Anatomy and Physiology of The Eye

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ANATOMY AND PHYSIOLOGY OF THE EYE

The globe-shaped eyeball occupies the anterior part of the orbit, bulging outward → this
outward projection represents about one-sixth of the total area of the eyeball and is the
transparent cornea.
Posterior to the cornea, from front to the back, there are:
- Anterior chamber
- Iris and Pupil
- Posterior chamber
- Lens
- Vitreous chamber
- Retina

Sagittal diameter → 24 to 25 mm
Transverse diameter → 24 mm

ANTERIOR AND POSTERIOR CHAMBERS


Anterior and posterior chambers are continuous with each other through the pupillary
opening → they are filled with the acqueous humor, secreted in the posterior chamber.
This fluid flows through the pupil in the anterior chamber, where is absorbed into the scleral
venous sinus → canal of Schlemm, found at junction between the cornea and iris.

The acqueous humor supplies nutrients to the avascular cornea and lens and maintains
intra-ocular pressure.
If the amount of fluid increases due to problems related to production and absorption of this
latter → increased intra-ocular pressure → glaucoma.

LENS AND VITREOUS HUMOR


Lens is a transparent, biconvex elastic disc attached circumferentially to muscles associated
with the outer wall of the eyeball → this lateral attachment provides the lens with the ability
to change its refractive ability to maintain visual acuity.
Lens is composed of three main parts:
- Capsule → thick basement membrane of GAGs, type IV collagen, laminin, forming the
outermost layer of the lens. Due to its great elasticity allows lens to assume a more spherical
shape when the tension of suspensory ligaments is reduced

- Epithelium → single layer of cells, providing lens fibers with nutrients and removing
waste → lens homeostasis

- Fibers → they form the bulk of the lens. They are long, transparent, thin cells stretching
from the posterior to the anterior poles. The lens is split into regions depending on the age
of the lens fibers of a particular layer

Posterior four-fifth of the eyeball, from lens to retina, is occupied by the vitreous chamber
→ it is filled with a transparent, gelatinous substance containing more than 98% of water
but with a viscosity 2-3 times higher than the water→ vitreous body.
Main functions are support of the eyeball shape and important role in the metabolism of
the lens.
Vitreous is attached to its surrounding structures by condensation of collagen fibrils:
- Vitreous base
- Hyaloideocapsular ligament of Weiger
- Margins of the optic disc
- At macula
- Along the retinal vessels

The central vitreous is traversed by Cloquets canal, extending from the posterior surface of
the lens to the optic nerve.

WALLS OF THE EYEBALL


Surrounding the internal structures of the eyeball are the walls of the eyeball, consisting of
three layers:
- Fibrous layer
It consists of two components:
1. Sclera → is an opaque layer of dense connective tissue that can be seen anteriorly as the
‘white of the eye’. It is pierced by numerous vessels and nerves, including optic nerve
posteriorly and provides attachment for numerous muscles involved in eyeball movements.

2. Cornea → continuous anteriorly with the sclera → being transparent allows light to enter
the eyeball. Main functions are protection and visio.
The refractive power is → 43-45 diopters (D)

The cornea has five distinct layers:


- Epithelium → it is stratified squamous epithelium, having three predominant layers:
- Bowman layer → composed of collagen fibers, not able to regenerate → if damaged,
scarring results

- Stroma → composed of type 1 collagen and glycosaminoglycans, with scattered


keratocytes. These latter secrete collagen and glycoproteins, therefore following injury,
keratocytes adjacent to the wound undergo transformation, proliferation, migration and
production of larger and disorganized fibers → scar formation

- Descemet membrane → it is the basement membrane deposited by the endothelium with


structural function. Excrescences of DM occur in the peripheral cornea in the elderly →
Hassal-Henle warts.

- Endothelium → is a monolayer of hexagonal cells that are not able to divide and
regenerate if damaged, but they are able to migrate and enlarge in order to cover the
endothelial defects → with the age the cell count declines → corneal oedema will occur
when cell fall below 500 cells/mm2.
Aqueous humor from the anterior chamber and surface tears provide nutrients and oxygen.

3. Tear film → composed of three major layers important in the maintenance of a healthy
corneal surface → normal pH of the tear film is 6.5 to 7.6

4. Conjunctiva → is a non-keratinizing stratified squamous epithelium with goblet cells,


closely adherent to the superior and inferior tarsus by fine septa.
- Uvea (vascular layer)
Main functions are nutrition, light regulation, accommodation and regulation of
intraocular pressure.
It consists of three continuous parts:
1. Choroid → is a thin, highly vascular, pigmented layer consisting of smaller vessels
adjacent to the retina and larger vessels more peripherally. Firmly attached to the retina
internally and to the sclera externally.
It has three vascular layers:
- Choriocapillaries → plexus of fenestrated vessels and on the inner side covered by the
membrane of Bruch

- Sattler’ s layer → medium sized vessels

- Haller’s layer → large sized vessels (outermost layer)

2. Ciliary body → it forms a complete ring around the eyeball, formed by ciliary muscle
and ciliary processes.
Formed by:
- Pars plicata → two layers of epithelium, non-pigmented secretory cells involved in
aqueous humor formation and blood-aqueous barrier and pigmented cells facing the
stroma

- Pars plana → smooth posterior portion formed by non-pigmented and pigmented


epithelium

Ciliary muscle consists of smooth muscle fibers arranged longitudinally, circularly and
radially, controlled by the parasympathetics traveling in the oculomotor nerve [III].
Ciliary processes are longitudinal ridges projecting from the inner surface of the ciliary
body, from which zonular fibers extend, attaching to the lens of the eyeball and collectively
forming the suspensory ligament of the lens.
- During contraction of ciliary muscle → reduced tension of suspensory ligament → lens
becomes more rounded, resulting in accommodation of the lens for near vision.
- During relaxation of ciliary muscle → increased tension of suspensory ligament → lens
becomes more flat, resulting in accommodation of the lens for far vision.
Ciliary processes also contribute to the formation of aqueous humor.

3. Iris → this circular part is the colored part of the eye with a central opening called pupil.
Controlling the size of the pupil are smooth muscle fibers within the iris:

Posterior and anterior ciliary vessels form major arterial circle.


- Retina
It consists of two parts:
1. Optic part → found posteriorly and laterally, it is sensitive to the light.
This part consists of two layers:
- Outer pigmented layer → firmly attached to the choroid and continues anteriorly over the
internal surface of the ciliary body and iris. It contains phagosomes and melanin granules
and its main functions are absorption of the stray light, regeneration of visual pigment,
phagocytosis, active transport and exchange of metabolites, outer blood-retina barrier.

- Inner neural layer → attached to the pigmented layer around the optic nerve and at the
ora serrata. This layer contains different cells, including:
A. Photoreceptors
B. Bipolar cells
C. Ganglion cells
D. Modulating cells
E. Muller’s cells

2. Non-visual part → covers the internal surface of the ciliary body and the iris

Junction between these parts is an irregular line called ora serrata.

Several features are visible on the posterior surface of the optic part of the retina:
- Optic disc → where the optic nerve leaves the retina and the central retinal artery
branches to supply the retina, lighter than the surrounding retina.
No light-sensitive receptor cells → blind spot of the retina.
- Macula lutea → found laterally to the optic disc, small area of yellowish coloration with a
central depression called fovea centralis → thinnest area of the retina and with highest
visual sensitivity due to higher concentration of cons rather than rods. One cone connects
with one bipolar cell and with one ganglion cell.

