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Follow-up of a left occipital cortical-subcortical AVM after partial embolization with cyanoacrylate

This 58 year old female presented with late onset of epileptic seizures.
Conventional MRI revealed a left occipital intracerebral lesion consistent with a vascular malformation. Conventional catheter based selective cerebral angiography was performed before therapeutic decision making and confirmed the diagnosis of a cerebral AVM. Endovascular treatment was elected and performed with partial occlusion of the lesion. MRA examination was performed afterwards in order to provide baseline data for further follow-ups.
Three weeks later the patient was hospitalized for acute myocardial infarct and was treated with local thrombolysis and systemic anticoagulation. The next day she suddenly became unconscious and a large intracerebellar hemorrhage was diagnosed. She died the same day.

Occipital AVM, post-embolization follow-up, 1.5 T
Fig.1 Sagittal non-enhanced T1-weighted spin echo images. Large abnormal area in the occipital region characterized by serpiginous signal void structures intermingled with a few slightly hypersignal structures. The latter might correspond to slow flow components or thrombosis.
Fig.2 Transverse proton-density-weighted fast spin echo images. The signal void structures in the left occipital region represent the patent components of the AVM that were not reached by the embolization. Increased signal intensity is observed in some, presumably venous, vascular structures (arrows) which might correspond to either very slow in-plane flow or fresh intravascular thrombosis, secondary to the embolization.
Fig.3 Transverse T2-weighted fast spin echo images. Note the mass effect (deformity of the brain stem, compression of the left ventricular trigonal area) of the AVM on the adjacent parenchymal structures.
Fig.4 Transverse FLAIR images. Uncertainty persists so as to the exact nature of the increased signal intensity areas, which are now apparent in the nidus as well, where they may also represent perivascular parenchymal lesions.
Fig.5 Sagittal source images from the Gadolinium-enhanced 3D Phase Contrast acquisition. On the averaged modulus images (on the left) the embolizing agent is clearly identified as a signal void intravascular structure (arrows). On comparing with the corresponding magnitude of complex differences images (on the right) no signal is detected in the appropriate areas, confirming the absence of flow in those components of the nidus. The patent vascular structures exhibit strong signal on the magnitude of complex differences images.
Fig.6 Comparison of different Phase Contrast MRA techniques. Good visualization of the AVM is obtained with a sagittal, single slice non-enhanced 2D Phase Contrast imaging sequence (upper left), using 512 matrix (Tac: 2 min 24 sec). Adding cardiac synchronization to the same sequence has a double effect (upper right). On the one hand it is meant to improve conspicuity of the vascular structures (better vascular contour delineation due to suppression of artifacts induced by pulsatile motion). On the other hand, because it considerably increases the acquisition time (Tac: 7 min 14 sec), artifacts induced by gross (involuntary and respiratory) motions of the patients are more likely to appear, therefore the overall image quality is not necessarily improved. Conversely, an apparent improvement in the signal-to-noise ratio (and especially in small vessel conspicuity) is achieved after intravenous Gadolinium injection (lower left) and without time penalty (Tac: 2 min 24 sec). However, best results are obtained both in terms of intravascular signal intensity and vessel definition with the Gadolinium-enhanced 3D Phase Contrast technique, but with a significant time penalty (Tac: 13 min 16 sec).
Fig.7 Sagittal MIP image from the Gadolinium-enhanced 3D Phase Contrast acquisition. The main feeders (red arrows) of the AVM, arising from the left middle and posterior cerebral arteries, are clearly identified. Draining veins superimposing on the superior sagittal sinus are not well seen in this projection.

 

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Fig. 1

Follow-up of a left occipital cortical-subcortical AVM after partial embolization with cyanoacrylate, Fig. 1
Follow-up of a left occipital cortical-subcortical AVM after partial embolization with cyanoacrylate, Fig. 2
Follow-up of a left occipital cortical-subcortical AVM after partial embolization with cyanoacrylate, Fig. 3
Follow-up of a left occipital cortical-subcortical AVM after partial embolization with cyanoacrylate, Fig. 4
Follow-up of a left occipital cortical-subcortical AVM after partial embolization with cyanoacrylate, Fig. 5
Follow-up of a left occipital cortical-subcortical AVM after partial embolization with cyanoacrylate, Fig. 6
Follow-up of a left occipital cortical-subcortical AVM after partial embolization with cyanoacrylate, Fig. 7