Physiology of vision
Vision: optics, retina, rods and cones, colour vision, accommodation and pupil reflexes
How the eye focuses light, how rods and cones convert it to signals, and how accommodation, dark adaptation and pupil reflexes work, for FCPS Part 1. Includes refractive errors, glaucoma, vitamin A deficiency, fundus changes and drug effects on vision.
One of the most tested topics in past papers
Optics and refractive errors
- Total refractive power is about 60 dioptres. The cornea provides about two-thirds (about 43 D) because the air–cornea interface has the largest change in refractive index; the lens adds about 15–20 D and is adjustable.
| Error | Problem | Correction |
|---|---|---|
| Myopia (short sight) | Eyeball too long; image falls in front of retina | Concave (diverging) lens |
| Hypermetropia (long sight) | Eyeball too short; image behind retina | Convex (converging) lens |
| Astigmatism | Unequal corneal curvature | Cylindrical lens |
| Presbyopia | Lens stiffens with age and cannot round up | Convex reading lens |
- Presbyopia: after about 45 the lens becomes too stiff to become more convex even though the ciliary muscle still contracts, so the near point recedes and reading glasses are needed.
Accommodation (near response)
- The ciliary muscle contracts (parasympathetic: oculomotor nerve, Edinger–Westphal nucleus, ciliary ganglion, short ciliary nerves), the ring of muscle narrows, the zonules slacken, and the elastic lens becomes more convex.
- The near response also includes convergence (medial recti) and pupil constriction, which increases depth of focus.
- Atropine and cyclopentolate paralyse accommodation (cycloplegia) as well as dilating the pupil.
Aqueous humour and glaucoma
- Aqueous is secreted by the ciliary epithelium (carbonic anhydrase dependent), flows through the pupil, and drains through the trabecular meshwork and canal of Schlemm. Normal IOP is about 10–21 mmHg.
- Acute angle-closure glaucoma: small, hypermetropic (short) eyes with shallow anterior chambers have narrow angles. When the pupil is mid-dilated (dim light, anticholinergics, dilating drops), the iris blocks drainage; IOP rises sharply, causing a painful red eye, haloes, vomiting and a fixed mid-dilated pupil.
- Acetazolamide inhibits carbonic anhydrase and reduces aqueous production (side effects: metabolic acidosis, hypokalaemia). Pilocarpine opens the angle; β-blockers reduce production; prostaglandin analogues increase uveoscleral outflow.
- Steroid-induced glaucoma: prolonged corticosteroid drops raise trabecular outflow resistance, giving silent open-angle glaucoma.
Retina
- Layers from outside in: pigment epithelium, photoreceptors, outer nuclear layer, outer plexiform layer, inner nuclear layer (bipolar, horizontal and amacrine cells), inner plexiform layer, ganglion cells and nerve fibre layer. Light crosses the inner layers to reach photoreceptors.
- Fovea centralis: only cones, tightly packed, with inner layers pushed aside and no vessels. Each cone links to its own bipolar and ganglion cell (one-to-one), giving the highest acuity. Loss of the macula (age-related macular degeneration) destroys reading and face recognition while peripheral rods allow navigation. Faint stars are seen best by looking slightly to the side.
- Optic disc: no photoreceptors (blind spot).
- Pigment epithelium recycles retinal, stores vitamin A and phagocytoses shed outer segments.
Rods and cones
| Feature | Rods | Cones |
|---|---|---|
| Number | About 120 million | About 6 million |
| Location | Periphery | Concentrated in the fovea |
| Sensitivity | High; dim light (scotopic) | Low; bright light (photopic) |
| Acuity | Low (many rods converge on one ganglion cell) | High |
| Colour | No | Yes (three types) |
| Pigment | Rhodopsin (11-cis retinal plus opsin) | Three cone opsins |
Phototransduction
- In the dark, cGMP keeps cation channels open (dark current); the photoreceptor is depolarised (about −40 mV) and releases glutamate continuously.
- Light isomerises 11-cis retinal to all-trans retinal, activating rhodopsin, which activates the G protein transducin, which activates phosphodiesterase 6 (PDE6). cGMP falls, channels close, the cell hyperpolarises and glutamate release falls.
- Sildenafil weakly inhibits retinal PDE6, so high doses can tint vision blue and increase light sensitivity for a few hours.
- Dark adaptation takes 20–30 minutes: cones adapt within about 7 minutes, then rods take over as rhodopsin regenerates. Light adaptation takes seconds to minutes.
Vitamin A deficiency
- Night blindness is the earliest symptom (rhodopsin needs retinal).
- Then xerophthalmia: conjunctival and corneal epithelium undergoes keratinising squamous metaplasia, giving dry, wrinkled conjunctiva and Bitot spots (foamy grey triangular patches), then keratomalacia and blindness.
