By Chandrashekhar Chawan 1 history

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Artificial Eye (Ocular Prosthesis)

By Chandrashekhar Chawan


Since ancient times Artificial Eyes have been used to escape the terror of stigmatisation due to Ocular Disfigurement. The Artificial Eyes used to be made of gold and precious stones.

In India there are references to artificial eye or eye transplant, dating back to 5600 BC from Shalivahan Shaka Parva in the book called “Garbhopanishad” written by Shri Garbbhacharya in 2 BC. One can find references to artificial eyes and eye transplants.

In Takshashila region during Shri Chanakyas time one Nilakumari mentions in her book called “Neelavati” an operation which she performed on an 8 year old girl who had lost her eye due to penetrating injury.

In 444 AD in Nalanda Vidyapith Shri Nagarjunbharda was in-charge of Human Medicine and Animal Medicine and used to perform eye surgery.

In 632 AD Shri Charak, Shri Shushrut and Shri Vagbhat were among the leading cosmetic surgeons who performed many operations on humans to cure disfigurement.

King Shashankdev of Vikramshila region has awarded an eye made of gold as a trophy to Acharya Prashastpad , in 633 AD, for his work in eye surgery on patients who had lost their eyes due to small pox.

Goat’s eyes wrapped in some ‘keratin’ substance and implanted in the eye socket gave the effect of a natural eye; however this type of cosmetic eye is smaller than the natural human eye. This is referred to in the book “Sughatan Shalyachikitsa”.

The Vikramshila Dynasty was destroyed in 1210 AD by the Moguls and all the knowledge and most of the books written on “Tadapatra” (large tree leaves dried and cured) were burnt by the Mogul invaders.

Since 1446 Portuguese Doctors introduced their system of medicine. From 1670 the British introduced the Greek Medicine which is followed to this day.

Technical developments, in the 18th and 19th centuries, in medicines and medical technologies accelerated the general developments.

It is an interesting thought that, if the best of all the medical systems available today, were to be integrated to develop a single system, for the betterment of the human society.

Ludwig Muller, a glass blower, used to make doll’s eyes, developed cryolite glass eyes. The breakage problems of glass led to the development of new materials.

Germany was the major supplier of glass eyes. During world II, the glass eye supply became scarce and technologist started experimenting with plastics.

Now all over the world Artificial Eyes are made of PMMA (poly methyl methacrylate) and only in some parts of Europe and Germany glass eyes are still manufactured.

PMMA is found to be biocompatible material, is non-allergic and gives life like effect to artificial eyes.

Readymade artificial eyes are made in large quantities to stock and are available in the market since 40-50 years. Though they are cheap and easily available they cannot be fitted to all, certainly not to special cases, and if fitted present problems such as excessive eye discharge, poor comfort, poor cosmetic matching, restricted wearing periods and reduced translate ocular movement. In the long run they cause sagging of the lower lid and in some cases contracted eye socket.

Depending on the chain of polymers the quality of PMMA is determined. A simple acryl ate is brittle and breaks easily. Whereas, High Density Medical Grade PMMA is very useful for making an artificial eye.

The stock eyes available in the market today are made from low-grade plastic. Hence they become discoloured and develop cracks after a few years and need frequent replacements.

For making Custom made artificial eyes a High-Density Medical Grade PMMA is used, in order to overcome all the problems of simple acrylic. It is not only tough but also very clear like glass, hence gives a more natural look to the Artificial Eye.

As the art and science of Ocular Prosthesis is making progress all over the world, people are becoming aware of the advantages of custom made artificial eye, and are using them for cosmetic rehabilitation. The role of the “stock eye” is becoming limited around the world and they are used as a “stop gap” arrangement initially, till a “Custom Made Artificial Eye” is prepared.

I India and other developing countries large number of patients have to depend on stock eye as the number of Ocularists fitting custom made artificial eye is limited.


The sense of vision is based on a step-wise process in which rays of light are focused on the Retina, where it is converted in to an electrical signal and is conveyed through the visual pathways to the brains occipital cortex. This signal is interpreted as a visual message by the brain. If any part of the system is affected by a disease, vision may be impaired.

