Carotid artery disease and carotid dissection

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

Atherosclerotic carotid stenosis is clinically important when it plausibly caused a recent ipsilateral retinal or hemispheric event. Percentage stenosis must state the measurement method because NASCET and ECST denominators differ.

The benefit of endarterectomy is time-dependent and greatest soon after a suitable TIA or non-disabling stroke, but severe disability, a large infarct, haemorrhage, medical instability and anatomy can modify timing or suitability.

Carotid dissection is an intramural haematoma/intimal injury, often in younger adults and sometimes after minor neck strain. Most extracranial dissections are managed medically; thrombolysis and thrombectomy remain options for otherwise eligible acute ischaemic stroke.

Key points

Symptomatic carotid disease causes ipsilateral retinal ischaemia or contralateral cerebral TIA/stroke; dizziness or syncope alone is rarely a carotid-territory syndrome.
Give aspirin 300 mg immediately for suspected TIA unless contraindicated, and arrange specialist assessment within 24 hours; do not use ABCD2 to delay referral.
A patient who may be suitable for carotid endarterectomy needs urgent carotid imaging after specialist assessment.
NICE recommends urgent carotid endarterectomy for recent stable TIA/non-disabling stroke with symptomatic 50–99% NASCET stenosis (equivalent 70–99% ECST), alongside best medical treatment.
Do not offer carotid surgery for symptomatic stenosis below 50% NASCET (below 70% ECST).
Carotid dissection often presents with unilateral neck/head/orbital pain, partial Horner syndrome, pulsatile tinnitus or delayed retinal/cerebral ischaemia.
CTA or MRA of head and neck demonstrates dissection, stenosis/occlusion and pseudoaneurysm; ultrasound alone can miss high cervical disease.
For symptomatic extracranial dissection, ESO supports either antiplatelet or anticoagulant therapy; the stroke specialist individualises choice, duration and follow-up imaging.

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

Atherosclerotic carotid disease

Age, smoking, hypertension, diabetes and dyslipidaemia promote plaque at the carotid bifurcation. Plaque burden and instability, together with a plausible ipsilateral retinal or cerebral event, determine clinical relevance; a bruit alone does not.

Spontaneous carotid dissection

An intimal injury or bleeding within the arterial wall may occur without major trauma, particularly in younger adults. Minor neck strain can precede symptoms but is not always present.

Mechanical arterial injury

Blunt neck trauma, marked neck movement or an arterial procedure can damage the carotid wall. The resulting intramural haematoma may narrow the lumen or form a pseudoaneurysm.

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

1
Plaque formation
Endothelial dysfunction permits lipid deposition, inflammation and fibrous plaque development, usually near the bifurcation. Progressive narrowing can reduce reserve, while an irregular surface encourages thrombus.
2
Atheroembolism or hypoperfusion
Plaque disruption can release platelet-rich thrombus or debris into the ipsilateral retinal or cerebral circulation. Severe stenosis or occlusion may additionally impair distal perfusion.
3
Dissection develops
Blood entering through an intimal defect, or bleeding within the vessel wall, separates arterial layers. The intramural haematoma narrows or occludes the true lumen.
4
Local and embolic effects
Thrombus forming on the dissected surface can embolise after pain begins. Expansion may cause pseudoaneurysm, pulsatile tinnitus or nearby cranial-nerve and sympathetic-plexus disturbance.

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

Carotid-territory TIARed flag

Transient monocular visual loss or contralateral face/arm/leg weakness or language disturbance; treat as an emergency even after symptoms resolve.

Acute ischaemic strokeRed flag

Persistent focal deficit, visual loss, aphasia, neglect or weakness requires immediate stroke reperfusion assessment before carotid-surgery planning.

Carotid bruit

Raises suspicion of atherosclerosis but neither grades stenosis nor proves causality; severe stenosis can be silent and a bruit can occur without severe narrowing.

Carotid dissection pain/Horner patternRed flag

Unilateral neck, facial, orbital or temporal pain plus partial Horner syndrome (ptosis and miosis without anhidrosis) is a classic warning pattern.

Dissection-related ischaemiaRed flag

Retinal TIA, hemispheric TIA/stroke, cranial-nerve palsy or pulsatile tinnitus may follow pain by hours or days.

