Anatomy of an Eye

Click on a term in the eye graphics below to read a definition of it in the Glossary
of Ocular Terms. From there, in some cases, you can link to more information.

1
2
3
4
5
6

posterior compartment
ora serrata
ciliary muscle
ciliary zonules
canal of Schlemm
pupil

11
12
13
14
15
16

lenticular nucleus
ciliary process
conjunctiva
inferior oblique muscle
inferior rectus muscle
medial rectus muscle

21
22
23
24
25
26

central retinal vein

optic nerve
vorticose vein
bulbar sheath
macula lutea
fovea centralis

7
8
9
10

anterior chamber
cornea
iris
lenticular cortex

17
18
19
20

retinal arteries / veins

optic disc
dura mater
central retinal artery

27
28
29
30

sclera
choroid
superior rectus muscle
retina

The eye manifests its refractive power via several curved surfaces, each separated
by media with different indices of refraction. The most significant refractive
surfaces are the anterior and posterior cornea and the anterior and posterior
crystalline lens.
In the emmetropic eye (which has no refractive error), the range of corneal
refracting power is between 39 and 48 diopters, while the range of lenticular
refracting power is between 15 and 24 diopters. In the emmetropic eye, the axial
length (from the posterior corneal surface to the retina) varies from 22 to 26
millimeters, or approximately an inch.
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, 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 eyes 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 the crystalline 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 upsidedown).

The light continues through the vitreous humor, the clear gel that makes up about
80% of the eyes 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 eyes 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 eyes 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). Nevertheless, presbyopia eventually
will affect the near focusing of every.

eye growth

The average newborns 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 19 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 1 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 the superior & 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.

Eyeglasses & Optics

Anatomy, Physiology and

Pathology of the Human Eye
Ted M. Montgomery,
Optometric Physician

, or scroll down the page.

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Anatomy, Physiology & Pathology of the Human Eye

Eyeglasses consist of specially ground spectacle lenses, placed into frames to wear
on the face. The lenses are prescribed and ground to specific standards. These
lenses are convex on the front surface and concave on the back surface.

Typically, eyeglass lenses compensate for the refractive error of the person
wearing them, enabling that person to see more clearly far away, at near, or both.
Such lenses usually are prescribed to compensate for a refractive error (myopia,
hyperopia, and/or astigmatism). They also can be prescribed to compensate for an
extraocular muscle imbalance, usually a strabismus.
frames
Probably the oldest eyeglass frames known are recorded in a painting by di
Modena in 1352. These were represented as two lenses set in metal rims and
joined together centrally.
After many years, metal frames were replaced by leather rims. In order to avoid
the tiring necessity of holding up the glasses rims manually, they often were tied
by a tape inserted under ones hat.
Lornettes soon appeared to aid the support of eyeglasses. However, it was not
until the latter part of the 19th century that temple pieces were used on eyeglass
frames. Soon thereafter, frames with springs in their nosepieces were introduced.
About this time, a variety of materials such as gold, silver, horn, fishbone, wood,
and steel were introduced in the manufacturing of eyeglass frames. Today,
scientific materials are employed that are lightweight, non-reactive, long-lasting,
and comfortable.
diopters and focal length
The power or strength of a lens is measured in diopters (D). The reciprocal
(inverse) of the dioptric power of a lens equals the focal length, in meters, of the
lens. A plus lens converges light. A minus lens diverges light.
For instance, consider a convex or converging (plus) lens with a power of +1.50 D
(see illustration below). The focal length, f, of that lens will be:
f = 1 +1.50 D = 0.667 meter = 66

centimeters.

With parallel light rays from a distant source entering this convex lens, from the
left, these light rays will converge to a focus as they leave the lens. The rays of
light will form a real image at a focal point, F, 66 centimeters in back (to the
right) of the lens.
Now, consider a concave or diverging (minus) lens with a power of 1.50 D (see
illustration below). The focal length, f, of that lens will be:

f = 1 1.50 D = 0.667 meter = 66

centimeters.

Parallel light rays entering this concave lens, from the left, will diverge as they
emerge from the right side of the lens. A virtual image will be formed at a focal
point, F, 66 centimeters in front (to the left) of the lens.

Convex Lens forms

a Real Image at F

Concave Lens forms

a Virtual Image at F

If the two animations are not synchronized, reloading the page may help.