As an Ocularist one should know the parts of the eye, its surrounding tissues, and its connections in the brain. As each part is described, you will know its structure (anatomy), function (physiology) and how it can become diseased (pathology).

The Ocular Adnexa (Fig. 1.1)

Ocular adnexa is the tissue surrounding the eye, it protects and preserves the normal function of the eyes. The Ocular Adnexa include:

  • Eyelids and Conjunctiva

  • Lacrimal apparatus

  • Orbit

  • Extraocular muscles

The Eyelids and Conjunctiva

The eyelids are moving folds of soft tissue that protect the outer portion of the eyeball from injury, exclude light and lubricate the front surface of the eye.

The blinking action of the upper lid spreads lubricating tear film over the front surface of the eye.

The elliptical opening between the upper and the lower lids is called the “Palpebral Fissure”. The normal size of the palpebral fissure is about 15 mm when the lids are open.

The inner junction of the lids is called the “Medial Canthus” and the outer junction is called the “Lateral Canthus”. The medial canthus contains folds of fleshy tissue. The deeper one is called the “Plica Semilunaris” (semi-lunar fold) and the more visible one is the “Caruncle” . The medial lid margins of the upper and lower lids contain small openings to the tear drainage system that is called the “Puncta”.

The anterior edge of the lid margins contains the hair follicles for the eyelashes (cilia). The lashes serve to sweep airborne particles away from the eye during a blink. Oil secreting glands called “Meibomian Glands” are situated on the posterior edge of the lid margin. Just in front of these glands is the grey line, which divides the inner (close to the eye), and outer portions of the lid margin.

Acute inflammation of a lash follicle is called a “Stye” (hordeolum exter num). It is a reddened, sore lump near the lid margin. Further from the lid margin, chronic inflammation may involve a meibomian gland producing a chalazion.

Blepharitis is the term applied to diffuse inflammation of the lid margin, which is usually the result of an overgrowth of the normal bacterial population of the lid. Patients with Blepharitis have reddened, crusted lid margins usually covering the entire extent of the lid.

The eyelids are composed of an outer layer of skin, an inner layer of palpebral conjunctiva and a layer of fibrous tissue and muscle between the two. The fibrous layer, called the “Tarsal Plate”, gives the lid its firmness. The orbicularis oculi is circular muscle that, upon contraction, results in forced eyelid closure, as in winking. The upper lid is raised by the levator plpebral superioris muscle, which attaches to the upper tarsal plate. The muscle is part of a group of extraocular muscels those are controlled by the third cranial (oculomotor) nerve.

Instead of lying in its normal position against the eyeball, the lid margin may turn away from or towards the globe. This turning out of the margin is called “Ectropion” and may lead to drying and irritation of the exposed cornea and conjunctiva.

An inward turning of the lid margin is called “Entropion”, in this condition, eye lashes may rub against the cornea and cause irritation and tearing, Inward turning of eye lashes is known as “Trichiasis”.

Loss of function of the levator muscle results in “Ptosis” a droopy upper eyelid that no longer elevates normally.

Diseases which affect the skin elsewhere on the body, may affect the skin of the lids. Careful examination may reveal dermatitis, cysts or tumours (especially basal cell carcinomas).

The conjunctiva is the translucent mucous membrane that lines the inner surface of the lids (the palpebral portion of the conjunctiva).

The bulbar conjunctiva ends at the limbus. The junction of the bulbar conjunctiva and the palpebral conjunctiva is called the “Fornix” or “Cul-de-Sac”.

The conjunctiva may become inflamed, due to bacterial or viral infection or because of an allergic reaction, is called “Conjunctivitis”, it is sometimes called “Red-Eye”, produces enlargement of surface blood vessels, causing the normally white part of the eye, the “Sclera”, to appear red. Sometimes, a blood vessel may rapture spontaneously and allow blood to flow under the conjunctiva. This is referred to as a “Subconjunctival haemorrhage and usually resolves in a few weeks without any treatment. Most often this haemorrhage occurs without explanation or after violent s sneezing or coughing, but rarely it may be associated with high blood pressure or bleeding disorders. A pingueculum, a yellowish mass on the bulbar conjunctiva just nasal or temporal to the limbus, probably represents irritation from sunlight. Continued irritation, especially by exposure to intense sunlight, may lead to formation of a pterygium, a fleshy wedge of bulbar conjunctiva that grows from the canthus (usually medial) towards the cornea. It may cause some irritation, but is not harmful unless it grows over the central cornea and impairs vision. If this happens, it must be surgically removed.

