Carotid dissection

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

Carotid dissection is blood within or separation of the arterial wall, producing intramural haematoma, luminal narrowing, occlusion or an outward dissecting aneurysm. It often affects the high cervical internal carotid rather than the atherosclerotic bifurcation. The principal early stroke mechanism is thrombus forming on the abnormal wall and embolising distally; severe narrowing can also impair flow. Local expansion can irritate the sympathetic plexus or lower cranial nerves. A young or middle-aged adult with new unilateral head, face or neck pain plus partial Horner syndrome, pulsatile tinnitus or cerebral ischaemia therefore needs urgent arterial imaging even when routine vascular risk factors are absent.

Dissections may follow major trauma or less dramatic neck stress, but many are spontaneous and a temporal association with coughing, exercise or manipulation does not prove causation. Fibromuscular dysplasia, arterial tortuosity, migraine and uncommon heritable connective-tissue disorders can increase susceptibility. Multiple or recurrent dissections, renal or other arterial abnormalities, striking hypermobility or a family history justify cause-directed assessment. Routine broad genetic testing after one isolated event has a low yield and should be guided by phenotype and specialist advice.

CTA from the arch through the intracranial circulation is fast and widely available. MRI with MRA and fat-suppressed T1 vessel-wall sequences can demonstrate intramural blood and clarify subacute or equivocal disease. Ultrasound may show abnormal flow in accessible segments but cannot reliably exclude a distal cervical lesion. Once haemorrhage is excluded, acute ischaemic stroke caused by extracranial dissection enters the usual thrombolysis and thrombectomy pathway. Subsequent prevention uses antiplatelet therapy or anticoagulation selected according to infarct burden, intraluminal thrombus, bleeding risk, intracranial extension and team judgement. The ESO guideline strongly supports either strategy for symptomatic extracranial dissection because two phase-two trials showed no clear difference in benefits or harms.

Duration is reviewed rather than assumed indefinite. The randomised CADISS and TREAT-CAD treatment phases were three months; older European guidance suggested six to twelve months, and contemporary practice uses repeat anatomy, clinical stability and the reason for choosing the agent to decide when to stop or simplify. A persistent stenosis or dissecting aneurysm often has a benign course and does not itself mandate stenting. Selected patients with recurrent embolism despite optimal treatment, critical haemodynamic compromise or an enlarging aneurysm causing compression need multidisciplinary neurointerventional discussion.

Key points

Treat any current retinal or hemispheric deficit as acute stroke: obtain brain imaging and complete head-and-neck angiography without delaying standard reperfusion assessment.
Painful partial Horner syndrome, new unilateral neck or orbital pain with ptosis and miosis, is a same-day carotid imaging indication even without limb weakness.
Thunderclap headache, meningism or intracranial extension raises subarachnoid haemorrhage; exclude bleeding before antithrombotic treatment.
CTA rapidly demonstrates tapered stenosis, occlusion, flap or dissecting aneurysm, while fat-suppressed vessel-wall MRI can confirm intramural haematoma.
Symptomatic extracranial dissection can be treated with antiplatelet therapy or anticoagulation; trials have not shown one strategy to be universally superior.
Extracranial carotid dissection does not by itself exclude otherwise eligible intravenous thrombolysis or mechanical thrombectomy.
Most post-acute residual stenoses and dissecting aneurysms are managed medically; intervene only for exceptional recurrent ischaemia, severe flow compromise or enlarging compression.
Agree a finite antithrombotic plan and repeat imaging when healing or residual anatomy will change its duration.

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

Spontaneous wall injury

Many carotid dissections occur without major trauma, reflecting interaction between arterial susceptibility and ordinary mechanical stress rather than one proven trigger.

Blunt cervical trauma

Direct impact, high-energy acceleration, cervical fracture or marked rotation can disrupt the artery and may precede neurological symptoms by hours.

Underlying arteriopathy

Fibromuscular dysplasia, marked arterial tortuosity and uncommon heritable connective-tissue disorders increase susceptibility, especially when disease is recurrent or multifocal.

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

1
Intramural haematoma
Blood enters the arterial wall through an intimal disruption or primary mural bleed, separating layers and expanding within the vessel wall.
2
Luminal narrowing
The mural collection compresses the lumen, producing tapering stenosis or occlusion and sometimes reducing perfusion beyond the lesion.
3
Thrombus and embolism
Abnormal endothelium and disturbed flow promote mural thrombus, whose fragments can occlude retinal, middle cerebral or anterior cerebral branches.
4
Outward aneurysmal expansion
Extension toward the adventitia forms a dissecting aneurysm that may compress sympathetic or lower cranial nerves and rarely enlarges progressively.

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

Painful partial Horner syndromeRed flag

New ipsilateral ptosis and miosis with orbital, facial or neck pain strongly suggests internal carotid dissection; facial sweating may be preserved.

Retinal or hemispheric ischaemiaRed flag

Transient monocular loss, retinal infarction, aphasia, neglect or contralateral motor and sensory deficits may follow artery-to-artery embolism.