Asymptomatic stenosis

An incidental carotid narrowing without a recent ipsilateral retinal/hemispheric event generally receives intensive risk-factor therapy and specialist selection rather than automatic surgery.

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
Non-contrast CT brain or MRI brainFirst step
Why
Distinguish haemorrhage, infarct burden and mimics in acute neurology.
Interpretation and limitations
Brain imaging informs thrombolysis/thrombectomy and timing/safety of antithrombotic or carotid intervention; a normal early scan does not exclude TIA.
02
Carotid duplex ultrasoundFirst line
Why
First-line quantification of extracranial carotid stenosis and plaque flow characteristics.
Interpretation and limitations
Report side and NASCET-equivalent category; confirm high-grade or intervention-relevant disease with a validated second modality according to the vascular/stroke pathway.
03
CTA head and neck
Why
Rapidly assess stenosis, occlusion, intracranial circulation, dissection and thrombectomy anatomy.
Interpretation and limitations
A tapered stenosis/occlusion, eccentric mural thickening or dissecting pseudoaneurysm supports dissection; calcification can affect stenosis measurement.
04
MRA head and neck with fat-suppressed vessel-wall sequences where available
Why
Demonstrate intramural haematoma and avoid radiation/iodinated contrast.
Interpretation and limitations
Useful when CTA is inconclusive or for follow-up; availability must not delay acute stroke care.
05
ECG/telemetry and vascular risk bloods
Why
Identify competing stroke mechanisms and modifiable risk.
Interpretation and limitations
AF or another high-risk cardiac source may alter antithrombotic strategy; carotid stenosis can coexist without being causal.

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

Cardioembolic TIA or stroke

Atrial fibrillation, recent myocardial injury or intracardiac thrombus can produce similar focal deficits. Infarcts in multiple vascular territories or no plausible ipsilateral carotid lesion favour a cardiac source.

Small-vessel cerebral disease

A pure motor or sensory lacunar syndrome without cortical or retinal features may reflect penetrating-artery disease. Brain imaging and vascular distribution help separate mechanisms.

Migraine aura or focal seizure

Spreading positive visual or sensory phenomena, stereotyped recurrence or post-event confusion favour migraine or seizure. Sudden negative loss of vision, language or power is more typical of ischaemia.

Vertebral artery dissection

Occipital or posterior neck pain with vertigo, ataxia, diplopia or other brainstem signs suggests posterior-circulation involvement. Head-and-neck angiography defines the affected arterial territory.

Non-vascular neck or orbital pain

Musculoskeletal pain or primary headache usually lacks focal retinal or cerebral deficit, pulsatile tinnitus and partial Horner syndrome. Persistent warning features still warrant arterial imaging.

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

01strokeOngoing focal deficitFirst stepPersistent retinal or cerebral neurological deficit.

1First: activate the acute stroke pathway, establish last-known-well time and obtain immediate brain plus vascular imaging.
2Next: assess for IV thrombolysis and mechanical thrombectomy; dissection itself does not automatically exclude standard reperfusion treatment.
3Next: begin antithrombotic therapy only after haemorrhage and reperfusion considerations are addressed by the stroke team.
4EscalationEscalation: coordinate urgent carotid/vascular review if symptomatic extracranial stenosis is identified and the stroke is non-disabling/stable.

02TIAResolved carotid-territory symptomsSuspected TIA or amaurosis fugax without current deficit.

1First: give aspirin 300 mg immediately unless contraindicated and refer for specialist assessment within 24 hours.
2Next: obtain urgent carotid imaging if the patient could be a candidate for endarterectomy; do not delay by ABCD2 scoring.
3Next: start best medical treatment, including specialist antiplatelet plan, high-intensity statin, BP/smoking/diabetes management.
4EscalationEscalation: urgent endarterectomy for symptomatic 50–99% NASCET stenosis when clinically suitable; no endarterectomy below 50% NASCET.

03dissectionSuspected extracranial carotid dissectionNew unilateral head/neck pain, partial Horner syndrome, pulsatile tinnitus or compatible retinal/cerebral ischaemia.

1First: same-day stroke/neurology assessment and CTA or MRA of head and neck, with brain imaging when neurological symptoms occur.
2Next: treat acute ischaemic stroke with standard reperfusion options if eligible.
3Next: choose antiplatelet or anticoagulation after specialist assessment of infarct size, thrombus, bleeding risk and anatomy; continue for the specialist-defined course, commonly 3–6 months.
4EscalationEscalation: multidisciplinary endovascular/surgical review only for exceptional recurrent ischaemia despite optimal therapy, expanding compressive pseudoaneurysm or another high-risk complication.

