Pupils Made Easy: Anisocoria, Horner, Adie and RAPD
Last updated: October 2026
Pupils confuse people because several pathways and four eye drops are taught at once. Untangle them with three questions: is there an afferent problem, is there anisocoria, and does the pupil react better to near than to light?
Three rules that solve most pupil cases
1. An afferent defect never makes the pupils unequalLight from either eye drives both pupils equally, so a blind eye still has a pupil the same size as the other. Afferent disease shows only as a RAPD.
2. Find the abnormal pupil with the lightsAnisocoria bigger in the dark = the small pupil cannot dilate (Horner or physiological). Bigger in bright light = the large pupil cannot constrict (III palsy, Adie, drugs, iris damage).
3. Light–near dissociation has few causesThe near pathway runs more ventrally and the ciliary muscle has 30 times more nerve fibres than the sphincter. So the pupil may react to near but not light in dorsal midbrain lesions, Argyll Robertson pupils, Adie pupils (after regrowth) and severe afferent loss.
The anisocoria algorithm
| Step | Finding | Meaning |
|---|---|---|
| 1 | Anisocoria the same in light and dark, ≤1 mm | Physiological (about 1 in 5 people); check old photographs |
| 2 | Greater in the dark; small pupil dilates slowly (dilation lag) | Horner syndrome: confirm with drops |
| 3 | Greater in bright light + ptosis and motility deficit | Third nerve palsy: urgent imaging if the pupil is involved |
| 4 | Greater in bright light, poor light reaction, slow tonic near reaction, sectoral palsy | Adie tonic pupil |
| 5 | Greater in bright light, fixed, no ptosis or motility problem | Pharmacological (atropine, scopolamine patch, plants) or iris damage: use 1% pilocarpine |
Memory hook: Dark exaggerates the Defective dilator; Light exaggerates the Lazy constrictor.
The eye drops, sorted
| Drop | Use | Result |
|---|---|---|
| Cocaine 4–10% | Confirm Horner (blocks noradrenaline reuptake) | Normal pupil dilates, Horner pupil does not: anisocoria ≥0.8 mm after drops is positive |
| Apraclonidine 0.5–1% | Confirm Horner (weak α1 agonist) | Reversal: the Horner pupil dilates (denervation supersensitivity) and the ptosis improves. Can be falsely negative in the first days to weeks |
| Hydroxyamphetamine 1% | Localise a Horner (releases noradrenaline from the 3rd neuron) | Dilates if the 3rd neuron is intact (1st or 2nd order lesion); fails if postganglionic (3rd order) |
| Pilocarpine 0.1% (or 0.125%) | Adie pupil (cholinergic supersensitivity) | Adie pupil constricts, a normal pupil barely does |
| Pilocarpine 1% | Fixed dilated pupil | Constricts in III palsy and Adie; does not constrict after atropine-like drugs or with iris sphincter damage |
Memory hook: Hydroxyamphetamine needs a living third neuron to work, so it fails only with a third-order (postganglionic) lesion.
Horner syndrome by neuron
| Order | Where | Sweating loss | Causes to think of |
|---|---|---|---|
| 1st (central) | Hypothalamus to C8–T2 | Whole side of the body | Lateral medullary (Wallenberg) stroke, syrinx, MS, cord tumours |
| 2nd (preganglionic) | Lung apex, neck | Face | Pancoast tumour, neck or thyroid surgery, chest drains, neuroblastoma in children |
| 3rd (postganglionic) | Internal carotid to the orbit | None, or a small patch of the forehead | Carotid dissection (painful Horner: urgent), cavernous sinus lesions, cluster headache |
- The triad is mild ptosis (1–2 mm, Müller's muscle), miosis with dilation lag, and anhidrosis; the lower lid may sit higher (inverse ptosis), giving apparent enophthalmos.
- Congenital Horner: the affected iris is lighter (heterochromia), because sympathetic input is needed for iris pigment in early life.
