VISION

Refraction of Light

Refractive Index of a Transparent Substance:

Light rays travel through air at a velocity of about

300,000 km/sec, but they travel much slower
through transparent solids and liquids. The
refractive index of a transparent substance is the
ratio of the velocity of light in air to the velocity in
the substance.

The refractive index of air itself is 1.00. Thus, if light The Eye as a Camera
travels through a particular type of glass at a
The eye is optically equivalent to the usual
velocity of 200,000 km/sec, the refractive index of
photographic camera
this glass is 300,000 divided by 200,000, or 1.50
• It has a lens system: > a variable aperture
system – pupil
> retina that corresponds to the film

The lens system of the eye is composed of four

refractive interfaces:

1. the interface between air and the anterior

surface of the cornea.
2. the interface between the posterior surface
of the cornea and the aqueous humor.
3. the interface between the aqueous humor
and the anterior surface of the lens of the
eye.
4. the interface between the posterior surface
of the lens and the vitreous humor.

The internal index of air is:

Refraction – the bending of light rays at an
angulated interface 1. the cornea, 1.38;
2. the aqueous humor, 1.33
• Concave Lens Diverges Light Rays 3. the crystalline lens (on average), 1.40
• Convex lens converges light rays 4. the vitreous humor, 1.34
Measurement of the Refractive Power of a About two thirds of the 59 diopters of refractive
Lens— “Diopter” power of the eye is provided by the anterior
surface of the cornea (not by the eye lens)
• The more a lens bends light rays, the
greater is its “refractive power.” • The principal reason for this is that the
• This refractive power is measured in terms refractive index of the cornea is markedly
of diopters different from that of air.
Formation of an Image on the Retina Accommodation Is Controlled by
Parasympathetic Nerves:
In the same manner that a glass lens can focus an
image on a sheet of paper, the lens system of the The ciliary muscle is controlled almost entirely by
eye can focus an image on the retina. parasympathetic nerve signals transmitted to the
eye through the third cranial nerve from the third
The image is inverted and reversed with respect to
nerve nucleus in the brain stem.
the object.
Stimulation of the parasympathetic nerves
However, the mind perceives objects in the upright
contracts both sets of ciliary muscle fibers, which
position despite the upside-down orientation on the
relaxes the lens ligaments, thus allowing the lens
retina because the brain is trained to consider an
to become thicker and increase its refractive
inverted image as the normal.
power.

With this increased refractive power, the eye

focuses on objects nearer than when the eye has
less refractive power.

Consequently, as a distant object moves toward

the eye, the number of parasympathetic impulses
impinging on the ciliary muscle must be
Mechanism of “Accommodation”
progressively increased for the eye to keep the
The shape of the lens is changed from that of a object constantly in focus.
moderately convex lens to that of a very convex
“Depth of Focus” of the Lens System Increases
lens.
with Decreasing Pupillary Diameter
The mechanism is as follows:
• When a lens system has great depth of
About 70 suspensory ligaments attach radially focus, the retina can be displaced
around the lens, pulling the lens edges toward the considerably from the focal plane or the
outer circle of the eyeball. These ligaments are lens strength can change considerably
constantly tensed by their attachments at the from normal and the image will still remain
anterior border of the choroid and retina. The nearly in sharp focus.
tension on the ligaments causes the lens to remain • When a lens system has a “shallow” depth
relatively flat under normal conditions of the eye. of focus, moving the retina only slightly
away from the focal plane causes extreme
When the lens is in a relaxed state with no tension
blurring.
on its capsule, it assumes an almost spherical
• The greatest possible depth of focus
shape, owing mainly to the elastic retraction of the
occurs when the pupil is extremely small.
lens capsule.
(With a very small aperture, almost all the
As the lens assume a more convex shape, the rays pass through the center of the lens,
DIOPTER strength becomes greater. and the central most rays are always in
focus)
Emmetropia (Normal Vision) Correction of Myopia and Hyperopia by Use of
Lenses
• the emmetropic eye can see all distant
objects clearly with its ciliary muscle • If the refractive surfaces of the eye have too
relaxed much refractive power, as in myopia, this
• However, to focus objects at close range, excessive refractive power can be
the eye must contract its ciliary muscle and neutralized by placing in front of the eye a
thereby provide appropriate degrees of concave spherical lens, which will
accommodation diverge rays.

