Pre- and postembolization evaluation of a right fronto-parietal cortical-ventricular AVM

This 39 year old patient suffered from partial motor seizures since the age of 11. At the age of 24 he had an episode of subarachnoid hemorrhage leading to the diagnosis to a right fronto-parietal AVM. The lesion was so voluminous and complex that no surgical treatment could be contemplated. He subsequently had several hemorrhagic events, one of them leaving him with a left hemiparesis.
The patient was readmitted for imaging reevaluation and possible endovascular treatment. Three successive embolization sessions to date have resulted in significant reduction of the venous congestion associated with this high flow lesion.

Right fronto-parietal cortical-ventricular AVM, 1.5 T
Examination 1 (before embolization)
Fig.1 Sagittal T1-weighted spin-echo images. The triangular shape and the cortical-ventricular extension of the large fronto-parietal AVM is demonstrated.
Fig.2 Transverse proton density and T2-weighted fast spin-echo images at the level of the circle of Willis. Abnormal tortuous and dilated vessels are seen on the left side (compare the diameter of the middle cerebral arteries), due to the high-flow conditions on the side of the AVM. Note the low-signal intensity lining (arrows) on the surface of the mesencephalon, consistent with leptomeningeal hemosiderosis, as a sequela of repeated previous subarachnoid hemorrhages.
Fig.3 Transverse proton density weighted fast spin-echo images. High signal intensity areas (secondary parenchymal lesions) are intermingled with the signal void of the nidus.
Fig.4 Transverse T2-weighted fast spin-echo images. Same observations as on Fig. 3.
Fig.5 Sagittal survey single-slice 2D PC MR angiograms with different Venc values. The upper image (Venc: 60 cm/s) yields better visualization of the nidus and venous components (including congested cortical veins) of the lesion. The lower image (120 cm/s) allows better identification of the arterial feeders, while the most important venous structures (arterialized cortical veins and the superior sagittal sinus) also remain clearly visible.
Fig.6 Sagittal collapsed MIP reconstruction from a Gadolinium-enhanced 3D PC MRA acquisition data set (Venc: 80 cm/s). Individual identification of the arterial feeders and draining veins is impossible in this complex case. Moreover, due to turbulent flow (rapid intravoxel phase dispersion), segmental intravascular signal drop-out is detected in several locations (arrows) rendering the evaluation of secondary high-flow angiopathy phenomena (e.g. arterial stenosis) inaccurate and unreliable.

Examination 2 (4 months after partial embolization of the AVM)
Fig.7 Sagittal T1-weighted spin-echo images. The large areas within the previously signal void lesion are now isointense with the cortex, corresponding to the occluded components of the nidus.
Fig.8 Transverse proton density weighted fast spin-echo images. Both the nidus and the parenchymal abnormal signal intensity areas show significant diminution compared to the pre-embolization status.
Fig.9 Transverse T2-weighted fast spin-echo images. Same observations as on Fig.2.
Fig.10 Sagittal survey single-slice 2D PC MR angiograms with different Venc values (above left: 40 cm/s, above right: 80 cm/s, below left: 120 cm/s, below right: 160 cm/s), each of them obtained in 1 min 06 sec (pilot study). At a Venc value of 40 cm/s the arterial feeders are not visualized, whereas at 160 cm/s, most of the nidus disappears. Here again, a Venc value of 80 was felt to represent the best compromise and was used for the more time-consuming 3D PC sequence. Note also the typical ghost artifacts on both sides of the cervical carotid arteries.
Fig.11 Sagittal collapsed MIP from a Gadolinium-enhanced 3D PC MRA acquisition data set (Venc: 80 cm/s, Tac: 8 min 38 sec). Some decrease in the size of the nidus and the intravascular signal intensity within the draining veins of the lesion and the superior sagittal sinus is observed, compared to the pre-embolization image. However, the segmental intravascular signal drop-outs in the internal carotid artery siphon and the arterial feeders (arrows) are still visible, consistent with persistence of the high-flow conditions in the right internal carotid artery system

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