is with an
“Amsler grid.” Two Amsler grids—one black-on-white and one white-on-black—are
shown below, following these instructions:

1. Situate one of the grids so that it is as close to the center of


this window frame as possible.
2. If you normally wear reading glasses or bifocals for near work,
put them on to view the grid.
3. Measure (or have someone else measure) a distance of about
20 inches from your eyes to the screen.
4. Cover your left eye, but do not close it or press on it.
5. With your right eye, stare directly at the spot in the center of
the grid, and do not look away from this spot.
6. As you notice the horizontal and vertical lines in your
periphery, see if you detect any of these things:
o curved lines
o distorted lines
o broken lines
7. Repeat the test with your other eye.
8. Repeat the testing on both eyes with the other grid.
If you have not noticed problems with your vision, yet you detected broken, curved,
or distorted lines (known as “metamorphopsia”) while using one or both of the above
Amsler grids, it could be that you have an early stage of macular degeneration.

Try doing the Amsler grid test later today or tomorrow. If the results are repeatable, it
probably would be a good idea to make an appointment to have your eyes examined
by a qualified eye doctor (optometrist, optometric physician, or ophthalmologist). In
any case, continue performing the Amsler grid test 2-3 times a week to monitor any
changes.

cystoid macular edema (CME)


Cystoid macular edema (CME) is a painless disorder affecting the macula. It is
marked by the presence of multiple cyst-like (cystoid) formations which cause edema
(swelling) in the macular area, resulting in blurred or decreased central vision.

Sometimes an eye with CME will be red and irritated, and a great deal of tearing may
occur. Also, the eye may be tender to the touch and sensitive to light.
Although the exact cause of CME is not known, it can accompany a variety of
diseases, such as retinal vein occlusion, uveitis, or diabetes. It also is present after
about 3% of cataract surgeries, often many months following the surgery, even if the
surgery had no complications.

If CME occurs in one eye, there is up to a 50% chance that it will appear subsequently
in the other eye. Fortunately, most people recover their vision after an indeterminate
period of time.

To confirm the diagnosis of CME, sometimes a test known as “fluorescein


angiography” is performed. During this procedure, a fluorescent yellow dye is
injected into the vein of an arm, and a series of retinal photographs are taken to show
pooling of the dye in the macular area with CME (or leakage of retinal blood vessels
in other conditions).

Retinal inflammation due to CME usually is treated with anti-inflammatory agents


(such as Indocin or a corticosteroid) and occasionally with diuretics (such as
Diamox). It may take weeks for there to be a noticeable improvement in vision.

Sometimes, the CME is caused by vitreous strands connected to and pulling on the
macula, in which case a YAG laser treatment, or even a vitrectomy (removal of the
vitreous), is required. Occasionally, the retinal inflammation and swelling from CME
can induce a secondary glaucoma, which must be treated as a separate condition.

central serous chorioretinopathy (CSCR)


Central serous chorioretinopathy (CSCR), a painless condition affecting the central
retina (macula or para-macular area), is caused by an accumulation of fluid under the
retina, causing blurry vision, distortion of shapes, and sometimes a change in the eye’s
refractive error (towards hyperopia). CSCR occurs when a small focal area of the
retinal pigmented epithelium becomes compromised and allows serous fluid, from the
choroidal vessels below, to leak underneath the retina, forming a sub-retinal “blister.”

The disorder affects mostly men in the age range of 20 to 50 and seems to be linked to
chronic stress, whether emotional or job-related, or even with steroid use. Some
experimental evidence suggests that high blood levels of epinephrine and cortisol
hormones may be indirectly responsible for some occurrences of CSCR.

Most cases of CSCR will resolve spontaneously in 3-6 months. However, about 40-
50% of the time, there will be recurrences of the condition. Even without a
recurrence, many people have residual symptoms after the first bout of CSCR, such as
visual distortion, decreased color and contrast sensitivity, and difficulty seeing at
night.