- Retinal periphery → high concentration of rods → more


than one rods connects with one bipolar cell and many
bipolar cells connect with one ganglion cells → one brain cell receive information from
many receptors (sum of impulses)

VESSELS OF THE EYEBALL


Arterial supply
- Short posterior ciliary arteries
- Long posterior ciliary arteries long posterior ciliary and
- Anterior ciliary arteries anterior ciliary arteries make
anastomoses in the choroid
- Central retinal artery
layer

Venous drainage
Vorticose veins are involved in this process → they exit through the sclera from each of the
posterior quadrants of the eyeball and enter the superior and inferior ophthalmic veins.
There is also a central retinal vein traveling with the central retinal artery.

The peripheral cortical vitreous is loosely attached to the internal limiting membrane of
the sensory retina at different sites:
- Vitreous base
- Optic disc margins
- Perifoveal

ANATOMY OF THE ORBIT


Orbits are bilateral structures below the anterior cranial fossa and anterior to the middle
cranial fossa that contain the eyeball, optic nerve, extra-ocular muscles, lacrimal apparatus,
fascia and nerves and vessels supplying these structures.

Seven bones contribute to the framework of each orbit:


- Maxilla
- Zygomatic
- Frontal
- Ethmoid
- Lacrimal
- Sphenoid
- Palatine

These bones give the pyramid-shape appearance to the orbit, with:


- Apex → extending in a posteromedial direction and formed by the optic foramen
- Base → opening anteriorly onto the face, formed superiorly by the frontal bone,
medially by the frontal process of the maxilla, inferiorly by the zygomatic process of the
maxilla, laterally by the zygomatic bone, the frontal process of zygomatic bone and the
zygomatic process of the frontal bone.
Completing the pyramid configuration are:
- Roof (superior wall) → made up of the orbital part of the frontal bone with a small
contribution from the sphenoid bone, separating the contents of the orbit from the the brain
in the anterior cranial fossa.
Posteriorly, the lesser wing of the sphenoid bone completes the roof.

- Medial wall → each consists of four bones: maxilla, lacrimal, ethmoid and sphenoid
bones. At junction between the roof and the medial wall are the anterior and posterior
ethmoidal foramina → anterior and posterior ethmoidal nerves.
Lacrimal bone and frontal process of the maxilla participate in the formation of the lacrimal
groove, which contains the lacrimal sac and is bound by the posterior and anterior
lacrimal crests.

- Floor (inferior wall) → consists primarily of the orbital surface of the maxilla, with small
contributions from the zygomatic and palatine bones → beginning posteriorly and
continuing along the lateral boundary of the floor is the inferior orbital fissure.

- Lateral wall → formed anteriorly by the zygomatic bone and posteriorly by the greater
wing of the sphenoid bone → the superior orbital fissure is between the greater wing and
the lesser wing of the sphenoid.

ANATOMY OF THE EYELIDS


Upper and lower eyelids are anterior structures that when closed protect the surface of the
eyeball → space between the eyelids when they are open is called palpebral fissure.
Layers of the eyelids, from anterior to posterior, consist of:
- Skin (epidermis) and subcutaneous tissue (dermis) → skin is not particularly substantial
and only a thin layer of connective tissue separates the skin from the underlying voluntary
muscle layer. Adnexa lie deep in the dermis or within the tarsal plates.
Epidermis comprises four layers of keratinocytes:
1. Keratin layer
2. Granular cell layer
3. Prickle cell layer
4. Basal cell layer

Dermis is much thicker than the epidermis, made of connective tissue and contains blood
vessels, lymphatics and nerve fibers.

- Meibomian glands → modified sebaceous glands found in the tarsal plates

- Gland of Zeis → modified sebaceous glands associated with lash follicles

- Orbicularis oculi → fibers encountered next in an antero-posterior direction belong to the


palpebral part of the orbicularis oculi. The other part of this muscle is the orbital part,
which surrounds the orbit.
Orbicularis oculi is innervated by the facial nerve [VII].

A third part, called lacrimal part, can be identified → consists of fibers on the medial
border, which pass deeply to attach to the posterior lacrimal crest → involved in the
drainage of tears.

- Orbital septum → it extends downward in the upper eyelid and downward into the lower
eyelid and is continuous with the periosteum outside and inside the orbit.

- Tarsus and levator palpebrae superioris


There is a large superior tarsus in the upper eyelid and a smaller inferior tarsus in the
lower eyelid → they are plates of dense connective tissue.
The main difference between the two tarsal plates is that the superior tarsus is associated
with the levator palpebrae superioris muscle, which raises the eyelid → it is innervated by
the oculomotor nerve [III].
In companion with the levator palpebrae superioris is a collection of smooth muscle fibers
→ superior tarsal muscle, innervated by the postganglionic sympathetic fibers from the
superior cervical ganglion.

- Conjunctiva → thin membrane that covers the posterior surface of each eyelid, before
reflecting onto the sclera of the eyeball. It attaches to the eyeball at the junction between the
sclera and the cornea.
Conjunctival sac is formed when the eyelids are closed and the upper and lower extensions
of this sac are the superior and inferior conjunctival fornices.
The arterial supply to the eyelids include:
- Supratrochlear artery
- Supra-orbital artery
Ophthalmic artery
- Lacrimal artery
- Dorsal nasal arteries

- Angular artery → Facial artery


- Transverse facial artery → Superficial temporal
artery
Venous drainage occurs following an external pattern
through veins associated with the various arteries and
following an internal pattern through connections with
the ophthalmic veins.

Sensory nerves are all branches from V1 and V2 divisions of the Trigeminal nerve [V].

ANATOMY OF THE LACRIMAL APPARATUS


This apparatus is involved in the production, movement and drainage of fluid from the
surface of the eyeball.
It is made of:
- Lacrimal gland and its ducts
- Lacrimal canaliculi
- Lacrimal sac
- Nasolacrimal duct

The lacrimal gland is anterior in the superolateral region of the orbit and it is divided into
two parts by the levator palpebrae superioris:
- Orbital part → found in a depression called lacrimal fossa
- Palpebral part → inferior to the levator palpebrae superioris

Fluid is continually being secreted by the lacrimal gland and moved across the surface of the
eyeball from lateral to medial as the eyelids blink → the fluid accumulates medially in the
lacrimal lake and is drained from the lake by the lacrimal canaliculi.
The lacrimal punctum is the opening through which fluid enters each canaliculus.
Lacrimal canaliculi eventually join the lacrimal sac between the anterior and posterior
lacrimal crests and anterior to the lacrimal part of the orbicularis oculi → when the
orbicularis oculi contracts during blinking, dilation of lacrimal sac occurs and tears are
drawn into it through canaliculi from the conjunctival sac.

The arterial supply to the lacrimal gland is by branches of the ophthalmic artery and
venous drainage is through the ophthalmic veins.

