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.