Obviously, the convex and concave lenses above would not work as eyeglass
lenses. Lenses worn in eyeglass frames are convex on the front surface and
concave on the back surface.
Below are depictions of two spectacle or eyeglass lenses:

a plus spectacle lens, which is thicker in the middle than on the edges,
and
a minus spectacle lens, which is thicker on the edges than in the middle.

Plus-Power
Spectacle Lens

Minus-Power
Spectable Lens

A plus lens compensates for hyperopia (farsightedness), while a minus lens

compensates for myopia (nearsightedness).

spherocylinder prescription
A lens prescription typically includes both a sphere (or spherical) component and
a cylinder (or cylindrical) component. This known as a spherocylinder (or
spherocylindrical) prescription.
The following is the typical format of a spherocylinder spectacle (glasses)
prescription, written in minus cylinder form:

OD = oculus dexter = right eye; OS = oculus sinister = left eye. In the above
prescription, for each eye,
1. the first number is the sphere or spherical component,
2. the second number is the cylinder or cylindrical component, and
3. the third number is the axis or axis of astigmatism component.
For OD, +1.25 D is the power of the lens in the 15 meridian, while +1.25 D 0.75
D = +0.50 D is the power of the lens 90 away, in the 105 meridian.
For OS, 0.50 D is the power of the lens in the 85 meridian, while 0.50 D 0.50
D = 1.00 D is the power of the lens 90 away, in the 175 meridian.
Here are optical crosses portraying the dioptric powers in the major meridians
for each lens:

sphere
The sphere or spherical component of a spectacle prescription indicates the degree
of hyperopia (farsightedness) or myopia (nearsightedness) in the axis meridian of
an eye. Plus (+) power indicates hyperopia, while minus () power indicates
myopia.

In OD (right eye) above, there is +1.25 D of hyperopia in the axis meridian (15).
In OS (left eye), there is 0.50 D of myopia in the axis meridian (85).
In the case where there is no cylinder component of a lens prescription (indicating
that the eye has no astigmatism, or maybe that the doctor has chosen not to
compensate for the astigmatism, in that eye, with the glasses), there is only a
sphere component to the prescription. For instance, if there were no cylinder
power in the above prescription, it commonly would be written as follows:

The DS notation means diopter sphere and indicates that there is no cylinder
(correction for astigmatism) in the lenses.
cylinder
The cylinder or cylindrical component of a spectacle prescription is an indication
of the amount of astigmatism in an eye. Astigmatism is the amount that the
refractive structures of the eye (primarily, the front and back surfaces of the cornea
and the front and back surfaces of the crystalline lens) vary or deviate from
sphericity or a spherical shape. That is, astigmatism indicates the degree of toricity
or cylindrical shape of all of the eyes refractive components, combined.

In OD (right eye) above, there is 0.75 D of astigmatism, so there is +1.25 D 0.75

D = +0.50 D of hyperopia in the 105 meridian (which is 90 away from the 15
meridian). In OS (left eye), there is 0.50 D of astigmatism, so there is 0.50 D
0.50 D = 1.00 D of myopia in the 175 meridian (which is 90 away from the 85
meridian).
Keep in mind that the power or strength of a glasses prescription is opposite to the
power of the eye itself, since the power of the glasses plus the power of the eye
equals zero. This means that, ideally, the light from a far away object passing
through the glasses, and then entering a non-accommodating eye, will be focused
on the retina. It is in this way that the glasses compensate for the eyes refractive
error.
Therefore, the powers of the two eyes for which the compensating glasses above
would be worn are as follows:

equivalent sphere
The equivalent sphere power of a lens prescription is the average of the dioptric
powers, in all meridians, of a lens. To obtain this value, add half of the cylinder
power to the sphere power. In other words, do the following:
1. Divide the cylinder power by 2.
2. Add this value to the sphere power.
3. The result is the equivalent sphere power of the lens.