The innervation involves three different components:


- Sensory innervation → through lacrimal branch of the ophthalmic nerve [V1]
- Secretomotor innervation → preganglionic parasympathetic fibers leave the CNS
through the facial nerve, enter the great petrosal nerve until it becomes the nerve of
pterygoid canal.
Once the nerve reaches the postganglionic parasympathetic neurons, postganglionic fibers
join the maxillary nerve [V2] and continue with it untile the zygomatic nerve branches
from it → then it become zygomaticotemporal nerve.
These fibers stimulate fluid secretion from the lacrimal gland.

- Sympathetic innervation → postganglionic sympathetic fibers from the superior


cervical ganglion travel along the plexus surrounding the internal carotid artery → they
leave this plexus as the deep petrosal nerve and join the parasympathetic fibers in the nerve
of pterygoid canal.
EXTRA-
OCULAR
MUSCLES
They are
muscles involved in movements of the eyeball or raising upper eyelids.
The extrinsic muscles include:
- Levator palpebre superioris → most superior muscle in the orbit, its contraction raises
the upper eyelid. Innervation is by the oculomotor nerve [III]

- Superior rectus → its contraction elevates, adducts and internally rotates the eyeball.
Innervated by the superior branch of the oculomotor nerve

- Inferior rectus → its contraction depresses, adducts and externally rotates the eyeball.
Innervated by the inferior branch of the oculomotor nerve

- Medial rectus → its contraction adducts the eyeball. Innervated by the inferior branch of
the oculomotor nerve

- Lateral rectus → its contraction abducts the eyeball. Innervated by the abducent nerve
[VI]

- Superior oblique → its contraction directs the pupil down and out. Innervated by the
trochlear nerve [IV]

- Inferior oblique → its contraction directs the pupil up and out. Innervated by the inferior
branch of the oculomotor nerve
The movements of the eyeball in three dimensions are:
- elevation → moving pupil superiorly
- depression → moving pupil inferiorly
- abduction → moving pupil laterally
- adduction → moving pupil medially
-

intorsion → rotating the pupil medially


- extorsion → rotating the pupil laterally

The arterial supply to the structures in the orbit,


including the eyeball, is by the ophthalmic artery,
branch of the internal carotid artery, given off
immediately after the internal carotid artery leaves the
cavernous sinus.
In the orbit the ophthalmic artery gives off numerous branches:
- Lacrimal artery → supplying the lacrimal gland and muscles
- Central retinal artery → occlusion of this vessels leads to blindness
- Long and short posterior ciliary arteries → supplying structures inside the eyeball
- Muscular arteries → supplying intrinsic muscles of the eyeball
- Supra-orbital artery → supplying forehead and scalp
- Posterior ethmoidal artery → supplying ethmoidal cells and nasal cavity
- Anterior ethmoidal artery → supplying septum and lateral wall of the nasal cavity
- Medial palpebral arteries → supplying medial area of the upper and lower eyelids
- Dorsal nasal artery → supplying upper surface of the nose
- Supratrochlear artery → supplying the forehead

As regards the venous drainage:


- Superior ophthalmic vein → receiving tributaries from companion veins to the branches
of the ophthalmic artery and veins draining the posterior part of the eyeball

- Inferior ophthalmic vein → receiving tributaries from muscles and the posterior part of
the eyeball as it crosses the orbit. Then it leaves the orbit posteriorly by joining with the
superior ophthalmic vein or passing through the superior orbital fissure on its own to join
the cavernous sinus

Numerous
nerves pass
into the
orbit and
innervate structures within its bony wall, including:
- Optic nerve [II]
- Oculomotor nerve [III]
- Trochlear nerve [IV]
- Abducent nerve [VI]
- Autonomic nerves
- Ophthalmic nerve [V1]

OPTIC OF VISION

If all the refractive surfaces of the eye are added together algebraically and then considered
to be one single lens → reduced eye.
In reduced eye, a single refractive surface is considered to exist, with a total refractive
power of 60 diopters (D) → about two-thirds of 60 diopters is provided by the anterior
surface of the cornea (40 D), while the total refractive power of the internal lens of the eye
is only 20 diopters.

The image is inverted and reversed with respect to the object but the mind perceives objects
in the upright position despite the upside-down orientation because the brain is trained to
consider an inverted image as normal.

MECHANISM OF ACCOMMODATION
When the lens is in a relaxed state, with no tension on its capsule, it assumes a spherical
shape → however about 70 suspensory ligaments attach radially around the lens and tension
of these latter causes the lens to remain relatively flat under normal eye conditions.
Also located at the lateral attachments of the lens ligaments to the eyeball is the ciliary
muscle, which has two separate sets of smooth muscle fibers → meridional fibers and
circular fibers:
contraction of meridional fibers allows release of ligaments’ tension on the lens as
contraction of circular fibers induce a sphincter-like action, decreasing the diameter of
circle of ligament attachments → ligaments pull less on the lens capsule.
Thus, contraction of either set of smooth muscle fibers relaxes the ligaments to the lens →
lens assumes a more spherical shape.

Stimulation of parasympathetic nerves contracts both sets of ciliary muscle fibers →


relaxation of lens ligaments → increased refractive power of the lens → improvement of
near vision.

As a person grows older, lens becomes larger and thicker, loosing its elasticity because of
denaturation of lens proteins.
The power of accommodation decreases from about 14 D in a child to essentialy 0 D at the
age of 70 years → lens remains almost totally nonaccommodating in a condition called
presbyopia.
The eyes can no longer accommodate for both near and far vision → to see clearly an older
person must wear bifocal glasses, with the upper segment focused for far vision and the
lower segment focused for near vision.

BINOCULAR VISION
A person normally perceives distance by three main means:
- sizes of the images of objects on the retina
- phenomenon of moving parallax
- phenomenon of stereopsis

This ability to determine distance is called depth perception.

Usually, the brain receives signals from both the eyes at the same time → because one eye is
a little more than 2 inches to one side of the other eye, images on the two retinas are
different from each other.
An object 1 inch in front of the nose forms an image on the left side of the retina of the left
eye and on the right side of the retina of the right eye, while a small object 20 feet in front
of the nose has its image at closely corresponding points in the centers of the two retinas.
Stereopsis → binocular parallax that gives a person with two eyes greater ability to judge
relative distances when objects are nearby than a person with only one eye.

PHYSIOLOGY OF VISION
The major functional segments of either rods and cones are:
- Outer segment
- Inner segment
- Nucleus
- Synaptic body

The light-sensitive photochemical is found in the outer segment


→ rhodopsin for rods and simply color pigment (one of three)
for cons.
In the outer segment we can find lots of discs, where rhodopsin
and color pigments are incorporated in the form of
transmembrane proteins.

The inner segment contains the usual cytoplasm → especially


important are the mitochondria which provide energy for
function of the photoreceptors.

The synaptic body is the portion that connects with subsequent horizontal and bipolar
cells.

Rhodopsin is a combination of the protein scotopsin and the pigment retinal, a particular
type called 11-cis retinal → only this type can bind to scotopsin to synthesize rhodopsin.
When light energy is absorbed by rhodopsin, this latter starts to decompose rapidly due to
transformation of cis form of retinal into an all-trans form, that doesn’t fit anymore with
scotopsin.

