Anatomy of the Eye
By visual examination we can see
Eyelids, cilia (eyelashes) and the openings of the tarsal (sebaceous) glands along the edges
Lateral and medial canthi
Lacrimal lake containing the lacrimal caruncle
Plica semilunaris (loose fold of bulbar conjunctiva)
Superior and inferior lacrimal puncta within their lacrimal papillae
Bulbar and palpebral conjunctiva
Corneoscleral junction (limbus)
Pupil and iris
Layers of the Eye
o Ciliary body
o Optic disc (blind spot)
Compartments and Chambers of the Eye
o Anterior chamber
Between the cornea and iris
o Posterior chamber
Between the iris, zonular fibres and lens
o Vitreous chamber
Between the lens and the retina
Optic Nerve & The Visual Pathway
Embryologically the optic nerve and retina develop as a diverticulum (outpouching) of the forebrain.
The retina is made up of 3 layers:
Receptor cells: rods & cones
Intermediate layer: bipolar cells
Ganglion cells whose axons converge at the optic disc, pierce the schlera and forms the optic nerve
The optic nerve passes through the optic foramen until it reaches the optic groove on the sphenoid. Here the fibres
Medial half of the retina (concerned with the temporal visual field) cross over in the optic chiasma
Lateral half of the retina (concerned with the nasal visual field) pass back in the optic tract of the same side
Most of the fibres of the optic tract end in the geniculate body. Some fibres are used for pupillary and visual body
(head and neck reflexes) and bypass the geniculate body but go to the superior colliculus or pretectal regions. The
Direct and Consensual Light Reflex
Optic nerve -> optic tract -> pretectal nucleus -> accessory oculomotor nucleus (Edinger-Westphal) -> CNIII -> pupils
When the eye follows a distant object brought close, three things happen
Lens thickens by contraction of the ciliary muscles
Medial rectus muscles cause convergence
This calls for a more complex pathway:
Visual Body Reflex
The visual body reflex is involved in:
o Automatic scanning movements of the eyes & head that are made when reading
o Automatic movements of the eyes, head & neck towards the visual stimulus
o Protective closing of the eyes & raising arm for protection (followed by the reflex vocalisation: “Oh shit”)
UV Light and the Eyes
The Cornea and Lens
The cornea and lens are the principal targets of UV radiation (UVR) damage, therefore, a brief mention of their
histology. In both cases, light is transmitted through both structures because they are predominantly acellular
internally and made up of parallel fibres allowing visible light to pass through them.
The cornea is made up of 5 layers but 90% of it is made up of a stromal layer made up of parallel collagen fibres
together with some sparsely separated keratinocytes.
The lens is covered by a collagen capsule and has a simple cuboidal epithelium on the anterior surface. At the
equatorial zone, they lose their organelles and elongate into fibres, which are pushed in towards the posterior pole
of the lens. New fibres compress one on top of another in parallel forming the bulk of the interior of the lens. This
differentiation is controlled by changing growth factor concentrations (Eg FGF, IGF, PDGF) along the surface of the
UVR is broken down into three main spectrums
UVA (320-390 nm)
UVB (290-320 nm) is most implicated in cancer formation.
UVC (230-290 nm)
UVB and UVA penetrate the cornea and exposure can come from
o Direct sunlight
o Reflections from
Glass, chrome, concrete, shiny surfaces
UVC is the shortest wavelength UV that is completely absorbed by the cornea. UVC exposure can come from
High altitude snow reflection
UVR causes tissue damage in two ways:
o Molecular Fragmentation: molecules containing alternating double bonds (proteins, nucleic acids) resonate
at UVR (especially UVB/C) frequencies and break. These then form new bonds causing DNA mutations and
loss of protein function.
o Free Radical Formation: pigmented molecules making up the vascular layer of the eye form long chains of
alternating double bonds that are susceptible to UVR. The bonds can eject electrons that are captured by
adjacent molecules (eg H2O + electron + H+ becomes H2O2), turning them into reactive oxides and peroxides
that can break or create bonds within proteins and nucleotides causing DNA mutations and function loss.
Basically, UV radiation catalyses reactions forming reactive molecules that are able to create or destroy bonds in
other molecules (proteins, nucleotides) leading to tissue damage and loss of function. The body’s defence
mechanisms protecting it from UV radiation include scavenger molecules:
Vitamins C and E
Caplains (mop up protein breakdown products in the lens(6)
These become depleted in the elderly and macular degeneration and cataract formation is accelerated. Eye
protection becomes even more crucial in this age group.