Pulsatile tinnitus

A new unilateral pulse-synchronous sound can arise from disturbed flow in an expanded or narrowed cervical internal carotid artery.

Lower cranial neuropathy

Dysphagia, tongue weakness, palatal dysfunction or hoarseness may reflect local compression by a high cervical dissecting aneurysm.

Traumatic pattern

Cervical fracture, high-energy acceleration, direct neck trauma or a seat-belt injury can produce carotid injury before neurological signs emerge.

Systemic arteriopathy clues

Multiple arterial beds, recurrence, marked tortuosity, renal artery disease or connective-tissue phenotype suggests an underlying arteriopathy requiring targeted assessment.

Red flags requiring action

Ongoing weakness, aphasia, visual loss, neglect or reduced consciousness requires immediate hyperacute stroke assessment and reperfusion imaging.
Painful partial Horner syndrome needs same-day cervical and intracranial arterial imaging even before weakness or speech disturbance appears.
Thunderclap headache, meningism or subarachnoid blood suggests intracranial dissection or rupture and changes antithrombotic safety completely.
Progressive dysphagia, airway symptoms or multiple lower cranial neuropathies may indicate an enlarging dissecting aneurysm with compression.
Recurrent ischaemia despite prescribed treatment needs repeat imaging and neurovascular review rather than empirical addition of more antithrombotic drugs.

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 luminal and wall-related signs while assessing intracranial vessels and potential stroke targets.
Interpretation and limitations
Long tapered narrowing, high cervical occlusion, intimal flap, double lumen or dissecting aneurysm supports diagnosis; complete arch-to-vertex coverage avoids missing tandem disease.
02
Non-contrast CT brain
Why
Exclude haemorrhage and assess established infarction before reperfusion and antithrombotic decisions.
Interpretation and limitations
A normal brain CT does not exclude carotid dissection and must be paired with angiography when the clinical syndrome is suspicious.
03
MRI brain with MRA and vessel-wall imaging
Why
Detect acute infarction and directly visualise intramural haematoma when CTA is uncertain or disease is subacute.
Interpretation and limitations
Fat-suppressed T1 mural signal evolves over time and can be confused with slow flow or venous structures; expert neuroradiology correlation is important.
04
Carotid duplex ultrasound
Why
Assess accessible cervical segments and provide selected haemodynamic follow-up information.
Interpretation and limitations
Normal bifurcation and proximal-flow appearances cannot exclude distal internal carotid dissection, so ultrasound must not close a high-probability case.
05
Digital subtraction angiography
Why
Clarify unresolved lumen anatomy or guide an already selected neuroendovascular procedure.
Interpretation and limitations
It defines the lumen superbly but is invasive and may not directly show mural haematoma; reserve it for a focused specialist question.
06
Follow-up CTA or MRA
Why
Assess recanalisation, persistent stenosis or dissecting aneurysm when the result will alter treatment.
Interpretation and limitations
Many lesions remodel over months; persistent narrowing without symptoms is not proof of treatment failure and does not require automatic intervention.

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

Atherosclerotic carotid disease

Calcified bifurcation plaque in an older vascular-risk patient differs from a high cervical tapered lesion, mural haematoma and acute painful local syndrome.

Primary headache disorder

Migraine can cause unilateral pain and transient neurology, but a new painful Horner syndrome, tinnitus or fixed arterial sign warrants vascular imaging.

Cerebral vasculopathy

Vasculitis and reversible cerebral vasoconstriction can cause multifocal narrowing; inflammatory context, thunderclap pattern and serial vessel behaviour help separate them.

Cavernous sinus or apical disease

Mass, inflammation or thrombosis can cause painful Horner or multiple ocular-motor palsies, usually with a different cranial-nerve and imaging distribution.

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

01LOCALPainful local carotid syndromeFirst stepUnilateral head or neck pain accompanies partial Horner syndrome, pulsatile tinnitus or lower cranial neuropathy.

1Perform urgent neurological, pupillary and cranial-nerve examination and ask specifically about transient monocular loss, language disturbance and recent trauma.
2Arrange same-day CTA or MRA of the head and neck rather than relying on auscultation, routine Doppler or symptom resolution.
3Discuss confirmed or strongly suspected extracranial dissection with the stroke service to select antithrombotic treatment and brain imaging.
4Give emergency advice for visual loss, weakness, speech change or reduced consciousness and advise avoiding neck manipulation during evaluation.

02STROKEDissection with acute ischaemiaA current focal neurological deficit occurs and angiography shows or strongly suggests extracranial carotid dissection.

1Activate the hyperacute stroke pathway, document last-known-well and obtain non-contrast CT plus complete head-and-neck angiography.
2Assess intravenous thrombolysis and mechanical thrombectomy under standard specialist criteria; extracranial dissection alone is not an exclusion.
3After reperfusion decisions, choose antiplatelet therapy or anticoagulation using infarct, anatomy, haemorrhage risk and specialist judgement.
4Monitor for recurrent embolism, haemorrhagic transformation, extension and mass effect, then arrange neurovascular follow-up.