For the glasses prescription

,
the equivalent sphere powers of each lens would be calculated as follows:
OD: +1.25 D + (0.75 D 2) = +1.25 D 0.375 D = +0.875 D
OS: 0.50 D + (0.50 D 2) = 0.50 D 0.25 D = 0.75 D.

minus cylinder vs. plus cylinder

An alternate way to write a spherocylinder prescription, which is equivalent to and
equally correct with the minus cylinder form, is the plus cylinder form. To
convert from minus cylinder to plus cylinder form, or visa versa, do the following:
1. Add the sphere and cylinder powers together; this becomes the new sphere power.
2. Change the sign of the cylinder power, from minus () to plus (+), or from plus (+) to minus ().
3. Change the axis value by 90, remembering that the axis must be a number from 1 to 180.

The following lens prescriptions, therefore, are equivalent and interchangeable:

Note that whether a lens prescription is written in minus cylinder or in plus

cylinder form, the equivalent sphere value of the lens is the same.

Visual acuity often is referred to as Snellen acuity. The chart and the letters are
named for a 19th-century Dutch ophthalmologist Hermann Snellen (18341908)
who created them as a test of visual acuity.
Ones visual acuity is an indication of the clarity or clearness of ones vision. It is
a measurement of how well a person sees. The word acuity comes from the
Latin acuitas, which means sharpness.
20/20 or 6/6 visual acuity
The reason that the number 20 is used in visual acuity measurements is because,
in the United States, the standard length of an eye exam room (that is, the distance
from the patient to the acuity chart) is about 20 feet.
In Great Britain, where meters are used instead of feet, a typical eye exam room is
about 6 meters long. Six meters is 19.685 feet, which is close to 20 feet, and
usually is considered to be close enough to optical infinity. Therefore, instead of
using 20/20 for normal vision, a notation of 6/6 is used in Britain.
Someone with 20/20 or 6/6 vision (visual acuity) is just able to decipher a letter
that subtends a visual angle of 5 minutes of arc (written 5') at the eye. (5' of arc is
5/60 of a degree, because there are 60' of arc in 1 degree.) What this means is that
if you draw a line from the top of a 20/20 letter to the eye and another line from the
bottom of the letter to the eye, the size of the angle at the intersection of these two
lines at the eye is 5' of arc.
Also, the individual parts of the letter subtend a visual angle of 1' of arc at the eye.
It does not matter how far away something is from the eye; if it subtends an angle
of 5' of arc at the eye, then a person with 20/20 visual acuity will just be able to
distinguish what it is.
A person with 20/20 vision could stand 30 feet away from a test chart and just
decipher a 20/30 letter on the chart, since at that distance a 20/30 letter would
subtend an angle of 5' of arc at the persons eye. That same person could stand 80
feet away from the chart and be able to decipher a 20/80 letter, or 200 feet away to
be able to decipher a 20/200 letter.
20/20 compared with other acuities
Someone with 20/20 visual acuity does not have perfect vision, since it is quite
possible to see better than 20/20. The less the bottom number in the visual acuity
ratio, the better the acuity; and the greater the bottom number, the worse the
acuity. Therefore, 20/15 acuity is better than 20/20 acuity, and 20/30 acuity is
worse than 20/20 acuity. Also, 20/15 acuity is equivalent to 6/4.5 acuity, while
20/30 acuity is the same as 6/9 acuity.

As noted before, although 20/20 is "normal" visual acuity for most people, it is
possible (and, in fact, very common) to be able to see better than that. For
instance, many people have 20/15 visual acuity. A person with 20/15 acuity can
stand 20 feet away from an object and see it as well as a person with 20/20 acuity
moving up to 15 feet away from the object to view it.
If that is true, lets take a person with 20/15 vision looking at an object from 100
feet away. Where would a person with 20/20 vision need to stand to see the object
just as well? The answer is 75 feet away from the object. (That is, 15/20 100
feet = 75 feet.)
It even is possible, although not too common, for someone to have 20/10 visual
acuity. Lets say a person with 20/20 vision can just detect a ship which is 25
miles away out on the ocean. A person with 20/10 acuity could be 50 miles away
from the ship and still be able to just detect it. That is, if a person with 20/10
acuity can just tell what an object is, a person with 20/20 vision would need to
stand half that distance away to be able to see what it is.
You can use the same rationale when considering someone with less than 20/20
acuity. Consider a person with 20/40 visual acuity (which is what someone needs
in most states to acquire a drivers license). If a person with 20/20 acuity can just
read a sign which is 60 feet down the road, the person with 20/40 acuity would
have to be 30 feet away to read the same sign. Also, a person with 20/15 acuity
could be 80 feet away, and a person with 20/10 acuity 120 feet away, to read the
same sign.
Compared to a person with 20/20 vision reading a sign 30 feet away, how far do
people with various visual acuities need to stand away from the sign to be able to
read it as well as the person with 20/20 acuity? See the following chart:
Visual Acuity