Errors of Refraction: Hyperopia

Conversely, in a person who has
(Farsightedness)
hyperopia—that is, someone who has too
• Hyperopia, which is also known as weak a lens system—the abnormal vision
“farsightedness,” is usually due to either an can be corrected by adding refractive
eyeball that is too short or, occasionally, a power using a convex lens in front of the
lens system that is too weak. eye.
• To overcome this abnormality, the ciliary
muscle must contract to increase the
strength of the lens.
• By using the mechanism of
accommodation, a farsighted person is
capable of focusing distant objects on the
retina.

In old age, when the lens becomes

“presbyopic,” a farsighted person is often
unable to accommodate the lens sufficiently to
focus even distant objects, much less near
objects.

Myopia (Nearsightedness)

• In myopia, or “nearsightedness,” when the

ciliary muscle is completely relaxed, the
light rays coming from distant objects are
focused in front of the retina.
• This is usually due to too long an eyeball,
but it can result from too much refractive
power in the lens system of the eye.
• A myopic person has no mechanism by
which to focus distant objects sharply on
the retina. However, as an object moves
nearer to the person’s eye, it finally gets
close enough that its image can be
focused. Then, when the object comes still Astigmatism:
closer to the eye, the person can use the
• is a refractive error of the eye that causes
mechanism of accommodation to keep the
the visual image in one plane to focus at
image focused clearly.
different distance from that of the plane at
• A myopic person has a definite limiting “far
right angles.
point” for clear vision
• most often results from too great a
curvature of the cornea in one plane of the
eye.
• It is obvious that light rays passing through • The reason for this is that the tears
an astigmatic lens do not all come to a between the contact lens and the
common focal point, because the light rays cornea have a refractive index almost
passing through one plane focus far in front equal to that of the cornea, so that the
of those passing through the other plane anterior surface of the cornea no longer
• The accommodative power of the eye can plays a significant role in the eye’s
never compensate for astigmatism optical system
because, during accommodation, the
*Instead, the outer surface of the contact lens
curvature of the eye lens changes
plays the major role. Thus, the refraction of this
approximately equally in both planes.
surface of the contact lens substitutes for the
• Therefore, in astigmatism, each of the two
cornea’s usual refraction.
planes requires a different degree of
accommodation. Thus, without the aid of • This is especially important in people
glasses, a person with astigmatism never whose eye refractive errors are caused by
sees in sharp focus. an abnormally shaped cornea, such as
those who have an odd-shaped, bulging
Correction of Astigmatism with a
cornea—a condition called keratoconus.
Cylindrical Lens
• Without the contact lens, the bulging
To correct for astigmatism, the usual procedure cornea causes such severe abnormality of
is to find a spherical lens by trial and error that vision that almost no glasses can correct
corrects the focus in one of the two planes of the vision satisfactorily; when a contact
the astigmatic lens. Then an additional lens is used, however, the corneal
cylindrical lens is used to correct the remaining refraction is neutralized, and normal
error in the remaining plane. To do this, both refraction by the outer surface of the
the axis and the strength of the required contact lens is substituted.
cylindrical lens must be determined.
The contact lens has other advantages:

1. the lens turns with the eye and gives a

broader field of clear vision than glasses
do.
2. the contact lens has little effect on the size
of the object the person sees through the
lens, whereas lenses placed 1 centimeter
or so in front of the eye do affect the size of
the image, in addition to correcting the
focus.

