MR T1-W Sequences
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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.
CA0571-MR T1-W Sequences
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CA0571-MR T1-W Sequences
Case ReportExam
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).
Findings
MR T1-W Sequence performed without and with IV Contrast
There is abnormal hyperintensity (thrombus) within at least two branches of the left vein of Labbe' on the noncontrast T1 MR. There is also abnormal cortical signal in the lateral temporal cortex consistent with post ischemic change (i.e. laminar necrosis). There is no hemorrhagic conversion.
The post contrast T1-w MR sequence demonstrates focal parenchymal contrast enhancement in the site of left cortical laminar necrosis likely reflecting regional reperfusion into veins with post ischemic damage and blood brain barrier leak. The deep medullary veins also exhibit hyperemic enhancement in the parenchymal surrounding the dense ischemic core (site of laminar necrosis) consistent with venous dysautoregulation.
There is prominence of the left lateral tentorial confluence representing one means being utilized as a venous collateral egress route. There is also enlargement of the left main trunk of the superior sylvian vein along with enlargement of the left sphenoparietal sinus/cavernous sinus representing another venous collateral egress route.
Impression
2. 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.
