Pupillary Pathways and Anomalies
Anatomical Localisation · Clinical Examination · Differential Diagnosis
Examination question · ~2500 words
Discuss the anatomy of pupillary pathways (afferent and efferent limbs) with emphasis on anatomical localisation of lesions. Classify pupillary anomalies, describe their clinical features, diagnostic approaches including pharmacological testing, and demonstrate systematic evaluation of anisocoria with reference to light-near dissociation differentials.
Try to outline your answer mentally before expanding sections below.
The pupil is a dynamic aperture governed by competing autonomic inputs — a tug-of-war between parasympathetic constrictor and sympathetic dilator. Its unique anatomy traverses the midbrain, cavernous sinus, orbit, and iris, making it an invaluable window into neurological disease. Understanding pupillary pathways enables precise anatomical localisation of lesions from the retina to the cortex and is one of the highest-yield topics in postgraduate ophthalmology examinations.
Light Reflex — Anatomical Pathway
- Receptor: Intrinsically photosensitive retinal ganglion cells (ipRGCs) — melanopsin-containing, located in inner retinal layer. Drive pupillomotor response independent of rods/cones (explaining why blind patients may retain light-near reflex).
- Afferent pathway: Retina → Optic nerve → Optic chiasm (nasal fibres decussate) → Optic tract → Pretectal nucleus (NOT lateral geniculate nucleus — diverges before LGN)
- Critical crossing: Pretectal nucleus → Bilateral Edinger-Westphal (EW) nuclei via posterior commissure
- Efferent limb: EW nucleus → Ciliary ganglion (via CN III, inferior division) → Short ciliary nerves → Sphincter pupillae
Key exam point: Pretectal fibres cross via the posterior commissure, ensuring BOTH pupils constrict to monocular light stimulation (consensual reflex). A lesion at the posterior commissure causes light-near dissociation (Parinaud/dorsal midbrain syndrome).
Near Reflex Triad
Accommodation, convergence, and miosis constitute the near triad. The near reflex pathway diverges from the light reflex: it involves cortical (occipital/frontal) input to EW nucleus without routing through the pretectal nucleus — this anatomical separation explains light-near dissociation (LND), where near response is preserved despite absent pupillary light reflex.
A. Parasympathetic (Constrictor)
- Pathway: EW nucleus (midbrain) → Pre-ganglionic fibres travel with CN III in superficial and superior position (vulnerable to compressive lesions) → Ciliary ganglion (synapse) → Post-ganglionic short ciliary nerves → Sphincter pupillae and ciliary muscle
- Surgical pearl: In posterior communicating artery (PComA) aneurysm, external compression affects superficial parasympathetic fibres FIRST — 'surgical' CN III palsy presents with dilated, fixed pupil + ptosis + EOM palsy. Contrast with 'medical' CN III (DM/HTN) — pupil typically spared (ischaemia affects central fibres).
B. Sympathetic (Dilator) — Three-Neuron Arc
| Order | Location | Key Landmark | Lesion Cause |
|---|---|---|---|
| 1st | Hypothalamus → C8-T2 | Brainstem lateral tegmentum | CVA, demyelination, syringomyelia |
| 2nd | C8-T2 → Stellate ganglion | Lung apex, subclavian artery | Pancoast tumour, cervical rib, thyroid Ca |
| 3rd | Stellate → iris | ICA, cavernous sinus | ICA dissection, cavernous sinus thrombosis, cluster headache |
Anhidrosis localisation: Anhidrosis of whole face = 2nd order (pre-ganglionic). Anhidrosis limited to medial forehead/nose = 3rd order. No anhidrosis = 3rd order post-carotid bifurcation.
Systematic Examination Protocol
- Inspection: Size, shape, symmetry in light and dark. Anisocoria physiological in ~20% of population.
- Direct PLR: Brisk, sluggish, or absent; amplitude and speed.
- Consensual PLR: Tests contralateral afferent and ipsilateral efferent pathways.
- Swinging Flashlight Test (SFT): Gold standard for relative afferent pupillary defect (RAPD).
- Near reflex: Assess for light-near dissociation.
- Pharmacological testing: Cocaine, apraclonidine, hydroxyamphetamine for Horner's; pilocarpine for Adie's.