“Cataracts”
Correction of Optical Abnormalities by Use • especially common eye abnormality that
of Contact Lenses: occurs mainly in older people.
• A cataract is a cloudy or opaque area or
• Glass or plastic contact lenses can be
areas in the lens.
inserted that fit snugly against the
• In the early stage of cataract formation, the
anterior surface of the cornea.
proteins in some of the lens fibers become
• These lenses are held in place by a thin
denatured. Later, these same proteins
layer of tear fluid that fills the space
coagulate to form opaque areas in place of
between the contact lens and the
the normal transparent protein fibers.
anterior eye surface.
• When a cataract has obscured light
• A special feature of the contact lens is
transmission so greatly that it seriously
that it nullifies almost entirely the
impairs vision, the condition can be
refraction that normally occurs at the
corrected by surgical removal of the lens
anterior surface of the cornea.
 • When this is done, the eye loses a large connection of more and more rods and
portion of its refractive power, which must cones to each optic nerve fiber in the
be replaced by a powerful convex lens in nonfoveal, more peripheral parts of the
front of the eye; usually, however, an retina.
artificial plastic lens is implanted in the eye
in place of the removed lens.

COATS OF THE EYE:

1. Sclera – outermost
2. Choroid – middle
3. Retina – inner

The Retina has:

1. Fovea – a minute area in the center of the retina

which is esp. capable of acute and detailed vision

- Central fovea = composed entirely of

cones

- in the foveal region, the blood vessels, RECEPTOR & NEURAL FUNCTION OF THE
ganglion cells, inner nuclear layer of cells, RETINA:
and plexiform layers are all displaced to
Retina = light-sensitive portion of the eye that
one side rather than resting directly on top
contains photoreceptors:
of the cones → allows light to pass
unimpeded to the cones (a) Cones- color vision (3 million)
- high degree of visual acuity in the central (b) Rods - vision in the dark (100 milion)
retina in comparison with the much poorer
acuity peripherally Layers of the Retina from outside → inside:

1. pigmented layer
2. Macula - contains both rods and cones
2. layer of rods and cones projecting to
VISUAL ACUITY: the pigment
3. outer nuclear layer containing the cell
• The normal visual acuity of the human eye
bodies of the rods and cones
for discriminating between point sources of
4. outer plexiform layer
light is about 25 seconds of arc.
5. inner nuclear layer
• That is, when light rays from two separate
6. inner plexiform layer
points strike the eye with an angle of at
7. ganglionic layer
least 25 seconds between them, they can
8. layer of optic nerve fibers
usually be recognized as two points instead
9. inner limiting membrane
of one.
• This means that a person with normal
visual acuity looking at two bright pinpoint
spots of light 10 meters away can barely
distinguish the spots as separate entities
when they are 1.5 to 2 millimeters apart.
• The fovea is less than 0.5 millimeter (less
than 500 micrometers) in diameter, which
means that maximum visual acuity occurs
in less than 2 degrees of the visual field.
• Outside this foveal area, the visual acuity
becomes progressively poorer, decreasing
more than 10-fold as the periphery is
approached. This is caused by the
 Rhodopsin-Retinal Visual Cycle:

• The outer segment of the rod that projects

into the pigment layer of the retina has a
concentration of about 40 per cent of the
light-sensitive pigment called rhodopsin,
or visual purple. It is a combination of the
protein scotopsin and the carotenoid
pigment retinal (also called “retinene”)
• The retinal is a particular type called 11-cis
retinal. This cis form of retinal is important
because only this form can bind with
scotopsin to synthesize rhodopsin. *When
light energy is absorbed by rhodopsin, the
Pigment Layer of the Retina
rhodopsin begins to decompose within a
• The black pigment melanin in the pigment very small fraction of a second
layer prevents light reflection throughout • The cause of this is photoactivation of
the globe of the eyeball electrons in the retinal portion of the
• This is extremely important for clear vision rhodopsin, which leads to instantaneous
• Without it, light rays would be reflected in change of the cis form of retinal into an all-
all directions within the eyeball and would transform that still has the same chemical
cause diffuse lighting of the retina rather structure as the cis form but w/ diff. physical
than the normal contrast between dark and structure.
light spots required for formation of precise • Because the three-dimensional orientation
images of the reactive sites of the all-trans retinal
• The importance of melanin in the pigment no longer fits with the orientation of the
layer is well illustrated by its absence in reactive sites on the protein scotopsin, the
albinos, people who are hereditarily lacking all-trans retinal begins to pull away from the
in melanin pigment in all parts of their scotopsin. The immediate product is
bodies. When an albino enters a bright bathorhodopsin.
room, light that impinges on the retina is • Bathorhodopsin is extremely unstable and
reflected in all directions inside the eyeball decays in nanoseconds to lumirhodopsin.
by the unpigmented surfaces of the retina This then decays in microseconds to
and by the underlying sclera, so that a metarhodopsin I, then in about a
single discrete spot of light that would millisecond to metarhodopsin II, and finally,
normally excite only a few rods or cones is much more slowly (in seconds), into the
reflected everywhere and excites many completely split products scotopsin and all-
receptors. trans retinal. It is the metarhodopsin II, also
• Therefore, the visual acuity of albinos, even called activated rhodopsin, that excites
with the best optical correction, is seldom electrical changes in the rods, and the rods
better than 20/100 to 20/200 rather than the then transmit the visual image into the
normal 20/20 values. central nervous system in the form of optic
• The pigment layer also stores large nerve action potential.
quantities of vitamin A. This vitamin A is Re-formation of Rhodopsin:
exchanged back and forth through the cell
membranes of the outer segments of the • The first stage in re-formation of rhodopsin,
rods and cones, which themselves are is to reconvert the all-trans retinal into 11-
embedded in the pigment. cis retinal.
• This process requires metabolic energy
and is catalyzed by the enzyme retinal
isomerase. Once the 11-cis retinal is
formed, it automatically recombines with
the scotopsin to re-form rhodopsin, which
 then remains stable until its decomposition • Vitamin A is present both in the
is again triggered by absorption of light cytoplasm of the rods and in the
energy. pigment layer of the retina.
• Therefore, vitamin A is normally always
available to form new retinal when
needed.
• Conversely, when there is excess
retinal in the retina, it is converted back
into vitamin A, thus reducing the
amount of light-sensitive pigment in the
retina.
• This interconversion between retinal
Role of Vitamin A for Formation of Rhodopsin:
and vitamin A is especially important in
• there is a second chemical route by which long-term adaptation of the retina to
all-trans retinal can be converted into 11- different light intensities.
cis retinal
Night Blindness:
• This is by conversion of the all-transretinal
first into all-trans retinol, which is one form • Night blindness occurs in any
of vitamin A person with severe vitamin A
• Then the all-trans retinol is converted into deficiency. The simple reason for
11-cis retinol under the influence of the this is that without vitamin A, the
enzyme isomerase amounts of retinal and rhodopsin
• Finally, the 11-cis retinol is converted into that can be formed are severely
11-cis retinal, which combines with depressed.
scotopsin to form new rhodopsin • This condition is called night
blindness because the amount of
light available at night is too little to
permit adequate vision in vitamin
A–deficient persons. For night
blindness to occur, a person usually
must remain on a vitamin A–
deficient diet for months, because
large quantities of vitamin A are
normally stored in the liver and can
be made available to the eyes.
Once night blindness develops, it
can sometimes be reversed in less
than 1 hour by intravenous injection
of vitamin A.

Excitation of the Rod When Rhodopsin Is

Activated by Light

• The Rod Receptor Potential Is

Hyperpolarizing, Not Depolarizing
• When the rod is exposed to light, the
resulting receptor potential is different from
the receptor potentials in almost all other
sensory receptors.
• That is, excitation of the rod causes
increased negativity of the intrarod
membrane
potential, which is a state of hyperpolarization, Tricolor Mechanism of Color Detection
meaning that there is more negativity than normal
All theories of color vision are based on the well-
inside the rod membrane.
known observation that the human eye can detect
• This is exactly opposite to the decreased almost all gradations of colors when only red,
negativity (the process of “depolarization”) green, and blue monochromatic lights are
that occurs in almost all other sensory appropriately mixed in different combinations.
receptors.
Spectral Sensitivities of the Three Types of
• But how does activation of rhodopsin cause
Cones:
hyperpolarization? The answer is that
when rhodopsin decomposes, it decreases On the basis of color vision tests, the spectral
the rod membrane conductance for sodium sensitivities of the three types of cones in humans
ions in the outer segment of the rod. This have proved to be essentially the same as the light
causes hyperpolarization of the entire rod absorption curves for the three types of pigment
membrane found in the cones.