- Measles precipitates deficiency; vitamin A is given to children with measles in deficient areas.
Colour vision
- Trichromatic theory: short (blue), medium (green) and long (red) wavelength cones. Opponent processing occurs in ganglion cells and the lateral geniculate body.
- Red–green colour blindness is X-linked recessive (about 8% of men); test with Ishihara plates.
- Ethambutol causes dose-related optic neuritis with reduced acuity and red–green colour loss; test vision before and during treatment. Other drug toxicities: vigabatrin (concentric, usually irreversible field loss), hydroxychloroquine (maculopathy), amiodarone (corneal deposits), long-term steroids (posterior subcapsular cataract).
Visual pathway reflexes
- Pupillary light reflex: retina, optic nerve, optic tract, pretectal nucleus, both Edinger–Westphal nuclei, oculomotor nerve, ciliary ganglion, sphincter pupillae. Bilateral connections give the consensual response.
- Pupil dilation: sympathetic chain from the hypothalamus via T1 and the superior cervical ganglion to the dilator pupillae.
- Light–near dissociation: pupils constrict on convergence but not to light. The light reflex fibres pass through the pretectal area, while near-response fibres travel more ventrally. Argyll Robertson pupils (neurosyphilis): small, irregular. Parinaud (dorsal midbrain) syndrome, classically from a pineal tumour compressing the tectum: failure of upgaze, light–near dissociation, convergence–retraction nystagmus.
- Superior colliculus: coordinates reflex turning of the eyes and head towards a sudden movement or flash in the peripheral field.
Fundus changes in vascular disease
| Finding | Mechanism | Significance |
|---|---|---|
| Arteriovenous nipping | Thickened arteriole compresses the vein at a crossing (shared sheath) | Chronic hypertension |
| Flame haemorrhages, cotton wool spots, disc swelling | Fibrinoid necrosis, ischaemia of nerve fibres, raised pressure | Malignant (accelerated) hypertension: emergency; check renal function |
| Microaneurysms (earliest lesion) | Loss of capillary pericytes and weakened walls | Early diabetic retinopathy |
| Neovascularisation | VEGF from ischaemic retina | Proliferative diabetic retinopathy |
Remember Cornea bends light most; light hyperpolarises photoreceptors; the ciliary muscle contracts for near vision.
Exam trap In accommodation the ciliary muscle contracts and the zonules relax; it is the lens that rounds up.
Exam trap Photoreceptors hyperpolarise in light and are depolarised in the dark.
How FCPS asks about this
- Greatest refractive power: cornea; myopia corrected with a concave lens.
- Reading glasses after 45: stiff lens cannot round up (presbyopia).
- Fine central vision: fovea with packed cones and one-to-one ganglion links.
- Angle-closure risk: short hypermetropic eye with a shallow anterior chamber; acetazolamide reduces aqueous production.
- Night blindness with Bitot spots: vitamin A deficiency; keratinising squamous metaplasia.
- Pineal tumour with upgaze palsy and light–near dissociation: dorsal midbrain compression.
- Ethambutol: optic neuritis with red–green colour loss.
Test yourself on this topic
5 of the 92 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 3-year-old boy develops an inward turning of one eye, mainly when looking at near objects. Refraction shows high hypermetropia, and glasses correct the squint. What is the mechanism of the squint?
Answer: Excess accommodation causes over-convergence
A hypermetropic eye focuses light behind the retina, so the child must accommodate even for distance and accommodate much more for near objects. Accommodation, convergence and pupillary constriction are linked in the near response, driven together from the midbrain. The excessive accommodation therefore brings excessive convergence, and one eye turns in (accommodative esotropia). Glasses remove the need to accommodate, and the squint straightens.
Accommodative esotropia
- Hypermetropia needs extra accommodation
- Near response: accommodation + convergence + miosis
- Extra convergence: eye turns in
- Treated with glasses
Remember Long-sighted child with a near squint: give glasses.
Exam trap An untreated squint in early childhood can cause permanent amblyopia.
Why the other options are wrong
- Weakness of the lateral rectus muscle Muscle weakness would not be corrected by glasses.
- Paralysis of the sixth cranial nerve A palsy causes a squint worse on looking to the side, not with near focus.
- Excess divergence caused by the lens The lens does not cause divergence.
- Loss of the pupillary light reflex The light reflex is unrelated to this squint.
A young man with retinitis pigmentosa asks how his rods signal light. When light activates rhodopsin in a healthy rod, its release of glutamate falls. Which of the following changes in the rod causes this?
Answer: It hyperpolarises as cGMP falls and Na⁺ channels close
In darkness, cGMP keeps cation channels in the outer segment open, so a steady 'dark current' of Na⁺ and Ca²⁺ holds the rod depolarised at about −40 mV and it releases glutamate continuously. Light converts 11-cis retinal to all-trans retinal, activating rhodopsin, which activates transducin and then phosphodiesterase 6. cGMP is broken down, the channels close and the rod hyperpolarises, so glutamate release falls. Photoreceptors produce graded potentials, not action potentials.
