What causes cervical artery dissection?

In about 80% of cases no clear cause is found — these are called spontaneous dissections and likely reflect underlying arterial wall fragility. In the remaining 20%, a trigger is identified: minor neck trauma is the most common, including sudden head turns, chiropractic cervical manipulation, a hairdresser appointment with prolonged neck extension, contact sport, or severe coughing. Connective tissue disorders such as fibromuscular dysplasia, Marfan syndrome, and vascular Ehlers-Danlos syndrome predispose, as does pregnancy. Most people who present with CAD are otherwise healthy adults between 30 and 55 years of age.

What are the symptoms I should watch for?

The most important warning symptom is new, severe, unilateral neck or head pain that feels different from any previous headache — often described as sharp, throbbing, or unlike anything before. For internal carotid dissection, look for a partial Horner syndrome (drooping eyelid and small pupil on one side), pulsatile tinnitus, or later weakness, speech disturbance, or visual loss on the opposite side. For vertebral artery dissection, symptoms include neck and occipital pain followed by dizziness, vomiting, facial numbness, or double vision. Any sudden neurological symptom alongside neck pain is a 000 emergency — call an ambulance immediately.

How is cervical artery dissection diagnosed?

Diagnosis is confirmed by imaging. In the emergency setting, CT angiography of the head and neck is the standard first-line test — it is fast, widely available, and highly sensitive. MRI with specialised fat-saturated sequences is the gold standard for showing the characteristic blood clot within the artery wall and is the preferred test for follow-up imaging because it avoids radiation. A standard carotid ultrasound alone is not adequate because it cannot see the upper part of the vertebral artery or the full course of the internal carotid artery. Your doctor will discuss which test is most appropriate.

What does treatment involve?

Treatment has two phases. In the acute stroke setting, clot-busting treatment (thrombolysis) and, if a large blood vessel is blocked, mechanical thrombectomy may be given — cervical artery dissection is not a contraindication to either of these. The antithrombotic phase then begins: either antiplatelet medication (such as aspirin, or aspirin plus clopidogrel for the first three weeks) or anticoagulation (warfarin or a direct anticoagulant such as apixaban) for three to six months. Both approaches are equivalent in preventing recurrent stroke. A follow-up MRI at three months checks whether the artery has healed, and most people step down to antiplatelet medication long-term.

Can I have chiropractic neck treatment in the future?

After a cervical artery dissection, Australian stroke guidelines recommend permanently avoiding chiropractic high-velocity neck manipulation. The association between cervical chiropractic adjustment and vertebral artery dissection is supported by case-control and case-crossover studies, and the RACGP shares this precautionary position. This does not mean all manual therapy is off limits — physiotherapy that does not involve thrusting neck movements, massage, and acupuncture at non-cervical sites are generally considered safe after the artery has fully healed. Discuss with your neurologist or GP before resuming any manual neck treatment.

What are my chances of a full recovery?

About 70% of dissected arteries recanalise (heal and reopen) fully within six months of treatment. For people who do have a stroke from the dissection, recovery varies with stroke severity and the area of brain affected — stroke rehabilitation is effective and most people with mild-to-moderate deficits make significant gains. Annual recurrence risk in the same vessel is around 1%, and lifetime recurrence risk is approximately 5–10%. Following secondary prevention measures — keeping blood pressure well-controlled, not smoking, avoiding neck manipulation, and maintaining a healthy weight — reduces the chance of a further event.

Cervical artery dissection

Cervical artery dissection: neck pain, Horner syndrome, and younger-adult stroke

By Dr HB Lo, FACRRM Reviewed 21 October 2026 7 min read

Cervical artery dissection (CAD) — a tear in the wall of the internal carotid or vertebral artery — accounts for 15–25% of ischaemic strokes in adults under 50. The classic warning is new unilateral neck pain that begins hours to days before neurological symptoms appear.

Australian stroke guidelines treat CAD as a stroke emergency: CT angiography and Code Stroke activation. Antithrombotic therapy is given for 3–6 months while the artery heals; around 70% of arteries recanalise fully.

Cervical artery dissection (CAD) is one of the most important causes of stroke in adults under 50, yet it is frequently missed because the early symptoms — unilateral neck pain or headache — mimic musculoskeletal or migraine presentations. The dissection itself is a tear within the wall of the internal carotid artery (~75% of cases) or the vertebral artery (~25%), forming an intramural haematoma that narrows or occludes the vessel and sheds clots downstream. The result is often an embolic stroke or TIA — sometimes days after the neck pain began. The Stroke Foundation Living Clinical Guidelines classify CAD as the aetiology in 15–25% of ischaemic strokes in those under 50, making it the under-50s stroke diagnosis no GP can afford to miss.

