The cornerstone of spontaneous CAD pathophysiology and diagnosis is the pres­ence of an intramural hematoma of unknown etiology, possibly caused by a tear in the tunica intima, a primary rupture of vasa vasorum in the medio-adventitial bor­derzone [20], or an underlying arteriopathy impairing vasomotion [6, 21]. The mural hematoma occurs within the media layer expanding distally and circumferen­tially. It is usually subintimal and causes arterial stenosis or occlusion, leading to cerebral ischemia due to embolization or less frequently due to hemodynamic fail­ure; sometimes, the subintimal hematoma can also rupture back through the intima, forming a perfused false lumen which is separated from a true lumen by a dissecting membrane. More rarely, the mural hematoma is subadventitial, causing only pain and local symptoms due to the compression of adjacent structures [22]. Ultrasound sensitivity in detecting CAD is quite high (80–95%). It frequently shows luminal and vessel wall alterations that suggest dissections, yet pathognomonic ndings are few and rarely detected [19, 23]. Furthermore, an ultrasound study might be normal in case of a subtle intramural hematoma, a low grade narrowing of the vessel lumen, and when the vessel segment is not accessible by ultrasound. Therefore, ultrasound alone is rarely denitively diagnostic. For this reason, the diagnostic work-up should include an axial cervical MRI using the T1 fat suppression technique that best detects intramural hematomas [24–26] as a hyperintense crescent-shaped sig­nal of various intensities depending on the stage and an eccentric ow void of the patent lumen, a pathognomonic nding in dissections (Fig.25.1).