Carotid and vertebral artery dissection

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

A dissection starts with injury or spontaneous failure of the arterial wall, allowing blood to enter and form an intramural haematoma. The vessel may narrow or occlude, generate thromboembolism or develop a pseudoaneurysm. Most neurological events arise from embolism rather than simple low flow. Hypertension, migraine, smoking and heritable connective-tissue disease may contribute, but many patients have no systemic disorder and no dramatic trauma. A careful history should ask about recent neck pain, exertion, manipulation, coughing, infection, childbirth and direct injury without implying causation from every everyday movement.

Local signs differ by artery. The internal carotid sympathetic plexus produces ptosis and miosis; facial sweating may remain intact because sudomotor fibres follow the external carotid, creating a partial Horner syndrome. Lower cranial neuropathy or pulsatile tinnitus can occur from mass effect. Vertebral lesions cause upper posterior neck or occipital pain and may embolise to the lateral medulla, cerebellum, pons or posterior cerebral artery. Symptoms can fluctuate and FAST may be negative.

CTA is fast and widely available; MRA with fat-suppressed vessel-wall sequences can demonstrate intramural blood and clarify uncertain or subacute cases. Acute management prioritises stroke reperfusion when eligible and antithrombotic prevention of recurrent embolism. Choice between antiplatelet and anticoagulation incorporates infarct size, intraluminal thrombus, bleeding risk, intracranial extension and local expertise. Endovascular stenting or surgery is uncommon and reserved for selected recurrent, haemodynamic or compressive complications.

Key points

Cervical artery dissection is an important cause of stroke in younger adults and can occur spontaneously or after seemingly minor neck strain, coughing, sport, trauma or manipulation.
Internal carotid dissection classically causes unilateral head, face or neck pain with partial Horner syndrome, pulsatile tinnitus, retinal ischaemia or hemispheric TIA or stroke.
Vertebral dissection more often causes occipital or posterior neck pain followed by vertigo, diplopia, dysarthria, ataxia, nystagmus, sensory change or other posterior circulation signs.
Pain can precede cerebral ischaemia by hours or days, so a normal initial limb examination does not make a new painful Horner syndrome or suspicious posterior neck syndrome benign.
Urgent CTA or MRA should cover head and neck vessels; carotid Doppler alone can miss high cervical, vertebral and intracranial disease and should not be used to exclude dissection.
Treat an acute disabling ischaemic stroke with the usual thrombolysis and thrombectomy pathways when eligible; dissection itself is not an automatic reperfusion contraindication.
For extracranial dissection, antiplatelet therapy or anticoagulation may be selected because no clear overall superiority has been established; current UK stroke guidance recommends antithrombotic treatment for at least 3 months, with any continuation beyond that reassessed by the specialist team.
Intracranial extension, dissecting aneurysm, subarachnoid haemorrhage or recurrent ischaemia despite therapy changes the risk and requires urgent neurovascular multidisciplinary management.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Spontaneous arterial wall failure

Many dissections arise without major trauma, sometimes in association with migraine, hypertension or subtle inherited connective-tissue susceptibility rather than a recognised systemic disorder.

Mechanical neck injury

Direct trauma, sudden rotation, sport, coughing or manipulation may precede symptoms, although common everyday movements can be coincidental and do not prove causation.

Pregnancy and arteriopathy

Postpartum vascular change and less common fibromuscular, inflammatory or heritable arteriopathies can weaken cervical arterial walls, particularly when dissections are recurrent or multifocal.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Wall disruption
A tear or spontaneous bleed allows blood to enter the arterial wall, creating an intramural haematoma between wall layers.
2
Luminal narrowing and thrombosis
The expanding haematoma compresses the lumen, disturbs flow and exposes thrombogenic surfaces, promoting local clot formation and sometimes vessel occlusion.
3
Distal embolisation
Thrombus fragments travel into retinal or cerebral arteries, making embolism the common mechanism of transient ischaemia and stroke.
4
Pseudoaneurysm formation
Outward wall expansion can form a dissecting pseudoaneurysm that compresses adjacent sympathetic or cranial nerves or rarely creates a haemorrhagic risk.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Painful partial Horner syndrome

New unilateral ptosis and miosis with ipsilateral neck, orbital or facial pain is strongly suggestive of internal carotid dissection even without weakness.