04incidentalAsymptomatic carotid stenosisStenosis found without a recent ipsilateral retinal or hemispheric event.

1First: confirm that symptoms are absent and that the stenosis estimate is reliable.
2Next: provide intensive smoking, BP, lipid, diabetes and appropriate antiplatelet management.
3Next: refer selectively for vascular/stroke review when severe disease, progression or high-risk plaque features may make intervention relevant.
4EscalationEscalation: any new retinal or hemispheric symptom converts the case to the urgent symptomatic pathway.

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

Immediate reduction of early recurrent ischaemic risk after suspected TIA.

Aspirin

300 mg orally once daily immediately for suspected TIA, unless contraindicated; the specialist then defines the ongoing antiplatelet regimen.

Exclude important contraindications and use the acute stroke imaging/reperfusion pathway for ongoing deficits; review bleeding, allergy and concurrent anticoagulation.

Long-term antiplatelet option after non-cardioembolic TIA/ischaemic stroke and for atherosclerotic vascular disease.

Clopidogrel

75 mg orally once daily for long-term secondary prevention when selected; short-term loading/dual therapy is stroke-specialist directed.

Bleeding risk, surgery timing and interacting anticoagulants; do not improvise long-term dual antiplatelet therapy.

Intensive lipid lowering after TIA/stroke or established carotid atherosclerosis.

Atorvastatin

80 mg orally once daily for secondary prevention, using a lower dose if interactions, adverse-effect risk or patient preference require it.

Check baseline liver tests, muscle symptoms and interactions; avoid in pregnancy and breastfeeding under the product information.

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

Recurrent cerebral ischaemia

Continued plaque embolisation, thrombus propagation or dissection-related emboli can cause recurrent TIA or disabling ischaemic stroke. Risk is particularly concerning soon after a symptomatic event.

Retinal ischaemia

Emboli entering the ophthalmic circulation may cause transient monocular visual loss or permanent retinal infarction. A retinal event can identify symptomatic ipsilateral carotid disease.

Haemodynamic infarction

Critical stenosis or occlusion can reduce cerebral perfusion, especially when collateral supply is poor or systemic pressure falls. Border-zone infarction may result without a fresh embolus.

Dissecting pseudoaneurysm

A weakened segment may dilate and remain a source of thromboembolism or local compression. Its significance depends on symptoms, evolution and specialist imaging review.

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

After TIA/stroke, monitor for recurrent focal symptoms and ensure the 24-hour specialist pathway and carotid decision are completed.
Document stenosis side, percentage, method (NASCET/ECST) and whether symptoms are ipsilateral and recent.
Monitor BP, lipids/non-HDL response, diabetes, smoking and tolerance/adherence to antithrombotic and statin therapy.
For dissection, review recurrent ischaemia, headache/neck pain and bleeding while on therapy; repeat CTA/MRA when the specialist pathway schedules it.
After endarterectomy, monitor neurological status, wound/cranial nerves and BP; follow vascular surveillance for restenosis according to the treating service.

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

Name the denominator

A percentage without NASCET or ECST method can place the same lesion in the wrong treatment band.

A bruit is not a stenosis grade

Duplex or angiographic imaging, not auscultation, determines severity.

Horner syndrome may be partial

Internal carotid dissection often causes ptosis and miosis without facial anhidrosis because sympathetic fibres to sweating travel with the external carotid.

Dissection pain can precede stroke

A normal neurological examination at the first pain presentation does not make the syndrome benign.

Carotid stenosis may be an innocent bystander

AF, small-vessel disease and other mechanisms must still be assessed; intervention requires a plausible ipsilateral symptomatic link.

11Common pitfallsFrequent interpretation and management errors.

01
Using ABCD2 to decide that a suspected TIA can wait several days.
02
Offering endarterectomy based on an unspecified percentage or for stenosis below 50% NASCET.
03
Calling non-focal dizziness a carotid TIA without seeking a better explanation.
04
Using a normal neck ultrasound to exclude high cervical dissection when clinical suspicion remains high.
05
Assuming anticoagulation is always superior to antiplatelet therapy for extracranial dissection.