Relative Afferent Pupillary Defect (RAPD)
On swinging flashlight test, paradoxical dilation of pupil when light swings to affected eye indicates relative optic nerve or severe retinal disease. RAPD requires optic tract or anterior-to-chiasm pathology; chiasmal or posterior lesions cause RAPD only if asymmetric. Grading (Levatin scale): 0 (absent) to 4+ (immediate dilation). Causes: optic neuritis, NAION, AION, glaucoma, optic nerve compression, large RD, CRAO, optic tract lesion.
| Anomaly | Affected Limb | Size | PLR | Near Reflex | Key Feature |
|---|---|---|---|---|---|
| RAPD (Marcus Gunn) | Afferent | Normal | Paradox dilation on SFT | Normal | Optic nerve/retinal disease |
| CN III palsy | Efferent (Para) | Dilated | Absent direct + consensual | Absent | Ptosis, EOM palsy |
| Horner Syndrome | Efferent (Sym) | Miosed | Normal (slow dilation) | Normal | Ptosis 2mm, anhidrosis, enophthalmos |
| Adie's Tonic Pupil | Efferent (Para) | Dilated | Absent/slow PLR | Slow tonic near | Cholinergic supersensitivity |
| Argyll Robertson | Efferent | Miosed | Absent PLR | Present (LND) | Neurosyphilis, DM |
| Dorsal Midbrain Syn. | Both | Mid-dilated | Absent PLR | Present (LND) | Collier's sign, upgaze palsy, pseudo-AR |
| Pharmacological dilation | Efferent | Dilated | Absent | Absent | No reversal with pilocarpine 1% |
| Physiological anisocoria | Neither | Asymmetric | Normal both | Normal | Constant difference in light/dark |
Wernicke's Hemianopic Pupil
Anatomical basis: Nasal fibres cross at the chiasm and represent the contralateral eye in each optic tract; temporal fibres are uncrossed and represent the ipsilateral eye. In the right optic tract, temporal fibres from the right (ipsilateral) eye + nasal fibres from the left (contralateral) eye are affected. For contralateral RAPD to occur, nasal fibres (contralateral eye) must carry greater pupillomotor weight than temporal fibres (ipsilateral eye). Therefore, a right optic tract lesion → LEFT (contralateral) eye has greater afferent loss → LEFT RAPD. The clinical rule (RAPD contralateral to optic tract lesion) is correct; the mechanism reflects nasal-fibre predominance in pupillomotor input.
Right optic tract lesion → left homonymous hemianopia + LEFT RAPD. This is OPPOSITE to students' initial expectation — a major MCQ trap. The RAPD is on the opposite side of the lesion.
Clinical Triad
- Miosis (pupil constriction, 1–2 mm difference)
- Ptosis (2 mm, due to superior tarsal muscle loss)
- Enophthalmos (apparent, due to lower lid elevation)
- Anhidrosis (variable; depends on lesion order)
Pharmacological Confirmation and Localisation
| Drug | Normal Eye | Horner Eye | Interpretation |
|---|---|---|---|
| Cocaine 4–10% | Dilates | Fails to dilate | Confirms Horner's (NE reuptake block); positive at any order |
| Apraclonidine 0.5–1% | Mild constriction | Dilates (anisocoria reversal) | Confirms Horner's via denervation supersensitivity; false-negative if acute (<2 weeks) |
| Hydroxyamphetamine 1% | Dilates | Dilates | 1st/2nd order lesion (intact NE stores) |
| Hydroxyamphetamine 1% | Dilates | Fails to dilate | 3rd order lesion (depleted NE terminals) |
VIVA PEARL: Apraclonidine works via denervation supersensitivity of alpha-1 receptors upregulated in dilator pupillae. False-negative apraclonidine test occurs in acute Horner's (<2 weeks) before supersensitivity develops.
Pathophysiology
Post-ganglionic parasympathetic denervation of ciliary ganglion (viral, autoimmune). Aberrant reinnervation — more fibres regenerate to ciliary muscle than sphincter (30:1 ratio), causing tonic near response but poor PLR.
Clinical Features
- Unilateral (80%), predominantly young women
- Vermiform iris movements on slit-lamp examination (sector palsy of sphincter)
- Tonic dilation after near effort (slow, sustained contraction)
- Cholinergic supersensitivity (responds to dilute pilocarpine)
- Diagnosis: Dilute pilocarpine 0.1% — Adie's pupil constricts (denervation supersensitivity); normal pupil does NOT constrict.
