MR Susceptibility SWI
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.
CA0620-MR Susceptibility SWI
View Images
CA0620-MR Susceptibility SWI
Case ReportExam
Prior Study
Acute to subacute thrombosis of multiple dural sinuses is evident including the transverse sinuses on both sides, and the straight sinus. Acute venous thrombosis is evident in both of the internal cerebral veins (ICV), the vein of Galen and the right basal vein of Rosenthal. There is edema in the dorsal right thalamus, but whether this is vasogenic edema or cytogenic edema (venous stroke) is indeterminate. There is also reduced CT density wihtin the superior vermis, but whether this is from prior radiation therapy (with leukomalacia) or whether it is related to retrograde propagation of clot from the vein of Galen into the superior vermian vein complex is indeterminate.
CT perfusion
There is deep central vein thrombosis producing venous congestion in the the subependymal venous system (i.e. caudate, thalamostriate, and deep medullary parenchymal vein), greater on the right than the left.
Thrombosis of the straight sinus is evident on the CTA, which is included with the CT perfusion data set, but there is no CT perfusion evidence of collateral flow in the dural sinus wall.
CTV neck
There is thrombosis (likely chronic) of the right cervical internal jugular vein and the right sigmoid/transverse sinuses.
CTV head
There is thrombosis of multiple dural sinuses including the right transverse/sigmoid sinuses and the adjacent right internal jugular vein plus thrombosis of the straight sinus.
There is either thrombosis or at least delayed filling of the deep central veins, the vein of Galen, and the right basal vein of Rosenthal on CTA of the head. However, there is thrombus in these veins on the CT head consistent with hyperacute CVT.
There is re-routing of venous egress through the left superior sylvian venous complex/sphenoparietal sinus/cavernous sinus and through the left lateral tentorial venous confluence.
Post contrast head CT
There is evidence of edema in the dorsal right thalamus which is part of the right ICV venous egress territory. Whether this edema is vasogenic edema alone related to venous congestion or includes cytogenic edema from venous infarction is indeterminate. However, the partial rise in right thalamic venocapillary pool density makes completed infarction unlikely; correlate with MR diffusion sequences.
Intraluminal clot is evident in the vein of Galen/straight sinus junction (empty delta sign), as well as in the right channel of the torcula and proximal right transverse sinus. There is subependymal venous congestion more prominent on the right than left. There is persistent CVT in the right transverse/sigmoid sinuses and right basal vein of Rosenthal with evidence of thickening (collateralized) dural sinus walls.
MR T1-w post contrast only
Persistent intraluminal thrombosis remains in the vein of Galen/straight sinus junction, straight sinus, right channel of the torcula and all of the transverse sinus. There is partially recanalized clot in the mesial segment of the left transverse sinus. There is expansion and enhancement of the dural sinus walls in the straight sinus and right transverse sinus and in the right lateral tentorial venous confluence, which are then re-routed through the dural wall collateral into the left patent transverse sinus. There is edema in the dorsal thalamus, as seen on prior exams. Whether this represent vasogenic alone or includes post ischemic cytogenic edema is indeterminate. There is evidence of deep medullary and subependymal venous congestion bilaterally.
MR diffusion
Focal, small volume, venous infarction in the right dorsal lateral thalamus. Whether it will proceed to completed infarction or not is indeterminate. The venocapillary pool density in this same area is not absent making it more likely this area will actually undergo tissue infarction.
There is lacunar infarction in the right parietal centrum semiovale. Whether this is caused by an arterial or venous thrombosis event is indeterminate.
MR Flair
There is positive FLAIR signal (i.e. post CVT vasogenic edema) in the right thalamus, caudate and basal ganglia. The positve FLAIR signal in the superior vermis may actually be chronic.
There is early right lateral ventriculomegaly with increased subependymal edema consistent the hydrocephalus (internal type).
Findings
MR SWI
There is abnormal blooming SWI signal (i.e. venous thrombosis) in the apex of the straight sinus, in the right lateral atrial vein, and in the right basal vein of Rosenthal. Abnormal SWI signal in the thrombosed parts of the right transverse sinus is lost in SWI bone artifact.
There are classic features of moderate grade deep venous congestion related to downstream venous outlet blockade at the apex of the straight sinus. The features of moderate venous congestion include dilatation of the deep central veins, the subependymal veins, and the choroidal veins without dilataion of the deep medullary veins and without any blooming artifact to confirm actual occlusion. In this case the deep medullary vein dilatation is more evident on the right than the left. There is no apparent physiologic hyperemia in the left superior sylvian vein complex to account for the CT perfusion changes.
There is vasodilatation (collateralization) of left sided choroidal veins and multiple right mesial occipital pial veins.
Impression
2. There is moderate grade venous congestion in the deep central venous system bilaterally, but is more prominent on the right than the left. The venous congestion is related to the venous egress block at the vein of Galen/straight sinus junction. Moderate venous congestion is consistent with fair deep venous egress collateral.
3. Deep venous collateral egress routes appear to be mainly through the deep medullary veins and likely some antegrade flow past the apex straight sinus thrombus.
Recommendations
Proceed to the summary video and case report to view all of the imaging findings in this case plus the "Lessons to be learned" from this specific instructional case.
