Pupillary Reflexes — Ultra–High-Yield MSRA Exam Blog (with ALL Important Conditions)

The pathways you must know

A. Light reflex pathway (the “torch test”)

Afferent limb (sensing light)

1. Light → retina

2. → optic nerve (CN II) → chiasm → optic tract

3. → pretectal nucleus (midbrain)

Interneurons (why consensual happens)

4. Pretectal nucleus projects to both Edinger–Westphal (EW) nuclei, so one torch stimulates both pupils.

Efferent limb (making the pupil constrict)

5. EW nucleus → CN III parasympathetic fibres

6. → ciliary ganglion

7. → short ciliary nerves → sphincter pupillae

8. → pupil constricts (miosis)

How to interpret the 3 tests

• Direct light reflex = illuminated eye constricts

• Consensual light reflex = other eye constricts

• Accommodation (near response) = pupil constricts when looking at near target (via cortex → EW)

B. Accommodation (near) pathway (why it can be spared)

• Retina → optic nerve → visual cortex

• Cortex → EW nucleus

• EW → CN III → ciliary ganglion → sphincter pupillae

• Accommodation can be preserved even if the light reflex circuitry (pretectal connections) is damaged = light–near dissociation.

Exam conditions: which part is hit → what you see → what tests are +/–

Legend: ✅ present, ❌ absent, ⬇️ reduced/slow

A) AFFERENT (CN II / retina) lesion: RAPD (Marcus Gunn pupil)

Where is the lesion? Retina/optic nerve (afferent limb)

Presentation

• Pupil sizes often equal

• Reduced light perception in affected eye

• Key finding on swinging flashlight test

Tests

• Light shone in normal eye → both constrict well ✅ (direct normal, consensual normal)

• Light shone in affected eye → both constrict less ⬇️ (because afferent input is weak)

• Accommodation ✅ (because efferent pathway intact)

Why? Input signal is weak; output wiring is fine.

B) EFFERENT PARASYMPATHETIC (CN III / ciliary ganglion / sphincter) lesions: typically DILATED pupil

Unifying mechanism: sphincter can’t constrict → sympathetic tone is unopposed → mydriasis.

1) CN III palsy — TWO exam phenotypes (diabetes vs PCom aneurysm)

Where are the fibres? Parasympathetic fibres are superficial on CN III; motor fibres are more central.

📌 Compression hits pupil fibres; ischemia often spares pupil fibres.

a) Diabetic (microvascular ischemic) CN III palsy = “pupil-sparing”

Lesion: central ischemia in CN III (motor fibres), superficial parasympathetics relatively spared

Presentation

• Ptosis, “down & out” eye, diplopia

• Pupil usually normal

Tests

• Direct light (affected eye) ✅

• Consensual (affected eye) ✅

• Accommodation ✅

Why? Parasympathetic fibres survive → constriction pathways still work.

b) PCom aneurysm (compressive) CN III palsy = “pupil-involving”

Lesion: external compression of superficial parasympathetic fibres

Presentation

• Ptosis, “down & out”

• Dilated pupil

• Often severe headache/eye pain (exam red flag)

Tests (affected eye has an efferent defect)

• Direct light (affected eye) ❌

• Consensual in affected eye when shining light in normal eye ❌

• Consensual response of the normal eye when light is shone in affected eye ✅ (because afferent CN II is fine)

• Accommodation ❌

Why? Efferent parasympathetic output is broken; afferent input still triggers the other eye.

2) Holmes–Adie pupil (tonic pupil)

Lesion: Ciliary ganglion / post-ganglionic parasympathetic fibres

Presentation

• Usually unilateral large pupil

• “Tonic” slow responses

Tests

• Direct light (affected) ⬇️/❌

• Consensual in affected eye (when light in other eye) ⬇️/❌

• Accommodation ✅ but slow/tonic ⬇️➡️ Light–near dissociation with a BIG pupil

Why? Post-ganglionic denervation + aberrant reinnervation favors near response.

3) Pharmacological mydriasis (e.g., atropine)

Mechanism: Muscarinic receptors blocked (effector can’t respond)

Presentation

• Dilated pupil, often very fixed

Tests

• Direct ❌

• Consensual in affected eye ❌

• Accommodation ❌ (cycloplegia)

Why? Sphincter cannot contract despite intact nerves.

4) Traumatic iridoplegia / sphincter damage

Lesion: Sphincter pupillae muscle (mechanical failure)

Presentation

• Dilated ± irregular pupil after trauma

Tests

• Direct ❌

• Consensual in affected eye ❌

• Accommodation ❌

Why? Muscle can’t constrict.

C) DORSAL MIDBRAIN light-reflex disconnection: Argyll

Robertson pupil

Lesion: Pretectal → EW light-reflex connections (midbrain)Efferent parasympathetics are intact.

Presentation

• Small, irregular pupils (often bilateral)

Tests

• Direct light ❌

• Consensual light ❌

• Accommodation ✅➡️ Light–near dissociation with a SMALL pupil

Why? Light pathway is cut, but near pathway (cortex → EW) still activates constriction.

D) SYMPATHETIC pathway lesions: typically CONSTRICTED pupil

1) Horner syndrome

Lesion: Sympathetic pathway to dilator pupillae

Presentation

• Miosis + mild ptosis ± anhidrosis

Tests

• Direct light ✅

• Consensual light ✅

• Accommodation ✅

Why? Parasympathetic constriction is intact; dilation is impaired.

E) Drug effect: Opiates

Mechanism: Central increase in parasympathetic dominance

Presentation

• Pinpoint pupils + systemic toxidrome

Tests

• Direct light ⬇️ (often sluggish)

• Consensual ⬇️

• Accommodation ⬇️

Why? Pupils are already maximally constricted; responses are blunted.

The exam “pattern matcher” (how to score quick marks)

• Dilated pupil + light & accommodation absent → efferent parasympathetic block (CN III compressive, atropine, trauma)

• Dilated pupil + light poor but accommodation better → Holmes–Adie

• Small pupil + normal light reflexes → Horner

• Small pupil + no light but accommodation present → Argyll Robertson

• Normal size + abnormal swinging flashlight → RAPD