PHYSIOLOGY OF VISION

Lecturer: Paul Dexter C. Santos, MD, FPCP, FPSMO (03-07-2013)

Physiology
Transcribed/Edited to Word Format by
Objectives
Describe the functional anatomy of the eye
Define and illustrate refraction of light
Define and illustrate mechanisms of accommodation
Define the different errors of refraction
Discuss the rhodopsin retinal visual cycle
State the abnormalities of color vision
Explain briefly the visual pathway
Discuss briefly the visual field and perimetry
State eye movements and explain their control

INTRODUCTION
According to:
Creationists: the very complex structure
of the eye is evidence for the existence of
a creator
Charles Darwin: at first glance, the
evolution of the eye by natural selection
seems absurd in the highest possible
degree
Evolutionists: if some omnipotent force is
responsible in creating the human eye, it
was something of a botched design since
the human eye is not even the best in
evolution
In lower forms of life, light sensitive spots:
concentration of photopigments
Evade predators
Give sense of night and day
Euglena eye spots

after just a few months inside the

womb, the human eyes breezed through
over 500 million years of evolution (PDS
2012)

*DEVELOPMENT OF THE EYE

Cup eyes
Can give sense of direction
Planaria eye pits
Photo chamber
Pinhole camera
No cornea and lens
Light inlet reduced
Nautilus photo chambers
Shape recognition

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*PARTS OF THE EYE

 Aqueous Humor
Maintains intraocular pressure (=15mmHg)
Provides nutrients (lens, cornea, anterior
vitreous body)
Continuously replenished
Contains glucose, amino acids, ascorbate
Increases refractive index
Immune functions
Vitreous Humor
Gelatinous material maintaining the shape
of the globe
Increases refractive index
Not continuously replenished

*Formation and flow of fluid in the eye

*Anatomy of the ciliary processes; aqueous humor is

formed on surfaces

Glaucoma
Increased intraocular pressure
Can cause blindness through death of optic
nerve axons
Blockage of trabecular spaces in most
cases
Treated by miotic agents (medical),
iridectomy or trabeculectomy (surgical),
laser trabeculectomy

*Eye of a patient who has undergone iridectomy to

free up space for aqueous humor drainage to decrease
intraocular pressure

------------------------------------------------OPTICS-----------------------------------------------REFRACTIVE INDEX
Ratio of the velocity of light in air (index of 1.0) to the velocity of light in a medium/substance
Light travels slower in solids or liquids

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 If light strikes an interface which is perpendicular to the beam, the rays enter the medium without
deviation
If light strikes an angulated surface with a higher refractive index, the beam is bent. The lower portion of
the beam enters the angulated medium first
Refraction: the bending of light rays at an angulated surface
Factors in refraction
1. How angulated is the
surface
2. The Refractive index of
the medium
The beam that passes
through the center: no
refraction
Towards the edge, light
beam
passes
through
progressively
more
angulated interface
Light rays bent enough
can meet at a certain
point called the Focal
point in a distance from
the
interface
focal
length

*Cylindrical lens: light converges in a focal line

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Refractive Index of the eye: 59 diopters

2/3 of refraction occurs in the Air-Cornea
interface
Other interface:
Posterior cornea and aqueous humor
Aqueous humor and anterior lens
Posterior lens and vitreous humor

Factors that can affect the focal length

Characteristic of light source: whether parallel
or divergent
Thickness of the lens (more angulated, shorter
focal length)

Any object in front of the lens is, in reality, a

mosaic of point sources of light. Some of these
points are very bright, some are very weak,
and they vary in color. Each point source of
light on the object comes to a separate point
focus on the opposite side of the lens in line
with the lens center.

