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)

• Light → retina

• → optic nerve (CN II) → chiasm → optic tract

• → pretectal nucleus (midbrain)

Interneurons (why consensual happens)

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

Efferent limb (making the pupil constrict)

• EW nucleus → CN III parasympathetic fibres

• → ciliary ganglion

• → short ciliary nerves (post-ganglionic parasympathetic fibres) → sphincter pupillae

• → 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.

But here is a question for you guys: Both the light reflex and accommodation start in the retina and travel via the optic nerve, then why is one reflex stronger than the other?

What is damaged in Marcus Gunn?

• Retina / optic nerve

• Signal is weakened, not abolished

So:

• Some impulses still get through

• Just fewer than normal

Why light reflex is abnormal

The light reflex:

• Is a low-threshold, brainstem reflex

• Depends on signal strength

• If afferent input is weak → poor constriction

So when light hits the affected eye:

• Brainstem receives a reduced signal

• Both pupils constrict less →That’s RAPD

Now the crucial part — accommodation

You’re right:

Accommodation ALSO needs retina + optic nerve

But accommodation:

• Is cortically mediated

• Requires conscious visual perception

• Has a much stronger neural drive

Even a weak afferent signal is:

• Enough to reach the visual cortex

• Amplified by cortical processing

• Sent robustly to Edinger–Westphal nucleus

👉 Therefore pupils constrict normally on accommodation

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 (pupil 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.

This is the core concept 👇

Aberrant reinnervation

After post-ganglionic damage:

• Nerve fibres regenerate incorrectly

• Fibres meant for accommodation reinnervate the pupil

Result:

• Near response pathways dominate

• Light reflex fibres are fewer

👉 Near response works better than light response

👉 This causes light–near dissociation

Why is it “TONIC” (slow)?

Because:

• Reinnervated fibres conduct slowly

• Pupil constricts gradually

• Relaxes very slowly

So:

• Accommodation = present but slow and sustained

• Hence the term tonic pupil

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.

Argyll Robertson pupil usually results from a bilateral lesion involving the pretectal–Edinger-Westphal (EW) light-reflex connections,

Normal light reflex pathway (simplified)

• Retina → optic nerve → optic tract

• → Pretectal nuclei (dorsal midbrain)

• Each pretectal nucleus projects bilaterally to both Edinger-Westphal nuclei

• → CN III → ciliary ganglion → pupil constriction

This bilateral projection is why shining light in one eye causes both pupils to constrict.

Causes: Diabetes mellitus (Chronic microvascular damage to midbrain) > Neurosyphilis

• Other causes: Multiple sclerosis, Pineal gland tumours (Compress dorsal midbrain (tectal plate)), Midbrain stroke or haemorrhage, Chronic alcoholism, Sarcoidosis, Encephalitis / infections

The descending sympathetic fibres run very close to the pretectal nuclei in the dorsal midbrain, specifically in the dorsolateral tegmentum.

So a dorsal midbrain lesion (classically causing Argyll Robertson pupil) can:

• Interrupt pretectal → EW light-reflex connections

• Also nick nearby descending sympathetic fibres→ causing small pupil (due to relatively unopposed parasympathetic tone)

Presentation

• pupils are small, irregular, bilateral pupils that do not react to light but constrict on accommodation.

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

• C8–T2 → sympathetic chain → superior cervical ganglion

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