Fluorescein angiography may be performed to determine the site of serous leakage,


and laser photocoagulation may be used to shorten the duration of the disease
condition. However, laser treatment may produce a noticeable, permanent blind spot
and most likely will not decrease the chance of a recurrence.

epiretinal membrane (ERM)


An epiretinal membrane is scar tissue that forms over a portion of the retina.
Although uncommon, it usually results from a posterior vitreous detachment. There
are other names for an ERM:

• macular pucker,
• cellophane retinopathy,
• internal limiting membrane disease,
• surface wrinkling retinopathy,
• premacular fibrosis, and
• retinal wrinkle.

When a posterior vitreous detachment occurs, sometimes minor


damage can occur to the surface of the retina. This can stimulate
an inflammation, exudate, and leucocyte response. Various types of
cells—glial cells, retinal pigment epithelial cells, macrophages,
fibrocytes, and collagen cells—can accumulate and form a
transparent membrane of scar tissue.

With time, the scar tissue can tighten. This creates tension and traction on the retina
underneath, often causing it to wrinkle or pucker. If this is in the macular area, it
results in a macular pucker and sometimes macular edema. (If the macula actually
tears from too much traction by the vitreous gel, a macular hole can result. However,
a macular pucker will not “progress” into a macular hole.)

The deformation of the macula results in mild to severe blurriness and visual
distortion. Straight lines can appear curved or wavy; this can be detected by using
an Amsler grid. Usually only one eye is affected, although the other eye may be
involved later in a similar way.

In many cases, the resultant blurriness and distortion of an epiretinal membrane,


involving the macula, is mild enough that no treatment is necessary. Sometimes the
scar tissue membrane will separate from the retina/macula and float away from the
area, restoring vision.

Less frequently, the reduced vision from the macular distortion can have an adverse
affect on daily activities, such as reading and driving. No eye drops, medications, nor
nutritional supplements can improve the vision distorted by a macular pucker.

Instead, a vitrectomy must be performed, where the vitreous humor gel is removed.
The epiretinal membrane is peeled, very carefully, away from the retina. Then a
saline solution is injected to replace the vitreous gel.

Usually, following this procedure, at least half of the lost vision is restored. However,
one possible complication of the surgery, though uncommon, is retinal detachment.
More commonly, a cataract may develop in that eye sooner than it otherwise would
have.

Anatomy, Physiology Ted M. Montgomery,


and Optometric
Pathology of the Human Physician
The Iris Eye

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The iris, visible through the clear cornea as the colored disc inside of the eye, is a
thin diaphragm composed mostly of connective tissue and smooth muscle fibers. It is
situated between the cornea and the crystalline lens. The color(s), texture, and
patterns of each person’s iris are as unique as a fingerprint.

The iris is composed of 3 layers, from the front to the back:

1. endothelium,
2. stroma, and
3. epithelium.

The iris divides the anterior compartment, the space separating the cornea and the
lens, into 2 chambers:

• the larger anterior chamber (between the cornea and the


iris), and
• the smaller posterior chamber (between the iris and the
lens).
eye color
The color of the iris, established
genetically, is determined by the amount of
pigment present in the iris structure. No
pigment at all (in the case of an albino)
results in a pink iris. Some pigment causes
the iris to appear blue. Increasing amounts
of iris pigment produce green, hazel, and
brown irises (or irides).

There actually are two pigments, melanin and lipochrome, which determine eye
color. Melanin (brown) deposition is controlled by a gene on chromosome 15.
Lipochrome (yellowish-brown) deposition is controlled by a gene on chromosome 19.

Rarely, one iris can be a different color than the other iris. This is known as
“heterochromia irides” and is determined genetically. Also, a section of one iris may
be a different color from the rest of that iris; this is known as “heterochromia iridum”
or “sectoral heterochromia iridis.” Usually, if one of these conditions is present, it is
noticeable at birth, although various ocular pathologies can cause any of these
conditions to be present.

Unlike what commonly is believed, the iris does not change colors in an adult (except
in the case of certain pathologies, such as pigment dispersion syndrome). Iris color
may appear to change, depending upon the color of clothing a person is wearing on a
particular day. However, this presumed color change does not actually take place; it
is a misperception by the observer, often due to variations in lighting.

pupil
The iris acts like the shutter of a camera. In the middle of a normal iris is the pupil,
typically a circular hole, comparable to the aperture of a camera. The pupil regulates
the amount of light passing through to the retina, which is at the back of the eye.