Distance Away
From Object

20/10

60 feet

20/15

40 feet

20/20

30 feet

(normal vision)

20/25

24 feet

20/30

20 feet

20/40

15 feet

20/50

12 feet

20/60

10 feet

20/80

7 feet

20/100

6 feet

20/200

3 feet

20/400

1 feet

near visual acuity

Besides a persons visual acuity being tested at a far distance, ones near acuity
also can be tested. Testing typically is done by holding a nearpoint Snellen acuity
card at 40 centimeters (about 16 inches). Just as on a far acuity chart, a 20/20 letter
on a near chart subtends a visual angle at the eye of 5' of arc (5 minutes of arc, or
1/12 of a degree).
Without a lens correction, a myopic (nearsighted) person generally will have better
visual acuity at near than at far, while a hyperopic (farsighted) person generally
will have better acuity at far than at near. Until the early to mid-forties, a person
with 20/20 distance acuity usually also has 20/20 acuity at near. However, once
presbyopia sets in, ones uncorrected near visual acuity decreases, creating the
need for reading glasses or bifocals.
size of a 20/20 letter
When an eye doctor sets up an examination room, care should be taken in
calibrating the size of the letters on the visual acuity chart (which usually is
projected onto a highly reflective screen).
The correct size of a 20/20 letter can be calculated using the diagram below, where

the letters visual angle subtended at the eye is 5' of arc (5 minutes of arc),
one-half of which is 2.5' of arc,
d is the distance (or virtual distance, if using a mirror), along the line of
sight, from the eye to the chart in feet, and
h is one-half the height of the 20/20 letter in millimeters.

As an example, lets say that the viewing distance, d, is 20 feet.

Since a right angle is formed by the line of sight and the plane of the acuity chart,
then simple trigonometry can be used:
1.
2.
3.
4.
5.
6.

2.5' of arc 60 = 0.04167

tangent 0.04167 = h d = h 20 feet
0.0007272 = h 6,096 millimeters
h = 0.0007272 6,096 millimeters
h = 4.433 millimeters
2h = total height of a 20/20 letter at 20 feet = 8.87 millimeters

In general, to find the size of a 20/20 letter (in millimeters), multiply .4433 by d
(where d is the viewing distance in feet). That is:
.4433 mm/ft d ft = height of 20/20 letter in mm.
optical infinity
When an eye is looking at a far away distance (such as at the horizon or at the
moon or at a star). The rays of light entering the eye are virtually parallel, and the
crystalline lens of the eye is thin and relaxed because, essentially, there is zero
accommodation.
When an optometrist or an ophthalmologist examines and performs a refraction on
someones eyes, it is optimal for the object being viewed (presumably an acuity
chart) to be as far away as possible from the patient. This is so that the incoming
rays of light are as close to parallel as possible, and the amount of accommodation
(increased curvature) of the crystalline lens of the eye will be negligible.
Due to space limitations, though, this viewing distance (= d in the diagram
above) can be only a few meters away from the patient in an examination room.
Therefore, the goal of an eye doctor should be to position the eye chart at optical
infinity, or the least distance at which there is no significant accommodation by
the crystalline lenses of a patients eyes.
Traditionally, optical infinity has been accepted to be 20 feet or, approximately, 6
meters. However, at this distance, there is an accommodative demand on the eye
of about 1/6 D (one-sixth of a diopter), which can be significant. For many people
(such as myself), an accommodative fluctuation during an eye examination of
more than 1/8 D can result in a variable endpoint in measuring a persons
refractive error, and 1/6 D is even greater than 1/8 D.

