Pupil Abnormalities
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Direct answer
Swing a torch from one eye to the other and watch both pupils: when the light lands on a damaged optic nerve, both pupils dilate slightly instead of constricting — a relative afferent pupillary defect (Marcus Gunn pupil), the most informative pupil sign in neuro-ophthalmology. On the efferent side, unequal pupils (anisocoria) resolve with two questions: which pupil is abnormal, and does the difference grow in light or in dark? A difference worse in light indicts the parasympathetic pathway (third nerve palsy, Adie tonic pupil, Argyll Robertson pupil); worse in dark indicts the sympathetic chain (Horner syndrome — miosis, ptosis, anhidrosis and apparent enophthalmos, confirmed when apraclonidine reverses the anisocoria). Light-near dissociation — pupils that fail to light but constrict to near — belongs to Adie pupil, neurosyphilis and dorsal midbrain lesions, a trio the exam recycles endlessly.
What you must remember
- Swinging torch test: afferent disease shows paradoxical dilatation of both pupils when the torch swings to the affected eye; it is the hallmark of optic nerve lesions (optic neuritis, ischaemic optic neuropathy, ischaemic central retinal vein occlusion) and is characteristically absent in pure media opacities such as cataract.
- Physiological anisocoria: difference under 1 mm, equal in light and dark, both pupils reacting normally.
- Horner syndrome: miosis, mild ptosis (Mueller muscle), apparent enophthalmos, ipsilateral anhidrosis when the lesion is proximal to the carotid bifurcation; causes include Pancoast tumour, carotid dissection, neck surgery and birth injury (congenital cases with iris heterochromia).
- Horner pharmacology: cocaine 10 per cent fails to dilate the affected pupil (classical confirmation); apraclonidine 0.5 to 1 per cent now preferred — it dilates the denervated pupil by supersensitivity and reverses the anisocoria.
- Adie tonic pupil: ciliary ganglion damage, young women; slit-lamp sectoral palsy with vermiform writhing, light-near dissociation, slow redilation after near effort; dilute pilocarpine 0.125 per cent constricts it (denervation supersensitivity) but not a normal pupil.
- Argyll Robertson pupil: small, irregular, both eyes, accommodates but does not react — neurosyphilis is the classical cause; screen accordingly.
- The fixed dilated pupil emergencies: third nerve compression (posterior communicating aneurysm, uncal herniation) — especially with ptosis and down-and-out eye; and anticholinergic or drug-induced mydriasis, which lacks ptosis and motility loss.
- Light-near dissociation trio: Adie tonic pupil, Argyll Robertson pupil, dorsal midbrain (Parinaud) syndrome — with convergence-retraction nystagmus and lid retraction completing the midbrain picture.
A systematic look at unequal pupils
A 35-year-old nurse notices her right pupil is larger than the left, spotted in a mirror. First confirm both pupils react and measure the difference in light and dark: the anisocoria is 2 mm and worse in the light, so the large right pupil is the abnormal one — a parasympathetic problem. Examine under the slit lamp: the right iris shows slow, wormlike segmental movements and constricts briskly to a near target but barely to light, redilating sluggishly afterwards — the vermiform movement and light-near dissociation of a tonic pupil. Dilute pilocarpine 0.125 per cent constricts the right pupil and leaves the left untouched, confirming denervation supersensitivity of the ciliary ganglion. Reassure her; the pupil often shrinks over years and reading glasses manage the near blur. Now contrast the man in the next bay with a small left pupil and drooping lid after neck radiotherapy: anisocoria worse in the dark, so the small pupil is abnormal — sympathetic failure. Apraclonidine testing confirms Horner syndrome, and imaging from chest apex to skull base hunts the lesion. Two unequal pupils, two nervous systems — the diagnosis flows from two bedside measurements.
Where candidates slip
The first error is calling every anisocoria pathological; the second is failing to use light-versus-dark to pick the culprit, which converts a two-step diagnosis into guesswork. The Adie versus Argyll Robertson discrimination is a favourite: both show light-near dissociation, but Adie is a large tonic pupil in a young woman while Argyll Robertson is small, irregular and bilateral with neurosyphilis — size alone answers it. Third, the painless fixed dilated pupil after surgery or aerosol drug exposure (anticholinergic mydriasis) gets over-investigated, while the dilated pupil with ptosis and headache gets under-investigated — the latter is the aneurysm until imaging says otherwise. Finally, dense media opacity does not produce a relative afferent pupillary defect — a "negative RAPD with poor vision" points away from the optic nerve.
Frequently asked questions
How is a relative afferent pupillary defect elicited?
By the swinging torch test — both pupils constrict when light falls on the good eye but dilate paradoxically when it swings to the affected eye, indicating asymmetric optic nerve or severe retinal disease.
Which drugs confirm and localise Horner syndrome?
Apraclonidine reverses the anisocoria by supersensitivity (confirmation), while cocaine 10 per cent classically fails to dilate the affected pupil; hydroxyamphetamine helps localise the lesion to the third-order neuron by its release mechanism.
What characterises the Adie tonic pupil?
Sectoral iris palsy with vermiform movements, light-near dissociation, slow redilation, and constriction to dilute 0.125 per cent pilocarpine from denervation supersensitivity.
Which three conditions cause light-near dissociation?
Adie tonic pupil, Argyll Robertson pupil (neurosyphilis) and dorsal midbrain (Parinaud) syndrome.
When is a dilated pupil a neurosurgical emergency?
A fixed dilated pupil with ptosis, ophthalmoplegia or headache suggests compressive third nerve palsy — posterior communicating aneurysm or uncal herniation — demanding urgent imaging.