Phototransduction
- Dark: cGMP high, cell depolarised
- Light: transducin, PDE6
- cGMP falls, channels close
- Rod hyperpolarises, less glutamate
Remember Light turns photoreceptors off.
Exam trap Photoreceptors are most active in the dark, not the light.
Why the other options are wrong
- It depolarises as cGMP rises and Na⁺ channels open This is the opposite of what light does.
- It hyperpolarises as K⁺ channels close Closing K⁺ channels would depolarise the cell.
- It depolarises as Ca²⁺ floods into the outer segment Ca²⁺ entry falls in light as channels close.
- It fires an action potential along its axon Photoreceptors use graded potentials.
Laser surgery that flattens the central cornea corrects a young woman's myopia. Why is the cornea chosen for correcting refraction?
Answer: It gives about two-thirds of the eye's power
Light bends most where it passes between media whose refractive indices differ the most. The largest difference is between air and the front of the cornea, so the cornea provides about 40–43 dioptres, roughly two-thirds of the eye's total power of about 60 dioptres. Its power is fixed, unlike the lens, which adds variable power in accommodation. Flattening the central cornea reduces its power, moving the focus back onto the retina in a myopic eye.
Refractive power
- Cornea: about 43 D, two-thirds
- Lens: about 20 D, variable
- Biggest bend at air–cornea surface
- Myopia: flatten the cornea
Remember The cornea is the main lens of the eye.
Exam trap Under water the cornea loses most of its power, which is why vision blurs while swimming without goggles.
Why the other options are wrong
- It changes its curvature during accommodation Only the lens changes shape in accommodation.
- It has the highest refractive index in the eye The lens has a higher refractive index, but sits between similar media.
- It lies closer to the retina than the lens The lens and vitreous lie closer to the retina.
- It controls the size of the pupil in light Pupil size is controlled by the iris muscles.
A teenager with a pineal tumour cannot look upwards, and his pupils constrict on convergence but not to light. Which region is compressed?
Answer: Dorsal midbrain
Parinaud (dorsal midbrain) syndrome: compression of the pretectal region and superior colliculi, typically by a pineal tumour (germinoma) or hydrocephalus, causes vertical (upward) gaze palsy, light-near dissociation (pupils react to accommodation but not to light), convergence-retraction nystagmus and eyelid retraction (Collier's sign). The aqueduct is also compressed, causing obstructive hydrocephalus. Argyll Robertson pupils (neurosyphilis) also show light-near dissociation but are small and irregular.
Parinaud syndrome
- Dorsal midbrain; pineal tumour
- Upgaze palsy, light-near dissociation
- Convergence-retraction nystagmus, lid retraction
- Aqueduct compression → hydrocephalus
Remember Pineal pushes on the eyes' up switch.
Why the other options are wrong
- Ventral pons Causes locked-in syndrome.
- Lateral medulla Wallenberg syndrome.
- Cerebellar vermis Truncal ataxia.
- Optic chiasm Bitemporal hemianopia.
An army doctor on night duty at a high-altitude post reads maps only by dim red torchlight, so that he can still see the dark ground outside straight afterwards. Which of the following explains why red light helps?
Answer: Rods are insensitive to long-wavelength red light
Night vision depends on rods, whose rhodopsin is bleached by light and takes 20–30 minutes to recover fully in the dark. Rhodopsin absorbs best at about 500 nm and very poorly at long red wavelengths, so dim red light barely bleaches it. Cones, including red-sensitive cones, still allow the map to be read. When the light goes off, the rods are still dark-adapted and he can see the dim ground at once.
Dark adaptation
- Rods need 20–30 min to dark-adapt
- Rhodopsin peaks near 500 nm
- Red light barely bleaches rods
- Cones still read the map
Remember Red light spares the rods.
Exam trap Bright white light bleaches rhodopsin at once and restarts dark adaptation.
Why the other options are wrong
- Red light speeds up rhodopsin regeneration Red light does not speed regeneration; it avoids bleaching.
- Red light dilates the pupil more fully Pupil size does not explain the effect.
- Cones adapt to the dark faster after red light Cones adapt quickly anyway but give poor night vision.
- Red light is filtered out by the macular pigment Macular pigment absorbs blue, not red.
Where this sits in the CPSP syllabus
- Paper 1: Special senses, Vision: optics, retina, photoreceptors, colour vision, accommodation, light reflex
- Surgery & Allied, Paper 2: Special senses, Vision: optics, retina, photoreceptors, colour vision, accommodation, light reflex
- Medicine & Allied, Paper 2: Special senses, Vision: optics, retina, photoreceptors, colour vision, accommodation, light reflex
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