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The exact mechanisms and etiology of spontaneous carotid artery dissection (sCAD) are unknown, but evidence supports both environmental exposures and ultrastructural abnormalities of collagen as contributing factors.1,2 MRI classically reveals a semilunar hyperintensity on fat-suppressed T1- and T2-weighted images, thought to be due to a tear in the intimal layer with extravasation of blood between this layer and the media.3 Recent evidence of microhemorrhages, other cellular debris, and phagocytes in between the medial and adventitial layers of undissected arteries in patients with sCAD suggests that injury is not limited to the medial layers and involves inflammatory immune responses.4 We present a case of sCAD with early progression and marked gadolinium enhancement suggestive of acute inflammation.
Case report.
A 61-year-old right-handed woman with hypertension and prior ductal carcinoma in situ of the right breast treated with lumpectomy, radiation therapy, and hormonal therapy presented with transient left eye blurriness followed by right hand weakness and trouble speaking. These symptoms lasted 25 minutes before spontaneously remitting. She had no other neurologic complaints except for mild …
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