š¦ Hornerās Syndrome is caused by the loss of sympathetic nerve supply to the face and eye.
It classically presents with ptosis, miosis, anhidrosis, and apparent enophthalmos.
ā ļø Important causes to exclude: lung apex malignancy (Pancoast tumour), carotid artery dissection, and lateral medullary infarct.
š Aetiology
- The sympathetic pathway originates in the hypothalamus, descends through the brainstem, exits at C8/T1, travels with the carotid artery, and finally enters the eye.
- Lesions along this 3-neuron pathway produce Hornerās syndrome.
š§ Causes (By Neuron Level)
- First-order (Central): Brainstem and cervical cord lesions
- Stroke (especially lateral medullary syndrome).
- Tumours, demyelination (e.g., MS).
- Syringomyelia, trauma.
- Second-order (Preganglionic): Apex of lung / chest outlet
- Pancoast tumour (lung apex squamous carcinoma).
- Thoracic trauma or post-surgical damage.
- Schwannoma.
- Third-order (Postganglionic): Neck / carotid artery to the eye
- Carotid artery dissection or aneurysm.
- Base of skull tumours or infections.
- Cluster headaches / migraines.
- Birth trauma in children.
š Anatomy of Autonomic Supply
This 3-neuron oculosympathetic pathway runs:
Hypothalamus ā Spinal cord (C8āT1) ā Superior cervical ganglion ā Eye (pupil dilator, eyelid smooth muscle, facial sweat glands).
𩺠Clinical Features
- šļø Ptosis: Drooping of upper eyelid (loss of sympathetic innervation to Müllerās muscle).
- šÆ Miosis: Constricted pupil that reacts normally to light.
- š§ Anhidrosis: Reduced sweating on affected side (distribution depends on lesion level).
- ā” Apparent enophthalmos: Sunken eye appearance.
- Additional: Conjunctival injection; cough and cachexia if lung cancer-related.
šø Case Studies
- Left Pancoast Tumour: Hornerās with ptosis from apical lung cancer.

- Idiopathic Hornerās: Left-sided, cause unknown.

- Classic Clinical Signs: Ptosis + miosis + anhidrosis.

š§Ŗ Investigations
- Bloods: FBC, U&E; calcium or sodium derangements may suggest paraneoplastic lung cancer.
- Imaging:
- MRI brainstem for stroke.
- MRA neck for carotid dissection.
- CT chest for apical lung tumour (Pancoast).
- Pharmacological Testing:
- 1% cocaine drops: failure of pupil dilation confirms Hornerās.
- Apraclonidine drops may also be used (denervation supersensitivity ā pupil dilates).
𩹠Management
- šÆ Treat the underlying cause:
- Surgery / radiotherapy for lung cancer.
- Anticoagulation or stenting for carotid dissection.
- Stroke management if central cause.
- šļø Symptom management: Usually benign, but underlying pathology must never be missed.
š” Clinical Pearls
- Think āPtosis + Miosis + Anhidrosis = Hornerās until proven otherwiseā.
- Always exclude š¬ Pancoast tumour in a smoker with Hornerās + arm/shoulder pain.
- š Carotid dissection is a stroke emergency: look for ipsilateral head/neck pain + Hornerās.
Cases ā Hornerās Syndrome
- Case 1 ā Apical Lung Tumour (First-Order Neuron) š«:
A 62-year-old man with a 40 pack-year smoking history presents with right-sided shoulder pain radiating to the arm. Exam: mild right ptosis, miosis, and anhidrosis. CXR shows a right apical mass.
Diagnosis: Hornerās syndrome due to Pancoast tumour invading sympathetic chain.
Management: Oncology referral; CT chest; biopsy for staging.
- Case 2 ā Carotid Artery Dissection (Second-Order Neuron) ā”:
A 45-year-old man presents with sudden neck pain and headache after minor trauma. Exam: left ptosis and miosis without anhidrosis; no extraocular palsy. MRI angiography: left internal carotid artery dissection.
Diagnosis: Painful Hornerās syndrome due to carotid dissection.
Management: Urgent vascular input; anticoagulation/antiplatelets; stroke prevention.
- Case 3 ā Cluster Headache (Third-Order Neuron) š„:
A 38-year-old man has recurrent severe left periorbital headaches lasting 1 hour, associated with ipsilateral lacrimation and nasal congestion. Exam during attack: mild ptosis and miosis on the left.
Diagnosis: Hornerās syndrome associated with cluster headache.
Management: High-flow oxygen, subcutaneous sumatriptan for acute attack; verapamil for prevention.
- Case 4 ā Stroke-Related Hornerās š§ :
A 59-year-old man with vascular risk factors presents with acute vertigo, dysphagia, hoarseness, and loss of pain/temperature sensation on the right side of his face and left body. Exam: right-sided ptosis and miosis. MRI brain: infarct in right lateral medulla (posterior inferior cerebellar artery territory).
Diagnosis: Hornerās syndrome secondary to lateral medullary (Wallenbergās) syndrome.
Management: Stroke care (antiplatelet therapy, risk factor modification, swallow assessment, rehab); supportive for Hornerās.
Teaching Commentary š§
Lateral medullary syndrome = classic brainstem stroke syndrome (PICA or vertebral artery occlusion).
Key features:
- Ipsilateral: facial pain/temperature loss (trigeminal nucleus), Hornerās syndrome (sympathetic tract), ataxia (cerebellar peduncle), palate weakness (nucleus ambiguus ā dysphagia/hoarseness).
- Contralateral: body pain/temperature loss (spinothalamic tract).
Mnemonic: āDonāt PICA horse (hoarseness) that canāt eat (dysphagia)ā.
Management: same as ischaemic stroke (antiplatelets, risk factor control, swallow therapy). Prognosis depends on severity of bulbar dysfunction.