Vision
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Direct answer
Light entering the eye passes through 59-60 dioptres of total refractive power, of which the cornea contributes about 43 dioptres — the single largest share, because refraction depends on the curvature and the air-tissue step — and the lens adds 15-17 dioptres at rest, with up to about 14 dioptres of accommodation available in youth (the near point of 9 cm at age 10 recedes to about 83 cm by 60). The retina holds roughly 120 million rods for scotopic vision and 6 million cones for photopic and colour vision, all cone-only at the fovea, where one-to-one bipolar-to-ganglion wiring delivers maximal acuity; about 1.2 million axons leave each eye in the optic nerve. Phototransduction is unique in being hyperpolarising: light converts 11-cis retinal to all-trans, the opsin cascade falls, cGMP drops, sodium channels close, and the photoreceptor hyperpolarises — the only receptor in the body that responds to its stimulus by hyperpolarising. Lesion localisation follows the optic pathway: chiasmal compression gives bitemporal hemianopia, temporal lobe (Meyer's loop) lesions give superior quadrantanopia, and occipital infarcts give homonymous hemianopia with macular sparing.
What you must remember
- Optics numbers: total refractive power about 59 D, cornea 43 D, lens 15-17 D resting with up to about 14 D of accommodation in a 10-year-old; near point 9 cm at 10 years, about 83 cm at 60.
- Receptor numbers: 120 million rods, 6 million cones; the fovea is cone-only; rods peak just off-centre for dim light; dark adaptation takes 20-30 minutes.
- Phototransduction cascade: light isomerises 11-cis to all-trans retinal (rhodopsin bleaching), transducin activates phosphodiesterase, cGMP falls, sodium channels close, and the outer segment hyperpolarises — with the highest concentration of rhodopsin making rods single-photon capable.
- Colour vision: trichromatic theory with three cone pigments peaking near 420, 530 and 560 nm; red-green colour blindness is X-linked recessive, affecting about 8 per cent of males, screened by Ishihara plates.
- Field defects by lesion: optic nerve — monocular blindness; chiasma — bitemporal hemianopia (pituitary adenoma from below, craniopharyngioma from above); optic tract — contralateral homonymous hemianopia; Meyer's loop — contralateral superior quadrantanopia; occipital cortex — homonymous hemianopia with macular sparing.
- Light reflex: retina to pretectal nucleus to both Edinger-Westphal nuclei — the bilateral projection explains the consensual response; the Argyll Robertson pupil accommodates but does not react (light-near dissociation).
- Intraocular pressure: normal 12-21 mm Hg, set by aqueous humour dynamics; acute angle-closure glaucoma is sight-threatening ocular emergency.
Following a photon from cornea to cortex
Track a photon from the left visual field: it strikes the right half of each retina, the image inverted by the lens. In daylight a foveal cone catches it — pigment shifts, cGMP collapses, the cone hyperpolarises and cuts glutamate release onto a bipolar cell wired one-to-one to a midget ganglion cell: high acuity, low convergence. At night a rod must catch it, dozens pooling onto one ganglion cell — high sensitivity, low resolution: rod summation. The ganglion potential runs the optic nerve, decussates at the chiasma if it began nasally, and relays through the lateral geniculate body to the visual cortex. Superior-field photons travel Meyer's loop through the temporal lobe — why a temporal tumour takes out the opposite superior field. In the cortex, the dorsal stream parcellates "where" from the ventral stream's "what".
The field-defect trap
The exam's trap is naming the side. A left temporal lobe lesion involving Meyer's loop produces a right superior homonymous quadrantanopia, and candidates lose the mark by writing the side of the lesion instead of the side of the field loss. Second trap: chiasmal lesions are named by their temporal (lateral) field loss — bitemporal — because nasal retinal fibres cross there; a pituitary adenoma pressing from below strikes inferior chiasmal fibres first, producing upper temporal defects initially. Third, macular sparing points to occipital cortex infarction, whereas a tract lesion spares nothing. Pair these with the reflex arc: a blind eye cannot initiate a light reflex but consensually responds if the other eye is lit — the afferent-efferent (Marcus Gunn) distinction.
Frequently asked questions
Why does the cornea contribute more refractive power than the lens?
Its curvature is steep and it interfaces air with tissue — the largest refractive index step — giving about 43 of the total 59 dioptres, while the lens sits between aqueous and vitreous.
How do rods differ from cones functionally?
Rods (120 million) serve dim-light scotopic vision with high convergence and no colour discrimination; cones (6 million, fovea-only at the centre) serve bright-light acuity and the three-pigment colour system.
Why is phototransduction called hyperpolarising?
Light closes cGMP-gated sodium channels so the photoreceptor hyperpolarises and releases less glutamate — the only sensory receptor that hyperpolarises to its adequate stimulus.
Which lesion causes bitemporal hemianopia?
Compression of the optic chiasma, classically a pituitary adenoma interrupting the crossing nasal retinal fibres from both eyes.
What explains the consensual light reflex?
Each pretectal nucleus projects to both Edinger-Westphal nuclei, so light in one eye constricts both pupils — and its dissociation localises afferent versus efferent lesions.