Lacrimal Apparatus (Fig. 1.2)

The lacrimal apparatus is composed of tear-producing glands and a tear drainage system. The lacrimal gland secretes the aqueous portion of tears and is located in the lateral segment of the upper lid just under the upper orbital rim. There are small, accessory lacrimal glands scattered throughout the upper fornix. The tear fluid is spread over the front surface of the eye when the upper lid closes during a blink. Tears then form a pool along both lid margins before passing through the upper and lower puncta (holes) into the canaliculi (little canals) of the drainage system. The upper and lower canaliculi merge into the common canliculus near the medial canthus, and the tears then flow into the lacrimal sac. The sac empties into the nasal cavity by means of the nasolacrimal duct. Where hot air being breathed out evaporates these tears.

The tear film is composed of three layers. The meibomian glands secrete the outer, oily layer, which helps prevent evaporation of the tears. The middle, aqueous (water) layer, secreted by the lacrimal gland, contains the oxygen and nutrients that nourish the cornea. The inner, mucinous layer is secreted by the goblet cells of the conjunctiva. The mucinous layer helps to maintain an even spread of tears over the cornea. The lacrimal system produces up to 1 ml (about 1/4th teaspoon) of tears during the waking hours, about 50% of which are lost to evaporation. No tears are produced during sleep. The tear-producing lacrimal gland is generally free of disease, but occasionally inflammation or tumours may occur in it. On the other hand, inflammation of the tear-collecting lacrimal sac, dacryocystits is relatively common. It usually occurs as a result of obstruction of the nasolacrimal duct. In infants, this obstruction is commonly the result of a congenital narrowing of the nasolacrimal duct where it opens into the nasal cavity. This often opens with time, if it does not it may require probing or other treatment. The signs of dacryocystitis are tenderness and swelling below the inner canthus, discharge or excessive tearing (epiphora). In the adult, obstruction of the tear outflow system occurs as a result of chronic lacrimal sac infection, facial trauma or tumours. If the blockage is severe, it may be necessary to bypass the nasolacrimal duct by surgically fashioning an opening between the sac and the nose (is called”Dacryocystorhinostomy”). Older persons and persons certain systemic diseases, may be subject to dry eyes (keratitis sicca). When one or more of the tear film components is insufficient, the tears cannot function properly and cornea becomes irritated. Patients usually treated with artificial tears.


The orbit is the cavity in the skull, which houses the eyeball. Its walls consist of seven bones, and it contains the eyeball, the extraocular muscles, blood vessels and nerves cushioned by a great deal of fat.

Four of the muscles form the muscle cone within the orbit through which pass the optic nerve and most of the blood vessels and nerves to the eye. The muscle cone originates in the posterior orbit as a circle of muscles called “Annulus of Zinn”.

Since the back of the orbit narrows, any increase in the orbital volume will cause the eyeball to protrude; this condition is called “Proptosis or Exophthalmos”. Proptosis is often seen in association with Graves’ disease, a condition of unknown cause that affects both the thyroid gland and the soft tissues around the eyes. Other causes include tumours, inflammation (including infection) or haemorrhage.

Diffuse infection of orbital tissue or orbital cellulitis, appears as grossly swollen lids, a red eye and sometimes proptosis. When the tissue bulk in the orbit is greater than normal, the eye muscles may not be free to move normally. If the eyes go out of alignment (strabismus), the patient may complain of double vision (diplopia). Misalignment of the eyes also results when one (or more) of the eye muscles become restricted in its movement because it has become inelastic from scarring or trapped by broken orbital bones. Muscle scarring occurs after any long-term inflammation, but the most common cause is Graves’ disease.