Retinal or hemispheric ischaemia

Amaurosis fugax, aphasia, neglect or contralateral motor and sensory loss may follow carotid thromboembolism after a period of local pain.

Vertebrobasilar syndrome

Posterior neck or occipital pain accompanied by diplopia, dysarthria, gait ataxia, nystagmus or crossed signs suggests vertebral dissection and posterior circulation ischaemia.

Local mass effect

Pulsatile tinnitus, dysphagia, tongue weakness or other lower cranial neuropathy may arise from an expanded dissected cervical carotid segment or pseudoaneurysm.

Trauma-associated pattern

High-energy acceleration, neck fracture or seat-belt injury can cause blunt cerebrovascular injury even when initial neurological examination is normal.

Systemic arteriopathy clues

Multiple dissections, marked arterial tortuosity, renal artery disease, easy bruising or a family history may suggest fibromuscular dysplasia or heritable connective-tissue disease.

Red flags requiring action

Ongoing or fluctuating focal deficit, aphasia, disabling posterior signs or reduced consciousness requires immediate acute-stroke activation and reperfusion imaging.
Painful Horner syndrome is a same-day arterial-imaging indication because cerebral embolism can occur after the local syndrome begins.
Thunderclap headache, meningism or intracranial dissection raises subarachnoid haemorrhage and changes antithrombotic safety completely.
Progressive dysphagia, airway symptoms or multiple lower cranial neuropathies may indicate an expanding pseudoaneurysm requiring urgent neurovascular review.
Recurrent ischaemic events despite confirmed therapeutic treatment needs repeat imaging and specialist endovascular discussion rather than unsupervised drug stacking.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
CT angiography of head and neckFirst step
Why
Demonstrate tapered stenosis, occlusion, intimal abnormality, pseudoaneurysm or mural change and assess intracranial vessels.
Interpretation and limitations
Coverage must include the aortic arch through intracranial circulation; normal carotid bifurcation imaging does not assess the distal cervical or vertebral arteries adequately.
02
MRI brain with MRA and vessel-wall imaging
Why
Detect acute infarction and visualise intramural haematoma when CTA is uncertain or a subacute dissection is suspected.
Interpretation and limitations
Fat-suppressed T1 signal evolves with time and venous or flow artefact can mislead; correlate with the lumen and expert neuroradiology review.
03
Non-contrast CT brain
Why
Exclude haemorrhage and identify established infarction before acute reperfusion or antithrombotic decisions.
Interpretation and limitations
A normal brain CT does not assess the cervical arterial wall; proceed to angiography when the clinical syndrome supports dissection.
04
Digital subtraction angiography
Why
Clarify uncertain anatomy or guide an endovascular procedure when non-invasive imaging is insufficient.
Interpretation and limitations
It gives detailed lumen information but is invasive and may not show mural haematoma directly; reserve it for specialist-defined questions.
05
Carotid and vertebral ultrasound
Why
Provide selected haemodynamic follow-up information for accessible cervical segments.
Interpretation and limitations
A normal result cannot exclude distal carotid, vertebral or intracranial dissection and must not replace CTA or MRA in a high-risk presentation.
06
Cause-directed vascular evaluation
Why
Assess for fibromuscular dysplasia or connective-tissue disease when multiple beds, recurrence or phenotype suggests systemic arteriopathy.
Interpretation and limitations
Do not request broad genetic testing for every isolated event; involve vascular genetics or the relevant specialty when findings would alter counselling or surveillance.
07
Follow-up arterial imaging
Why
Assess healing, persistent stenosis or enlarging pseudoaneurysm when the result will affect antithrombotic duration or intervention.
Interpretation and limitations
Many extracranial dissections remodel over months; residual imaging abnormality alone does not define symptoms or mandate indefinite anticoagulation.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Primary headache or musculoskeletal neck pain

Reproducible mechanical tenderness without focal signs is reassuring, but new unilateral pain with Horner syndrome, tinnitus or posterior-circulation symptoms requires arterial imaging.

