Carotid dissection

Overview

Carotid dissection is one of the most important causes of ischaemic stroke in patients under 45. A tear in the tunica intima allows blood into the vessel wall, causing luminal narrowing/occlusion and thromboembolism to the intracranial circulation.

Presentation

Pain (headache + neck pain) typically precedes the neurological deficit by hours to days - this window represents ongoing thrombus formation before embolisation.

•Headache - present in 60-75%; unilateral, severe, gradual onset (not thunderclap); ipsilateral to dissection

•Partial Horner's syndrome - present in ~58%; ptosis and miosis WITHOUT anhidrosis (post-ganglionic fibres in carotid sheath compressed; anhidrosis-carrying fibres travel with external carotid and are spared)

•Pulsatile tinnitus - ~27%; turbulent flow through narrowed lumen transmitted to middle ear

•Ipsilateral neck pain - ~25%; haematoma stretches vessel wall

•Amaurosis fugax - ~25%; embolism to ophthalmic artery (ICA branch)

•Lower cranial nerve palsy (IX-XII) - ~12%; mass effect of haematoma in parapharyngeal space

•Contralateral hemiplegia / hemisensory loss - MCA territory ischaemia from embolism or haemodynamic compromise

💡

Ptosis + miosis WITHOUT anhidrosis in a young patient with ipsilateral head/neck pain = carotid dissection until proved otherwise. The Horner's is post-ganglionic - distinguishing it from central or pre-ganglionic causes.

Investigations

🥇 First-line

•Non-contrast CT head - urgently exclude haemorrhagic stroke/SAH before antithrombotic therapy

•Carotid duplex ultrasound - non-invasive; high sensitivity for extracranial ICA dissection; poor for intracranial disease

🏆 Gold standard

•MRA with fat-suppression MRI - directly visualises intramural haematoma (crescent of high T1 signal); shows string sign (tapered narrowing) and double-lumen sign

🥈 Second-line

•CT angiography - faster, more available; shows double-lumen sign or flame-like tapering; preferred if MRI contraindicated

Management

•Assess thrombolysis eligibility immediately if within 4.5-hour window with disabling ischaemic stroke

•Antithrombotic therapy for 3-6 months - choice between antiplatelet and anticoagulation remains unresolved (CADISS trial: no significant difference)

•Standard first-line: aspirin or clopidogrel (antiplatelet) - most UK centres

•Anticoagulation reserved for high thrombus burden or progressive neurological symptoms

•Surgical/endovascular intervention - reserved for specific indications only

Complications

•Ischaemic stroke - most serious; accounts for up to 20% of strokes in under-45s

•Pseudoaneurysm - blood pools between adventitia and media forming false aneurysm; most decrease spontaneously

•SAH - rare; more likely after head/neck trauma

Prognosis

•Generally favourable - dissection heals spontaneously with lumen recanalisation over weeks to months

•Principal determinant of outcome is whether stroke has already occurred at presentation

•Recurrence risk is significantly higher in patients with connective tissue disorders or fibromuscular dysplasia - require long-term vascular surveillance

Risk factors / precipitants

Precipitants and associations

Marfan syndrome - defective fibrillin-1

Ehlers-Danlos syndrome (type IV) - defective type III collagen

Fibromuscular dysplasia - younger women

Oral contraceptive pill / pregnancy

Chiropractic manipulation / yoga

Direct neck trauma / RTC

Vigorous coughing / sneezing

Migraine