As the amount of light entering the eye diminishes (such as in a dark room 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.” This allows 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) so that the eye can view something at a near distance. This reaction is
known as the “near reflex.” A representation of parasympathetic pathways in the
pupillary light reflex can be seen here: parasympathetic response. Sometimes the
pupil does not react properly, due to cranial nerve or muscle problems (seePupillary
Defects and Conditions Affecting the Face).

Watching television in a dark room gives some people eye aches or headaches. This
is because as the brightness of the television screen fluctuates considerably every few
seconds. This causes the dilator and sphincter iris muscles controlling the pupil to
have to work overtime, constantly adjusting the ever-changing levels of light entering
the eye.

Therefore, it is recommended that a uniform background light source is present in the


room while watching television. This will cause the pupils to be slightly constricted,
thus causing less variance in the size of the pupil as the television illumination
changes. As a result, the muscles controlling the pupil size should 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). Other structures, posterior to the iris, also
are part of the uveal tract. Thus, the uvea is composed of the following:

• iris,
• ciliary body (within which is the ciliary muscle that controls
the shape of the crystalline lens), and
• choroid (located underneath the retina and which contains the
retina’s blood supply).

iritis/uveitis/chorioretinitis
It is not uncommon for the iris, the entire uvea, and/or the choroid/retina complex to
become inflammed. Here are types of inflammation of the uveal tract:

• iritis: inflammation of the iris alone,


• iridocyclitis: inflammation of the iris and ciliary body,
• choroiditis: inflammation of the choroid alone,
• chorioretinitis: inflammation of the choroid and retina, and
• uveitis: inflammation of the entire uveal tract
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 (that is, a
systemic problem). Sometimes these (and other) diseases can cause uveal
inflammation: arthritis, tuberculosis, syphilis, ankylosing spondylitis, Reiter’s
syndrome, toxoplasmosis, histoplasmosis, cytomegalovirus (CMV), sarcoidosis, and
toxocariasis. 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 around the limbus (the junction of the
cornea and sclera), often is present when there is an iritis. Some people may see
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 develop as
a result of iritis and/or the medications used to treat the disorder.

malignant melanoma
A melanoma is cancer that forms in melanocytes, the cells that produce melanin.
Melanin is a pigment responsible for skin color and eye color. A nevus, containing
normal malanocytes, should be watched carefully, as it may develop into a malignant
melanoma.

Most commonly formed on the skin, a malignant meloma also can be found within the
eye, in the uveal tract, most commonly in the choroid, but sometimes in the iris. Less
commonly, a melanoma can form on the conjunctiva. Increased exposure to ultra-
violet radiation in sunlight often is a factor in melanoma formation in the skin and iris,
but probably not in the choroid.

A choroidal melanoma, forming just beneath the retina, usually pushes up the retina.
It can spread extensively throughout the choroid. The biggest concern is that the
malignant cells will metastisize (spread) to other areas of the body and cause
cancerous tumors elsewhere.

Large tumors, especially if they are near the optic nerve, are the most likely to
metastasize. An adverse affect on vision, as well as documented tumor growth over
time, also are risk factors for metastasis.

Small tumors generally are monitored for growth, using dilated fundus examinations,
photography, and ultrasound. Sometimes laser photocoagulation or transpupillary
thermotherapy (TTT) can be used to treat a small to medium tumor.

Medium to large tumors may be treated using a radioactive plaque (a small, gold-
covered device containing a radioactive source). It even may be necessary to
enucleate (remove) the eye completely, especially if tumor metastisis is suspected or
confirmed.

Anatomy, Physiology Ted M. Montgomery,


and Optometric
The Vitreous Pathology of the Human
Eye
Physician

Humor
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The vitreous humor is a clear gel which occupies the posterior compartment of the
eye, located between the crystalline lens and theretina and occupying about 80% of
the volume of the eyeball. Light initially entering the eye through the cornea, pupil,
and lens, is transmitted through the vitreous to the retina.

Vitreous humor has the following composition:

1. water (99%),
2. a network of collagen fibrils,
3. large molecules of hyaluronic acid,
4. peripheral cells (hyalocytes),
5. inorganic salts,
6. sugar, and
7. ascorbic acid.

hyaloid artery
The “hyaloid artery” (a branch of the primitive dorsal ophthalmic artery) grows, in the
fetus, outward from the optic cup of the optic nerve into the vitreous cavity. It extend
forward to the crystalline lens to aid its development.

