Cervical artery dissections are defined by the presence of a mural hematoma in the arterial wall. Most occur in the internal carotid artery more than 2 cm after the bifurcation, although they can also occur in the vertebral artery.1

Cervical artery dissections account for 20% of ischemic strokes occurring before age 45 years; patients have a mean age of 40 years and a male:female ratio of 1.5. The internal carotid artery is the most commonly affected vessel. Cervical artery dissection causes cerebral ischemia attributable to homodynamic factors or embolism. The incidence in the general population is low, estimated to be 2.6/100,000 inhabitants/year (95% CI 1.9-3.3), as reported in a recent population-based study.2 A high index of suspicion and early diagnosis and treatment is essential in the identification and management of cervical artery dissection.

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Trauma and primary diseases of the arterial wall are the main predisposing factors of these dissections. Cervical artery dissections are associated with hematoma in the wall of a cervical artery (carotid or vertebral), secondary either to an intimal tear or to direct bleeding within the arterial wall caused by ruptured vasa vasorum. The intramural hematoma can expand toward the intima or the adventitia, resulting in a stenosis or in an aneurysmal dilation of the artery.3,4 A spontaneous dissection is assumed when no or only minor trauma preceded the onset. However, the differentiation between spontaneous and traumatic dissections is artificial because of a continuum between both forms.1,4

Rare risk factors include infection, migraine, hyperhomocysteinemia, and the 677TT genotype of the 5,10-methylenetetrahydrofolate reductase gene, although evidence is sparse. An underlying arteriopathy, caused by such hereditary connective-tissue disorders as Marfan’s syndrome, Ehlers-Danlos syndrome type 4, pseudoxanthoma elasticum, and others, is believed to have a role in the development of cervical artery dissections.1,4


The clinical presentation of cerebral ischemia caused by a cervical artery dissection does not differ from that of cerebral ischemia attributable to other factors.

The clinical presentation of spontaneous dissections of the internal carotid artery includes cerebral ischemia, cervical or cranial pain, Horner’s syndrome, cranial nerve palsy, and tinnitus. Cervical artery dissections may also be silent. Occipital pain and lateral medullary syndrome resulting in speech and swallow difficulties caused by brainstem ischemic deficits are the most common findings in vertebral artery dissections.

In rare instances, carotid artery dissection can lead to retinal ischemia, and rare cases of cervical spinal cord infarcts resulting from vertebral-artery dissections have been reported.5


The favorable natural history of cervical artery dissections emphasize the need for a noninvasive approach to detection, monitoring, and follow-up. Apart from the mural hematoma (best seen on axial cervical MRI), typical features of cervical artery dissections can be visualized with ultrasound, magnetic resonance angiography, and CT angiography—although conventional angiography remains the gold standard for the diagnosis of arterial dissections.1,4 Anticoagulants or antiplatelets are usually recommended in the acute phase to prevent primary or recurrent ischemic events.

Follow-up studies suggest a fairly good overall prognosis in adults and in children. In many centers, Cervical artery dissections are treated with heparin at the acute stage, although the benefit of such a potentially dangerous treatment has never been proven by a randomized trial.4,6


Optimal management of cervical artery dissections strongly relies on diagnostic accuracy. Although the functional outcome of the condition is good in most patients, socioprofessional effects can be important. The incidence of the disorder in the general population is underestimated. Mortality and short-term recurrence rates are low, but possibly also underestimated. Further research is warranted to improve our understanding of the underlying pathophysiology, to assess the long-term outcome, and ultimately to provide treatment and prevention strategies.1

Dr. Sharma is a hospital medicine physician with Mayo Health System: Franciscan Skemp Healthcare in La Crosse, Wisc.


1. Debette S, Leys D. Cervical-artery dissections: predisposing factors, diagnosis, and outcome. Lancet Neurology. 2009;8:668-678.

2 Lee VH, Brown, Jr., RD, Mandrekar, JN, Mokri B. Incidence and outcome of cervical artery dissection: a population-based study. Neurology. 2006;67:1809-1812.

3. Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med. 2001;344:898-906.

4. Kim YK, Schulman S. Cervical artery dissection: Pathology, epidemiology and management. Thrombosis Research. 2009;123:810-821.

5. Hundsberger T, Thomke F, Hopf HC, Fitzek C. Symmetrical infarction of the cervical spinal cord due to spontaneous bilateral vertebral artery dissection. Stroke. 1998;29:1742.

6. Leys D, Lucas G, Gobert M, et al. Cervical artery dissection. Eur Neurology. 1997;37:3-12.

All electronic documents accessed January 15, 2011.