Adie Syndrome: Tonic pupil + absent deep tendon reflexes (Holmes-Adie). Ross syndrome: Adie's + hyporeflexia + segmental hypohidrosis.
Classic description: 'Prostitute's pupils' — accommodate but do not react to light (light-near dissociation).
Pathophysiology and Features
Syphilitic lesion at pretectal nucleus / posterior commissure interrupts light reflex fibres while sparing near reflex fibres (which travel ventrally). Also seen in diabetic neuropathy, MS, sarcoidosis. Clinical features: Bilateral, small (miosed), irregular, eccentric pupils with COMPLETE absence of light reflex and preserved near/accommodation response. Poor dilation to mydriatics.
Critical distinction: Do NOT confuse true Argyll Robertson pupils (small, miosed, bilateral, neurosyphilis-specific) with pseudo-Argyll Robertson pupils / Parinaud syndrome pupils (mid-dilated, from posterior commissure compression by pinealoma, hydrocephalus, MS). Pupil size (small vs mid-dilated), light response completeness (absent vs partial), and aetiology are all different. This is a major exam differentiator.
Pathophysiology
Compression or ischaemia of posterior commissure / pretectal area (pinealoma, obstructive hydrocephalus, MS, tectal stroke). Results in disruption of light reflex fibres while sparing near reflex pathway.
Clinical Features — Classic Tetrad
- Upgaze palsy — vertical supranuclear gaze limitation
- Convergence-retraction nystagmus (CRN) — on OKN testing, downward pursuit is normal but upward saccadic recovery triggers co-contraction of extraocular muscles (NOT true nystagmus)
- Eyelid retraction (Collier's sign) — overactivity of levator palpebrae superioris
- Mid-dilated pupils with light-near dissociation — bilateral mid-dilated pupils with impaired light reflex but preserved near/accommodation response (pseudo-Argyll Robertson appearance)
Distinction from true Argyll Robertson: Dorsal midbrain pupils are mid-dilated (normal to slightly dilated) with partial light response. True AR pupils are small/miosed with complete absence of light reflex. Morphologically and clinically distinct — students must differentiate for MCQ accuracy.
Surgical (Compressive) CN III Palsy
Parasympathetic fibres run superficially on CN III. External compression (PComA aneurysm, uncal herniation) affects pupil FIRST — dilated, fixed pupil ('blown pupil'), complete ptosis, external ophthalmoplegia. Emergency imaging (CTA/MRA) mandatory.
Medical (Ischaemic) CN III Palsy
DM/HTN ischaemia affects central core of nerve, sparing peripheral parasympathetic fibres. Pupil typically spared in ~80% of medical CN III palsies. Presents with ptosis + EOM palsy but normal pupil.
RULE: Any CN III palsy with pupil involvement = neuroimaging urgently (CTA/MRA to exclude aneurysm). Pupil-sparing in young diabetic = medical palsy (observe). Any uncertainty = image.
| Condition | PLR | Near Reflex | Mechanism | Other Features |
|---|---|---|---|---|
| Argyll Robertson | Absent | Present | Pretectal lesion (neurosyphilis, DM) | Miosed, bilateral, irregular, poor dilation |
| Adie's Tonic Pupil | Sluggish/absent | Tonic (slow) | Ciliary ganglion post-ganglionic denervation | Unilateral, young F, vermiform iris, supersensitivity |
| Dorsal Midbrain Syndrome | Absent/impaired | Present | Posterior commissure compression | Mid-dilated, upgaze palsy, CRN, Collier's sign |
| Aberrant CN III Regeneration | Absent | Present (pseudo) | Misdirected parasympathetic fibres | History of CN III palsy, adduction synkinesis |
| Diabetes Mellitus | Sluggish/present | Sluggish/present | Ciliary nerve neuropathy | Bilateral, often miosed, systemic DM |
| Severe Optic Neuropathy | Reduced/RAPD | Normal | Afferent loss; near is cortical-driven | RAPD present; near spared because cortical bypass |
| Drug | Mechanism | Clinical Use | Interpretation |
|---|---|---|---|