The hyaloid artery regresses during the last trimester of fetal formation, leaving
behind the “Cloquet’s canal” through the vitreous. Sometimes, the hyaloid artery
remains after birth and is viewable by a doctor looking into the eye as a “persistent
hyaloid artery,” but it rarely is noticeable to the person who has it.

Sometimes, remains of the lenticular attachment of the hyaloid artery can be found on
the back surface of the crystalline lens. These tiny remnants appear gray or white and
are located just inferior and nasal to the posterior pole of the lens. These
“Mittendorf’s dots,” which are congenital (present at birth), continue throughout life.
They have no effect on vision.

posterior vitreous detachment (PVD)


With age, the vitreous humor changes from a gel to a liquid. As it does so, the
vitreous mass gradually shrinks and collapses, separating and falling away from
the retina. This is called a “posterior vitreous detachment” (PVD) and is a normal
occurrence between ages 40 and 70.

Commonly, a person having experienced a PVD will report seeing flashing lights
and/or floaters in his or her field of vision. The flashes of light occur when the
vitreous tugs on the sensory layer of the retina, as the vitreous is detaching. The
floaters—which are cells or debris released, when the vitreous detaches—can appear
as little dots, circles, lines, cobwebs, clouds, or a puff of smoke.

Floaters can be apparent especially when looking at a bright background, as the light
entering the eye casts shadows of the floaters onto the retina. Sometimes a large,
single floater actually can obstruct print that is being read. The observance of flashes
and floaters can last two or more weeks. Episodes lasting even as long as six months
can occur.

It is said that the percent chance of having a vitreous detachment is at least the same
as one’s age. However, a PVD may occur earlier than normal in moderately to
extremely nearsighted people, as well as in people who have had cataract surgery. A
dilated eye exam should be performed to make sure the symptoms are not due to
a retinal detachment, which is a much more serious and potentially sight-threatening
condition.
floaters (muscae volitantes)
As a posterior vitreous detachment (PVD) occurs—that is, as the vitreous fluid
separates from the retina—organic debris or particles known as “floaters” are
released. Another name for floaters is “muscae volitantes” (flying flies).

Most floaters are merely compressed cells or strands of the vitreous gel which have
clumped together so that they are less transparent than the rest of the vitreous. Some
floaters are remnants of the hyaloid artery, which usually disintegrates before birth.
These types of floaters are harmless.

Floaters sometimes interfere with vision, often during reading, and they can be quite
annoying. If a floater appears directly in the line of sight, the best thing to do is to
move the eye from side to side or up and down. Doing so can create a current within
the internal fluids to move the floater temporarily away from the line of sight.

If a floater is suspended in a portion of vitreous humor which is very viscous, it can be


particularly persistent and bothersome. Unfortunately, in most instances, there is
nothing to do but learn to tolerate the floater’s presence. Surgical removal, which is
risky, is considered only in the most extreme cases.

Usually, the vitreous makes a clean break as it pulls away from the retina. Rarely,
however, the vitreous will adhere tightly onto the retina in certain places; and a small,
often horseshoe-shaped rip in the retina can result from persistent tugging and tearing
by the vitreous. Unless the retinal tear is repaired, fluid can seep through this hole
into or underneath the retina and cause a retinal detachment, a very serious, sight-
threatening condition.

As the vitreous membrane tugs on the retina, at points where the two structures
remain attached, the tension can cause “flashing” sensations, because some of the
retinal nerves are stimulated. Occasional flashes of light usually are nothing to be
concerned about, unless they increase in frequency and/or occur in conjunction with a
sudden onset of a large number of floaters. In this case, it may be that a retinal
detachment has occurred.

asteroid hyalosis
Not uncommonly, tiny spherical or disc-shaped, “soapy” globs, can be located in the
vitreous of one eye or occasionally in both eyes. This is known as “asteroid
hyalosis.” When present, these calcium-containing lipid complexes usually are
suspended throughout the vitreous.
Usually, these “asteroids” are not observable by a person who has them, and they
normally do not cause any decrease in vision, since light generally passes through
them unaffected. Rarely, however, if the asteroids coalesce on the visual axis,
especially at or near the nodal point immediately behind the lens, there can be a
profound decrease in vision. In such a case, removal of the asteroids, via a
vitrectomy, is an option to restore vision.