Refractive power: DIOPTERS

1 meter divided by focal length
(+) diopter: convergence by a convex lens
() diopter: divergence by a concave lens
For cylindrical lens: specify axis:
Horizontal line 0 degrees
Vertical line 90 degrees
Diopter principle is the same as the spherical
lens

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*REFRACTIVE INDICES

*Both human and camera lenses see objects upsidedown, leading to a debate whether or not the entire
world is upside-down

ACCOMODATION
Increase in the refractive power of the eye
Lens increase in convexity
Ciliary muscle contracts
Under parasympathetic control
Refractive power increased by 14diopters
Eyes converge
Pupils constrict

*Mechanism of accommodation

PUPILLARY CONSTRICTION

*Effect of small (top) and large (bottom) pupillary

apertures on depth of focus

PRESBYOPIA
Loss of lens elasticity due to denaturation of
lens protein
Lens becomes thicker and larger but less
elastic
From 14 diopters accommodating power, it
drops to about 2 by age 50
A non-accommodating lens = presbyopia
ERRORS OF REFRACTION (EOR)
Emmetropia
Myopia
Hyperopia

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HYPEROPIA
Short eyeballs or weak lens system in a
relaxed ciliary muscle, image is focused at the
back of the retina
The eye has to use some effort of
accommodation to bring the image forward
and be focused on the retina
Person can still focus on near objects as long
as he has not used up all of the lens
accommodation power
Problem starts if presbyopia sets in, so that he
cant use even the smallest effort of
accommodation to see far objects
MYOPIA
Eyeballs too long
In a completely relaxed state, a distant image
is focused in front of the retina.
Problem is that, to bring the image on the
retinal layer, the ciliary muscles cannot
relax much more.
Natural solution is to bring object closer.
PINHOLE TEST FOR EOR
Light passing through the center is not
refracted

*Astigmatism, demonstrating that light rays focus at

one focal distance in one focal plane (plane AC) and
at another focal distance in the plane at the right
angle (plane BD)

*Biconcave lenses correct myopia, while biconvex

glasses correct hyperopia

TREATMENT FOR EOR

Eyeglasses
Contact lenses
Laser treatment

*Chart composed of parallel black bars at different

angular orientations for determining the axis of
astigmatism. People with astigmatism, upon closure
of one eye and focusing on this image, will see some
lines thicker than the others or fuzzier than the
others.

Additional Info (Wikipedia):

LASIK or Lasik (Laser-Assisted in Situ Keratomileusis)
Refractive
surgery for
the
correction
of
myopia, hyperopia, and astigmatism
Ophthalmologist uses a laser or microkeratome to
reshape/etch the eye's cornea in order to
improve visual acuity

Corrected using combination of spherical and

cylindrical lens
Axis of cylindrical correction is parallel to the
fuzzy bars
Accommodation cannot correct astigmatism as
different planes would require different
degrees of accommodation
Treated by a cylindrical lens
DEPTH PERCEPTION
Determination of the distance of an object
from the eyes
Sizes of known objects on the retina
Moving parallax
Movement of near objects is perceived
more compared to movement of
objects afar
Stereopsis (binocular vision)
Takes advantage of the fact that the
eyes are 2 inches apart.
Images fall on different areas of the
retina depending on the distance

*Not really sure what ablation profiles mean, but they

seem (according to Internet sources) to calculate the
amount of tissue required to be removed to produce a
favorable refractive result

ASTIGMATISM
Caused by increased curvature of the cornea
in one plane
Image in one plane is focused on a different
distance compared to the perpendicular plane.
Parts of the cornea acting as a cylindrical lens

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------------------------------------------------RETINA-----------------------------------------------TEN MUST KNOW LAYERS (FROM OUTER TO INNER) should be remembered until you die (PDS, 2013)
1) Pigment layer
2) Layer of rods and cones photoreceptors
3) External limiting membrane
4) Outer nuclear layer (cell bodies of rods and cones)
5) Outer plexiform layer (axons of cone and rods, dendrites of bipolar and horizontal cells)
6) Inner nuclear layer (cell bodies of bipolar, horizontal and amacrine cells)
7) Inner plexiform layer (axons of bipolar, amacrine cells, dendrites of ganglion cells)
8) Ganglionic cell layer
9) Optic nerve layer (axons of ganglion cells)
10) Inner limiting membrane
Melanin in pigment layer prevents reflection of light inside the eye. Lack of melanin (albinos)
dramatically decreases visual activity. Instead of just activating a few rods and cones, light will be
bounced around inside the eye activating more rods and cones
Pigment layer stores vitamin A.