Extraocular Muscles (Fig. 1.3)

The eyeball is moved by the action of six extraocular muscles. The medial rectus pulls the eye towards the nose in adduction and inserts on the globe 5.5 mm from the medial limbus. The lateral rectus moves the eye away from the nose in abduction and inserts about 7 mm from the lateral limbus. The eye is elevated primarily by the superior rectus (insertion at 8 mm) and depressed primarily by the inferior rectus (insertion at 6 mm). The oblique muscles insert behind the equator of the globe and assist in elevation (inferior oblique) and depression (superior oblique).

The superior oblique also intorts the eye and the inferior extorts the eye. To understand intorsion and extorsion, imagine that the eye rotates on a pole piercing it from front to back. Intorsion means clockwise rotation of the right eye, counter-clockwise rotation of the left eye; extortion is rotation in the opposite direction.

The function of the six extraocular muscles are evaluated by asking the patient to move his eyes from straight ahead gaze, i.e. primary position in to upward gaze, downward gaze and into the six cardinal positions of gaze, which are right gaze, left gaze, up and right gaze, down and right gaze, up and left gaze, down and left gaze. The movement of the two eyes into this diagnostic gaze positions are called “Versions”.

The Eye

The main components of the eye are the

  • Cornea

  • Sclera

  • Anterior chamber

  • Uveal tract

  • Pupil

  • Lens

  • Vitreous

  • Retina

  • Optic disc


The cornea is the transparent anterior structure of the globe. Its transparency results from a highly ordered cell structure and low water content. The cornea loses its transparency if either of these factors is altered.

There are five layers of the corneal tissue, but the outermost and innermost layers are most important. The outermost layer is called the “Epithelium” which consists of cells that are constantly regenerating.

A superficial injury to this layer, by a contact lens or small foreign bodies, will usually heal within 24 to 48 hours. But infections with viruses, bacteria or fungi will require vigorous medical treatment. The innermost layer, the “Endothelium”, prevents the intraocular fluid from penetrating the cornea. If disease or trauma has damaged the endothelial cells, they may no longer be able to regulate the amount of water that reaches the internal tissue of the cornea. When this occurs, the cornea swells and becomes cloudy, this condition is called “Edema”.

Situated between the outermost epithelium and the innermost endothelium are three layers, called “Bowman’s Membrane”, the “Stroma” and “Descemet’s Membrane”. They each add rigidity to the cornea and provide additional barriers to infection.

The front surface of the cornea focuses light rays and contributes about two-thirds of the optical power of the eye. Because it must remain clear, the cornea contains no blood vessels. The cells are nourished by the aqueous humour and by the tear film, which also serves to maintain a smooth optical surface. The cornea is about 11.5 mm in diameter and 0.5 mm thick at its centre. Its junction with the sclera is called the “Limbus”. The limbus is also the location of the attachment of the bulbar conjunctiva to the globe. Tiny conjunctival capillaries at the limbus supply nutrients to the peripheral cornea.

Corneal inflammation is referred to as “Keratitis” and may result from a great variety of conditions such as a tear deficiency, toxic chemicals or infections. With any keratitis the patient usually experiences a foreign body sensation, eye pain aggravated by bright light, the condition called ”Photophobia”, blurred vision, redness and excessive tearing. In severe cases of keratitis, the anterior corneal tissue is destroyed and a corneal ulcer develops. Bacterial ulcers may be mild or severe, but the reaction to them is striking. The bulbar conjunctiva, which covers the white of the eye, becomes quite red, and there is often a copious discharge from the eye.

The active ulcer produces an opaque area on the cornea. As it heals, it leaves a scar that may result in permanently decreased vision. The surface of the ulcer must be scraped and cultured in order to discover the specific causative organism, which is treated with the appropriate antibiotic. Fungi may also cause corneal ulcers, usually as a result of a corneal injury with some type of vegetable matter (thorns, branches, pieces of wood). Without adequate treatment, the ulcers may extend through the cornea and cause infection inside the globe.

Herpes simplex keratitis caused by the virus responsible for “cold sores” produces branch-like (“dendritic”) erosion of the corneal epithelium that may progress to form an ulcer. Symptoms of an early infection are often mild, but careful examination reveals that the eye is red and watery. This ulcer must be treated promptly with special anti-viral drugs to prevent spreading to deeper corneal tissues. Once the disease has spread beneath the epithelium, the scar that remains after the healing process may seriously impair vision and leave a total corneal opacity, which may require corneal transplant surgery.