Anatomy, Physiology Ted M. Montgomery,


and Optometric
Pathology of the Human Physician
The Conjunctiva Eye

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The conjunctiva is a clear mucous membrane that lines the inner surfaces of the
eyelids and and continues on to cover the front surface of the eyeball, except for the
central clear portion of the outer eye (the cornea). The entire conjunctiva is
transparent.

The conjunctiva is composed of 3 sections:

1. palpebral conjunctiva (covers the posterior surface of the


eyelids),
2. bulbar conjunctiva (coats the anterior portion of the eyeball),
and
3. fornix (the transition portion, forming the junction between
the posterior eyelid and the eyeball).

Although the palpebral conjunctiva is moderately thick, the bulbar conjunctiva is very
thin. The latter also is very movable, easily sliding back and forth over the front of
the eyeball it covers. Since it is clear, blood vessels are easily visible underneath it.

Within the bulbar conjunctiva are “goblet cells,” which secrete “mucin.” This is an
important component of the pre-corneal tear layer that protects and nourishes
the cornea.

conjunctivitis (pink eye)


An “infectious conjunctivitis” (or “pink eye”) is an inflammation of infected
conjunctiva. An infection typically is caused by a bacterium or a virus. Less
commonly, a fungus or an amoeba can cause the infection. The same bacteria and
viruses that cause colds, ear infections, and sinus infections also can cause an
infectious conjunctivitis. Even bacteria that cause sexually transmitted diseases
(STDs) such as chlamydia and gonorrhea can cause an infectious conjunctivitis.

Someone with an infectious conjunctivitis must be careful not to touch the infected
eye. If that occurs, it is imperative to wash the hands well, because the infection
easily can be transferred to the other eye and/or to the eyes of other people.

A “noninfectious conjunctivitis” is an inflammation of noninfected conjunctiva.


Unlike an infectious conjunctivitis, a noninfectious conjunctivitis cannot be spread to
someone else by hand-to-eye contact.

One type of noninfectious conjunctivitis is “irritant conjunctivitis.” It is caused by


irritants to the eye, such as pollution particles in the air, chlorine in swimming pools,
or an acid or base accidentally dropped or rubbed onto the eye.

More frequently, a noninfectious conjunctivitis is caused by an allergic reaction to


something. It can produce conjunctival redness, extreme itching, and excessive ocular
mucous production. This reaction, called “allergic conjunctivitis,” commonly is
caused by a seasonal allergy to pollen or plant bi-products, most often in the Spring
and Summer (“vernal conjunctivitis”). An allergic conjunctivitis also can be caused
by an allergic reaction to preservatives in eye drops or solutions.

An allergic conjunctivitis also can result from a reaction to proteins or other


contaminants deposited on the surface of contact lenses, most commonly extended
wear soft lenses. The latter can result in “giant papillary conjunctivitis” (GPC),
mostly evidenced by the appearance of large “papillae” on the superior conjunctival
tarsal plate (underneath the upper eyelid). Each papilla is a collection of lymphocytes
and plasma cells.

Elimination of conjunctival papillae often is not easy. Obtaining new contact lenses,
with reduced wearing time and with regular enzymatic cleaning of the lenses, is
recommended. Sometimes it is best to be refit with disposable soft lenses or with
rigid gas permeable (RGP) lenses. With these lenses, protein build-up is not as much
of a problem as it is with daily wear lenses, though it still can occur.

Many people develop callous-like thickenings of the conjunctiva on the front of the
eye, usually located on the nasal portion of the conjunctiva. Such eyes are susceptible
to irritation caused by dry climates (especially with windy conditions), as well as toxic
vapors, salt water spray, excessive exposure to the sun (ultraviolet radiation), and
even inadequate natural lubrication of the eye (tears).
There are 2 types of these raised, yellowish or yellowish-white patches. One type is a
“pinguecula” and the other a “pterygium.”

pinguecula
A pinguecula often is referred to as a fatty degeneration of the conjunctival tissue.
The fine, nearly transparent collagen fibers of the conjunctiva degenerate and are
replaced by thicker, yellowish, more durable fibers, sometimes containing calcium
crystals. This causes the elevated, yellow and sometimes glistening whitish area
located near the cornea.