Lightly Pigmented Individuals
The lighter the eye pigmentation, the greater the prevalence of age related macular degeneration (it is almost
unknown in genetically pure Negroes)
Use of Photosensitizing Drugs
A number of drugs absorb UV light and produce free radicals, damaging the retina and lens. These include:
Phenothiazines (“Phenergan” and “Mersyndol” antihistamines, older antipsychotics)
Allopurinol (common gout treatment)
Pathologies Likely To Be Caused By Exposure to the Different UV Spectra
UVB exposure causes
o Conjunctival damage
Squamous cell carcinoma caused by prolonged and repeated damage to DNA by creating
bonds between CC which DNA polymerase interprets as AA. TT forms in the growing strand,
creating the C-T mutation signature of SCC caused by UVB
Actinic conjunctivitis (acute inflammation caused by excessive exposure)
Pinguecula (yellow deposit adjacent to the limbus)
Pterygium (release of stress induced cytokines producing a wedge shaped area of fibrosis,
chronic inflammation, cell growth and angiogenesis(1)
o Lens damage
Def: clouding or opacification of the lens
10% of cataracts are directly caused by UVB. Altogether 160,000 are treated
annually in Australia(2)
Pathophysiology of cataracts
o UVB (and possibly UVA) causes changes in lens proteins either directly
through molecular transformation or by production of free radicals, mainly,
H2O2 , causing them to precipitate and become opaque. This process is
exacerbated in certain chronically ill or elderly patients by the addition of
small molecules to the proteins (post translational modifications):
photooxidation products which accumulate in the elderly and bind
Glycation in diabetics
Cyanate from high urea levels in renal failure
Excessive retention of copper (Wilson’s disease) and iron
(haemochromatosis) produce reactive hydroxyl radicals
o Changes to balance of growth factor concentrations at the surface of the
lens (affected by corticosteroids, chemotherapy, cancers, metabolic
disorders such as diabetes) prevents differentiation into fibres, causing
nucleated cells to cover the posterior surface of the lens, causing a type of
cataract (posterior subcapsular cataract).
o Alteration of intracellular calcium metabolism causing the formation of
calcium salts and binding to proteins causing light scattering. Corticosteroids
mobilise Ca++ salts and are a major culprit.
o Because the proteins at the centre of the lens are the oldest (as old as the
individual), cataracts often form here in the elderly and this type of cataract
is called nuclear sclerosis.
o Vascular Layer damage
Choroidal melanoma is the most common cancer of the eyeball(3).
UVA penetrates further and can cause damage to deeper structures within the eye
Together with UVB contributes to cataract formation
o Vascular layer
Was originally considered the likely cause melanoma but this has since been found to be
unlikely, with UVB remaining the main culprit(4).
o Neural layer
UVC is completely absorbed by the cornea and causes
o Photokeratitis: acute damage to corneal epithelium, stroma and in severe cases, endothelial cells of
the cornea resulting in “snow blindness” or “welders arc eye”. Epithelial cells are shed into the tear
film which can be seen as dots of debris.
The exposed nerve fibre ending resulting in intense pain and an ongoing corneal reflex where the
sufferer becomes “blinded” by blepharospasm (inability to open his eyelids). The main clinical signs
and symptoms (which can appear several hours after exposure) of photokeratitis are:
o Foreign body sensation
o Gritty feeling
o Tearing (containing conjunctival discharge and cellular debris)
o Symptoms abate within two days with no permanent damage to the cornea.
1. Di Girolamo N, Wakefield D, Coroneo MT. UVB-mediated induction of cytokines and growth factors in
pterygium epithelial cells involves cell surface receptors and intracellular signaling. Invest Ophthalmol Vis Sci.
2. Council TC. Eye Protection From Ultraviolet Radiation. 2006.
3. American Society of Clinical Oncology. Eye Cancer | Cancer.Net. 2010; Available from:
4. De Fabo A, Noonan F, Fears T, Merlino G. Ultraviolet B But Not Ultraviolet A Initiates Melanoma. Cancer Res.
September 15, 2004;64(6372).
5. Ultraviolet Vulnerability. In: Yanoff, Duker, editors. Ophthalmology. 3rd ed2008.
6. PATHOPHYSIOLOGY OF CATARACTS. In: Yanoff, Duker, editors. Ophthalmology2008.