Light must traverse the entire thickness of the retina to get to the rods and cones. This limits visual acuity
There is an area called the fovea where the plexiform, inner nuclear and the ganglion layers are pushed to
one side
The fovea consists of mainly cones
THE

FOVEA
Around 1 sq. mm. in area
Provides detailed vision
Plexiform, inner nuclear, and ganglion layers are
pushed to one side
Light reaches the cones unimpeded
Contains mostly cones which are more slender

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THE PHOTORECEPTORS

*The different three-dimensional orientation of the

cis and trans.

*LEFT: Rod; RIGHT: Cone

RODS AND CONES

Outer segment: folded shelves of membrane
that contain the pigments
Pigments are transmembrane proteins,
constitute around 40 percent of the mass
of the outer segment
Inner segment: mitochondria that provides
energy
PHOTOCHEMISTRY

Reformation of Rhodopsin: Scotopsin binds to

reformed 11-cis retinal
11-cis-retinal can be generated from:
all trans retinal via retinal isomerase
Vitamin A pathway
Vitamin A is present in the pigment layer and
cytoplasm of the rods

*Regeneration of rhodopsin occurs in few minutes

Night Blindness
Severe deficiency of vitamin A
Deficient amounts of retinal
Small quantities of light are unable to
stimulate the photoreceptors
THE ELECTRICAL SIGNAL
Membrane potential of photoreceptor in the
dark is = -40 mV
This is due to leaking back of sodium ions
from outside to inside (from cGMP gated Na
channels in the OUTER segment) despite the
Na-K pump expelling sodium (through the Na-K
pump in the INNER segment)

Rhodopsin = cis-retinal + scotopsin. Light

energy causes decomposition of rhodopsin.
Retinal is converted to the trans
configuration
Metarhodopsin II = the active rhodopsin,
responsible for the electrical signal

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 Increased sensitivity to even small amounts of

light
FROM BRIGHT LIGHT TO DARK

*Cones: chemical vision events occur 4x as fast

compared to rods
*Rods: slowly adapting rods continue to adapt for
several minutes or even hours

COLOR VISION
Three Types of Cones

*Different ratios of cone stimulation give the perception

of color
*Equal stimulation of all 3 cones gives a white light

ACTIVATED RHODOPSIN (METARHODOPSIN II)

ACTIVATES TRANSDUCIN
Once Na channels are closed by dwindling
amounts of cGMP, the inside of the cells
become more electronegative as compared to
the outside with electrical charge reaching 70= -80mv upon maximal light exposure
MEMBRANE IS HYPERPOLARIZED
Hyperpolarization allows for varying
DEGREES of response as compared to a
depolarization which is an ALL or NONE
RESPONSE
Allows for discrimination of light intensity:
more light intensity = more hyperpolarization
Flash of light generates a potential in 0.3s and
lasts for about 1 second (Afterimage Effect)

Color blindness
Absence of certain color of cones
Lacking either red or green cones: unable
to distinguish green, yellow, orange, and
red colors (red-green color blindness)
Loss of red cone: protanope
Loss of green cone: deuteranope
Women are the carriers of a defective X
chromosome
The other X chromosome of the female
usually carries the normal genes so women
do not exhibit color blindness
Phenotype expressed only in males who
inherit the defective X, since the Y
chromosome does not contain the normal
set of genes

LIGHT ADAPTATION
Prolonged exposure to light
Decreased levels of photosensitive chemicals
More opsins and retinals
More vitamin A
Sensitivity of the eye to light is reduced
DARK ADAPTATION
Photosensitive chemicals (rhodopsins and color
pigments) are regenerated and stored.
Vitamin A converted back to retinal

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*Sample of an Ishihara chart, for

testing color blindness

---------------------------------------THE VISUAL PATHWAY-------------------------------------THE VISUAL PATHWAY - should be remembered until you die (PDS, 2013)
Rods
Cones

