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AJNR - American Journal of Neuroradiology

A and B, Left internal carotid artery (ICA) angiograms in frontal and lateral projections demonstrating a parieto-occipital high-flow AVM with multiple feeders and cortical veins draining to the superior sagittal sinus (pre-embolization).

C and D, Axial rCBFs illustrating the increased perfusion in the AVM nidus (arrow) as well as in the widespread distribution of the cortical draining veins before treatment.

E and F, Almost corresponding rCBFs made after 2 uneventful sessions of embolization. The images show a decrease in AVM nidus size and rCBF in the area of the previously enlarged and draining veins. The patient was then sent for subsequent radiation therapy.

A and B, Frontal projections of internal carotid angiogram done before and after an uneventful embolization. One of 2 draining veins is patent after the treatment.

C and D, Illustrate the cast of glue on unsubtracted DSA and on coronal MR (2D FLASH, performed 26 hours after treatment). The susceptibility artifacts caused by the glue are well illustrated but an associated hematoma could not be definitely defined.

E–G, Axial MR (T2-weighted, DWI b 1000, and ADC maps) performed after treatment show a vasogenic edema in the surroundings of the AVM nidus (arrowhead).

H, Axial CT, performed 2 days later in conjunction with sudden onset of minor symptoms, shows a small hematoma in the area of previous edema. The AVM showed a complete and spontaneous occlusion at follow-up.

A–D, Frontal left internal carotid angiogram, early and late phase, before and after the second embolization. Patent venous drainage is seen after the treatment.

E–L, Axial MR (E–H, T1-weighted, and I–L, DWI [b 1000]) immediately posttreatment, at 23 days, 35 days after treatment, and before a third treatment, 3 months later. The images illustrate the development of venous thrombosis 3 weeks after treatment in the deep and contralateral cortical veins with a complete resolution at follow-up.

M–U, rCBF (M–O) and rCBV (P–R) with the corresponding MTT (S–U): unchanged PI images after treatment (left column) are followed by a dramatic increase in MTT (severe drop in rCBF with a mild rCBV increase) 3 weeks later (middle column). A slow but almost total normalization of PI pattern was seen 9 days later (ie, after hypervolemic hemodilution) (right column). The patient was left with no symptoms.

A, Frontal right vertebral angiogram demonstrates a small, high-flow, parieto-occipital AVM with an enlarged feeder supplying 2 intranidal fistulas (arrows) before embolization.

B and C, Same projection after partial embolization. Glue can be seen at the site of the fistulas, and the venous drainage remained patent.

D, DSA, performed 6 weeks later (same projection) in conjunction with and before an additional embolization. A spontaneous occlusion of the feeder supplying the fistula is noted with a partial reduction of the nidus. The vein is still patent but reduced in size.

E–P, Axial T2-weighted, DWI, ADC maps, and rCBF done after the first embolization (E–H), before (I–L), and after (M–P) the second treatment. A vasogenic edema (black arrow) evolved in between the treatments, because of a spontaneous thrombosis of the feeder, nidus plus draining vein (white arrow), and decreased immediately after the second embolization. A small, perinidal ischemic lesion is seen after the last treatment (arrowhead). The patient experienced minor and transient headaches in between the embolizations.

A, Axial CT performed the day after treatment illustrates the severe artifacts caused by the glue, but no obvious ischemic lesion is noted.

B and C, Corresponding sections on postprocedural MR-DWI/ADC demonstrate a rather large ischemic lesion (arrows) within the left thalamic nucleus (not seen on the CT image).

D, Axial T2-weighted MR image at follow-up shows a small and permanent infarct in the posterior portion of the left thalamus (arrowhead).