Abstract

Carotid artery dissection (CAD) is a leading cause of ischemic stroke in young and middle-aged adults. CAD is an uncommon disease with an approximate incidence of 2.6/100,000 cases per year. CAD can occur either in intracranial or extracranial portions of the carotid artery, with extracranial being more often due to its mobility and contact with bone. It is usually spontaneous secondary to a tear in the intimal layer of the carotid artery but can be traumatic secondary to a blunt or penetrating trauma as well. Spontaneous dissections are usually idiopathic. Connective tissue and vascular disorders (e.g., fibromuscular dysplasia and Ehlers–Danlos syndrome type IV) and positive family history increase the risk of incidence. Aortic root dilatation and Eagle syndrome may also increase the risk of CAD. Genetic predisposition is also suspected with underlying arteriopathy. Clinical presentation can range from being asymptomatic to acute ischemic stroke, but headache and neck pain are the most common presenting symptoms. Patients can also complain from transient ischemic attacks, Horner or partial Horner syndrome, visual symptoms, and symptoms secondary to cranial nerve injury. Carotid bruit can be heard and expanding neck hematoma may be present on physical examination. Diagnosis can be confirmed by many imaging modalities. Being noninvasive and bedside, duplex ultrasound is considered the best initial screening tool for CAD. Computed tomographic arteriography (CTA) provides accurate visualization of the intramural hematoma and classical flame sign. Magnetic resonance imaging (MRI) and magnetic resonance arteriography (MRA) can substitute CTA if contraindicated. Conventional angiography was considered as the gold standard, but it is now replaced with CTA or MRI/MRA. CAD can be treated initially with antithrombotic medications. If failed or contraindicated, endovascular with angioplasty and stenting or surgical treatment can be considered.

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