Bipolar Amacrine cells Ganglion cell optic nerve (axons of ganglion cells) Brain
Bipolar ------------------ Ganglion cell optic nerve (axons of ganglion cells) Brain

Horizontal cells: provides lateral inhibitory

signals
Bipolar cells: transmit signals vertically from
rods, cones, horizontal cells amacrine and
ganglion cells
Amacrine cells: bipolar ganglion cells

LATERAL INHIBITION
Provides visual contrast
Horizontal cells always provide inhibitory
signals
Two types of bipolar cells (depolarizing and
hyperpolarizing) adds to contrast

GANGLION CELLS
1.6M ganglion cells serving 100M rods and 3M
cones
Ratio of rods/cones to ganglion cells decreases
towards the central retina (almost 1:1 coneganglion ration at the fovea)
Peripheral retina most sensitive to light
Ganglion cells transmit signals to the brain
through repetitive action potentials
W cells:
40% of ganglion cells. Small fibers
Conducts mostly rod signals. Dendrites are
widely spread
Slow transmission
Crude rod vision in dark conditions
X cells:
55% of ganglion cells. Medium fibers
Receives input from at least one cone
Responsible for all color vision
Y cells:
Largest
in
diameter;
fastest
conduction/transmission
Responds to rapid changes in the visual
signals
Alerts the CNS if a new visual event occurs
Color blind
TRANSMISSION OF COLOR SIGNALS
One cone type stimulates one ganglion cell
through a depolarizing bipolar cell.
This cone can be inhibited by the opponent
color through a hyperpolarizing bipolar cell
Optic Nerves Optic Chiasm Dorsal
Lateral Geniculate Nucleus DLGN (thalamus)
Optic radiation Visual cortex (calcarine
fissure of occipital lobe)
- should be remembered until you die
(PDS, 2013)

AMACRINE CELLS
Interneurons that analyze visual signals before
they leave the retina

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 Primary visual cortex is in the medial

occipital lobe along the calcarine fissure
Fibers from the macula: most posterior
occipital pole. Largest representation for
highest degree of visual acuity
Peripheral retina fibers: more anterior
Secondary visual cortex: visual association
areas, images dissected and analyzed

Ipsilateral temporal: layers II, III, V

Contralateral nasal: layers I, IV, VI
Magnocellular
Contains large neurons
Transmit fast Y ganglion signals
Color blindness
Parvocellular
Contains slow to medium sized neurons
Transmit X ganglion color signals
FUNCTIONS OF DLGN
Relays signal to the visual cortex with high
degree of spatial fidelity
Gating function: controls which visual signals
to pass through inputs from corticofugal fibers
and reticular fibers from mesencephalon (both
provide inhibitory signals)
PRIMARY VISUAL CORTEX

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Visual cortex arranged in six layers, and in

vertical neuronal columns consisting of
thousands of neurons
Geniculo-calcarine fibers (optic radiations)
terminate in layer IV. From layer signals are
transmitted outward towards the cerebral
surface and inwards
Color blobs: receives lateral signals. Activated
by color signals for deciphering color
PROCESSING OF VISUAL SIGNALS
Position and Motion Pathway
Visual cortex posterior midtemporal
area occipitoparietal cortex
Overlap with posterior somatic association
areas analyze 3D aspects of somatosensory
signals
From Y ganglion cells. Fast but no color
vision
Three dimensional position, form, and
motion of objects
Accurate color pathway
Visual cortex inferior, ventral, medial
occipital and temporal cortex
Colors, letters, reading, texture

 Other visual fiber projections from DLGN

Suprachiasmatic
Nuclei of
Hypothalamus

o Circadian rhythm

Pretectal Nuclei
of Midbrain

o Reflex movements
o Focus on important objects
o Pupillary light reflex

Superior
Colliculus
Ventral Lateral
Geniculate
Nucleus

o Rapid directional movements

o Behavioral functions

PERIMETRY
Visual Field: area seen by the eye in a given
instant
Nasal field of vision
Temporal field of vision
Blind spot
Part of the retina with no rods and cones
Corresponds to the location of the optic
disc
15 degrees lateral to the central point of
vision