A. Core clinical — the AU general-practice framework

Who presents and with what

CAD most commonly affects otherwise healthy adults between 30 and 55 years. About 80% of cases are spontaneous with no identifiable trigger; the remainder follow minor neck trauma — chiropractic cervical manipulation, sudden head rotation, prolonged hyperextension at a hairdresser or dental chair, contact sport, or forceful coughing. Connective tissue disorders (fibromuscular dysplasia, Marfan syndrome, vascular Ehlers-Danlos, osteogenesis imperfecta) predispose, as does pregnancy and the post-partum period.

The clinical signature depends on which artery is involved:

Internal carotid artery dissection (ICAD) — anterolateral neck pain ± ipsilateral retro-orbital or temporal headache; partial Horner syndrome (ptosis + miosis without anhidrosis — pathognomonic, present in up to 50% of ICAD); pulsatile tinnitus; lower cranial nerve palsies (IX–XII, rare); followed by anterior circulation TIA or stroke (contralateral hemiparesis, hemisensory loss, dysphasia, transient monocular blindness).

Vertebral artery dissection (VAD) — posterior occipital or nuchal pain; vertigo; Wallenberg syndrome (lateral medullary infarct: ipsilateral facial sensory loss, crossed contralateral body sensory loss, ipsilateral Horner, dysphagia, hoarseness, ataxia, nausea, nystagmus); cerebellar or brainstem signs.

The critical window — neck or head pain often precedes the ischaemic event by hours, days, or even weeks. Recognising CAD in this pre-stroke phase, before neurological deficits appear, is the highest-value intervention.

History to take in general practice

The eTG Cardiovascular module and Stroke Foundation Living Guidelines guide the focused assessment:

Character, onset, and location of headache or neck pain — is it different from any previous headache?
Side of symptoms — unilateral neck + ipsilateral Horner or tinnitus is a red flag combination
Recent neck trauma within the past 2–4 weeks, including chiropractic adjustment, sport, MVA, coughing fits
Neurological symptoms — visual change, speech, swallowing, facial numbness, arm or leg weakness
Connective tissue features — joint hypermobility, tall thin build, family history of dissection or arteriopathy
Pregnancy status and contraceptive pill use

Examination

Targeted examination:

Cranial nerve examination — upper (II–VIII) and lower (IX–XII); partial Horner (ptosis + miosis — confirm anhidrosis absent by asking about facial sweating)
Motor, sensory, cerebellar, and speech assessment — NIH Stroke Scale if stroke suspected
Blood pressure in both arms — discrepancy may indicate subclavian or aortic pathology
Auscultation — carotid bruit (present in some ICAD); fundoscopy if visual symptoms

Investigations

Acute/emergency:

CT angiography (CTA) of the head and neck — first-line in Australian EDs; available 24/7; sensitivity >95%; identifies intimal flap, vessel narrowing, pseudoaneurysm, and simultaneous intracranial assessment for thrombectomy planning
MRI brain — diffusion-weighted imaging for stroke confirmation
MRI with T1 fat-saturated axial sequences — gold standard for detecting the intramural haematoma (hyperintense crescent); preferred for follow-up imaging at 3 and 6 months

General practice initial workup (before urgent referral):

If CAD is suspected in a patient without acute neurological deficit, the appropriate action is same-day urgent referral or ED assessment — general practice does not independently confirm the diagnosis; it refers promptly

B. Diagnosis and the evidence for imaging

Schievink’s landmark review in NEJM established that CTA is both practical and accurate in the acute ED setting. MRA with fat-saturated T1 axial sequences over the cervical vessels remains superior for detecting intramural haematoma — the pathological hallmark — but requires more time. Australian centres therefore use CTA acutely and MRA for monitoring healing.

Carotid duplex ultrasound alone is insufficient: it cannot adequately assess the high-cervical segments of the internal carotid artery or the V3–V4 segment of the vertebral artery, where most CAD occurs. Do not use it to exclude CAD.

