MR FLAIR
Claim CME CreditPOINT OF CARE INFORMATION
This CME activity consists of the student reviewing the video of the professor reviewing the case as well as the associated DICOM image set related to the case in question.
Learning Objectives
As a result of participation in this activity, participants should be able to:
- Provide improved patient care.
- Greater knowledge of the imaging characteristics of the patient's disease.
- Understand a better approach to interpretation of studies.
Faculty Disclosure
Mehmet Albayram, MD, Ivan Davis, MD, Mariam Hanna, MD, Anthony Mancuso, MD, Ronald Quisling, MD, Dhanashree Rajderkar, MD, Priya Sharma, MD, Roberta Slater, MD and Joann Stamm, MBA have disclosed that they have no relevant financial relationships. No one else is a position to control content have any financial relationship to disclose.
CME Advisory Committee Disclosure:
Conflict of interest information for the CME Advisory Committee members can be found on the following website: https://cme.ufl.edu/disclosure/.
Continuing Medical Education Credit
Accreditation: The University of Florida College of Medicine is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.
Credit: The University of Florida College of Medicine designates this enduring material for a maximum of 0.5 AMA PRA Category 1 Credits. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
CA0573-MR FLAIR
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CA0573-MR FLAIR
Case ReportHistory
Exam
Prior Study
Focal left retrosylvian vasogenic edema matching the vein of Labbe' venous egress territory. Whether there is cytogenic edema in this area representing venous stroke remains indeterminate. There is acute thrombus in multiple branches of the left vein of Labbe' without apparent concurrent left transverse sinus thrombosis. There is no hemorrhagic conversion.
CT Perfusion
There is a focal area of reduced brain perfusion in the left retrosylvian area corresponding to oligemia resulting from thrombosis of the left vein of Labbe' (evident on the noncontrast head CT).There is both collateral zone physiologic hyperemia in the collateral zone surrounding the retrosylvian oligemic area plus evidence of re-routing of venous egress into the left superior sylvian vein complex and left lateral tentorial venous confluence. This accounts for the increased blood volumn (increased CBV) in the cavernous sinus and left transverse sinus.
CTA of the Neck
Negative for venous occlusion; negative for otomastoid or paranasal sinus infection/tumor. The CTA of the neck included the head with good opacification of the major dural sinuses, all of which were patent.
CTA of the Head
CTA head evidence of re-routed venous egress into the lateral tentorial venous confluence. The cortical veins are not well seen on either sided, because of the timing of a CTA versus a CTV. No arterial stenosis nor occlusion was evident.
Delayed Post Contrast CT Venocapillary Pool
There is a 2 cm. focal area of virtually absent CT density in the venocapillary pool within the left retrosylvian area plus nonfilling of the vein of Labbe'; findings are consistent with venous stroke. There is no evidence of left transverse sinus thrombosis, nor evidence of arterial occlusion in the same area. The dominant routes for re-routing of the remain retrosylvian veins is into the cavernous sinus via left superior sylvian vein/sphenoparietal sinus route and into the left lateral tentorial venous confluence/left transverse sinus route.There is altered blood brain barrier with leak of contrast into the area of vasogenic edema (vein of Labbe' oligemic zone).
MR pre and post contrast T1-w sequence
There are focal changes in the left retrosylvian area consistent with thrombosis of the vein of Labbe' and evidence of focal tissue edema and cortical laminar necrosis (completed venous infarction).
The area of ischemic penumbra surrounding the dense ischemic core exhibits features of dysautoregulation, including minimal contrast leak, plus venous congestion in both cortical and deep temporal parenchymal medullary veins.
MR DWI
Acute, venous related, cortical infarction is evident in the left lateral retrosylvian regions. Most of the area of vasogenic edema (ischemic penumbra) evident on prior imaging is not MR diffusion positive.
Findings
MR T2 of FLAIR
There is focal retrosylvian vasogenic edema matching the left vein of Labbe' venous egress zone. There is also positive FLAIR in the area of laminar necrosis which is distinguishable withinthe larger 2-3 cm. area of vasogenic edema.
There is positive FLAIR abnormality within the site of positive DWI (dense ischemic core site of laminar necrosis). However, the positive FLAIR is also present in area surrounding the dense ischemic core, but is not limited to that area.
There is positve FLAIR signal (consistent with BBB leak of protein) within the sulci in a wider area than included in the area of vasogenic edema. This is consistent with the venous dysautoregulation of the ischemic event in the retrosylvian area. There is also thickening of the dura limited to this area related to pial/dural venous collateralization.
There is minimal local mass effect flattening the left ventricular trigone; there is no malignant edema nor herniation.
There is a background of age-related ischemic demyelination within the centrum semiovale bilaterally.
Impression
2. FLAIR is also positive for vasogenic in the region surrounding the site of dense ischemic core, and regional dural thickening from pial/dural venous collateral egress.
