Last reviewed: March 2026
Contents
MDM Templates
Physiologic Anisocoria
Patient presents with anisocoria without associated neurologic symptoms. Pupils are both reactive to light with preserved consensual response. No ptosis, no extraocular movement deficit, no pain. Difference between pupils is <1 mm and has been present per patient history (or old photographs confirm prior asymmetry).
History and exam reassure against dangerous causes of anisocoria including CN III palsy from posterior communicating artery aneurysm, Horner syndrome from carotid dissection, and pharmacologic exposure. No features of brainstem pathology.
Plan: No further workup indicated.
Disposition: Discharge with PCP follow-up. Return precautions for new headache, vision changes, ptosis, or weakness.
Anisocoria — Workup Indicated
Patient presents with new anisocoria without clear prior history of pupil asymmetry. No evidence of direct iris trauma or pharmacologic exposure. Pupils are reactive but asymmetric by >1 mm.
Given new onset and absence of clearly benign features, I have considered CN III palsy (posterior communicating artery aneurysm), Horner syndrome (carotid dissection, apical lung lesion), pharmacologic cause, and Adie tonic pupil. No ptosis or EOM deficit to suggest CN III palsy. No ipsilateral ptosis with miosis to suggest Horner syndrome.
Plan: CT/CTA head and neck to evaluate for aneurysm and dissection.
Disposition: Pending imaging results. Ophthalmology follow-up within 1 week if workup negative.
Horner Syndrome Concern
Patient presents with new unilateral miosis with ipsilateral ptosis, concerning for Horner syndrome. No anhidrosis appreciated on exam. Patient does endorse ***.
Given concern for Horner syndrome, I have considered dangerous causes along the oculosympathetic pathway: first-order (brainstem stroke, spinal cord lesion), second-order (apical lung tumor, mediastinal mass), and third-order (carotid dissection, cavernous sinus pathology). Neck pain or recent trauma raises concern for carotid dissection.
Plan: CTA head and neck to evaluate for carotid dissection. CT chest if second-order lesion suspected.
If neck pain, trauma, or acute onset: CTA is emergent given dissection concern.
Disposition: Pending imaging. Neurology consultation if confirmed.
CN III Palsy Concern
Patient presents with unilateral mydriasis with ipsilateral ptosis and/or extraocular movement deficit, concerning for CN III palsy. A dilated, unreactive pupil with “down and out” gaze is the classic presentation.
Given pupil-involving CN III palsy, this is an emergent concern for posterior communicating artery aneurysm until proven otherwise. I have also considered uncal herniation, cavernous sinus pathology, and diabetic mononeuropathy (though diabetic CN III palsy classically spares the pupil).
Plan: Emergent CTA head to evaluate for posterior communicating artery aneurysm.
Neurosurgery consulted regarding imaging findings and disposition.
Disposition: Pending imaging and neurosurgical evaluation.
Clinical Education
Approach to Anisocoria
The critical first question: which pupil is abnormal? Test in both light and dark conditions. If anisocoria is greater in the dark, the smaller pupil is the problem (it fails to dilate — think Horner syndrome). If anisocoria is greater in bright light, the larger pupil is the problem (it fails to constrict — think CN III palsy or pharmacologic mydriasis).[1]
Check old photographs. A driver’s license or old selfie showing pre-existing asymmetry is the fastest way to confirm physiologic anisocoria and avoid unnecessary imaging.
Physiologic Anisocoria Pearls
Up to 20% of the population has physiologic anisocoria (<1 mm difference). Both pupils react normally to light and accommodation. The asymmetry remains relatively constant in light and dark. If the difference fluctuates or exceeds 1 mm, it is less likely physiologic.[1]
Horner Syndrome
Classic triad: ipsilateral miosis, ptosis, and anhidrosis. Anhidrosis is often subtle or absent (especially in third-order lesions). The ptosis in Horner’s is mild (1–2 mm) — it involves Muller’s muscle, not the levator. The involved pupil is the smaller one, and dilation lag in dim light is a classic exam finding.[2]
| Order | Neuron Location | Dangerous Causes |
| 1st (central) | Hypothalamus → brainstem → C8-T2 cord | Stroke, demyelination, spinal cord lesion |
| 2nd (preganglionic) | T1 root → lung apex → superior cervical ganglion | Pancoast tumor, mediastinal mass, trauma |
| 3rd (postganglionic) | Along ICA → cavernous sinus → orbit | Carotid dissection, cavernous sinus lesion |
Acute Horner + neck pain or headache = carotid dissection until proven otherwise. This demands emergent CTA head and neck.[2]
CN III Palsy
Pupil-involving CN III palsy is an aneurysm until proven otherwise. The parasympathetic pupillary fibers run on the outside of CN III and are compressed first by an expanding posterior communicating artery aneurysm. This produces a “down and out” eye with a fixed, dilated pupil and complete ptosis. CTA head is the emergent study.[3]
Pupil-sparing CN III palsy is more commonly ischemic (diabetic mononeuropathy). However, this is an imperfect rule — up to 14% of aneurysmal CN III palsies may initially spare the pupil. If there is any ptosis or EOM deficit with a relative pupil-sparing pattern, imaging is still warranted. “Complete” pupil-sparing with complete ptosis and complete EOM deficit in a diabetic patient may be observed, but this requires confident assessment and close follow-up.[3]
Adie Tonic Pupil
Adie pupil is a benign cause of unilateral mydriasis. Caused by damage to the ciliary ganglion (often post-viral). The affected pupil is dilated, reacts sluggishly to light, but shows a tonic (slow, vermiform) constriction to prolonged near focus. Absent deep tendon reflexes (Adie syndrome) may be associated. Not dangerous but requires ophthalmology follow-up for confirmation.[1]
Pharmacologic Anisocoria
Always ask about eye drops, scopolamine patches, nebulizer treatments, and occupational exposures. Ipratropium nebulizer mask leak is a classic cause of unilateral mydriasis in hospitalized patients. Scopolamine patches (especially if the patient touches the patch then touches their eye) are another common culprit. A pharmacologically dilated pupil will not constrict with 1% pilocarpine — this is the definitive bedside test.[1]
Disposition
Known or confirmed physiologic anisocoria: discharge, no workup needed. Isolated new anisocoria without red flags: ophthalmology follow-up within 1 week. Anisocoria with ptosis, EOM deficit, headache, or neck pain: emergent imaging (CTA head and neck) and neurology or neurosurgery consultation in the ED.[1]
References
- Gross JR et al. Anisocoria and Horner Syndrome. In: Tintinalli’s Emergency Medicine, 9th ed. McGraw-Hill; 2020.
- Walton KA, Buono LM. Horner syndrome. Curr Opin Ophthalmol. 2003;14(6):357-363. PubMed
- Fang C et al. Pupil-involving versus pupil-sparing third nerve palsy: an updated meta-analysis. Br J Ophthalmol. 2023;107(4):556-561. PubMed
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