| Pilocarpine 0.1% (dilute) | Direct cholinergic agonist | Adie's diagnosis | Constricts Adie's (supersensitivity); does NOT constrict normal pupil |
| Pilocarpine 1% (strong) | Direct cholinergic agonist | CN III vs pharmacological dilation | Constricts CN III palsy; does NOT constrict pharmacological blockade |
| Cocaine 4–10% | Blocks NE reuptake | Confirm Horner's | Horner eye fails to dilate; normal eye dilates |
| Apraclonidine 0.5–1% | Alpha-2/1 agonist; denervation supersensitivity | Confirm Horner's | Reversal of anisocoria = Horner's; false-negative if acute (<2 weeks) |
| Hydroxyamphetamine 1% | Releases NE from pre-synaptic terminals | Localise Horner's (1st/2nd vs 3rd) | Dilation = 1st/2nd order; non-dilation = 3rd order |
| Phenylephrine 1% | Alpha-1 agonist | Localise Horner's (2nd vs 3rd) | Dilation = 3rd order (supersensitivity); minimal = 2nd order |
Step 1 — Determine Which Pupil Is Abnormal: Light vs Dark
- Greater anisocoria in bright light: Larger pupil is abnormal → Efferent parasympathetic defect (CN III palsy, Adie's, pharmacological dilation)
- Greater anisocoria in darkness: Smaller pupil is abnormal → Sympathetic defect (Horner's syndrome)
- Equal difference in light and dark (~1 mm): Physiological anisocoria (no pathology)
Step 2 — Dilation Lag Test (For Suspected Horner's)
In darkened room, photograph pupils at 4–5 seconds and 15–20 seconds after room light is extinguished. Horner's pupil dilates slowly (dilation lag) compared to normal eye due to absent sympathetic drive. Simple, elegant test confirming sympathetic involvement.
EVOLVING CONCEPT: High-resolution smartphone-based infrared pupillometry is being validated as bedside tool for quantifying RAPD and dilation lag, potentially replacing neutral density filter testing in resource-limited settings.
| Condition | Feature | Association / Gene |
|---|---|---|
| Leukocoria | White pupillary reflex | Retinoblastoma, PHPV, cataract, Coats disease, ROP |
| Iris Coloboma | Keyhole pupil inferonasally | CHARGE syndrome (CHD7 mutation); trisomy 13, 4p-deletion. NOTE: PAX2 mutations → optic disc coloboma + renal anomalies, NOT iris coloboma |
| Aniridia | Absent iris / rudimentary rim | PAX6 mutation; associated with Wilms tumour (WT1 gene — 11p13 WAGR locus) |
| Polycoria | Multiple true pupils | Rare; Axenfeld-Rieger syndrome |
| Ectopia lentis et pupillae | Pupil displacement + ectopia lentis | Autosomal recessive; lens displaced opposite to pupil |
| Persistent pupillary membranes | Iris strands across pupil | Failed regression of tunica vasculosa lentis |
Trap 1 — FALSE
“Dense cataract, corneal opacity, and mild-to-moderate amblyopia cause a relative afferent pupillary defect (RAPD).”
RAPD requires optic nerve disease, extensive retinal damage (e.g., CRAO, large RD), or optic tract lesion. Anterior segment opacities (cataract, corneal scar) and mild amblyopia do NOT cause RAPD because afferent pupillomotor pathways (ipRGCs → optic nerve → pretectal) remain intact. A clear pupil-to-pretectal pathway = no RAPD.
Trap 2 — FALSE
“Convergence-retraction nystagmus is a true nystagmus reflex (involuntary oscillation) seen in dorsal midbrain syndrome.”
Convergence-retraction nystagmus (CRN) is NOT true nystagmus — it is synchronous co-contraction of extraocular muscles during attempted upgaze. On OKN drum rotated downward, downward pursuit is normal but upward saccadic recovery triggers CRN. It is pathognomonic for dorsal midbrain syndrome, not a brainstem oscillation.
Trap 3 — FALSE
“In a right optic tract lesion, a right relative afferent pupillary defect (RAPD) is expected because the lesion is ipsilateral.”
A RIGHT optic tract lesion causes a LEFT (contralateral) RAPD. Nasal fibres (representing the contralateral eye) cross at the chiasm and carry greater pupillomotor weight; an optic tract lesion therefore produces contralateral RAPD (Wernicke's hemianopic pupil). This is opposite to students' initial expectation — a classic MCQ trap.
