Synopsis
Recognise sympathetic pathway failure from the pupil and eyelid findings, distinguish it from physiological anisocoria and rapidly investigate painful or acute Horner syndrome for vascular, central, apical and neck causes.
- Horner syndrome reflects interruption of the three-neuron sympathetic pathway from hypothalamus through brainstem and cervical cord, over the lung apex and up the neck with the carotid arteries to the eye.
- The core signs are ipsilateral miosis and mild ptosis, often with apparent elevation of the lower lid; anisocoria is usually more obvious in darkness because the affected pupil dilates slowly.
- Anhidrosis varies with lesion level because facial sweating fibres separate along external and internal carotid routes; its absence does not exclude the syndrome.
- Measure pupils in bright and dim light after allowing dilation, record eyelid position and look for dilation lag. Compare old photographs because lifelong physiological anisocoria is common.
- Painful acute Horner syndrome—especially unilateral neck, facial or orbital pain—requires urgent arterial imaging for carotid dissection even if limb examination is initially normal.
- Brainstem or first-order lesions may add vertigo, nystagmus, dysphagia, ataxia, crossed sensory loss or long-tract signs and should enter an emergency posterior-circulation pathway.
- Preganglionic lesions can arise at the lung apex, thoracic inlet or cervical sympathetic chain and may accompany shoulder or arm pain, hand weakness, neck mass, surgery or trauma.
- Postganglionic lesions follow the internal carotid into the cavernous sinus and orbit and can accompany trigeminal pain, ocular motor palsies or headache syndromes.
- Pharmacological pupil testing can confirm sympathetic denervation in appropriate specialist settings but should not delay emergency vascular or structural imaging when onset or pain is concerning.
- Congenital Horner syndrome may include heterochromia, but heterochromia is neither required nor a reliable discriminator in acquired adult presentations.
- Do not confuse Horner syndrome with a third-nerve palsy: Horner produces a small pupil and mild ptosis without extraocular weakness, whereas third-nerve disease often impairs eye movements and may enlarge the pupil.
- When duration is genuinely longstanding and no red flags exist, imaging strategy remains specialist-led because the whole sympathetic pathway may require assessment and incidental testing can be extensive.
Key red flags
New partial Horner syndrome with ipsilateral neck, face or orbital pain, headache or transient retinal or cerebral symptoms strongly suggests carotid dissection and requires emergency head-and-neck vascular imaging.
Horner syndrome with vertigo, nystagmus, ipsilateral facial sensory loss, contralateral body pain-temperature loss, dysphagia or limb ataxia supports a first-order lesion such as lateral medullary stroke.
Horner syndrome plus persistent shoulder or medial arm pain, hand weakness or wasting, cough, constitutional symptoms or an apical chest finding suggests lower brachial-plexus and sympathetic-chain involvement from a thoracic-inlet lesion.
Miosis and ptosis accompanied by ocular motor palsies or trigeminal V1 or V2 sensory change points to the cavernous sinus or orbital apex and raises vascular, inflammatory, infectious and neoplastic causes.
Neck, chest, spinal or carotid procedures and penetrating or traction injury can interrupt the pathway. Timing and accompanying vascular or plexus injury determine whether postoperative observation or urgent imaging is appropriate.
Transient partial Horner signs can accompany strictly unilateral orbital pain with autonomic features, but a first or atypical painful episode still requires exclusion of carotid and structural disease.
Investigation priorities
Determine which pupil is abnormal and whether anisocoria increases when sympathetic dilation is required.
Management branches
New miosis and mild ptosis accompanies ipsilateral neck, facial, orbital or head pain, with or without transient neurological symptoms.
- Establish last known well and trauma or manipulation history, perform ABCDE and a complete stroke and cranial examination and compare pupils in bright and dim light without delaying escalation.
- Contact the stroke or neurovascular service and obtain urgent head-and-neck CTA or the locally preferred arterial imaging for carotid dissection and associated infarction.
- Use antithrombotic and follow-up treatment only under the responsible stroke team after haemorrhage and vascular anatomy are defined, and safety-net recurrent retinal or cerebral symptoms.