The first stage in reformation of rhodopsin is to convert again all-trans retinal into 11-cis
retinal → this process requires metabolic energy and is catalyzed by the enzyme retinal
isomerase.
When 11-cis retinal is formed, recombines automatically with scotopsin to re-form
rhodopsin.
There is also another pathway where all-trans retinal is converted into all-trans retinol,
which is one form of vitamin A → all-trans retinol is converted into 11-cis retinol through
the enzyme isomerase → finally 11-cis retinol is converted into 11-cis retinal, which can
combine with scotopsin to form new rhodopsin.
Night blindness occurs in person with severe deficiency of vitamin A, because without
vitamin A the amounts of retinal and subsequent rhodopsin produced are severely depressed
→ called night blindness because the amount of light available at night is too little to permit
adequate vision.

LIGHT AND DARK ADAPTATION


- Light adaptation (Photopic vision)→ if a person has been in bright light for hours, large
portions of the photochemicals in both the rods and the cons will have been reduced to
retinal and opsins → furthermore, much of the retinal will have been converted into
vitamin A.
In this way the concentrations of the photosensitive chemicals are considerably reduced and
the sensitivity of the eye to the light is reduced too.

- Dark adaptation (Scotopic vision)→ if a person remains in darkness for a long period,
retinal and opsins in the rods and cones are converted back into the light-sensitive
pigments.
Furthermore, vitamin A is converted back into retinal → finally opsins in rods and cons
combine with the retinal.
Observing the dark adaptation curve we can deduce that:
The early portion of of the curve is caused by adaptation of the cones because all the
chemical events of vision occurs four times as rapidly in cones as in rods.
Cones cease adapting after only a few minutes, whereas the slowly adapting rods continue
to adapt for many minutes and even hours, with their sensitivity increasing tremendously.

Dark adaptation takes about 30 minutes to be complete, while light adaptation happens very
quickly, usually in less than 1 minute.

Other important mechanisms for light and dark adaptations are:


- Change in pupillary size
- Neural adaptation → signals transmitted by different cells found in the different layers of
the retina decrease
rapidly in the
various stages of
transmission in
neural circuit when
light intensity
increase. Neural
adaptation occurs in
a fraction of
second.

- Impaired dark
adaptation →
AGE-RELATED
MACULAR
DEGENERATION
VISUAL ACUITY
The average diameter of the cons in the fovea of the retina is about 1.5 micrometers,
however a person can normally distinguish two separate points if their centers lie up to 2
micrometers apart on the retina.
The normal visual acuity of the human eye for discrimination between point sourced of light
is about 25 seconds of arc → light rays from two different points strike the eye with an
angle of at least 25 seconds between them, they can be recognized as two points instead of
one.

The fovea is less than 0.5 millimeters in diameter, which means that maximum visual
acuity occurs in less than 2 degrees of the visual field → outside this foveal area, visual
acuity becomes more progressively poorer.

The chart for testing eyes (SNELLEN TEST) usually consists of letters of different sizes
placed 20 feet away from the person being tested:
- if person can see well letters placed 20 feet far from him/her → 20/20 vision

Clinical method for expressing visual acuity is to use a mathematical fraction that expresses
the ratio of two distances.

Other examination tests are:


- Counting fingers
- Hand motion

COLOR VISION
The color-sensitive pigments of the cones are combination of retinal and photopsins →
only one of the three color pigment is present in each of different cones, thus making the
cones selectively sensitive to different colors.
These color pigments are called:
- Blue-sensitive pigment → 445 nanometers
- Green-sensitive pigment → 535 nanometers
- Red-sensitive pigment → 570 nanometers

All theories of color vision are based on the well-known observation that the human eye can
detect almost all gradations of colors when blue, green and red monochromatic lights are
appropriately mixed in different combinations:
- a monochromatic blue light with a wavelength of 450 nm stimulates the red cones to a
stimulus value of 0, the green cones to a value of 0 and the blue cones to a value of 97 →
this set of ratios 0:0:97 is recognized by the nervous system as blue

- a monochromatic orange light with a wavelength of 580 nm stimulates the red cones to a
value of 99, the green cones to a value of 42 but the blue cones are not stimulated at all →
this set of ratios 99:42:0 is recognized by the nervous system as orange

About equal stimulation of all the red, green and blue cones gives one the sensation of
seeing white → no single wavelength of light corresponding to white → combination of all
the wavelengths of the spectrum.

When a single group of color-receptive cones is missing from the eye, the person is unable
to distinguish some colors from the others:
- a person with loss of red cones is called a protanope
- a person with loss of green cones is called deuteranope

Red-green color blindness is a genetic disorder that occurs almost exclusively in males →
genes in the female X chromosomes code for the respective cones → because the male has
just a single X chromosome, a missing gene can lead to color blindness. (X-linked
recessive disorder)

VISUAL PATHWAYS AND CENTERS


The visual nerve signals leave the retinas through
the optic nerves → at the optic chiasm, the optic
nerve fibers from the nasal retinas cross the
opposite sides where they join the fibers from the
opposite temporal retinas to form the optic tracts.
The fibers of each optic tract then synapse in the
dorsal lateral geniculate body of the thalamus and
from there, geniculocalcarine fibers pass via the
optic radiation to the primary visual cortex in the
medial occipital lobe.
Visual fibers also pass to several older areas of the
brain:
- Suprachiasmatic nucleus of the hypothalamus
→ to control the circadian rhythms

- Pretectal nuclei in the midbrain → to elicit reflex


movements of the eyes to focus on objects of
importance and activate the pupillary light reflex

- Superior colliculus → to control rapid directional movements of the eyes

- PRIMARY VISUAL CORTEX


It lies in the calcarine fissure area and is the terminus of direct visual signals from the eyes
→ signals from the macular area (highest degree of visual acuity) of the retina terminate
near the occipital pole, whereas signals from the more peripheral retina terminate in
concentric half-circles anterior to the pole

- SECONDARY VISUAL AREAS OF THE CORTEX


They lie lateral, anterior, superior and inferior to the primary visual cortex → secondary
signals are transmitted to these areas for analysis of visual meanings.
An important area where virtually all signals from the primary visual cortex are transmitted
next is Brodmann’s area 18.

PHYSICAL AND CLINICAL REFRACTION


The light change its speed and direction at the interface between the two materials
depending on their composition → all mediums have a characteristic index of light rays
refraction (IOR)

- Physical refraction → the IOR of cornea and lens is almost the same → 1.38/1.40
Cornea refracts more because IOR between air and cornea is great → +0.38
Lens refracts weakly because IOR between the aqueous humor and the lens is only +0.07
Aqueous humor and vitreous take a minimal part in refraction → -0.05
The axial eye length of the normal eye is about 23-24 mm → for every 1 mm of axial
length difference, you can anticipate a 3.0 D difference in the refractive error.
- Clinical refraction → ratio between the refraction power of the eye (physical
refraction) and axial length of the eye when its accommodation is paralyzed.
There are two different types of clinical refraction:
1. Static refraction → refraction of the eye without accommodation
When parallel light rays refracted from optic system are focused on the retina →
emmetropia → the optical power must correspond exactly to the axial length

When the parallel rays of light cannot focus on the retina, refractive error develops →
ametropia

There are three common types of static refractive errors:


1. Myopia → focus of light rays is in front of the retina →
far-away objects look blurry

2. Hyperopia → focus of light rays is behind the


retina → vision is blurry at any distance

3. Astigmatism → different curvatures of the meridians of the cornea with multiple focus
points → cornea is shaped more like an egg than a sphere → all objects at far-away and
nearby positions look blurry

