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11.11 — The Eye and Vision

A dark-adapted rod cell can respond to a single photon. Under ideal conditions a human observer can reliably detect a flash of five to nine photons. That is close to the physical limit of what any detector could achieve, and it is done by a wet organ 24 millimetres across.

The eye also transmits about 10 million bits per second up the optic nerve, of which your conscious visual experience is a heavily processed and largely constructed fraction.

The structure

Cross-section of the eye labelled with cornea, aqueous humour, iris, lens, vitreous humour, retina, macula, optic disc and optic nerve
The eye in cross-section. Light passes through the cornea, the pupil, the lens and the vitreous before reaching the retina at the back — and, as Chapter 3.6 explained, it must then pass through the retina's own nerve layers before reaching the light-sensitive cells at the very back. Image: Wikimedia Commons.

Three coats.

Outer — sclera and cornea. The sclera is the tough white protective shell. The cornea is the transparent front sixth, and it is transparent because of an extremely regular arrangement of collagen fibres and because it contains no blood vessels.

Middle — choroid, ciliary body and iris. The choroid is a vascular layer nourishing the retina. The ciliary body makes aqueous humour and holds the lens. The iris is the coloured diaphragm, and the pupil is simply the hole in it.

Inner — retina, the light-sensitive layer.

Two fluid compartments. The aqueous humour in front of the lens is watery, continuously produced and drained, and it maintains the eye's pressure. The vitreous humour behind the lens is a clear gel, formed before birth and never replaced.

And that permanence is why floaters happen. The vitreous gradually liquefies and shrinks with age, and clumps of collagen cast shadows on the retina — the drifting specks and threads most people over 40 notice. They are harmless.

But a sudden shower of new floaters, especially with flashes of light, is different. As the vitreous shrinks it can pull on the retina, and the pull can tear it. Flashes plus a sudden increase in floaters, and particularly a shadow or curtain spreading across the vision, means possible retinal detachment and needs same-day assessment, because a tear treated early with laser prevents a detachment that would otherwise need surgery and might not fully recover.

Focusing

The eye must bend light by about 60 dioptres to focus it on the retina, and it is worth knowing where that comes from.

The cornea provides about 40 to 45 dioptres — around two thirds of the total. It does most of the focusing, and it does it at a fixed strength.

The lens provides about 15 to 20 dioptres, and it is adjustable.

This is why laser eye surgery reshapes the cornea rather than the lens — the cornea is where most of the refractive power is and it is accessible from the outside.

Accommodation — focusing on near objects — works in a way that is counter-intuitive and worth getting right.

The lens is naturally elastic and would be round if unconstrained. It is held flattened by tension in the fibres suspending it from the ciliary body.

To focus near, the ciliary muscle contracts. Because it is a ring, contracting it makes the ring smaller, which slackens the suspending fibres and allows the lens to become rounder and more powerful.

So the muscle works to see close up and relaxes to see far away, which is why prolonged close work causes eye strain and why looking into the distance rests the eyes.

Presbyopia is the loss of this. The lens stiffens progressively from childhood, and by around 40 to 45 it can no longer round up enough for comfortable near vision. This is why reading glasses become necessary in the mid-forties, essentially universally, and why people start holding menus at arm's length.

It is not a disease and it is not preventable, and knowing it is a mechanical consequence of lens stiffening rather than a sign of decline takes some of the sting out of it.

Refractive errors

Myopia (short sight) — the eye is too long, or the cornea too curved, so light focuses in front of the retina. Distance is blurred; near is clear. Corrected by a concave lens.

Myopia has increased dramatically, from around 20 to 25 percent of young adults in many populations a generation ago to over 80 percent in parts of East Asia today. That change is far too fast to be genetic.

And the strongest identified factor is time spent outdoors in childhood. Multiple studies and several trials find that children who spend more time outside develop less myopia, apparently because bright light stimulates dopamine release in the retina, which restrains axial elongation. The effect appears to be about light exposure rather than about distance viewing. Two hours outdoors a day is the figure usually cited, and some school systems have changed break policies on the basis of it.

Hyperopia (long sight) — the eye is too short, so light would focus behind the retina. Young people can compensate by accommodating, which is why it often goes unnoticed until the accommodative reserve declines. Corrected by a convex lens.

Astigmatism — the cornea is not evenly curved, so different meridians focus at different distances. Corrected by a cylindrical lens.

The retina

The photoreceptors sit at the back, facing away from the light (Chapter 3.6), so light must pass through the nerve layers to reach them.

Two receptor types, and the division of labour is complete.

Rods — about 120 million. Extremely sensitive, working in dim light. No colour information. Concentrated in the periphery, absent from the very centre.

Cones — about 6 million. Need bright light. Provide colour and fine detail. Concentrated in the centre.

Three cone types, responding maximally to short (blue), medium (green) and long (red) wavelengths.

Colour is computed from the ratios, not read off directly. A single cone cannot report colour at all — it only reports how much it was stimulated, and a bright dim-wavelength light and a dim optimal-wavelength light produce the same output. Colour requires comparing across types, which is why colour vision fails in dim light when only rods are working.

The fovea is a small pit at the centre of the macula, about 1.5 millimetres across, containing only cones, packed at maximum density, with the overlying nerve layers pushed aside so light reaches them directly.