Tunnel vision
Loss of peripheral vision
Glaucoma, retinitis pigmentosa, drugs

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Scotomas
Blind Spots
Optic nerve damage
Glaucoma
Lead poisoning
Excessive tobacco consumption
EYE MOVEMENTS

Reciprocal innervation: one of the muscle

pair contracts while the other relaxes
The nerves have their nuclei in the brain stem
which are interconnected through the Median
Longitudinal Fasciculus (MLF)
Oblique muscles rotate the eyeballs to keep
the visual fields in upright position

 Cortical inputs
Primary visual cortex
Visual association area
Involuntary fixation area
Voluntary fixation area
Equilibrium inputs from the vestibular nuclei
transmitted through the MLF

*When a spot of light has become fixed on the foveal region

of the retina, the tremulous movements cause the spot to
move back and forth at a rapid rate across the cones, and
the drifting movements cause the spot to drift slowly across
the cones. Each time the spot drifts as far as the edge of the
fovea, a sudden reflex reaction occurs, producing a flicking
movement that moves the spot away from this edge back
toward the center of the fovea. Thus, an automatic response
moves the image back toward the central point of vision.

FIXATION MECHANISMS
Voluntary fixation area
Premotor cortex of frontal lobes
Unlock from a point of fixation and move
to another point
Involuntary fixation area
Secondary visual areas in occipital lobes
through the superior colliculus
Lock the eyes on a given spot
Involuntary eye movements during fixation:
Continuous tremor
Slow drift
Sudden flicking movement

Saccadic movements
Eyes fixing from one highlight to the next
during a moving visual scene
Evident during reading or when riding a car
and looking out the window
Pursuit movements
Following a moving object
A cortical mechanism detects movement of
the object and develops a similar course of
movement of the eyes
Image Fusion
Interference neurons are activated if
images from both retinas are not seen as
fused in the cortex (not in-register)
These neurons send signals to the
oculomotor apparatus to cause divergence,
convergence, or rotation of the eyeballs so
that the images can be properly fused
*Remember stereopsis or depth perception? This uses
the degree of non-fusion or non-register to gauge
distance of the object

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 Strabismus
Lack of fusion of the eyes
Horizontal, torsional, and vertical types
Amblyopia
Lazy eye: results if one eye is repressed
and does not develop its full visual
potential
Essentially, only one eye (the dominant
eye) will be working
Poor stereopsis

Parasympathetic: Edinger-Westphal nucleus

Sympathetic: Intermedial horn cells of T1

Parasympathetic
Ciliary muscle
Iris sphincter (decrease pupil diameter or
MIOSIS)
Sympathetic
Radial iris muscle (increase pupil diameter
or MYDRIASIS)
Pupillary light reflex
Limits the amount of light through
pupillary constriction
Direct and consensual light reflex
Abnormal
pupillary
reactions/states
indicative of CNS disease
Afferent: Optic nerve
Processing center: Pretectal area, EW nucleus
Efferent:
Oculomotor
nerve
carrying
parasympathetic signal

*Strabismus: abnormal pattern of conjugate eye

movements is set, so the eyes never fuse

AUTONOMIC INNERVATION

Horners syndrome:
Interruption of sympathetic signals
MIOSIS: constricted pupils
PTOSIS: drooping eyelids (some muscles to
keep eyelids open are controlled by
sympathetic signals)
ANHYDROSIS: no sweating on the affected
side
Dilation of blood vessels on the affected
side (flushed skin)

-ENDWhen I said that the Minerals lecture in Biochemistry would be my last handout, I obviously lied.
This is the complete lecture of Dr. Santos converted from PPT to Word, and about 5/6 of it comes from Guyton & Halls
Textbook of Medical Physiology. I added some new information to supplement some of the pictures, as well as notes from
Doc himself. Though Dr. Santos said he mostly derives questions from the book, it would be still best to read the book.
Ganongs Review of Medical Physiology and Berne & Levys Physiology are good reads, but Guyton & Halls discussion is way
better, more complete, and ample.
Best of luck on this one, Batch 2016.
Kamehameha! No, I mean, na na na na na na na na!

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