Intracranial dissection rupture

Thunderclap headache, meningism and subarachnoid blood favour aneurysmal or intracranial dissecting haemorrhage rather than uncomplicated extracranial dissection.

Cerebral vasculitis or RCVS

Multifocal arterial narrowing and recurrent headaches can overlap; inflammatory cerebrospinal fluid supports vasculitis, while repeated thunderclaps and reversible beading favour RCVS.

Atherosclerotic carotid disease

Calcified plaque at a typical bifurcation with vascular risk factors supports atherosclerosis, whereas mural haematoma, tapering stenosis and acute neck pain favour dissection.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01LOCALPainful local syndromeFirst stepNew unilateral head or neck pain occurs with partial Horner syndrome, pulsatile tinnitus or lower cranial neuropathy.

1Perform urgent neurological, pupillary and cranial-nerve examination and ask about transient retinal or cerebral symptoms and recent neck stress or injury.
2Arrange same-day CTA or MRA of the head and neck rather than relying on carotid Doppler or waiting for weakness.
3Discuss confirmed or strongly suspected dissection with stroke or neurology to determine antithrombotic treatment and whether brain MRI is needed.
4Give emergency return advice for visual loss, speech change, imbalance or weakness and advise against further neck manipulation during evaluation.

02STROKEDissection with acute ischaemiaThe patient has a current disabling focal deficit and angiography shows or strongly suggests cervical artery dissection.

1Activate the hyperacute stroke pathway, document last-known-well and obtain non-contrast brain CT plus complete head-and-neck angiography.
2Assess intravenous thrombolysis and mechanical thrombectomy using standard specialist criteria; extracranial dissection is not by itself an exclusion.
3After reperfusion decisions, select antiplatelet or anticoagulant treatment based on infarct, arterial anatomy, bleeding risk and the stroke service protocol.
4Monitor for recurrent embolism, haemorrhagic transformation, extension or pseudoaneurysm and arrange specialist follow-up imaging.

03TRAUMABlunt cerebrovascular injurySignificant trauma pattern, cervical fracture or neurological findings raise traumatic carotid or vertebral injury.

1Follow the trauma protocol for airway and spinal protection and identify high-risk injury criteria without delaying neurological assessment.
2Obtain trauma CTA with suitable cervical and intracranial arterial coverage and assess coexisting brain, spine and solid-organ bleeding.
3Agree antithrombotic timing jointly between stroke, trauma, neurosurgery and vascular or neurointerventional teams because bleeding risks compete.
4Plan repeat imaging and intervention only according to injury grade, symptoms and healing rather than one universal schedule.

04RECURSymptoms despite treatmentNew retinal or cerebral ischaemia occurs while the prescribed antithrombotic is being taken.

1Treat the new event as an acute stroke, confirm adherence and dosing and obtain repeat brain and arterial imaging urgently.
2Assess extension, intraluminal thrombus, haemodynamic compromise, pseudoaneurysm and a competing cardiac or arterial mechanism.
3Review antiplatelet versus anticoagulant strategy through the multidisciplinary team instead of combining agents empirically.
4Consider endovascular stenting or another rescue intervention only for selected recurrent or flow-limiting disease in an experienced centre.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Reduces artery-to-artery thromboembolism during healing of an extracranial carotid or vertebral dissection.

Aspirin

When antiplatelet treatment is selected, use the acute loading and subsequent daily dose specified by the stroke service, then convert to the planned maintenance regimen.

Exclude intracranial haemorrhage and consider infarct size, allergy, active bleeding and planned intervention; do not combine with anticoagulation without a defined indication.

Provides single-antiplatelet prevention of recurrent embolism during extracranial dissection healing in selected patients.