As a result, it is recommended that the viewing distance (d) in an examination

room should be long enough to create no more than a 1/8 D accommodative
demand on any patients eyes. I maintain, then, that optical infinity, for purposes
of examining the refractive error of the human eye, is at least 8 meters or 26 feet,
rather than merely 6 meters or 20 feet.
If lack of space is a problem, front-surface reflective mirrors usually can be
utilized to increase the virtual viewing distance in an exam room. From the
previous section, it can be seen that the height of a 20/20 letter on an acuity chart,
located at a viewing distance from a patients eyes of d = 26 feet, is as follows:
.4433 millimeters/foot 26 feet = 11.63 millimeters.
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.
2.
3.
4.
5.
6.

medial rectus (MR),

lateral rectus (LR),
superior rectus (SR),
inferior rectus (IR),
superior oblique (SO), and
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
Sherringtons 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 Rectus

LR = Lateral Rectus

SR = Superior Rectus

IR = Inferior Rectus

SO = Superior Oblique IO = Inferior 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 ringlike 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 Herings 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:

convergenceboth eyes moving nasally or inward

divergenceboth 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 ones 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 persons 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 strabismusesotropia and
exotropiaare displayed:
OD (Right Eye) Esotropia

OD (Right Eye) 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.

The Cornea

Anatomy, Physiology and

Pathology of the Human Eye
Ted M. Montgomery,
Optometric Physician

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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.
2.
3.
4.
5.

epithelium,
Bowmans (anterior limiting) membrane,
stroma (substantia propria),
Descemets (posterior limiting) membrane, and
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 eyes

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,
and
containing an enzyme called lysozyme which destroys bacteria and
prevents the growth of microcysts on the cornea.

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 eyes 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, Sjogrens syndrome,
keratoconjunctivitis sicca, xerophthalmia, lupus erythematosus, Graves
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
Keratoconuswhich is a combination of two Greek words: karato, meaning
cornea, and konos, meaning coneis 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.

The Optic Nerve

Anatomy, Physiology and

Pathology of the Human Eye
Ted M. Montgomery,
Optometric Physician

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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 and rods) in the optic nerve
head, this area of the retina cannot respond to light stimulation. As a result, it is
known as the blind spot, and everybody has one in each eye.
The reason we normally do not notice our blind spots is because, when both eyes
are open, the blind spot of one eye corresponds to 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 arms 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);
Lebers 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 the crystalline lens, through the
pupil (the central opening in the iris), and into the irido-corneal angle, the
anatomical angle formed where the iris and the cornea come together. Then the

fluid passes through the trabecular meshwork in the angle and leaves the eye, via
the canal of Schlemm.
If 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 the sclera 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 IOPs 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 IOPs 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 Quadrant Visual Field Loss
1. Inferior Quadrant

Superior Field

2. Superior Quadrant

Inferior Field

3. Temporal Quadrant

Nasal Field

4. Nasal Quadrant

Temporal 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 nerves
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.

The Crystalline Lens

Anatomy, Physiology and

Pathology of the Human Eye
Ted M. Montgomery,
Optometric Physician

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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.
2.
3.
4.

capsule,
subcapsular epithelium,
cortex, and
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
eyes 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 errorno hyperopia,
myopia, nor astigmatismor 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
Age

Amplitude of Accommodation

Nearpoint of Accommodation
(in an Emmetropic Eye)

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 ones 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 ones far-distance vision to become
clear again.
Sometimes, though, this process can undergo significant stress after having done a
few 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 food section signs down the aisles of supermarkets or, at night, street and
freeway signs.
The mechanics of nearpoint-stress-induced myopia vary from person to person. In
most cases, though, the intraocular ciliary muscle controlling the eyes 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-stressinduced myopia.
Often, rather than both eyes being overworked an equal amount, the persons
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 ones 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 eyes 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 intraocular
muscle strain 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 arms-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 awaythe 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 ones 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.
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. The idea behind such
a lens prescription is that these convex (plus) lenses, worn only while performing
near visual tasks, will refocus the entering light, thus doing some of the focusing
for the persons crystalline lenses and reducing some of the ongoing stress on the
ciliary muscles.
In most cases, the relief of tension on the focusing system, via the use of plus
lenses for near work, is enough to prevent over-contraction of these intraocular
muscles and, thus, avert a nearpoint-stress event. Prevention or reversing of
nearpoint-stress-induced myopia, though, is much more likely to occur very soon
after the condition has been discovered, 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 eyes
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 rigid contact lenses can retard or stop the
progression of myopia, in many cases. 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 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 arms 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,

ones 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, ones 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 peoples 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 1980s, 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 (the macula). 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 lenslutein 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 secondary cataract. 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 and pupil 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.