Ametropia develops by three main mechanisms:


- Axial ametropias → the eye has a normal refractive power but the length of the eye is
too long (myopia) or too short (hyperopia) → axial length is the most influential factor for
emmetropization of the human eye

- Refractive ametropias → the eye has normal axial length but the refractive power is too
strong (steeply curved lens – myopia) or too weak (flat curved lens – hyperopia).
About 80% of refraction occurs in the cornea while the remaining 20% in the inner
crystalline → newborns are hyperopic (+ 2.00 to + 4.00 D) and emmatropisation is
completed at the age of 5-6 years.
If the cornea is not perfectly spherical → astigmatism

- Correlational ametropias → when the components of physical refraction deviate from


normal → it results of improper combination of normal parameters of:
1. Physical refraction → 55-65 D
2. Axial length → 23-24 mm

55 D + 23 mm → focus behind the retina → hyperopia


65 D + 24 mm → focus in front of the retina → myopia

Both genetic and environmental factors may be involved in development of refractive


errors:
- The spectral composition of light can influence development of myopia → short waves
(external light) seems to slow down the growth of the eyes, while long waves seems to
increase the growth of the eyes leading to the development of myopia

- During close proximity, represented by a relatively large accommodation stimulus, the


accommodative response lags behind the stimulus → chronic hyperopic defocus

- Of course genetics plays a fundamental role in development of refractive errors → for


example, a myopic person may be born with an eye more long than normal → increased
axial length

2. Dynamic refraction → refraction of the eye using accommodation


If the ciliary muscle is relaxed → ligaments of Zinn are stretched and the lens becomes
flat with less refractive power.
During contraction of the ciliary muscle → ligaments of Zinn are relaxed and the lens
assumes a more convex shape, with an increased refractive power

In this case, refractive errors are associated to deficit of accommodation.


The most common dynamic refractive error is Presbyopia, physiologic phenomenon related
to increasing of age → after the age of 60 the lens completely loses its elasticity and cannot
change its shape anymore → loss of accommodation.

METHODS FOR EXAMINATION OF REFRACTION


1. Subjective refraction → major method of examining patients’ eye refraction,
beginning by testing visual acuity.
An eye test chart with rows of letters (optotypes) with a gradually decreasing size is used,
located in front of the patient at 20 feet (5/6 meters) → the lowest row of optotypes clearly
seen by the patient is recorded.
Normal vision → 20/20 , 5/5 or 1.0

VA = distance of the patient from the chart / distance at which a healthy eye can see those
optotypes

A preliminary test is performed using a Pinhole occluder: light passes only through the
center of the lens of the eye and errors in lens refraction do not affect visual acuity.
If the visual acuity of the eye improves, the presence of refractive error is assumed → we
continue with correction of the refractive error through different lenses.
The study begins by testing the patient’s vision with a series of + and – lenses, with
increasing power and asking the person to make a comparison between these latter, telling
with which lens the image is clearer.

You need to start by putting on + 0.50 spherical lenses → if vision doesn’t improve instead
worsens, you should continue with – lenses.
If a clear image with spherical lenses is not achieved → astigmatism → cylindrical lenses.

- When correcting myopia → the weakest – lens is chosen → if you correct with a stronger
minus diopter, the focus shifts behind the retina, which leads to inclusion of
accommodation and the appearance of discomfort when looking away

- When correcting hyperopia → the strongest + diopter is prescribed → in order to be


completely excluded accommodation especially in young people

It is important to compare the new refraction back and forth with the old glasses and to
consider the problems that patients need to adapt to the new glasses.

- AUTOREFRACTOMETRY
It’s a computer-controlled machine used during an eye examination to provide an objective
measurement of a person’s refractive error and prescription for glasses or contact lenses.
The amount of light reflected from the retina is measured.

- RETINOSCOPY
It is an objective method that measures the refractive error of the eye, done by looking
through an optical instrument called retinoscope to observe the movement of reflected light
in a patient’s pupil.
There are four main refractive states of the eye:
- Emmetropia → refractive state wherein parallel light rays are focused on the fovea,
emerging as parallel light rays → if this is the case, neutralization will be observed

- Myopia → refractive state wherein light rays are focused in front of the retina, emerging
as converging light rays → with-motion will be observed

- Hyperopia → refractive state wherein light rays are focused behind the retina, emerging
as diverging light rays → against-motion will be observed

- Astigmatism → light rays form two points of focus in the eye → both with-motion and/or
against-motion can be observed

For relaxation of patient’s accommodation → asking the patient to fixate on a distant target
or by using cycloplegic agent dilating the eyes.
SYSTEMATIC ORDER OF EYE EXAMINATION

There are three major part of examination of eye and related structures:
PATIENT HISTORY
1. Sensory complaints
- Irritation and feeling of foreign body → conjunctivitis, foreign body, conjunctival
tumour
- Pain in the forehead → refractive anomalies, accommodative asthenopia
- Trigeminal pain → glaucoma, neuralgia, shingles
- Eye pain → disease of adnexa, cornea, anterior uvea

Pain may be:


- Acute → orbital cellulitis, acute keratitis, glaucoma attack
- Chronic → chronic iridocyclitis, stromal keratitis
- Intermittent pain → corneal epithelial dystrophy, bullous keratopathy
- Pain with eye movement → retrobulbar neuritis, posterior scleritis, chronic
osteoperiostitis

2. Visual complaints
Symptoms in eye diseases with normal visual acuity:
- Mobile opacity ‘spiders’ or stripes → degeneration and detachment of the vitreous
- Sudden onset of rain of spots and flies → vitreous detachment, haemorrhage or
inflammatory exudate in the vitreous body

- Photopsies → retinal traction or retinal inflammation


- Micropsies/Macropsies/Polymorphopsies → image distortion → macular inflammation
and degeneration

Symptoms in eye diseases with impaired visual acuity:


- Total decreased vision → from blurred to complete loss → sudden loss of vision with
occlusion of central retinal artery
- Central vision disorder → corneal leukemia, cataract, macular disease
- Peripheral vision disorder → peripheral retinal disease, visual pathway damage,
glaucoma
3. Red-eye
- Sudden single eye redness without other complaints → subconjunctival haemorrhage
- Sudden binocular redness with severe swelling of the eyelids, profuse tearing and
preserved vision → allergic conjunctivitis
- Gradual one-eye redness with irritation, secretion and preserved vision →
conjunctivitis

- Gradual single-eye redness with pain, photophobia, blepharospasm, tearing and gradual
decrease in vision → keratitis and iridocyclitis

- Gradual single-eye redness with pain, exophthalmos, secretion and initial preservation
of vision → orbital cellulite

- Rapid eye redness


with severe
trigeminal pain and
severe vision loss →
acute glaucoma
attack
FAMILY HISTORY
Hereditary eye diseases:
- Myopia
- Corneal dystrophies
- Retinal degenerations
- Cataracts
- Primary glaucoma
- Diabetic retinopathy

PAST ILLNESSES
- Allergic diseases → asthma
- CV diseases → arterial hypertension, atherosclerosis
- Diabetes
- Blood diseases → anaemia, leukemia
- Autoimmune diseases → rheumatoid arthritis, thyroiditis
- Systemic infections → TB, toxoplasmosis, hepatitis, brucellosis

FUNCTIONAL RESEARCH
1. Visual acuity
- Snellen visual acuity
- Counting fingers (CF)
- Hand movements (HM)
- Perception of light (PL)

2. Colour perception
Normal colour perception requires all three primary colours (red, green, blue) to match
them within the spectrum.
Any given cone pigment may be deficient – protanomaly or entirely absent – protanopia.
Trichromats posses all three types of cones, while absence of one or two types of cones
renders an individual dichromat or monochromat, respectively.
Most individuals with congenital colour defects are anomalous trichromats:
- Red-green deficiency → caused by abnormality of red-sensitive cones → protanomalous
while caused by abnormality of green-sensitive cones → deuteranomalous
- Blue-green deficiency → very rare → cause by abnormality of blue-sensitive cones →
tritanomalous

The Ishihara test is designed to screen for congenital protan and deuteran defects.

