It has been suggested that spontaneous cervical carotid artery dissection (sCAD) may result from
arterial inflammation. Periarterial
edema (PAE), occasionally described in the vicinity of the mural
hematoma in patients with sCAD, may support this hypothesis. Using cervical high-resolution magnetic resonance imaging, three readers, blinded to the mechanism of carotid artery dissection, searched for PAE, defined as periarterial T2-hyperintensity and T1-hypointensity, in 29 consecutive CAD patients categorized as spontaneous CAD (sCAD, n = 18) or traumatic CAD (
tCAD, n = 11; i.e., major head or neck
trauma within 2 weeks before the clinical onset). The relationships between PAE, inflammatory
biological markers, history of
infection and CAD mechanism were explored. Multiple CADs (n = 8) were found only in sCAD patients. Compared with
tCAD, patients with sCAD were more likely to have a recent history of
infection (OR = 12.5 [(95%)CI = 1.3-119], p = 0.03), PAE (83% vs. 27%; OR = 13.3 [(95%)CI = 2.2-82.0], p = 0.005) and to have elevated CRP (OR = 6.1 [(95%)CI = 1.2-32.1], p = 0.0002) or ESR (OR = 8.8 [(95%)CI = 1.5-50.1], p = 0.002) values. Interobserver agreement was 0.84 or higher for PAE identification. sCAD was associated with PAE and
biological inflammation. Our results support the hypothesis of an underlying
arterial inflammation in sCAD.