Key differentials

Presentation	Distinguishing feature
Migraine with aura	Recurrent stereotyped pattern; no neck-pain quality; no Horner; imaging normal
Cluster headache	Strictly periorbital/temporal, 15–180 min; restlessness; no neck pain
Subarachnoid haemorrhage	Thunderclap (peak severity within 60 sec); meningismus; CT positive in 95% within 6 h
Cervical radiculopathy	Dermatomal/myotomal; no cranial nerve or stroke features; disc pathology on imaging
Ischaemic stroke from other cause	No neck pain; older age; atrial fibrillation or vascular risk profile

C. Treatment — the antithrombotic evidence

Acute stroke from CAD — Code Stroke activation is the immediate response. IV thrombolysis (alteplase or tenecteplase) and endovascular thrombectomy follow standard eligibility criteria — CAD is not a contraindication to either, per the Stroke Foundation Living Guidelines.

Antithrombotic therapy is the cornerstone of subacute CAD management. The key evidence:

CADISS trial (Markus, JAMA Neurology 2019) — 250 patients randomised to antiplatelet (aspirin/clopidogrel/DAPT) or anticoagulation (heparin then warfarin) for 3 months — no significant difference in recurrent stroke (2.5% vs 1.6%) or death. Recurrence risk was low in both arms.
TREAT-CAD (Engelter, Lancet Neurology 2021) — aspirin vs VKA — non-significant trend toward fewer ischaemic events with anticoagulation but more major bleeding.
STOP-CAD (Yaghi, Stroke 2024) — large observational registry — no significant superiority of anticoagulation, with higher haemorrhagic risk.

Bottom line per the Stroke Foundation Living Guidelines: antithrombotic therapy is strongly recommended; antiplatelet and anticoagulation are equivalent in preventing recurrent stroke. Many Australian stroke services default to antiplatelet therapy given equivalent efficacy and a lower bleeding risk profile.

Practical regimens (per eTG and AMH):

Antiplatelet — aspirin 100 mg/day; or DAPT (aspirin + clopidogrel) for 21 days then aspirin; or clopidogrel 75 mg/day
Anticoagulation — warfarin (INR 2.0–3.0) or apixaban 5 mg twice daily (off-label for CAD but widely used) for 3–6 months, then step to antiplatelet

Duration and follow-up: 3–6 months of antithrombotic therapy; repeat MRA at 3 months. If the vessel has healed (~70% recanalise), step down to antiplatelet. If pseudoaneurysm or persistent stenosis, continue and re-image at 6 months.

D. Australian operations

MBS-rebatable pathways:

GP attendance — items 23/36/44; GP management plan (GPCCMP) item 965/967 for ongoing chronic-disease coordination post-stroke
Mental Health Care Plan item 2715 — post-stroke depression and anxiety are common and qualify
CT angiography neck — item 57353; MRI brain — item 63007; MRA cervical vessels — item 63385
Specialist consultation (neurology/stroke) — items 110/116

PBS-listed antithrombotics for ischaemic stroke/TIA: aspirin (general/OTC), clopidogrel (Streamlined Authority), warfarin (general). Direct oral anticoagulants (apixaban, rivaroxaban) are PBS-listed for atrial fibrillation and VTE; use in CAD is off-label — private prescription may apply.

Statins and antihypertensives for secondary prevention are PBS-listed for established cardiovascular disease.

Austroads fitness to drive — post-stroke restrictions apply: non-commercial licence typically suspended for 4 weeks (TIA) to 3 months (stroke); commercial for longer. Document advice given.

E. Special populations

Connective tissue disorders — Vascular Ehlers-Danlos (COL3A1 mutation), Marfan syndrome, and fibromuscular dysplasia substantially increase recurrence risk. Clinical genetics referral is appropriate when features are present; family members may also warrant assessment.

Pregnancy and post-partum — CAD risk is elevated in the third trimester and first 6 weeks post-partum. Anticoagulation with low-molecular-weight heparin is generally preferred; avoid warfarin in the first trimester. Co-manage with obstetrics and stroke neurology at a tertiary centre.

Oral contraceptive pill — the causal link to CAD recurrence is debated, but most stroke neurologists recommend switching to non-hormonal contraception after CAD. A copper-IUD is the standard alternative.

Younger adults (under 35) — exclude connective tissue disorder, thrombophilia workup in recurrent cases, and discuss long-term secondary prevention in the context of a potentially longer life ahead.