EXCITATION CASCADE: Interpretation of Color in the Nervous System:

Photoreceptors have a very sensitive chemical • One can see that an orange
cascade that amplifies effects: monochromatic light with a wavelength of
580 nanometers stimulates:
1. A single photon of light decomposes
- the red cones to a stimulus value of about
rhodopsin to form metarhodopsin II
99 (99 per cent of the peak stimulation at
2. Metarhodopsin II activates Transducin
optimum wavelength)
3. Activated transducin activates
- the green cones to a stimulus value of
phosphodiesterases
about 42
4. Phosphodiesterase hydrolyzes CGMP
- the blue cones not at all
5. CGMP when destroyed leads to closure of
- the ratios of stimulation of the three types
Na+ channels → Hyperpolarization
of cones in this instance are 99:42:0
6. occurs which activate the rod
7. W/in seconds, rhodopsin kinase inactivates
the activated rhodopsin

LIGHT AND DARK ADAPTATION:

Light Exposure for a long time → Decrease in

photoreceptors in the Rods & Cones → Sensitivity
of eye to light decreases → = Light Adaptation

Exposure to dark for a long time → Retinal &

Opsins in Rods & Cones are converted into light
sensitive pigments → Vitamin A converted into
Retinal to give additional light-sensitive pigments =
Dark Adaptation

Color Vision
A monochromatic blue light with a wavelength
• Different cones are sensitive to different
of 450 nanometers stimulates:
colors of light
• The mechanisms by which the retina • the red cones to a stimulus value of 0
detects the different gradations of color in • the green cones to a value of 0
the visual spectrum: • the blue cones to a value of 97
• This set of ratios—0:0:97—is
interpreted by the nervous system as
blue.
 • Likewise, ratios of 83:83:0 are 2. Blue Weakness
interpreted as yellow
• Blue cones are missing or
• 31:67:36 as green
underrepresented
Perception of White Light = About equal • is a genetically inherited state
stimulation of all the red, green, and blue cones
Color Test Charts
gives one the sensation of seeing white. Yet
there is no single wavelength of light • A rapid method for determining color
corresponding to white; instead, white is a blindness is based on the use of spot charts
combination of all the wavelengths of the • ISHIHARA CHARTS: These charts are
spectrum. arranged with a confusion of spots of
Color Blindness: several different colors. In the person with
normal color vision= reads “74,” whereas
1. Red-Green Color Blindness the red-green color-blind person reads
“21.”
• When a person is especially unable to
• In the bottom chart,the person with normal
distinguish red from green and is
color vision reads “42,” whereas the red-
therefore said to have red-green color
blind person reads “2,” and the green-blind
blindness.
person reads “4.”
• A person with loss of red cones is called
a protanope; the overall visual
spectrum is noticeably shortened at the
long wavelength end because of a lack
of the red cones.
• A color-blind person who lacks green
cones is called a deuteranope; this
person has a perfectly normal visual
spectral width because red cones are
available to detect the long wavelength
red color.
• Red-green color blindness is a genetic
disorder that occurs almost exclusively VISUAL PATHWAYS:
in males. A. New System
• That is, genes in the female X
chromosome code for the respective The visual nerve signals leave the retinas
cones through the optic nerves → At the optic chiasm,
• Color blindness almost never occurs in the optic nerve fibers from the nasal halves of the
females because at least one of the two retinas cross to the opposite sides, where they join
X chromosomes almost always has a the fibers from the opposite temporal retinas to
normal gene for each type of cone. form the optic tracts → The fibers of each optic
• Because the male has only one X tract then synapse in the dorsal lateral geniculate
chromosome, a missing gene can lead nucleus of the thalamus, and from there, →
to color blindness. geniculocalcarine fibers pass by way of the optic
• Because the X chromosome in the radiation (also called the geniculocalcarine tract) to
male is always inherited from the the primary visual cortex in the calcarine fissure
mother, & never from the father: area of the medial occipital lobe
➢ color blindness is passed from B. Old System
mother to son
➢ the mother is said to be a color Visual fibers also pass to several older areas of the
blindness carrier brain: (1) from the optic tracts to the
➢ this is true in about 8 per cent of all suprachiasmatic nucleus of the hypothalamus,
women presumably to control circadian rhythms that
synchronize various physiologic changes of the
body with night and day; (2) into the pretectal Function of the Lateral Geniculate Body:
nuclei in the midbrain, to elicit reflex movements of
1. Serves as relay station to relay visual
the eyes to focus on objects of importance and to
information from the optic tract to the visual cortex
activate the pupillary light reflex;(3) into the
superior colliculus, to control rapid directional Characteristic of Relay Transmissions:
movements of the two eyes; and (4) into the ventral
lateral geniculate nucleus of the thalamus and - Accurate
surrounding basal regions of the brain, presumably - Exact point-to-point transmission
to help control some of the body’s behavioral - High degree of spatial fidelity
functions. 2. “gate” the transmission of signals to the visual
cortex (controlling the signal)