In colour-blind people, all the dots in one or more plates will appear similar or the same.

Dyschromatopsia (colour blindness)


may be acquired in patients with eye
diseases that affect the optic nerve or the
retina.
3. Visual field assessment
- Donder’s test → patient and examiner cover their opposite eyes while other eyes are fixed
between them. Examiner moves his hand and the patient must determine the boundary of
his/her field of vision

- Standard automated perimetry


The normal eye can detect stimuli over a 120° range vertically and a nearly 160° range
horizontally.
From the point of fixation, stimuli can be detected:
- 60° superiorly
- 70° inferiorly
- 60° nasally
- 100° temporally

Nerve fibres pass through sclera at the optic nerve head, typically 10°-15° nasal to fixation
→ at this location no photoreceptors are present, creating a normal absolute scotoma (point
of total loss of vision).

Perimetry refers to the systematic measurement of the visual field and is an essential
component of defining mainly the extent and progression of glaucoma.
All perimeters measure sensitivity to stimuli at multiple locations in the visual field →
usually a white stimulus is projected on a white background to determine the threshold
values.

Stimuli presented by perimeters can be:


- Static → stationary stimuli are presented at defined points in the visual field
- Kinetic → a stimulus is moved from a non-seeing area to a seeing area and the location
where the object is first seen is recorded

Summary measures of visual field performance include:


- Visual field index (VFI) → expresses the visual field status as a percent of a normal age-
adjusted visual field

- Mean deviation → categorized as normal or abnormal p-value, which lower p values


corresponding with a greater clinical significance

Several measures should be incorporated into an assessment of how reliable or meaningful


the results of a single visual field test are:
- Fixation losses → identified as a result of positive responses to stimuli presented in the
blind spot

- False positives → occur when patient responses are noted in the absence of a presented
stimulus

- False negatives → identified when, retesting a previously tested location with a stimulus
brighter than the measured threshold value, no response is detected
Visual fields were not included into the normative database if rates of FL, FP and FN
exceeded 33%.

4. Examination of refraction
- Retinoscopy → is an exam technique that measures the refractive error of the eye, done by
looking through an optical instrument called retinoscope to observe the movement of
reflected light in a patient’s pupil.
There are four main refractive states of the eye:
- Emmetropia → refractive state wherein parallel light rays are focused on the fovea,
emerging as parallel light rays → if this is the case, neutralization will be observed

- Myopia → refractive state wherein light rays are focused in front of the retina, emerging
as converging light rays → with-motion will be observed

- Hyperopia → refractive state wherein light rays are focused behind the retina, emerging
as diverging light rays → against-motion will be observed
- Astigmatism → light rays form two points of focus in the eye → both with-motion and/or
against-motion can be observed

For relaxation of patient’s accommodation → asking the patient to fixate on a distant target
or by using cycloplegic agent dilating the eyes.

- Autorefractometry
It’s a computer-controlled machine used during an eye examination to provide an objective
measurement of a person’s refractive error and prescription for glasses or contact lenses.
The amount of light reflected from the retina is measured.
- Keratometry
It’s a technique used to measure the anterior curvature of the cornea, allowing the doctor to
determine the corneal refractive power, which can be expressed as an optical power or as a
radius of curvature of the cornea.
The degree of curvature of the vital corneal meridians is measured by the way light is
indicated on the mirror.
Automated keratometry uses optical sensors and specialized software to compare the
patient’s cornea with a standard value database.

5. Examination of extra-ocular muscles


- Hirschberg test → screening test that can be used to assess whether a person has
strabismus.
It is performed by shining a light in the person’s eyes and observing where the light reflects
off the corneas:
- Exotropia → light lands on the medial aspect of the cornea
- Esotropia → light lands on the lateral aspect of the cornea
- Hypertropia → light lands on the inferior aspect of the cornea
- Hypotropia → light lands on the superior aspect of the cornea

- Krimsky test → very similar to the Hirschberg test


- Cover test → done by covering one of the eye and asking the patient to look an object
placed at about 40 cm. After few seconds, the covered eye is uncovered and its movement
should be observed to differentiate a tropia from a phoria:
- Tropia → misalignment of the eyes always present, even when they are both open and try
to work together
- Phoria → misalignment of the eyes that only appear when the binocular vision is broken
and the two eyes are no longer looking at the same object

Cover test helps to differentiate between different types of phorias:


- Exophoria→ eye turns outward
- Esophoria → eye turns inward
- Hyperphoria → eye turns upward
- Hypophoria → eye turns downward

6. Examination of binocular vision


- Worth’s four dot test → clinical testing assessing binocular vision, including diplopia,
suppression and anomalous retinal correspondence.
Patient should wear the red-green glasses, conventionally with the red lens covering the
right eye, then are shown to him/her 4 illuminated dots in a diamond shape → 1 red on top,
2 green on the sides and 1 white on the bottom.
The patient is then asked to describe what they see, including number, location and color of
the lights:
- Four dots → normal result in patients with normal alignment in patients with manifest
strabismus indicated anomalous retinal correspondence

- Two red dots → left eye suppression

- Three green dots → right eye suppression


- Five dots with red on the right and green on the left → uncrossed diplopia → esotropia

- Five dots with red on the left and green on the right → crosses diplopia → exotropia

- Synoptophore

7. Examination of adenxa
- Ophthalmometry
- Examination of lacrimal apparatus and lacrimal production
- Examination of upper and lower eyelids conjunctivas

8. Examination of the anterior eye segment


- Slit-lamp microscopy → purpose of slit lamp examination is to determine the position,
depth and size of any abnormalities.
Direct illumination with a diffuse light is used to visualize a cross-section of the cornea →
further narrowing of the beam to a very thin optical section moved across the cornea can
determine the depth of a lesion.
The use of red-free filter makes red objects appear black → useful for observing vascular
structures.
Usually a cobalt blue filter is normally used in conjunction with fluorescein.

Scleral scatter involves decentring the slit beam laterally → light is transmitted within the
cornea by total internal reflection.
This technique is especially useful to detect stromal haze or cellular/lipid infiltration.

Retroillumination uses reflected light from the iris or fundus after pupil dilation to
illuminate the cornea → allows detection of fine epithelial and endothelial changes, like
epithelial cysts.