Trap 4 — FALSE
“True Argyll Robertson pupils (small, miosed, light-near dissociation) are caused by any posterior commissure lesion, including pinealoma and hydrocephalus.”
True Argyll Robertson pupils are small, bilateral, irregular, miosed pupils with COMPLETE absence of light reflex — a specific sign of neurosyphilis (rarely diabetic neuropathy). Generic posterior commissure lesions (pinealoma, obstructive hydrocephalus, MS, tectal stroke) produce Parinaud/dorsal midbrain syndrome with mid-dilated pupils and partial light response (pseudo-Argyll Robertson appearance). Pupils are morphologically distinct: small/miosed (AR) vs mid-dilated (Parinaud). Do NOT conflate.
Q: Why is the pupil spared in medical (ischaemic) CN III palsy but dilated in surgical (compressive) CN III palsy?
A: Parasympathetic fibres travel in the superficial, peripheral portion of CN III with better collateral blood supply. Medical (DM/HTN) ischaemia affects the central core of the nerve, sparing peripheral fibres — pupil is spared in ~80%. Surgical compression (PComA aneurysm, uncal herniation) affects superficial parasympathetic fibres FIRST → dilated, fixed pupil + ptosis + EOM palsy.
Q: A patient has acute left Horner's syndrome after carotid dissection. Which drug confirms Horner's and which drug localises the lesion to the 3rd order neuron?
A: Apraclonidine 0.5% confirms Horner's by reversing anisocoria (denervation supersensitivity). Hydroxyamphetamine 1% localises to 3rd order if it fails to dilate the Horner's pupil — indicating depleted NE stores in post-ganglionic terminals. (Note: Acute Horner's <2 weeks may show false-negative apraclonidine; cocaine 4–10% is most reliable confirmatory test.)
Q: Explain the anatomical basis for contralateral RAPD in optic tract lesion (Wernicke's hemianopic pupil).
A: Nasal fibres cross at the chiasm (representing contralateral eye); temporal fibres do not cross (representing ipsilateral eye). Nasal fibres carry greater pupillomotor weight. In a right optic tract lesion, nasal fibres from the LEFT (contralateral) eye + temporal fibres from the RIGHT (ipsilateral) eye are damaged. The contralateral-eye nasal fibres (greater weight) are lost → LEFT (contralateral) RAPD. Optic tract lesions produce RAPD on the contralateral side — opposite the lesion side.
Q: What is Wernicke's hemianopic pupil and how is it tested?
A: In complete optic tract lesion, the pupillary light reflex is absent when light illuminates the hemianopic (blind) half of the retina, but normal when illuminating the seeing half. Tested with a narrow pencil of light directed nasally (hemianopic side) vs temporally (seeing side) — asymmetric pupil response. Difficult to elicit clinically due to light scatter across retinal boundaries.
Q: Which pupillary conditions present with light-near dissociation (LND)? List the key differential features.
A: Argyll Robertson pupil (neurosyphilis, small/miosed); Adie's tonic pupil (ciliary ganglion, unilateral, young F, supersensitivity); Dorsal midbrain syndrome (posterior commissure compression, mid-dilated, upgaze palsy, CRN); Aberrant CN III regeneration (misdirected fibres, adduction synkinesis); Diabetes mellitus (ciliary nerve neuropathy, bilateral, miosed); Severe optic neuropathy (afferent loss, RAPD present, near is cortical-driven).
Q: Explain the pathophysiology of Adie's tonic pupil and why dilute pilocarpine differentiates it from other conditions.
A: Adie's: Post-ganglionic parasympathetic denervation of ciliary ganglion (viral/autoimmune). Aberrant reinnervation follows — 30:1 ratio of fibres to ciliary muscle vs sphincter → tonic near response, poor PLR. Denervation supersensitivity develops to acetylcholine. Dilute pilocarpine 0.1% directly activates hypersensitive muscarinic receptors on Adie's pupil → constricts. Normal pupil (with intact innervation, high acetylcholinesterase activity) does NOT constrict to 0.1% pilocarpine. Differential response confirms Adie's.
Q: What is the apraclonidine test for Horner's syndrome and what is a potential pitfall?