Corneal dystrophies are hereditary defects in the structure of cornea due to which the cornea loses its clarity. Corneal dystrophies become apparent at all ages. One example is keratoconus, in which the central cornea becomes thin and cone-shaped. The increase in corneal curvature at the centre of the cone causes an increasing nearsightedness (myopia) and astigmatism. The process begins in the teenage years and is usually completed by the late twenties. The decreased vision may be corrected in early stages by Rigid Gas Permeable Contact Lenses, but corneal thinning may become severe enough to require a corneal transplant.

A common change in the cornea of older patients is an opaque ring, called “Arcus Senilis”, seen near the limbus. It represents deposition of fatty substances from the blood. While it causes no symptoms, it may be a signal of an abnormally high fat content of the blood.


The sclera, the white of the eye, is the rigid outer portion of the wall of the eye that protects and supports the delicate inner structures. The sclera meets the cornea at the limbus. Occasionally the sclera or overlaying episcleral tissue becomes inflamed (scleritis and episcleritis) and may require treatment. Patients with rheumatoid arthritis may develop areas of marked sclera thinning (scleromalacia) which allows the purple colour of the underlying choroid to show through.

Anterior Chamber

The anterior chamber is the space between the back of the cornea and the front of the iris. It is filled with clear aqueous fluid humour produced by the ciliary body lying behind the iris.

The aqueous fluid is secreted by the processes of the ciliary body and flows through the pupil into the anterior chamber. It exits from the eye at the junction of the cornea and the iris, where it flows through a filter called the “Trabecular Meshwork” and into the canal of “Schlemm”. From here it empties into episcleral veins.

The balance between aqueous production and drainage normally maintains the intraocular pressure between 12 and 20 mm Hg (mercury). If aqueous drainage is impaired, the intraocular pressure rises and may cause optic nerve damage and loss of vision, this condition is called “Glaucoma”.

Inflammation or infection within the eye may cause a pool of pus (hypopyon) to layer out at the bottom of the anterior chamber. When blood is found in the anterior chamber, after an injury or in certain diseases, it is called “Hyphema”.


The uvea or “uveal tract” is the middle layer of the wall of the eye and is composed of the iris, the ciliary body and the choroid. The iris is the coloured part of the eye that controls the size of the central opening, the “Pupil”. The front layers of the iris contain its blood supply, muscles and pigment. The dialator muscle, which extends radially from the iris root to the pupil margin, opens the pupil (mydriasis) when it contracts.

The sphincter muscle encircles the pupil margin and makes the pupil smaller (miosis) when it contracts. A blue iris contains a relatively small amount of pigment while brown iris contains a relatively large amount. Pigment is deposited in the iris as the nervous system is developing. Because some of this development occurs after birth, most newborn babies have light eyes. Since the appearance of the net of new blood vessels on the iris gives it reddish cast, it is called “Rubeosis. Rubeosis may be responsible for blood leakage into the anterior chamber or obstruction of the filtration angle. Several diseases (especially diabetes) may cause an abnormal growth of new blood vessels (neovascularisation) on the surface of the iris. The iris may also be the site of nevi (freckles), tumours, cysts or nodules. The ciliary body is a band-like structure of muscle and secretory tissue that encircles the inside of the eye from behind the root of the iris to the anterior edge of the retina (the ora serrata). Most of the function of the ciliary body is concentrated in the anterior part, a folded muscle mass called the “Pars Pilicata”, which is composed of finger like ciliary processes that are responsible for secretion of the aqueous fluid. The posterior portion of the ciliary body is flat and is called the “Pars Plana. This latter area is a frequent site for surgical entry into the back of the eye because it contains relatively few delicate structures. Some of the muscle fibers of the ciliary body are arranged in a circular fashion and these control the eye’s ability to focus on near objects (the phenomenon is called “accommodation”).

The ciliary body may become inflamed in diseases that affect the iris and choroid as well (uveitis), it may also give rise to tumours or cysts.

