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

This 27 year old patient presented with sudden onset of headache with nuchal rigidity and vomiting. At neurological examination he had a right homonymous hemianopsia.
Initial CT disclosed left occipital intracerebral hemorrhage with intraventricular extension. Subsequent MRI-MRA confirmed the diagnosis of an arteriovenous malformation.
After clinical recovery, endovascular treatment was proposed. Embolization through two pedicles resulted in total elimination of the lesion.

Left occipital cortical-subcortical AVM, 1.5 T
Examination 1
Fig.1 Sagittal T1-weighted spin-echo images. Irregular serpiginous signal void structures are seen in the left inner temporo-occipital region suggesting an arteriovenous malformation.
Fig.2 Transverse proton density (above) and T2-weighted fast spin-echo images. The abnormal vascular signal voids are better appreciated on these images.
Fig.3 Transverse turbo FLAIR images. No associated abnormal signal intensity parenchymal lesion is seen.
Fig.4 Transverse 2D PC MR angiogram (Venc: 50 cm/s). The pathological vascular structures are clearly demonstrated with this rapid (Tac: approximately 2 minutes) survey sequence, allowing positive diagnosis of the arteriovenous malformation. Note the markedly different appearance of the two posterior cerebral arteries. The increased diameter and intravascular signal intensity signify higher flow in the left posterior cerebral artery.
Fig.5 Sagittal targeted MIP reconstruction from a Gadolinium-enhanced 3D PC MRA acquisition data set. The arteriovenous malformation is drained towards the vein of Galen.

Examination 2 (early post-embolization follow-up)
Fig.6 Sagittal T1-weighted spin-echo images. High signal intensity components are observed within the nidus of the arteriovenous malformation, consistent with thrombosed vessels.
Fig.7 Transverse proton density (above) and T2-weighted fast spin-echo images. Inhomogeneous appearance of the embolized nidus, where the low signal intensity components might correspond to both patent vessels or the embolic agents, whereas the high signal intensity components represent either intravascular thrombosis or secondary parenchymal lesions.
Fig.8 Sagittal 2D PC MR angiograms (Venc: 345 cm/s) without (above) and with (below) intravenous Gadolinium injection. The conspicuity of the intracranial vessels is considerably improved on the contrast-enhanced image. No clearly pathological vessel is seen on these survey images.
Fig.9 Transverse targeted MIP reconstruction from a non-enhanced 3D TOF (with 512 matrix and MOTSA) MRA acquisition data set. The normalization of the caliber of the left posterior cerebral artery is well demonstrated. The left inner temporo-occipital arteriovenous malformation appears to be practically eliminated, although a fine vascular network is still observed.
Fig.10 Transverse targeted MIP reconstruction from a Gadolinium-enhanced 3D TOF MRA acquisition data set. There is no clear evidence for a residual nidus.

Examination 3 (1-year post-embolization follow-up)
Fig.11 Sagittal T1-weighted spin-echo images. The high signal intensity components are not seen at this time.
Fig.12 Transverse proton density weighted fast spin-echo images. Irregular, serpiginous low-signal intensity structures are still detected in the left temporo-occipital region (residual abnormal vascular structures vs. intravascular embolic agent vs. focal cortical hemosiderosis?).
Fig.13 Transverse T2-weighted fast spin-echo images. The dilatation of the right lateral ventricle and the subarachnoid spaces adjacent to the site of the lesion suggest focal parenchymal atrophy, consistent with the sequelae of the previous hemorrhage and subsequent embolization.
Fig.14 Transverse turbo FLAIR images. Confirmation of the focal cortical-subcortical atrophy in the left inner temporo-occipital region. No associated parenchymal abnormal signal intensity area is seen around the embolized nidus.
Fig.15 Sagittal survey single-slice 2D PC MR angiogram (Venc: 45 cm/s). No abnormal vessels are seen in conjunction with the left posterior cerebral artery.
Fig.16 Sagittal Gadolinium-enhanced survey 2D PC MR angiogram. Same observations as on Fig.5. Note the better overall vessel conspicuity compared to the previous non-enhanced 2D PC image.
Fig.17 Transverse anatomical averaged modulus type source images from a Gadolinium-enhanced 3D PC MRA acquisition. Excellent demonstration of the secondary parenchymal lesions and atrophy in the left inner temporo-occipital region.
Fig.18 Transverse MIP reconstruction from the Gadolinium-enhanced 3D PC MRA acquisition data set (Venc:45 cm/s). Although the inner temporo-occipital branch of the left posterior cerebral artery is still more apparent, no clearly pathological vascular structure is seen.
Fig.19 Transverse targeted MIP reconstruction from a Gadolinium-enhanced 3D TOF (with 512 matrix and MOTSA) MRA acquisition data set. Same observations as on Fig.18.
N.B. Total elimination of the arteriovenous malformation was later confirmed by conventional, catheter based selective cerebral angiography.

The ESNR CD-Rom Series