-The second major function of the dorsal lateral

geniculate nucleus is to “gate” the transmission
of signals to the visual cortex—that is, to
control how much of the signal is allowed to
pass to the cortex.

-The nucleus receives gating control signals

from two major sources:

(1) corticofugal fibers returning in a backward

direction from the primary visual cortex to the
lateral geniculate nucleus

(2) reticular areas of the mesencephalon

- both are Inhibitory

- when stimulated, turn off transmission,
Effect of Lesions in the Optic Pathway on the controlling visual information
Fields of Vision - receives input almost entirely from type X
retinal ganglion cells
- Destruction of an entire optic nerve
- transmit color
causes blindness of the affected eye
- transmit accurate point-to-point spatial
- Destruction of the optic chiasm prevents
information at moderate velocity of
the crossing of impulses from the nasal half
conduction
of each retina to the opposite optic tract.
Therefore, the nasal half of each retina is The dorsal lateral geniculate nucleus is divided
blinded, which means that the person is in another way:
blind in the temporal field of vision for each
(1) Layers I and II are called magnocellular
eye because the image of the field of vision
layers because they contain large neurons
is inverted on the retina by the optical
system of the eye; this condition is called - These receive their input almost entirely from the
bitemporal hemianopsia large type Y retinal ganglion cells
*Such lesions frequently result from tumors of - This magnocellular system provides a rapidly
the pituitary gland pressing upward from the conducting pathway to the visual cortex
sella turcica on the bottom of the optic chiasm
- However, this system is color blind, transmitting
- Interruption of an optic tract denervates the only black-and-white information
corresponding half of each retina on the same
side as the lesion; as a result, neither eye can - Its point-to-point transmission is poor because
see objects to the opposite side of the head- there are not many Y ganglion cells, and their
This condition is known as homonymous dendrites spread widely in the retina
hemianopsia
(2) Layers III through VI are called parvocellular Secondary Visual Areas of the Cortex
layers because they contain large numbers of
- The secondary visual areas, also called
small to medium-sized neurons
visual association areas
- These neurons receive their input almost entirely - lie lateral, anterior, superior, and inferior to
from the type X retinal ganglion cells the primary visual cortex
- Most of these areas also fold outward over
- transmit color
the lateral surfaces of the occipital and
- convey accurate point-to-point spatial parietal cortex
information, but at only a moderate velocity of - Secondary signals are transmitted to these
conduction rather than at high velocity areas for analysis of visual meanings
- For instance, on all sides of the primary
visual cortex is Brodmann’s area 18, which
is where virtually all signals from the
primary visual cortex pass next