When to escalate

Refer to ED immediately — or activate 000 — when:

Any suspected CAD presentation (neck/head pain + neurological symptoms) — this is a stroke emergency
Acute focal neurological deficit at any point
Intracranial CAD with features of subarachnoid haemorrhage — anticoagulation is contraindicated; needs neurosurgery

Refer to stroke neurology for all confirmed or suspected CAD diagnoses — including those presenting with isolated neck pain and Horner syndrome without yet having had a stroke, which represents the highest-value prevention window.

Refer to clinical genetics when connective tissue disease features are present or when dissection recurs.

What this article is and is not

This is general health information drawn from the Stroke Foundation Australian and New Zealand Living Clinical Guidelines for Stroke Management, Therapeutic Guidelines, AMH, the CADISS and TREAT-CAD trials, and RACGP general practice resources. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about individual investigation and management — including antithrombotic choice, duration of therapy, and imaging follow-up — are made with your own GP, neurologist, and treating team.

For acute stroke: call 000 immediately. For AU consumer information: Stroke Foundation Australia, HealthDirect, Better Health Channel.

Sources cited

Frequently asked questions

What causes cervical artery dissection?

In about 80% of cases no clear cause is found — these are called spontaneous dissections and likely reflect underlying arterial wall fragility. In the remaining 20%, a trigger is identified: minor neck trauma is the most common, including sudden head turns, chiropractic cervical manipulation, a hairdresser appointment with prolonged neck extension, contact sport, or severe coughing. Connective tissue disorders such as fibromuscular dysplasia, Marfan syndrome, and vascular Ehlers-Danlos syndrome predispose, as does pregnancy. Most people who present with CAD are otherwise healthy adults between 30 and 55 years of age.
What are the symptoms I should watch for?

The most important warning symptom is new, severe, unilateral neck or head pain that feels different from any previous headache — often described as sharp, throbbing, or unlike anything before. For internal carotid dissection, look for a partial Horner syndrome (drooping eyelid and small pupil on one side), pulsatile tinnitus, or later weakness, speech disturbance, or visual loss on the opposite side. For vertebral artery dissection, symptoms include neck and occipital pain followed by dizziness, vomiting, facial numbness, or double vision. Any sudden neurological symptom alongside neck pain is a 000 emergency — call an ambulance immediately.
How is cervical artery dissection diagnosed?

Diagnosis is confirmed by imaging. In the emergency setting, CT angiography of the head and neck is the standard first-line test — it is fast, widely available, and highly sensitive. MRI with specialised fat-saturated sequences is the gold standard for showing the characteristic blood clot within the artery wall and is the preferred test for follow-up imaging because it avoids radiation. A standard carotid ultrasound alone is not adequate because it cannot see the upper part of the vertebral artery or the full course of the internal carotid artery. Your doctor will discuss which test is most appropriate.
What does treatment involve?

Treatment has two phases. In the acute stroke setting, clot-busting treatment (thrombolysis) and, if a large blood vessel is blocked, mechanical thrombectomy may be given — cervical artery dissection is not a contraindication to either of these. The antithrombotic phase then begins: either antiplatelet medication (such as aspirin, or aspirin plus clopidogrel for the first three weeks) or anticoagulation (warfarin or a direct anticoagulant such as apixaban) for three to six months. Both approaches are equivalent in preventing recurrent stroke. A follow-up MRI at three months checks whether the artery has healed, and most people step down to antiplatelet medication long-term.
Can I have chiropractic neck treatment in the future?

After a cervical artery dissection, Australian stroke guidelines recommend permanently avoiding chiropractic high-velocity neck manipulation. The association between cervical chiropractic adjustment and vertebral artery dissection is supported by case-control and case-crossover studies, and the RACGP shares this precautionary position. This does not mean all manual therapy is off limits — physiotherapy that does not involve thrusting neck movements, massage, and acupuncture at non-cervical sites are generally considered safe after the artery has fully healed. Discuss with your neurologist or GP before resuming any manual neck treatment.
What are my chances of a full recovery?

About 70% of dissected arteries recanalise (heal and reopen) fully within six months of treatment. For people who do have a stroke from the dissection, recovery varies with stroke severity and the area of brain affected — stroke rehabilitation is effective and most people with mild-to-moderate deficits make significant gains. Annual recurrence risk in the same vessel is around 1%, and lifetime recurrence risk is approximately 5–10%. Following secondary prevention measures — keeping blood pressure well-controlled, not smoking, avoiding neck manipulation, and maintaining a healthy weight — reduces the chance of a further event.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.