Pre- and postembolization evaluation of a left frontal cortical-subcortical AVM

This 48 year-old male presented with an initial epileptic seizure. Neurologically he was found to be normal.
The MRI examination suggested the presence of a left frontal cortical-subcortical AVM, which was subsequently confirmed by MRA.
Endovascular embolization was recommended for therapy.

Left frontal cortical-subcortical AVM, 1.5 T
Examination 1
Fig.1 Sagittal T1-weighted spin-echo images. The left frontal opercular AVM is demonstrated.
Fig.2 Transverse proton density weighted fast spin-echo images. The topography of the signal void nidus is well delineated.
Fig.3 Transverse T2-weighted fast spin-echo images. The high signal intensity areas, intermingled with the signal void nidus vessels, suggest enlarged CSF spaces, rather than associated parenchymal lesions.
Fig.4 Transverse turbo FLAIR images. No intraparenchymal high signal intensity lesion is found, confirming the previous findings.
Fig.5 Sagittal survey Gadolinium-enhanced single-slice 2D PC MR angiogram (Venc: 65 cm/s, Tac: 36 sec). This image, although lacking appropriate vessel definition, allows a rough appreciation of the geometric characteristics of the AVM and especially of its major draining veins (arrows), which is sufficient for guiding the design of the subsequent 3D PC MRA acquisition.
Fig.6 Sagittal averaged modulus (left) and corresponding magnitude of complex differences (right) type source images from a Gadolinium-enhanced 3D PC MRA acquisition (Venc: 65 cm/s). The topography of the nidus (below) and the course of the two major cortical draining veins of the AVM are clearly identified.
Fig.7 Sagittal (left) and coronal (right) collapsed (above) and targeted (below) MIP reconstructions from the Gadolinium-enhanced 3D PC MRA acquisition data set. The AVM is fed by branches of the left middle cerebral artery (red arrows) and drained towards the ipsilateral transverse sinus (blue arrows) and the superior sagittal sinus (green arrows).
Fig.8 Coronal averaged modulus (left) and corresponding magnitude of complex differences (right) type source images from a second Gadolinium-enhanced 3D PC MRA acquisition (Venc: 65 cm/s).The cortical-subcortical location of the nidus is better appreciated in this projection.
Fig.9 Coronal collapsed (left) and targeted (right) MIP reconstructions from the second coronal Gadolinium-enhanced 3D PC MRA acquisition data set. With identical (coronal) acquisition and reconstruction planes the MIP reconstruction yield significantly better vessel delineation and conspicuity. Compare these images to those of Fig.7. Note also the typical magnetic susceptibility artifacts, mimicking stenosis, affecting both internal carotid arteries at the entrance of the carotid canal at the skull base (arrows). Indeed, the characteristic level and the symmetric appearance of these abnormalities are very suggestive of artifactual origin.

Examination 2 (embolization)
Fig.10 DSA images (lateral and A-P views) after selective injection of the left internal carotid artery, which are in good agreement with the previous MRI-MRA findings.
Fig.11 Plain x-ray image after embolization of the AVM, showing the radiopaque embolizing agent within the nidus.
Fig.12 DSA images (lateral views) with selective injection of the left internal carotid artery, immediately after the embolization. A significant reduction in the size of the lesion and the velocity of the pathological flow is achieved.

Examination 3 (2 months postembolization follow-up)
Fig.13 Sagittal T1-weighted spin-echo images. The signal void of the nidus is almost fully replaced by increased signal intensity structures, consistent with subtotal thrombosis of the nidus.
Fig.14 Transverse proton density weighted fast spin-echo images. Same observations as on Fig.13
Fig.15 Transverse T2-weighted fast spin-echo images. Same observations as on Fig.13 and Fig.14.
Fig.16 Transverse turbo FLAIR images. A few punctate signal voids are still detected on these images, consistent with a small residual nidus. The surrounding increased signal intensity areas presumably correspond to thrombosed nidus compartments.
Fig.17 Sagittal Gadolinium-enhanced survey single-slice 2D PC MR angiogram (matrix: 512, Venc: 40 cm/s, Tac: 1 min 6 sec). The suspected residual nidus is not visualized.
Fig.18 Sagittal averaged modulus (left) and corresponding magnitude of complex differences (right) type source images from a Gadolinium-enhanced 3D PC MRA acquisition. The signal void embolizing agent and the enhancing thrombosed compartments of the nidus are well demonstrated on the anatomical images. The flow images show a few punctate vascular structures (arrows) within the nidus, corresponding to residual patent blood vessels.
Fig.19 More lateral sagittal averaged modulus (left) and corresponding magnitude of complex differences (right) type source images from the same Gadolinium-enhanced 3D PC MRA acquisition. The patency of the two main draining veins of the AVM is confirmed (arrows), although their caliber is significantly decreased.
Fig.20 Sagittal collapsed (above left) and increasingly targeted MIP reconstructions (above left and below) from the Gadolinium-enhanced 3D PC MRA acquisition data set (matrix: 256, Venc: 40 cm/s), showing the residual nidus (yellow arrows) and the patent cortical draining veins (blue arrows).

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