03ANTITHROMBOTICSelect and review preventionSymptomatic extracranial dissection is confirmed after intracranial haemorrhage and subarachnoid blood have been excluded.

1Assess infarct size, intraluminal thrombus, intracranial extension, bleeding risk, renal function, interacting medicines and planned procedures.
2Choose an antiplatelet strategy or therapeutic anticoagulation with the stroke specialist, explaining that neither is universally superior.
3Record agent, dose, start date, planned duration and review point, avoiding combined anticoagulant and antiplatelet treatment without a separate indication.
4At approximately three months or the specialist-defined interval, review symptoms and imaging to stop, simplify or continue for a documented reason.

04RECURRENCESymptoms despite treatmentNew retinal or cerebral ischaemia develops while the prescribed antithrombotic is being taken.

1Treat the episode as acute stroke, verify dose and adherence, and repeat brain plus arterial imaging urgently.
2Assess extension, intraluminal thrombus, flow compromise, an enlarging aneurysm and competing cardioembolic or atherosclerotic mechanisms.
3Review the antithrombotic plan through the neurovascular team rather than empirically stacking antiplatelet and anticoagulant agents.
4Consider stenting or surgery only for exceptional recurrent, haemodynamic or compressive disease in an experienced multidisciplinary centre.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Provides antiplatelet prevention of recurrent embolism during early arterial healing.

Aspirin

When an antiplatelet strategy is selected after acute ischaemic stroke, give 300 mg orally or rectally once daily after haemorrhage is excluded, continuing for fourteen days before the documented long-term regimen; if thrombolysed, start only after the twenty-four-hour scan excludes bleeding.

Check allergy, active bleeding, ulcer risk and concomitant anticoagulation; intracranial dissection with subarachnoid haemorrhage requires a different pathway.

Provides an evidence-supported alternative strategy to antiplatelet therapy for symptomatic extracranial dissection.

Specialist-selected oral anticoagulant

No universal licensed dissection dose exists; the stroke specialist selects a named oral agent and its product-specific regimen, documents whether use is off label, and sets a three-month reassessment.

Exclude subarachnoid and intracranial haemorrhage; consider infarct size, intracranial extension, renal and hepatic function, trauma, bleeding, pregnancy, interactions and planned procedures before selecting the agent.

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

Retinal or cerebral infarction

Distal embolism or severe flow reduction can cause transient monocular blindness, disabling hemispheric stroke or watershed infarction.

Subarachnoid haemorrhage

Intracranial extension or rupture of a dissecting aneurysm can release blood around the brain and make antithrombotic treatment hazardous.

Persistent dissecting aneurysm

Residual outward dilatation may retain embolic, compressive or surveillance significance, although most remain stable or remodel without intervention.

Local nerve compression

Expansion can injure the carotid sympathetic plexus or lower cranial nerves, causing Horner syndrome, dysphagia, dysarthria or hoarseness.

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

Ask about recurrent monocular loss, aphasia, weakness, headache, pulsatile tinnitus and cranial-nerve symptoms during the early healing period.
Monitor the chosen antithrombotic for adherence, bleeding, haemoglobin, renal function and interactions using its usual safety framework.
Repeat CTA or MRA when recanalisation, persistent stenosis or dissecting-aneurysm behaviour will change duration or intervention decisions.
Review pain trajectory while ensuring analgesia does not delay reassessment of new focal symptoms or thunderclap headache.
Discuss driving, safety-critical work, contact sport and forceful neck manipulation with the stroke team using current individual advice.
For multifocal or recurrent disease, review blood pressure and any targeted arteriopathy or genetics assessment plan.

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

Horner can spare sweating

Sudomotor fibres largely travel with the external carotid, so internal-carotid dissection often causes ptosis and miosis without prominent facial anhidrosis.

Pain may precede stroke

The local arterial-wall syndrome can begin hours or days before embolic ischaemia, creating a valuable opportunity for diagnosis and prevention.

Location separates mechanisms

Extracranial dissection mainly causes thromboembolism, while intracranial dissection has a greater subarachnoid-haemorrhage risk because the vessel wall differs.

Residual abnormality can persist

A narrowed artery or dissecting aneurysm on follow-up may remain clinically quiet and should not be equated automatically with failed treatment.

Ultrasound has blind segments

The distal cervical internal carotid lies beyond reliable routine insonation, so a normal duplex cannot exclude a high lesion.

Trials tested finite therapy

CADISS and TREAT-CAD randomised antithrombotic treatment for three months, supporting a planned reassessment rather than unexamined lifelong treatment.

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 dissection because the patient lacks major trauma or traditional atherosclerotic risk factors.
03
Do not use a normal carotid duplex to rule out high cervical internal-carotid disease.
04
Do not deny otherwise eligible thrombolysis or thrombectomy solely because extracranial dissection caused the stroke.
05
Do not assume anticoagulation is universally superior to antiplatelet treatment after extracranial dissection.
06
Do not apply an extracranial antithrombotic plan when intracranial extension or subarachnoid haemorrhage is possible.
07
Do not stent every persistent narrowing or pseudoaneurysm; reserve intervention for specialist-selected exceptional disease.

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