The choroid is the posterior portion of the uveal tract. It is largely composed of blood vessels and lies between the sclera and the retina. It provides the blood supply for the outer cells of the retina. Inflammation of the choroid (choroiditis, posterior uveitis), may result from infection or from unknown (idiopathic) causes. The choroid may be the site of tumours such as malignant melanoma or metastatic cancer. Malignant melanoma is recognised as an elevated pigmented lesion that may cause the retina to detach. It is important to diagnose malignant melanomas early, so they can be treated before they spread to the rest of the body and cause death.


The pupil is the central opening in the iris that regulates the amount of light reaching the retina. The size of the pupil is controlled by the sphincter and dilator muscles of the iris. Each of these muscles is governed by a different part of the autonomic nervous system.

The sympathetic system controls the dilator muscle that opens the pupil and the parasympathetic system controls the sphincter muscle that closes the pupil. Ordinarily the pupils are about 4 mm in diameter in a dimly illuminated environment and equal in size in both eyes. It is not unusual for the pupil sizes, in an individual, to differ, from o.5 to 1.0 mm. When the two pupils of an individual differ in size by more than 1.0 mm (anisocoria), there is an abnormality of one pupil or other (or both). If the inequality is greater in dim illumination where the pupils usually larger, then the dilator muscle is not working in the eye with the smaller pupil. On the other hand, if the anisocoria is greater in bright light, when the pupils are usually smaller, then the sphincter is not working in the eye with the larger pupil. Once the weak muscle has been determined, the part of the nervous system that is affected can be identified.


The crystalline lens is a normally transparent, biconvex structure that is located in the posterior chamber between the iris and the vitreous body. The lens is composed of an inner nucleus, a surrounding cortex and an enveloping capsule.

The lens is responsible for about 1/3rd of the total focussing power of the eye and accounts for the ability to change focus from distance to near objects. The lens is suspended just behind the pupil by fibers called “Zonules” that are attached to the ciliary processes. When the ciliary muscles muscle contract, it relaxes the tension on the zonuls and allows the lens to become more round. The increased curvature of the lens makes it a more powerful refracting surface.

The process of ciliary muscle contraction and increased lens curvature is called accommodation. The ability of the lens to change its shape depends on its elasticity. As it ages, the lens tissue becomes increasingly more rigid and accommodation power is gradually lost (presbyopia). This is the reason that most people, as they age, have to wear corrective bifocal spectacles; the lower segment helps the eye focus on near objects.

When the lens proteins degenerate, the lens loses its transparency, this is called a “Cataract”. Thus synonyms for cataract are lens opacification. Cataracts may be present at birth, though this is rare. Most commonly, cataracts occur as part of the normal aging process (senile cataract). Lens opacities may also be the result of an injury to the eye or may be associated with ocular or systemic disease or with chronic use of certain drugs. When vision has become significantly impaired, the lens is surgically removed. An eye with a lens in place is called “Phakic”. Once the lens has been removed, the eye becomes “Aphakic”. When the eye’s own lens has been removed, its refractive power must be replaced with a powerful artificial lens, either as a spectacle, a contact lens or an intraocular lens (implant).


The vitreous body is a clear, gelatinous mass that fills the intraocular cavity behind the lens and helps maintain the spherical shape of the globe. When small particles drift across the vitreous, patients report that they see floaters. Floaters are a normal occurrence and need not be investigated unless they suddenly increase in number, if so, they may represent condensations of a portion of vitreous that has become detached from the retina. This vitreous detachment occurs as a normal part of aging, but may lead, in rare cases, to a retinal detachment, a vision threatening emergency.

The vitreous material is an excellent culture medium for bacteria. When infectious agents are accidentally introduced into the eye, either by injury or surgery, their growth may be so rapid as to destroy an eye within days. Infection of the vitreous and the adjacent tissue is called “Endophthalmitis” and constitutes an emergency. The infection is treated with large doses of antibiotics, but may also require the surgical removal of the infected vitreous (vitrectomy).

Abnormal retinal blood vessels may produce a haemorrhage into the vitreous that obscures vision. Usually this blood is absorbed over time. However, if the blood or resulting fibrous tissue remains, the vitreous may have to be removed surgically.