The Macula

Anatomy, Physiology and

Pathology of the Human Eye
Ted M. Montgomery,
Optometric Physician

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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 ones 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 eyes 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 ones cones are clustered together as a group, within the macula, the
sharper that persons vision, potentially, will be. Some peoples cones are spread
out more (resulting in lesser acuity), while other peoples 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. Redsensitive cones are most stimulated by light in the red to yellow range, greensensitive 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 cones

Green-sensitive or M 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, ones 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 maculas
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 rapidover months or even weeksas 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 peoples 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 gridsone black-on-white and one white-onblackare 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 eyes 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 cellsglial cells, retinal pigment

epithelial cells, macrophages, fibrocytes, and collagen cellscan 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.

The Iris

Anatomy, Physiology and

Pathology of the Human Eye
Ted M. Montgomery,
Optometric Physician

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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 persons 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 (see Pupillary 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 retinas
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, Reiters
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, goldcovered device containing a radioactive source). It even may be necessary to
enucleate (remove) the eye completely, especially if tumor metastisis is suspected
or confirmed.

The Vitreous Humor

Anatomy, Physiology and

Pathology of the Human Eye
Ted M. Montgomery,
Optometric Physician

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Anatomy, Physiology & Pathology of the Human Eye

The vitreous humor is a clear gel which occupies the posterior compartment of the
eye, located between the crystalline lens and the retina 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.
2.
3.
4.
5.
6.
7.

water (99%),
a network of collagen fibrils,
large molecules of hyaluronic acid,
peripheral cells (hyalocytes),
inorganic salts,
sugar, and
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 Cloquets 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
Mittendorfs 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
floaterswhich are cells or debris released, when the vitreous detachescan
appear as little dots, circles, lines, cobwebs, or clouds.
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 ones 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) occursthat is, as the vitreous fluid
separates from the retinaorganic 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 floaters 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.
Occasionally, 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.

The Conjunctiva

Anatomy, Physiology and

Pathology of the Human Eye
Ted M. Montgomery,
Optometric Physician

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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)
Bacterial or viral conjunctivitis (or pink eye) is an inflammation of irritated or
infected conjunctiva. Someone with such a 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.
An allergic reaction to something can cause conjunctival redness, extreme itching,
and excessive ocular mucous production. The reaction, called allergic

conjunctivitis or vernal conjunctivitis, can occur due to seasonal allergies

(usually in the Spring and Fall of the year).
Not uncommonly, allergic conjunctivitis can result from a reaction to proteins
deposited on the surface of contact lenses, most commonly daily 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.

The Retina

Anatomy, Physiology and

Pathology of the Human Eye
Ted M. Montgomery,
Optometric Physician

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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 gelatinous vitreous humor):
1. pigmented epithelium,
2. photoreceptors; bacillary layer (outer and inner segments of cone and rod
photoreceptors),
3. external (outer) limiting membrane,
4. outer nuclear (cell bodies of cones and rods),
5. outer plexiform (cone and rod axons, horizontal cell dendrites, bipolar
dendrites),
6. inner nuclear (nuclei of horizontal cells, bipolar cells, amacrine cells, and
Mller 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.
2.
3.
4.

sclera (white part of the eye),

large choroidal blood vessels,
choriocapilaris, and
Bruchs 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 nanometernmis 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 retinaan
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,

freezing it with cryotherapy, or
securing it with a tiny belt or scleral buckle around the equator of the
eye.

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.
Anisocoria:
It means that the pupil in the right eye and left eye are not the same size. A small amount of
anisocoria or difference in pupil size is normal. On some days, a persons right pupil might be larger
than the left and on other days, the pupils might be the same size or the left might be larger than
the right. But if more than a small difference in pupil size is present and persists, you may have a
neurologic problem.