Secondary Visual Areas of the Cortex

- The secondary visual areas, also called

visual association areas lie lateral, anterior,
superior, and inferior to the primary visual
cortex
- Most of these areas also fold outward over
the lateral surfaces of the occipital and
parietal cortex
- Secondary signals are transmitted to these
areas for analysis of visual meanings
- For instance, on all sides of the primary
Organization and Function of the Visual
visual cortex is Brodmann’s area 18, which
Cortex
is where virtually all signals from the
- the visual cortex located primarily on the primary visual cortex pass next →
medial aspect of the occipital lobes Therefore, Brodmann’s area 18 is called
- Like the cortical representations of the visual area II, or simply V-2
other sensory systems, the visual cortex is - The other, more distant secondary visual
divided into a primary visual cortex and areas have specific designations—V-3, V-
secondary visual areas 4, and so forth—up to more than a dozen
areas
Primary Visual Cortex ( Visual Area I, V-I, - The importance of all these areas is that
Striate Cortex) various aspects of the visual image are
- The primary visual cortex lies in the progressively dissected and analyzed.
calcarine fissure area, extending forward Pupillary Light Reflex
from the occipital pole on the medial aspect
of each occipital cortex - When light is shone into the eyes, the
- This area is the terminus of direct visual pupils constrict, a reaction called the
signals from the eye pupillary light reflex
- Signals from the macular area of the retina - When light impinges on the retina, a
terminate near the occipital pole, while few of the resulting impulses pass from
signals from the more peripheral retina the optic nerves to the pretectal nuclei.
terminate at or in concentric half circles From here, secondary impulses pass to
anterior to the pole but still along the the Edinger-Westphal nucleus and,
calcarine fissure on the medial occipital finally, back through parasympathetic
lobe nerves to constrict the sphincter of the
iris.
 - Conversely, in darkness, the reflex also, very small (an Argyll Robertson pupil)
becomes inhibited, which results in is an important diagnostic sign of central
dilation of the pupil. nervous system disease—often syphilis.
- The function of the light reflex is to help
Horner’s Syndrome
the eye adapt extremely rapidly to
changing light conditions The sympathetic nerves to the eye are
- The limits of pupillary diameter are occasionally interrupted. Interruption frequently
about 1.5 millimeters on the small side occurs in the cervical sympathetic chain. This
and 8 millimeters on the large side causes the clinical condition called Horner’s
- Therefore, because light brightness on syndrome, which consists of the following effects:
the retina increases with the square of
pupillary diameter, the range of light • First,because of interruption of
and dark adaptation that can be sympathetic nerve fibers to the
brought about by the pupillary reflex is pupillary dilator muscle, the pupil
about 30 to 1—that is, up to as much as remains persistently constricted to a
30 times change in the amount of light smaller diameter than the pupil of the
entering the eye. opposite eye.
• Second,the superior eyelid droops
Pupillary Reflexes or Reactions in Central because it is normally maintained in an
Nervous System Disease: open position during waking hours
partly by contraction of smooth muscle
• A few central nervous system diseases
fibers embedded in the superior eyelid
damage nerve transmission of visual
and innervated by the sympathetics.
signals from the retinas to the Edinger-
Therefore, destruction of the
Westphal nucleus, thus sometimes
sympathetic nerves makes it
blocking the pupillary reflexes.
impossible to open the superior eyelid
• Such blocks frequently occur as a result of
as widely as normally.
central nervous system syphilis,
• Third, the blood vessels on the
alcoholism, encephalitis,and so forth
corresponding side of the face and
• The block usually occurs in the pretectal
head become persistently dilated.
region of the brain stem, although it can
• Fourth, sweating (which requires
result from destruction of some small fibers
sympathetic nerve signals) cannot
in the optic nerves.
occur on the side of the face and head
• The final nerve fibers in the pathway
affected by Horner’s syndrome.
through the pretectal area to the Edinger-
Westphal nucleus are mostly of the
inhibitory type. When their inhibitory effect
is lost ,the nucleus becomes chronically
active, causing the pupils to remain mostly
constricted, in addition to their failure to
respond to light.
• Yet the pupils can constrict a little more if
the Edinger-Westphal nucleus is stimulated
through some other pathway.

For instance, when the eyes fixate on a near

object, the signals that cause accommodation
of the lens and those that cause convergence
of the two eyes cause a mild degree of pupillary
constriction at the same time. This is called the
pupillary reaction to accommodation.

• A pupil that fails to respond to light but

does respond to accommodation and is