The retina is a transparent structure that lines the inner surface of the globe posteriorly, and is actually an extension of the brain. It converts light to electrical (nerve) impulses and transmits these impulses to the brain’s visual cortex where they are integrated into the sensation of sight. When viewed through an ophthalmoscope, the normal retina appears orange, the retina though transparent, appears orange due to the blood vessels of the underlying choroid. Lying on the inner surface of the retina are the retinal arterioles (bright red) and veins (dark red).

The retina is composed of an inner sensory portion and an outer pigment epithelium. The most important part of the sensory retina is the photoreceptor layer. It contains two types of photoreceptor cells, the cones and the rods, each with a different function in the visual process. Cones provide sharp central vision (acuity) and colour vision and function best in daylight. Rods are largely responsible for peripheral vision and function even in dim illumination. The innermost part of the retina consists of ganglion cells. Fibres from the ganglion cells for m the nerve fibre layer of the retina that converges at the optic disc. A specialised area of the retina containing most of the cone cells is located lateral to the optic disc and is called the “Macula”. The centre of the macula is called the “Fovea”. Damage to the macula will greatly reduce visual acuity and the eye will be left with only peripheral vision. When any other area of the retina is damaged, blind spots occur in off-centre position of the visual field. During development of the embryo, a cleft forms between the sensory and pigment epithelial portions of the retina that, under certain circumstances, may lead to an actual separation of these layers. Such a separation is called a “Retinal Detachment”. Trauma inflammation, eye surgery or the natural aging process may result in a tear in the sensory retina. Vitreous fluid leaks through the tear and spreads under the sensory retina causing it to become detached from the pigment epithelium. Patients who have a retinal detachment notice floaters, light flashes, blurred vision and sometimes the sensation of a “curtain” obscuring a portion of their field of vision. The detachment must be repaired surgically as soon as possible to prevent irreparable damage to sight.

Of the many disorders that affect the retina, senile macular degeneration is probably the most common. It occurs in the elderly and produces a slow decline in visual acuity usually in both eyes. The cause appears to be poor choroidal blood supply. In this condition, abnormal blood vessels (neovascularisation) that form beneath the macula leak and deform this delicate structure. In some cases such neovascularisation may be treated with the laser beam to prevent further vision loss.

A rare tumour called a “Retinoblastoma” can arise in the retina of very young children. Because retinoblastoma is life threatening, the eye containing this tumour is treated promptly, either by radiation or surgical removal (enucleation).

Optic Disc

After passing through the transparent inner layers of the retina, light is converted by the rods and cones to a nerve impulse that travels forward to the ganglion cell layer and then to the optic disc by way of the nerve fiber layer. The optic disc is situated in the nasal portion of the fundus, 15 degrees off-centre. Because no rods and cones are present in this area, it is sightless and termed the physiologic blind spot in the field of vision. Inflammation and stroke (blood vessel blockage) can damage the optic disc and produce defects in any portion of the field of vision. When the intracranial pressure is abnormally high, the disc tissue will swell (papilledema). There are other causes of optic disc swelling, including inflammations and strokes of the disc tissue itself. The optic disc tissue becomes excavated (cupped) in advanced glaucoma.

Retrobulbar Visual Pathway (fig. 1.4)

The eye is only the first part of the visual pathway, which extends to the back of the brain. The pathway that conducts visual messages after they leave the eye is termed the retrobulbar visual pathway.

The nerve impulse triggered by light striking the retina exits from the eye through the optic nerve, travelling to the optic chiasma. Here only the nasal nerve fibres from each eye cross to the opposite side, while the temporal fibres continue along on the same side. After the chiasma, the temporal nerve fibres from one eye and the nasal fibres from the other eye travel together in the optic tract and end in the lateral geniculate body.

From there the impulse is carried via the optic radiations to the occipital lobe in the posterior part of the brain. The destination of these fibres within the occipital lobe is called the “Visual (calcarine) Cortex”, where the visual message is integrated with information derived from other parts of the brain in a process called “Perception”.

Disorders affecting other parts of the visual pathway produce characteristic changes in the field of vision. The most common disorders are tumours of the pituitary gland (which lies directly under the chiasma) and strokes, aneurysms, inflammations, infections and trauma.

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