MR Susceptibility SWI
CA0416-MR Susceptibility SWI

CA0416-MR Susceptibility SWI
Case ReportExam
Prior Study
There is evidence of a left high-cervical ICA dissection. There is very subtle edema in the left hippocampus.
MRA Head and Neck
There are changes consistent with left high-cervical and vertical intapetrous ICA dissection. There is a short segment with non-filling of the genu segment of the ICA likely representing occlusion. However, the left ICA becomes patent in the horizontal, intrapetrous segment and beyond reflecting patent EC-IC collateralization.
Focal areas of absent MRA signal (consistent with down-stream thromboemboli) were evident in the proximal right ACA, the proximal left PCA, and the left MCA at the M2 trunk division (affecting flow into both the superior and inferior MCA perfusion zones).
MR Diffusion
Positive diffusion in the left hippocampus consistent with post-ictal effects of a recent seizure. A grand mal seizure may have precipitated the left high-cervical ICA dissection.
MR Flair
Known Lt. high-cervical ICA dissection with high-grade stenosis with positive FLAIR signal.
Positive FLAIR signal is evident in the left hippocampus consistent with post-ictal hippocampal edema.
Findings
MR susceptibility
There is SWI blooming artifact in the left M1 and M2 MCA segments consistent with hyperacute thromboemboli arising from the proximal Lt. ICA dissection/luminal thrombus. This positive signal on SWI in the MCA matches the region of non-opacification on the MRA head exam. The right A1/2 and the left P1-PCA thrombus sites are obscured by bone artifact;
There is venous hyperemia without blooming and without a correspond positive MR diffusion, is consistent with the hyperemia associated with physiologic response to the proximal ICA intrapetrous occlusion or it could be related to a post ictal state or both could be present. There was no parenchymal stroke on the diffusion to suggest post ischemic dysautoregulation.
The findings in this case are related to seizure related hippocampal signal changes, and the seizure contractures likely precipitated the carotid dissection and segmental thrombosis. Clot lysis is clearly the basis for the intradural arterial thromboemboli.
Impression
2. The left cerebral venous hyperemia could be post ictal or a physiologic response to the intrapetrous left ICA occlusion or both.
Recommendations
A summary video discussion of all CT, CTA, and MR elements is available, which reviews all the pertinent findings and summarizes their importance in this clinical case.