9. Examination of the posterior eye segment


- Direct ophthalmoscopy → very helpful for viewing the retina, retinal blood vessels and
optic nerve, and very useful in identifying ocular as well as systemic pathology.
The light beam from the ophthalmoscope cane be used to illuminate the cornea, allowing
detection of foreign body, check the pupil for irregularity and determine the light reflexes.
Some ophthalmoscopes incorporate a cobalt blue filter which allows visualization of
corneal abrasions and ulcers after the insertion of fluorescein.

There are two important rules for a correct examination:


- Right-right-right → the observer should examine the right
eye of the patient using his/her right eye and holding the
ophthalmoscope with his/her right hand

- Left-left-left → the observer should examine the left eye of


the patient using his/her left eye and holding the
ophthalmoscope with his/her left hand

- Indirect ophthalmoscopy → produces a reversed, inverted


image magnified 2 to 5 times using a BIO (binocular indirect
ophthalmoscope) device.
10. Examination of anterior chamber angle
- Gonioscopy → used for evaluation of the anterior chamber (AC) angle.
This angle cannot be visualized through intact cornea, because light from angle structures
undergoes total internal reflection at the anterior surface of the precorneal tear film →
because the refractive index of a goniolens is similar to that of cornea, it eliminates total
internal reflection by replacing the tear film-air interface with a tear film-goniolens
interface.
Light rays can then be viewed as they exit the contact lens.

1. Direct gonioscopy → direct because light rays from the angle are viewd directly, without
reflection inside the lens and they do not require slit lamp.

2. Indirect gonioscopy → lenses used in indirect gonioscopy use mirrors to overcome total
internal reflection, by redirecting light from the angle so that it exits the eye perpendicularly
to the lens-air interface.
Goldmann three-mirror lens has one mirror dedicated to viewing the angle, with the other
two mirrors for examination of the peripheral retina → they are coupled to the cornea by
means of a viscous methylcellulose fluid.
Anatomy of the anterior angle of the eye
- Scleral spur → most anterior projection of the sclera and site of attachment of
longitudinal muscle of the ciliary body → narrow whitish band

- Ciliary body band → just behind the scleral spur, to which is attached, seen as a pink,
dull brown band → tends to be narrowed in hypermetropic eyes and wider in myopic
eyes.

- Trabecular meshwork → it has a ground-glass translucent appearance


- Schlemms canal →it communicates with the anterior chamber through the trabecular
meshwork, while externally it is perforated by aqueous collector channels which branch
into intrascleral and deep scleral plexi → may be identified in the angle as a slightly
darker line deep to the posterior trabeculum

- Schwalbe line → appearing whitish to variably pigmented.


Anatomically it demarcates the peripheral termination of Descemet membrane and the
anterior limit of the trabeculum.

- Iris processes
- Blood vessels

Pathological findings
- Primary angle-closure glaucoma
- Anterior uveitis
- Angle recession
- Foreign bodies
- Iris or angle melanoma

11. Assessment of intra-ocular pressure


Goldmann applanation tonometry is based on the Imbert-Fick principle:

pressure inside the sphere equals the force necessary to flatten its surface divided by the area
of flattening

The intra-ocular pressure (IOP) is proportional to the pressure applied on the cornea an its
thickness.
Small amount of fluorescein is placed into the conjunctival sac and the patient is positioned
at the slit lamp with his/her head firmly against the headrest.
With the cobalt blue filter in place and
illumination of maximal intensity, the prism is
centred in front of the apex of the cornea and is
advanced until it just touches the apex.
A pattern of two green semi-circular mires will be
seen, one above and one below the horizontal
midline.
12. Imaging diagnostic
- Echography
- X-ray
- Computerized axial tomography (CAT)
- Magnetic resonance imaging (MRI)

- Optical coherence tomography (OCT) → Optical coherence tomography (OCT) and


optical coherence tomography angiography (OCTA) are non-invasive imaging tests. They
use light waves to take cross-section pictures of your retina.
With OCT, your ophthalmologist can see each of the retina’s distinctive layers. This allows
your ophthalmologist to map and measure their thickness. These measurements help with
diagnosis.
They also guide treatment for glaucoma as well as retinal disease, like age-related macular
degeneration (AMD) and diabetic eye disease.
Optical coherence tomography angiography (OCTA) takes pictures of the blood vessels in
and under the retina. OCTA is like fluorescein angiography. But it is a much quicker test and
does not use a dye.
MOST FREQUENTLY USED DRUGS IN OPHTHALMOLOGY AND METHODS
OF THEIR ADMINISTRATION
REFRACTIVE ERRORS

PHYSICAL AND CLINICAL REFRACTION


The light change its speed and direction at the interface between the two materials
depending on their composition → all mediums have a characteristic index of light rays
refraction (IOR)

- Physical refraction → the IOR of cornea and lens is almost the same → 1.38/1.40
Cornea refracts more because IOR between air and cornea is great → +0.38
Lens refracts weakly because IOR between the aqueous humor and the lens is only +0.07
Aqueous humor and vitreous take a minimal part in refraction → -0.05
The axial eye length of the normal eye is about 23-24 mm → for every 1 mm of axial
length difference, you can anticipate a 3.0 D difference in the refractive error.

- Clinical refraction → ratio between the refraction power of the eye (physical
refraction) and axial length of the eye when its accommodation is paralyzed.
There are two different types of clinical refraction:
1. Static refraction → refraction of the eye without accommodation
When parallel light rays refracted from optic system are focused on the retina →
emmetropia → the optical power must correspond exactly to the axial length

When the parallel rays of light cannot focus on the retina, refractive error develops →
ametropia

Ametropia develops by three main mechanisms:


- Axial ametropias → the eye has a normal refractive power but the length of the eye is
too long (myopia) or too short (hyperopia) → axial length is the most influential factor for
emmetropization of the human eye

- Refractive ametropias → the eye has normal axial length but the refractive power is too
strong (steeply curved lens – myopia) or too weak (flat curved lens – hyperopia).
About 80% of refraction occurs in the cornea while the remaining 20% in the inner
crystalline → newborns are hyperopic (+ 2.00 to + 4.00 D) and emmatropisation is
completed at the age of 5-6 years.
If the cornea is not perfectly spherical → astigmatism
- Correlational ametropias → when the components of physical refraction deviate from
normal → it results of improper combination of normal parameters of:
1. Physical refraction → 55-65 D
2. Axial length → 23-24 mm

55 D + 23 mm → focus behind the retina → hyperopia


65 D + 24 mm → focus in front of the retina → myopia

Both genetic and environmental factors may be involved in development of refractive


errors:
- The spectral composition of light can influence development of myopia → short waves
(external light) seems to slow down the growth of the eyes, while long waves seems to
increase the growth of the eyes leading to the development of myopia

- During close proximity, represented by a relatively large accommodation stimulus, the


accommodative response lags behind the stimulus → chronic hyperopic defocus

- Of course genetics plays a fundamental role in development of refractive errors → for


example, a myopic person may be born with an eye more long than normal → increased
axial length

2. Dynamic refraction → refraction of the eye using accommodation


If the ciliary muscle is relaxed → ligaments of Zinn are stretched and the lens becomes
flat with less refractive power.
During contraction of the ciliary muscle → ligaments of Zinn are relaxed and the lens
assumes a more convex shape, with an increased refractive power

In this case, refractive errors are associated to deficit of accommodation.