This is where your acuity lives. Visual acuity falls off extremely steeply away from the fovea — at 10 degrees off centre it is roughly a fifth of the maximum. Your impression of a detailed visual world is constructed, from a small high-resolution spot being moved rapidly around by eye movements while the brain assembles the results.

The optic disc is where the nerve fibres exit and the vessels enter. No photoreceptors, hence the blind spot — 5 to 6 degrees across, filled in by the brain so convincingly that most people never notice it.

Dark adaptation takes about 20 to 30 minutes to complete, as the photopigments regenerate. Cones adapt within a few minutes; rods take much longer, which is why full dark adaptation is slow.

And it is destroyed instantly by bright light, which is why red light is used in situations where dark adaptation must be preserved — rods are insensitive to red, so red light does not bleach them.

Vitamin A is required to make the photopigment. Deficiency causes night blindness first, then dryness of the cornea, then irreversible blindness — and it remains a leading cause of preventable childhood blindness worldwide. The intervention is cheap and effective: vitamin A supplementation programmes have prevented enormous numbers of cases, and it is one of the clearest public health successes available.

The visual pathway

Covered in Chapter 11.7, and the key point bears repeating: fibres from the nasal half of each retina cross at the chiasm and those from the temporal half do not, which is why a field defect localises so precisely.

The retina processes before it transmits. Around 126 million photoreceptors feed about 1 million ganglion cell axons, so there is roughly 100-fold convergence and substantial computation happening in the eye itself.

Centre–surround organisation means retinal cells respond to contrast rather than absolute light — a cell excited by light in the centre of its field is inhibited by light in the surround. This is edge detection, performed in the retina, and it is why many visual illusions of brightness work.

The common eye conditions

Cataract — clouding of the lens. The leading cause of blindness worldwide, and it is completely curable.

The lens proteins aggregate over decades, scattering light. Painless, gradual blurring, glare from headlights, and colours appearing faded.

Surgery removes the lens and replaces it with a plastic one, takes 15 to 20 minutes under local anaesthetic, and is one of the most successful operations in all of medicine — around 95 percent achieve good vision. The main global problem is access rather than technique, and cataract surgery programmes are among the most cost-effective health interventions that exist.

Glaucoma — damage to the optic nerve, usually associated with raised eye pressure.

Aqueous humour is produced continuously and must drain. If drainage is impaired, pressure rises and the nerve fibres are progressively damaged.

Open-angle glaucoma is gradual and painless, and this is what makes it dangerous. Peripheral vision is lost first, and the brain fills in the gaps, so people often notice nothing until a large proportion of the field is gone — and lost vision does not return.

Which is why routine eye examinations matter. Glaucoma detected early and treated with pressure-lowering drops preserves vision essentially indefinitely. It is a condition where screening genuinely works.

Acute angle-closure glaucoma is the opposite — sudden, painful, and an emergency. Severe eye pain, a red eye, blurred vision, halos around lights, nausea and vomiting, with a fixed mid-dilated pupil and a stony hard eye.

It is often mistaken for a migraine or a stomach upset, because the nausea can dominate. Untreated it causes permanent blindness within days, and it needs immediate pressure reduction.

Age-related macular degeneration — the leading cause of blindness in older people in wealthy countries. Central vision is lost while peripheral vision is preserved, so people cannot read or recognise faces but can still move around.

Two forms, with very different outlooks. Dry AMD is gradual and has no established treatment, though a specific vitamin and mineral combination slows progression in intermediate disease.

Wet AMD involves abnormal new vessels growing and leaking. It was rapidly blinding until the mid-2000s. Injections of anti-VEGF drugs into the eye — blocking the signal that drives new vessel growth — now stabilise vision in most patients and improve it in a substantial minority. This is one of the genuine transformations in medicine of the last twenty years, and it turned a diagnosis of inevitable central blindness into a manageable condition.

Diabetic retinopathy — damage to retinal vessels from diabetes, and a leading cause of blindness in working-age adults.

And it is almost entirely preventable. Good glucose and blood pressure control prevent most of it, and screening detects it before vision is affected, when laser or injections can preserve sight. Annual retinal screening for everyone with diabetes is one of the best-evidenced screening programmes in existence, and the reduction in diabetes-related blindness where it is implemented has been substantial.

Conjunctivitis — inflammation of the surface membrane. Usually viral, self-limiting, and highly contagious. Bacterial conjunctivitis usually resolves without antibiotics too, though drops shorten it slightly.

The red flags that separate a trivial red eye from a serious one are worth knowing: pain rather than irritation, reduced vision, photophobia, a pupil that is not round or not reacting, and a history of contact lens wear or of injury. Any of these means same-day assessment.

Contact lens wearers with a painful red eye are treated as having a corneal infection until proven otherwise, because bacterial keratitis can destroy the cornea within days.

Colour vision deficiency

Around 8 percent of men and under 0.5 percent of women, because the genes for the red and green pigments are on the X chromosome (Chapter 2.6).

Red–green deficiency is much the commonest. It is not seeing in grey — it is difficulty distinguishing certain colours, particularly reds, greens and browns.

It rarely causes practical difficulty, though it excludes people from a small number of occupations and can cause problems with poorly designed colour-coded information — which is why accessibility guidelines require that colour never be the only channel carrying meaning.

What the next page fixes

The other special sense with its own dedicated nerve does two entirely different jobs in one organ. Chapter 11.12 covers the ear — how sound is converted from air vibration to nerve impulse across three different media, and how the same organ tells you which way up you are.