Clopidogrel

Use 75 mg orally once daily for maintenance when chosen, with any loading dose and intended duration set by the acute stroke or neurovascular protocol.

Review bleeding, blood dyscrasia, concurrent anticoagulants and surgery; evidence does not justify escalating every recurrent symptom without repeat diagnostic assessment.

Offers an alternative antithrombotic strategy when intraluminal thrombus, recurrent embolism or the overall specialist assessment favours anticoagulation.

Therapeutic anticoagulation

Select heparin followed by warfarin or a specialist-approved oral anticoagulant regimen only after considering infarct, anatomy, renal function and bleeding risk; when anticoagulation is chosen, current UK stroke guidance recommends 3 months before specialist reassessment.

Avoid when subarachnoid haemorrhage, major bleeding or high-risk intracranial dissection is present; no universal superiority over antiplatelet therapy has been shown, and continuing beyond 3 months requires an individual reason.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Cerebral or retinal ischaemia

Thromboembolism or severe flow limitation can cause transient monocular blindness, TIA or disabling anterior or posterior circulation infarction.

Subarachnoid haemorrhage

Intracranial extension or rupture of a dissecting aneurysm can release blood into the subarachnoid space, changing antithrombotic risk and requiring urgent neurovascular care.

Persistent pseudoaneurysm

Residual wall dilatation may maintain embolic, compressive or surveillance concerns, although many cervical dissections heal or stabilise on follow-up imaging.

Local nerve dysfunction

Carotid sympathetic-plexus injury produces partial Horner syndrome, while larger lesions can cause pulsatile tinnitus or lower cranial neuropathies through local mass effect.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Ask about recurrent monocular loss, aphasia, weakness, diplopia and ataxia during the early high-risk period and route any recurrence to emergency care.
Monitor antiplatelet or anticoagulant adherence, haemoglobin, bleeding, renal function and interactions using the chosen agent's usual safety framework.
Repeat arterial imaging at the specialist-defined interval when healing, pseudoaneurysm behaviour or treatment duration depends on the result.
Review headache and neck pain trajectory while avoiding repeated opioid escalation that could obscure neurological deterioration.
Assess driving, high-risk occupation, contact sport and neck manipulation restrictions with the stroke team and current DVLA guidance.
For recurrent or multifocal disease, follow blood pressure and any systemic arteriopathy or genetic referral plan without over-medicalising an isolated healed event.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Horner can lack anhidrosis

Sweating fibres often leave the internal carotid route earlier, so ptosis and miosis without facial anhidrosis remains a classic carotid dissection clue.

Pain may lead ischaemia

The local arterial wall syndrome can precede thromboembolism, creating a valuable imaging window before a completed stroke occurs.

Ultrasound has blind segments

High cervical internal carotid and vertebral arteries are incompletely visualised, so a reassuring Doppler cannot close a high-probability case.

Most strokes are embolic

Mural thrombus shedding into distal cerebral arteries is often more important than low flow through the narrowed dissected segment.

Everyday movement is not proof

Temporal association with exercise or coughing can be relevant, but many spontaneous dissections occur without a demonstrable causal injury.

Healing changes duration

Clinical stability, repeat vessel anatomy and the original treatment rationale inform when to stop or simplify antithrombotic therapy.

11Common pitfallsFrequent interpretation and management errors.

01
Do not wait for limb weakness before imaging a new painful partial Horner syndrome.
02
Do not exclude vertebral dissection because FAST is negative or dizziness is initially labelled peripheral.
03
Do not use a normal carotid ultrasound as definitive exclusion of high cervical or vertebral disease.
04
Do not assume anticoagulation is always superior to antiplatelet treatment for extracranial dissection.
05
Do not apply an extracranial antithrombotic plan uncritically when intracranial extension or SAH is possible.
06
Do not deny standard thrombolysis or thrombectomy assessment solely because a dissection caused the occlusion.
07
Do not stent every residual pseudoaneurysm; reserve intervention for specialist-selected symptomatic or high-risk anatomy.