There is no effect on vision from a pinguecula, which can appear after only a brief
exposure to damaging irritation, such as excessive dryness or sun (ultraviolet
radiation). The tissue damage increases with continued exposure. It might take only a
day or two to notice a new pinguecula but weeks or months for it to resolve.

Removing the source(s) of irritation and providing artificial lubricating drops may
shrink and eliminate pingueculae in their early stages. However, long-standing
pingueculae do not respond well to treatment and may be permanent.

pterygium
A pterygium, although produced by the same things which cause a pinguecula, often
has inflammed blood vessels infusing into it. A pterygium does not emerge from a
pinguecula.

Unlike a simple pinguecula, a pterygium often is progressive and will involve


the cornea, if left unchecked. It is triangular in shape, with the base of the triangle
located in the conjunctiva and the apex of the triangle encroaching onto the cornea. A
pterygium virtually always is located on the nasal conjunctiva.

With corneal involvement, even if arrested surgically, a pterygium can affect vision
by warping the surface of the cornea and inducing astigmatism. In some cases, the
pterygium actually may grow all the over to the central cornea, in front of the pupil,
and obstruct the entering light.

Removing the source(s) of irritation and providing artificial lubricating drops may
slow down or halt the growth of pterygia. However, sometimes surgical intervention
is necessary to prevent a further decrease in vision.

subconjunctival hemorrhage
A somewhat common condition, caused by direct or indirect trauma to the eye, is a
“subconjunctival hemorrhage.” This manifestss as a spot or pool of blood underneath
the clear conjunctiva. It can be seen in distinct contrast to the sclera or white part of
the eye. The hemorrhage may be present on only one side or on both sides of
the cornea, and it almost always is on only one eye, unless the trauma has affected
both eyes.

The trauma causing the hemorrhage may be due to a blunt hit, hard coughing,
pushing, straining, heavy lifting, or even hypertension. Any of these things can cause
a small blood vessel to break and to leak blood underneath the conjunctiva. A
subconjunctival hemorrhage is one of the worst looking things that is harmless and
will not affect vision. No treatment is necessary. The blood should reabsorb and
disappear in 1-2 weeks, depending on the extent of the bleeding.
Anatomy, Physiology Ted M. Montgomery,
and Optometric
Pathology of the Human Physician
The Retina Eye

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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. That is, 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 gelatinousvitreous 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. nerve fiber layer (axons from ganglion cells traversing the
retina to leave the eye at the optic disc), and
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, and
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.

This 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). Then, amazingly, 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 (activated in photopic or bright conditions) and with
“rhodopsin” in rods (activated in scotopic or dark conditions), 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 packet of energy available) 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 one is most sensitive to a certain wavelength
of light: short (430 to 440 nm), medium (535 to 540 nm), and long (560 to 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 result in color deficiency;
whereas, defective or damaged rods result in problems seeing in the dark and at night.

retinal detachment (RD)


Normally, with age, the vitreous gel 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
beneath 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. Sometimes the floaters are described as being like a “shower of pepper”
before the eyes.

Sudden flashes of light, as well as a “web” or “veil” in front or else in the periphery of
the eye, also may appear in conjunction with the onset of floaters. The retinal tear and
subsequent detachment must be repaired as soon as possible, usually with one of these
procedures:

• sealing it using an argon laser (“photocoagulation”),


• freezing it (“cryotherapy” or “cryopexy”),
• securing it, after cryotherapy, with a tiny belt around the
equator of the eye (“scleral buckle” surgery),
• injecting a gas bubble into the eye (in conjunction with
photocoagulation or cryopexy) so that the bubble rests against
the hole or tear (“pneumatic retinopexy”), requiring the person
to keep his/her head in the same position for several days, or
• removing the vitreous gel and filling the eye with a gas
bubble or silicon oil (“vitrectomy”).

If the tear and detachment are not repaired, permanent vision loss
can result. The worst vision loss occurs if the macula becomes
detached.

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.”