The iris is the colored (brown, blue, etc.) portion of the eye and the pupil is the black, circular area in
the center of the iris.
The pupil is actually a hole in the iris which controls the amount of light that gets into the eye. In dim
light, the hole, or pupil, gets larger (dilates) to let in more light, while in bright light, the pupil gets
smaller (constricts) in order to protect the eye from too much light.
The size of the pupil is controlled by muscles in the iris
the iris dilator and the iris constrictor muscles. The
muscles are controlled by nerves from the brain to the eye.
Problems with these nerves cause the size of the pupil to be abnormal. A problem with the nerve
that normally dilates the pupil in the dark, causes a small pupil. A problem with the nerve that
normally constricts the pupil, produces an abnormally large pupil.
An Abnormally Small Pupil
The nerve that dilates the pupil in the dark, the oculosympathetic nerve, also controls a little muscle
that holds the eyelid open. When the oculosympathetic nerve is not working, the pupil on that side
is abnormally small and the upper eyelid droops a bit. This is called Horner Syndrome.
Although having Horner Syndrome by itself will not damage the eye or cause loss of vision, it may be
a signal of damage to one of the structures along the nerve. The nerves that dilate the pupils in dark
come in contact with many structures. They begin in the brain and pass down to the spinal cord.
They exit from the spinal cord and run up over the lung and into the neck, where they travel with the
carotid artery. They follow the carotid artery back into the
brain, from where they enter the eye and go to the dilator
muscle of the iris. Damage anywhere along this path will cause Horner Syndrome. It is important to
find out where the damage is and what is causing it because sometimes it can be serious. Examples
of serious conditions causing
Horner syndrome are a stroke in the brain or a tumor in the lung or a break in the wall of the carotid
artery called a carotid dissection. In other cases, the Horner syndrome is due to birth trauma.
Sometimes no cause can be found and the patient remains well.
Your doctor may do one or two eye drop tests to confirm that a Horner Syndrome is present and to
determine the location of the nerve damage. Detailed radiologic studies, usually magnetic resonance
imaging (MRI), are done to look at the places the nerves pass through for possible causes of the
damage.
An Abnormally Large Pupil
The nerve that goes to the constrictor muscle is part of the IIIrd cranial (oculomotor) nerve. The IIIrd
cranial nerve controls several of the muscles that move the eye. It also controls the muscle that
opens the eyelid and the muscle that constricts the pupil. A problem with the IIIrd nerve can result in
a droopy eyelid, double vision and/or enlarged pupil.
Pupil enlargement in addition to lid droop and eye muscle weakness may signal an aneurysm and is a
medical emergency. The patient should immediately have neuroimaging (CT, MRI, MRA, and/or
angiogram) to look for the aneurysm.
When only the pupil portion of the IIIrd nerve is not working, the pupil is large and does not constrict
in bright light. This might be caused by a medicine or chemical that dilates the pupil. Examples

include motion-sickness patches, chemicals used in the garden, and certain eye drops. The patient
often is unaware of what she touched that caused the problem but careful questioning by the doctor
may reveal the cause. A pupil that is chemically dilated will return to normal size as the chemical
wears off and eventually will react normally to light. Depending on the specific chemical, this can
take hours or days.
Adie Pupil is another type of pupil that is large and constricts poorly in light.
An eye with an Adie pupil initially has difficulty focusing on objects held close, for example, for
reading. Adie pupil is commonly seen in young adult women but men can develop it, too. In most
cases, the cause of the damage is unknown and radiology studies rarely show any abnormality.
A person can have Adie pupils in one or both eyes. Adie syndrome is the combination of Adie pupils
and reduced reflexes such as knee jerks. The cause of Adie syndrome, like Adie pupil, is unknown.
There is no treatment for Adie pupils. With time, the ability to focus up close usually returns. The
Adie pupil may remain enlarged but more often
shrinks in size gradually over several years, even becoming smaller than the normal pupil in the
other eye. The Adie pupil will never react well to a light shined in the eye. It is important that you
remember this for future eye exams.
Anisometropia:
is a condition where there is a significant difference in the
refractive errors of the two eyes. If this condition is present in infancy and is
undetected or untreated, it often results in the development of lazy eye or amblyopia in the more
hyperopic (far-sighted) eye. The greater the amount
of the difference, the more likely the development of lazy eye will be.Another problem can occur
when glasses are made for an anisometropic individual. The difference in the powers of the lenses
induce a prismatic difference that can cause double vision in off-center areas of the lens, which can
be compensated for by the use of slab-off prism.
A brighter right reflex indicates the need for glasses
Unequal refractive errors in the two eyes result in unequal vision. A brighter right reflex indicates the
need for glasses
Anisokonia:
A difference of the image size on the retina of each eye. It is due to anisometropia.

Dr Sarhan
World Medicine Forums