STATIC AMETROPIAS
- MYOPIA → patient won’t be able to focus on far-away objects because the light rays will
be placed in front of the retina.
There are two main categories of myopia:
1. Axial myopia → due to increased axial length, dived into mild form (under 6 D) and
degenerative form (over 6 D).

2. Refractive myopia → due to a change in IOR

The most common form is the axial myopia.

Risk factors
- Genetic factors → if one or both parents have myopia, there is an increased chance their
children will have it too
- Working at a computer
- Playing videogames
- Reading
Generally starts in the childhood until about the age of 20 years old, when the eyeball stop
to grow.

Symptoms
Myopia symptoms may include blurry vision when looking far objects, headache, eyestrain
and need to partially close the eyelids to see clearly

High myopia is a more serious form of the condition, where the eyeball grows more than it
is supposed to and becomes very long front to back.
It can raise your chance of having other conditions like:
- Detached retina
- Cataracts
- Glaucoma

Myopia is corrected by using biconcave minus lenses (divergent) by glasses or contact


lenses or through eye surgery techniques like LASIK.

- HYPEROPIA → light rays will focus behind the retina, the opposite phenomenon of
myopia → this will cause blurred vision both for near and far vision.
There are two main categories of hyperopia:
1. Axial hyperopia
We can divide this main category into three sub-categories:
- Physiologic hyperopia of newborns → newborns present a hyperopia of 2/3 D until
eyeball reaches normal axial length around the age of 6 years.
If the newborn presents emmetropia or less marked hyperopia → more predisposed to
myopia.

- Congenital microphtalmos → ocular structures are smaller than normal, subject present
elevated hyperopia → greater than 6 D

- Acquired hyperopia → may be due to different conditions such as retrobulbar tumors


or retinal detachment

2. Refractive hyperopia → usually associated to conditions like cortical cataract, flat


cornea or abnormal distance between cornea and lens

Symptoms
- Asthenopia (eyestrain)
- Headache
- Watering of the eyestrain
- Mild aversion to the light

Hyperopia is corrected by using biconvex plus lenses (convergent) by glasses or contact


lenses or through surgical treatments like Photorefractive keratectomy (PRK) or
Hypermetropic LASIK.

- ASTIGMATISM
It’s a condition found both in subjects with myopia or hyperopia or can be found as a single
refractive error.
Manifested as a distorted perception of near and far-away objects, with pronounced
alteration of horizontal, vertical and oblique lines.
This condition is usually associated to an irregular curvature of the cornea → egg shape
with meridians having different curvatures → multiple focal points.
Astigmatism may be also irregular when all meridians are irregular and each point on the
meridian has own IOR.

Risk factors
Astigmatism is usually hereditary and it isn’t related to health conditions. Some conditions
that can cause astigmatism are eye injuries, keratoconus or complications after eye
surgery.

Symptoms
- Blurry vision
- Headaches
- Eyestrain
- Trouble seeing at night

Astigmatism is corrected through cylindrical lenses, which can be both convex or concave.
The axis should always be translated of 90° from the position of the most curved meridian
→ therefore should be perpendicular.

In case of simple astigmatism → we should use a cylindrical lens with perpendicular axis
respect to the axis of the most curved meridian

In case of compound astigmatism → we should use a spherical lens (correction of myopia


or hyperopia) + a cylindrical lens perpendicular to the axis of the most curved meridian →
sphero-cylindrical lens.

DYNAMIC AMETROPIAS
- Presbyopia
It’s a physiopathological process concerned to ‘all humans of the Earth’.
If the ciliary muscle is relaxed → ligaments of Zinn are stretched and the lens becomes
flat with less refractive power.
During contraction of the ciliary muscle → ligaments of Zinn are relaxed and the lens
assumes a more convex shape, with an increased refractive power

In this case, refractive errors are associated to deficit of accommodation.


The most common dynamic refractive error is Presbyopia, physiologic phenomenon related
to increasing of age → after the age of 60 the lens completely loses its elasticity and cannot
change its shape anymore → loss of accommodation.
Usually it begins at the age of 40 years until 60 years, when the eye loses completely its
power of accommodation.
Sclerosis of the lens will occur progressively, loosing 0.5 D each 5 years → usually at 60
years old, spherical lenses with + 3 D should be wore.

In myopic subjects usually this condition occurs lately or it doesn’t occur at all, because
their next point is nearer than emmetropic subjects.

In hyperopic subjects usually presbyopia occurs earlier (before 40 years) and it develops
more rapidly (3 D before 60 years)
Risk factors
- Having hyperopia
- Taking some medications like antidepressants
- Certain conditions like diabetes, multiple sclerosis or CV disease

As regards correction of presbyopia:


- in myopic subject → we should add positive diopters to power of his/her negative
spherical lenses → if subject has -1 D of myopia and he/she needs +3 D, final power of
lenses will be +2 D

- in hyperopic subject → opposite situation → if subject has +2 D and he/she needs +3 D,


final power of lenses will be +5 D

There are different types of lens:


- Reading glasses → for subjects who don’t have myopia, hyperopia or astigmatism

- Bifocal lenses → lens has two different focuses, one for near vision and one for far-away
vision

- Multifocal/ Progressive → the upper portion of the lens will allow far vision, while going
down the lens, spherical power will increase, allowing near vision

Following laser procedures correct presbyopia by using monovision → one eye corrected
for distance, the other corrected for near vision:
- PRK surgery
- LASIK surgery
NORMAL VS PATHOLOGICAL PUPILLARY REACTIONS

The physiology behind a normal pupillary constriction is a balance between the SNS and the
PNS:
- PNS → leads to pupillary constriction. A circular muscle called the sphincter pupillae
encompasses the pupil → the pathway of pupillary constriction begins at the Edinger-
Westphal nucleus near the oculomotor nucleus

- SNS → leads to pupillary dilation. Dilation is controlled by dilator pupillae, a group of


muscle in the peripheral 2/3 of the iris → fibres from the superior cervical ganglion of the
sympathetic trunk travel through the carotid plexus and enter into the orbit through the
ophthalmic division [V1] of the trigeminal nerve

Normal size varies from 1-8 mm.

ANISOCORIA
Refers to the asymmetric sizes of pupils → the variation should not be more than 1 mm
between the two eyes and both eyes should react to light normally.
RELATIVE AFFERENT PUPILLARY
DEFECT
It is a defect in direct response → due to
damage in optic nerve or severe retinal
disease.
If an optic nerve lesion is present, the
affected pupil will not constrict to light when
it is pointed towards the pupil during the
swinging flashlight test.

Some causes of RAPD include:


- Optic neuritis
- Retinal disease
- Severe glaucoma
- Retinal detachment
- Traumatic optic nerve damage

ADIE’S TONIC PUPIL


It is an anisocoria where the abnormal pupil is larger and does not constrict to light, but
slowly constricts to accomodation.

HORNER’S SYNDROME
Loss of sympathetic innervation, causing the clinical triad of:
- Ptosis
- Miosis
- Anhidriosis → decreased seating of the face

Main causes of Horner’s syndrome include:


- Carotid artery dissection
- Pancoast tumours
- Brachial plexus injury
- Cavernous sinus thrombosis

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