Pupillary Defects and Conditions Affecting the Face


Afferent Pupillary Defect

• afferent pupillary fibers affected


• slight dilation of pupil with direct stimulation and cessation of direct
stimulation to the other eye (“Swinging Flashlight” test or Marcus-Gunn
Pupil)

Adie’s Syndrome
• fixed, dilated, tonic pupil
• weak or absent direct and consensual pupil reactions
• unknown etiology

Anisocoria

• unequal pupil sizes

Argyle-Robertson Pupil

• miotic pupils O.U.


• no direct or consensual pupil reflex
• near reflex normal
• suggests syphilis

Bell’s Palsy

• VII nerve damage


• paresis and drooping of one side of face

Cavernous Sinus Syndrome

• III, IV, V, VI nerves affected


• proptosis
• exophthalmos
• papilledema
• headache

Crocodile Tears

• misdirected nerve fibers after damage to facial nerve enervating the


lacrimal gland, resulting in tearing with anticipation of eating

Cushing’s syndrome

• steroid or adrenal gland induced


• moon face
• buffalo hump
• posterior subcapsular cataracts

Duane’s syndrome

• attempted adduction leads to retraction and ptosis

Efferent Pupillary Defect

• III nerve or pupillary muscle affected


• loss of consensual and direct pupillary reflex in affected eye
• consensual and direct pupillary reflex in unaffected eye

Foster-Kennedy Syndrome

• ipsilateral optic atrophy


• contralateral papilledema

Gradengo Syndrome

• VI nerve palsy
• esotropia
• V nerve irritation
• pain

Horner’s syndrome

• miosis
• ptosis
• anhydrosis
• enophthalmos
• lesion of the sympathetic pathway in the brain stem to cervical area

Marcus-Gunn Syndrome
• “jaw-winking” syndrome
• ptotic lid raises when ipsilateral pterygoid muscle is stimulated, as in
chewing, sucking, or opening the mouth
• amblyopia and strabismus common

Mobius Syndrome

• III, VI, VII nerve palsy (proptosis, ptosis, esotropia)

Oculogyric Crisis

• spastic upward conjugate movement of eyes


• head held back

Ophthalmoplegia – Internal

• III nerve paralysis


• dilated fixed pupils
• stroke

Ophthalmoplegia – External

• III, IV, and VI nerve damage


• muscle palsies
• no upgaze
• accommodative spasm

Parinaud’s Syndrome

• no upgaze
• nystagmus on attempted convergence
• pseudo-Argyll-Robertson pupils (large with sluggish reaction to light)
• bilateral papilledema common
• pinealoma and other tumours affecting the mid-brain, multiple sclerosis,
vascular lesions

Close Window
Color Vision Testing
Pseudoisochromatic plates frequently are used by eye specialists to get an idea of
one’s color efficiency or deficiency. The Ishihara color test, used to
detect protanopia and deuteranopia color deficiencies, was designed by Dr. Shinobu
Ishihara (1879–1963), a professor at the University of Tokyo.

The test includes several pseudoisochromatic plates, each composed of a pattern of


differently shaded dots. Within each pattern, a number is present.

To a color-deficient person, all the dots in one or more of the plates will appear
similar or the same—“isochromatic.” To a person without a color deficiency, some of
the dots will appear dissimilar enough from the other dots to form a distinct figure
(number) on each of the plates—“pseudoisochromatic.”

In the following plate, even a color-deficient person will be able to distinguish an


orange “25” on a turquoise background:

In the table below, click on each of the twelve links to view a new
pseudoisochromatic plate. Try to determine what number is encompassed within each
plate; then go to the answer to see if you are correct.

Afterwards, close the small window and return to this page to link to the next
pseudoisochromatic plate. Some of the numbers are difficult to see, even for people
with normal color vision. Just do your best!

Table of Pseudoisochromatic
Plates
Plate Plate Plate Plate
#1 #2 #3 #4

Plate Plate Plate Plate


#5 #6 #7 #8

Plate Plate Plate Plate


#9 #10 #11 #12

Plate Plate Plate Plate


#13 #14 #15 #16

If you missed being able to detect the number(s) in one or more of the above plates,
it may be that you have a color deficiency. It might be a good idea to obtain further
color vision testing by an eye care professional. Another site for color vision testing
is Colorblind Home Page.