Fig. 3

Variable pattern of vessel wall enhancement among different affected segments in a single patient. A 47-year-old female with a 1-year history of recurrent infarcts in the bilateral MCA territories had a history remarkable for a heterozygous factor V Leiden mutation. Otherwise, the patient had no laboratory findings of hypercoagulability (including protein C, protein S, antithrombin III, antiphospholipid antibody). No vascular risk factors, such as smoking, hyperlipidemia/hypercholesterolemia, hypertension, or diabetes. A trans-esophageal echocardiogram was unremarkable. Rheumatologic history and laboratory work-up were also unremarkable with no evidence of vasculitis or autoimmune disorder. Axial VWI demonstrates narrowing and negative remodeling of the supraclinoid left ICA without vessel wall enhancement (white arrow, a), while there was grade I circumferential wall enhancement of the distal left ICA (not shown). There was also eccentric grade I enhancement of the posterior wall of the distal right ICA (white arrowhead) as well as grade I circumferential wall enhancement of the left A1 segment at the same level (white arrow, b). The left M1 segment demonstrates negative remodeling throughout without vessel wall enhancement (white arrow, c). There is marked focal negative remodeling at the junction of the right M1 and A1 segments with faint grade I enhancement (white arrowhead) and sparing of the mid to distal right M1 segment and distal right A1 segment (c). Two-year follow-up VWI for descriptive purposes showed that there were no identifiable remnants of the terminal ICAs, proximal M1 or proximal A1 segments (white arrows) (d). An axial gradient echo image shows chronic blood product in the left lentiform nucleus (black arrow, e). An axial T2 FLAIR image shows chronic infarcts of the bilateral cerebral hemispheres (f). Right frontal (g) and left frontal (h) DSA images (CCA injections) further show the bilateral areas of stenosis and proliferation of lenticulostriate vessels, more marked on the right