Cervical artery dissection: A real pain in the neck

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Author: Blake Briggs, MD

Peer Reviewer: Travis Smith, DO


Cervical artery dissections are a common cause of stroke in young people <50 years old with some reports of up to 20% being from dissections. They can occur at any age. Much like aortic dissections, there is some loss of structure along the wall of either the internal carotid artery (ICA) or vertebral artery (VA), allowing blood to collect within the intima. This review will focus on spontaneous dissections, not traumatic, as well as the pathophysiology, risk factors, presentation, diagnosis, and management.

In patients <50 years old, cervical artery dissections account for 20% of ischemic strokes. The overall incidence is about 2.5 per 100,000 annually in the US alone, with a mean age of 45 years. ICA dissections are 3-5x more common that VA dissections. For comparison, subarachnoid hemorrhage (SAH), another can’t-miss neurological diagnosis, has an incidence of ~7 per 100,000 worldwide.


As stated above, a separation of the arterial wall layers results in dissection. They occur extracranial or intracranial. Extracranial internal carotid dissection is more common, typically it occurs 2 cm or more distal from the carotid bifurcation (near the skull base). Vertebral artery dissection most commonly occurs at the V3 segment of the vertebral artery, at the C1-C2 level.

The false lumen that forms will continue to dissect, or “unzip”, resulting in cerebral ischemia. Ischemia is caused by both hypoperfusion or thromboembolism, with the latter being more important. The compression of the expanding hematoma presses on sympathetic fibers on the outside of the blood vessel and adjacent nerves, resulting in partial Horner syndrome (see below), cranial neuropathies, and pain.

Very rarely these vessels dissect intracranially, rupturing to cause a SAH.

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Risk Factors

Minor trauma: the key word is “mild” trauma, associated with up to 40% of cases. This does not include motor vehicle crashes that end up at a level 1 trauma center with a cervical spine fracture. These are usually activity-related: skating, basketball, volleyball, swimming, scuba diving, dancing, yoga, chiropractors (1 in 20,000 cervical manipulations), sexual intercourse, trampoline use, amusement park rides, vaginal delivery, etc.

With that being said, most CADs develop in the absence of any discernible mechanical event thus making it very difficult to indict a particular incident or factor as the cause of a particular stroke.

The most compelling risk factors likely have to do with an underlying connective tissue abnormality, which likely contribute to a weakening of the vascular wall. These genetic predispositions are the usual culprits (Ehlers-Danlos, Marfan’s, PCKD, etc). The most common of these is fibromuscular dysplasia.

While both vertebral and cervical dissections are associated with minor trauma, vertebral dissection has a higher rate and they are more associated with rapid head movements.


Think headache, neck pain, and potentially ischemic, neurologic symptoms.

It is important to add this pathology to your differential of patients with headache and neck pain, as headache and neck pain are the most common symptoms, ranging from 60-90%. Headache is more common in carotid dissections, while neck pain is more common in vertebral dissection. See image 1 for the common associated pain locations.

The headache onset is usually gradual, with <20% being a “thunderclap” onset. Both vertebral and carotid dissections have no difference in terms of occurrence and frequency of headache as a presenting symptom, as well as thromboembolism or mural thrombus hematoma.

Ischemia manifesting in TIA/stroke symptoms are present in about 70% of patients but this may not be present on initial presentation. The risk is highest during the first 2 weeks of symptoms (77% present at the time of diagnosis).

On exam, look for the obvious motor or sensory deficits in addition to the more subtle nystagmus, truncal ataxia (can’t sit up in bed), ipsilateral Horner’s syndrome, tongue deviation, or an ophthalmoplegia.

For vertebral dissections think of lateral medullary syndromes (Wallenberg Syndrome) and cerebellar infarctions.

Think amaurosis for carotid artery dissection.

As mentioned above, ipsilateral Horner syndrome is only in ~25% of cases. Even so, it is usually partial, with only unilateral ptosis and miosis. Anhidrosis is rarely seen.

Other possible symptoms include unilateral hearing loss, pulsatile tinnitus, auscultated bruit, dizziness, the “Deadly D’s”(dysarthria, diplopia, dysphagia), other cranial neuropathies, and scalp tenderness.


Made by neuroimaging, MRA or CTA. Both are more or less equal in performance and sensitivity/specificity. CTA is faster and has wider availability in most EDs. Historically, the gold standard was digital subtraction angiography, but this is rarely used today.

Key findings on CT imaging: vessel stenosis, tapered occlusion, dissecting aneurysm (pseudoaneurysm), intimal flap, double lumen, or intramural hematoma.

Rarely, CTA and MRA can be falsely negative. If you have a strong suspicion for cervical artery dissection, proceed with arranging digital subtraction angiography.

Ultrasound can be used but its limitations include intracranial extension and imaging of the vertebral artery system. Additionally, the fact that it has been found to show evidence specific to dissection in only 20% of patients makes it an imaging modality to forego.


As discussed above, cervical artery dissection increases the risk of thromboembolism, causing stroke. This can be a deadly diagnosis as there is up to a 10% mortality prior to even initiating treatment.

In those patients who present with acute ischemic stroke, standard approaches to management of stroke should be followed. Discussion of thrombolytics should take place with the code stroke team.

There is no increased harm in giving IV thrombolytics (outside of the usual harm associated with acute stroke management), but no clear benefit has been found as well (i.e. no difference in intracranial hemorrhage, mortality, or favorable outcome).

One critical caveat is that thrombolytics are relatively contraindicated in those with intracranial extension of the dissection. Another complication that is quite obvious: a cervical artery dissection involving the aorta…we’ll let you think about why that would be bad.

Anti-thrombotic therapy with either antiplatelet agents or anticoagulation are the preferred methods for preventing ischemic stroke and TIA complications. They have been studied and there is no difference in their efficacy.

There is debate on the preferred antiplatelet agents: aspirin, clopidogrel, dipyridamole, or a combination of these agents. We suggest consulting your neurologic team on this.

There is no consensus on how long patients need to be on therapy. Some studies suggest after 3-6 months as most arterial abnormalities stabilize by then. Repeat imaging is necessary at that time to evaluate for improvement in the dissection complications.

Endovascular or surgical repair are last resort options in those who have recurrent ischemia or failed antithrombotic therapy. The subject of endovascular surgery is institutionally dependent, along with who runs the service and CTA findings.


Recurrence rate is uncertain, and hotly debated. We do know that unfavorable outcomes are more common in carotid artery dissections versus vertebral. Excellent recovery has been found in 70-85% of patients, with major disabling deficits in 10-25% and death in <10%.


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