- New painful Horner = carotid dissection until proven otherwise: same-day CT or MR angiography of head and neck.
- Horner in a child without a clear cause: look for neuroblastoma (abdomen, chest, neck imaging and urine catecholamines).
The large pupil
| Feature | III palsy | Adie tonic pupil | Pharmacological |
|---|---|---|---|
| Ptosis / motility | Yes (partial or complete) | No | No |
| Light reaction | Poor or absent | Poor; sectoral | None |
| Near reaction | Poor | Slow, sustained (tonic) and better than light | None |
| 0.1% pilocarpine | Little effect | Constricts | No effect |
| 1% pilocarpine | Constricts | Constricts | No effect |
| Key worry | Posterior communicating aneurysm if the pupil is involved | Benign; reduced tendon reflexes = Holmes–Adie | Ask about patches, inhalers, plants, eye drops |
- Pupil sparing: pupil fibres run on the outside of the nerve, so compression hits them early, while ischaemia (diabetes, hypertension) damages the core and usually spares the pupil. A complete III palsy with a normal pupil is reassuring; a partial palsy with a normal pupil still needs imaging and close follow-up.
- Adie pupil starts large and becomes smaller over years ("little old Adie"). Vermiform movements of the iris border are seen at the slit lamp.
The small pupils
| Pupil | Features | Cause |
|---|---|---|
| Horner | Unilateral, ptosis, dilation lag, reacts to light | Sympathetic lesion (see above) |
| Argyll Robertson | Bilateral, small, irregular, light–near dissociation, dilate poorly | Neurosyphilis (also diabetes) |
| Pharmacological | Pilocarpine, opioids, organophosphates | History |
| Old Adie | Small, tonic near reaction | Long-standing Adie |
| Inflammatory | Posterior synechiae, irregular | Uveitis |
Memory hook: ARP: Accommodation Reflex Present, light reflex absent.
RAPD in practice
- Swing the light every 2–3 seconds; when it reaches the bad eye, both pupils dilate.
- Grade with neutral density filters over the good eye (0.3, 0.6, 0.9, 1.2 log units) or in a simple 1+ to 4+ scale.
- If one pupil is fixed or dilated, watch only the working pupil (reverse RAPD): it still tells you which eye is bad.
- Gives a RAPD: optic nerve disease, large retinal lesions (CRAO, RD, extensive PRP), asymmetric chiasmal compression, optic tract (opposite eye), dense amblyopia (mild).
- Does not: cataract, corneal scars, refractive error, macular hole or small macular lesions, functional loss. A dense cataract may even give a small RAPD in the other eye.
Dorsal midbrain (Parinaud) syndrome
Mid-dilated pupils with light–near dissociation, upgaze palsy, convergence–retraction nystagmus on attempted upgaze, eyelid retraction (Collier sign) and skew deviation. Think pinealoma in a young man, stroke or MS in adults, and hydrocephalus or shunt failure in children.
Where residents slip
- Looking for anisocoria in a blind eye: an afferent defect alone never makes the pupils unequal.
- Testing anisocoria only in room light: always compare dim and bright light.
- Using 1% pilocarpine to diagnose Adie: only the dilute drop (0.1%) shows supersensitivity.
- Calling a painful new Horner a migraine: image the carotid the same day.
- Doing an apraclonidine test the day after a carotid dissection: supersensitivity takes time, so cocaine is more reliable early.
Test yourself: flip cards
Quick quiz
Related: Neuro-ophthalmology hub, Visual pathway made easy, Ocular motility made easy, Ophthalmic emergencies.
Key sources
- American Academy of Ophthalmology. Basic and Clinical Science Course, Section 5: Neuro-Ophthalmology (current edition)
- Kawasaki A. Approach to the patient with abnormal pupils. Semin Neurol. 2008;28(5):683-689
- Koc F, et al. Topical apraclonidine testing discloses pupillary sympathetic denervation in Horner syndrome. Neurology. 2005;65:1305-1307
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