A: Apraclonidine 0.5–1% is an alpha-2/1 agonist that activates denervation supersensitive alpha-1 receptors upregulated in Horner's dilator pupillae. In Horner's, anisocoria reverses (miosed pupil dilates) → confirms Horner's. Pitfall: Acute Horner's (<2 weeks) may show false-negative apraclonidine — supersensitivity takes time to develop. Cocaine 4–10% (blocks NE reuptake) is most reliable confirmatory test in acute Horner's.
Q: Describe the three-neuron sympathetic arc and how lesions at each level cause anhidrosis in different patterns.
A: 1st order: Hypothalamus → C8-T2 lateral tegmentum (brainstem CVA, syringomyelia). 2nd order: C8-T2 → Stellate ganglion along lung apex/subclavian (Pancoast tumour, thyroid Ca). 3rd order: Stellate → ICA → cavernous sinus → orbit (ICA dissection). Anhidrosis pattern: Whole-face anhidrosis = 2nd order (pre-ganglionic). Anhidrosis limited to medial forehead/nose (nasociliary V1 distribution) = 3rd order. No anhidrosis = 3rd order post-carotid bifurcation.
A 45-year-old woman presents with a 2-week history of left ptosis and a small left pupil. She also complains of left-sided neck pain. On examination, her anhidrosis is limited to the medial forehead. Apraclonidine 0.5% reverses the anisocoria, confirming left Horner's syndrome. Hydroxyamphetamine 1% fails to dilate the left pupil. What is the diagnosis? Discuss the pathophysiology, anatomical localisation logic, immediate investigation, and current management.
Diagnosis & Localisation
Diagnosis: Left 3rd order (post-ganglionic) Horner's syndrome due to Internal Carotid Artery (ICA) dissection. Localisation logic: - Anhidrosis pattern: Limited to medial forehead (nasociliary/V1 territory) indicates sympathetic lesion at or after the point where fibres join the ICA in the cavernous sinus/orbital apex — 3rd order location. - Hydroxyamphetamine failure: Non-dilation of the Horner's pupil confirms 3rd order lesion. Hydroxyamphetamine releases NE from pre-synaptic terminals; if terminals are depleted (3rd order post-ganglionic denervation), no dilation occurs. Intact 1st/2nd order lesions would show pupil dilation. - Clinical presentation: Acute onset + left-sided neck pain + Horner's = high suspicion for ICA dissection (spontaneous or traumatic; more common in middle-aged women, often triggered by minor trauma or manipulation).
Pathophysiology of ICA Dissection
Spontaneous or traumatic ICA dissection causes intramural haematoma in the arterial wall. The expanding haematoma compresses the sympathetic plexus that travels along the ICA surface from the carotid bifurcation upward through the cavernous sinus. Sympathetic involvement only (Horner's without motor/sensory deficit) occurs when compression is localised to the arterial wall. Propagating intramural thrombus or arterial occlusion can extend into cerebral vasculature → cerebral ischaemia (stroke, TIA). Acute neck pain preceding neurological signs is typical — reflects arterial wall stretch and inflammation.
Immediate Investigation
Gold standard: MRI/MRA of the neck - T1 fat-suppressed sequence: Demonstrates hyperintense crescent sign (intramural haematoma) - MRA: Shows tapered narrowing of ICA lumen ('string sign') Alternative: CTA neck/head for faster acquisition (good sensitivity/specificity; less tissue detail than MRI) Avoid: Conventional angiography unless MRI/CTA equivocal (invasive; reserve for challenging cases or when intervention planned)
Management & Prognosis
Anticoagulation vs Antiplatelet therapy: - Anticoagulation: Heparin (initial, IV) → transitioned to warfarin (oral, INR 2–3 for 3–6 months). Theoretical benefit: prevents propagating thrombus and cardioembolic stroke. - Antiplatelet therapy: Aspirin (daily) or other antiplatelet agents. Simpler, lower haemorrhagic risk. Evidence: CADISS trial (2015, Lancet Neurology, n=250) compared antiplatelet vs anticoagulation in cervical artery dissection — no significant difference in stroke/death outcomes at 3 months or long-term. Current practice favors antiplatelet therapy as first-line given similar efficacy and lower haemorrhagic risk. Monitoring: Serial neuroimaging (MRA) at 1, 3, 6 months to assess arterial remodelling (most dissections stabilise within 3 months). Horner's typically resolves within 6–12 months with arterial recanalization/collateral development. Full neurological recovery is common.
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