Abstract

Spontaneous cervical artery dissection (sCAD) is an important cause of stroke and transient ischemic attacks in young and middle-aged patients. Although spontaneous dissections of the carotid or the vertebral arteries account for only about 2% of all ischemic strokes, sCAD accounts for 10% to 25% of ischemic strokes in young patients.1 The pathogenesis of sCAD is often unclear. An underlying arteriopathy has been accepted as a possible cause, with trivial trauma including coughing, sneezing, or vomiting,2 and infections as possible other etiologies.3 A family history of arterial dissection, genetically determined alterations of the extracellular matrix, hyperhomocysteinemia, and the 677TT genotype of the 5,10-methylenetetrahydrofolate reductase gene may be important predisposing factors. However, these preexisting abnormalities do not explain all the pathophysiologic features of sCAD.4 Accurate diagnosis of sCAD and monitoring of its progression are crucial for adjusting medical management and affecting overall disease outcomes. Imaging plays a major role in diagnosis and follow-up of patients with sCAD. Radiologic hallmarks of sCAD include a luminal flap, a false lumen, the presence of a mural hematoma or a long tapered stenosis/occlusion, or a dissecting aneurysm.5 Neurosonology techniques, particularly the …

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