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.
CA0611-MR Susceptibility SWI
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CA0611-MR Susceptibility SWI
Case ReportExam
Prior Study
Acute thrombosis is evident within the posterior (parietal/occipital) segments of the superior sagittal sinus extending into the torcular herophile and the straight sinus. There is no apparent cortical or deep central vein CVT.
CT perfusion No CT perfusion is available
CTV of the neck No CTV neck is available
CTV of the head
Evidence of partial recanalization of dural sinus thromboses, which include the parietal-occipital segments of the SSS, the torcular herophile, the initial segment of the transverse sinuses, and the straight sinus. Multiple effective routes of collateral venous egress are present, as listed above. There is also some antegrade venous blood flow after partial recanalization.
Delayed post contrast CT
Dural sinus thrombosis is evident affecting the distal SSS, the straight sinus, the torcula, and both mesial segments transverse sinuses proximal to the lateral tentorial venous confluences. There is moderate venous congestion in the deep central venous system. The venous congestion accounts for the size effacement of the upper third ventricle.
There is no evidence of venous stroke nor hemorrhagic conversion.
Noncontrast T1-w MR
There is evidence of recent thrombus within the distal SSS, straight sinus, torcula, and initial transverse sinuses. The age of the thrombus is acute, since the clot evolution has not yet change into the met-hemoglobin phase (which would appear hyperintense).
There is evidence of deep central venous congestion now affecting the deep medullary veins indicating at least moderate venous congestion. There is no hemorrhagic conversion nor acute hydrocephalus nor clear evidence of optic hydrops.
MR dwi MR diffusion is negative for venous stroke.
MR flair
There is some FLAIR abnormality in the vein of Galen, the apex of the straight sinus, and within the left channel within the torcula consistent with recent thrombus. However, many areas of known thrombus appear as flow voids and potential dural sinus patentcy.
There is no subependymal edema to confirm early hydrocephus.
There is no parenchymal edema in the centronuclear structures.
Findings
MRI SWI
There is evidence of moderate-grade venous congestion with dilatation of the deep central veins, the subepndymal veins, and minimal dilatation of the deep medullary veins. there is no blooming artifact to suggest enought venous stasis to reach the features of moderately-severe deep central venous congestion. There is generalized physiologic cortical venous dilatation bilaterally.
There is enlargement of the lateral venous confluence venous complexes in particular, acting as an active venous egress route. However, the degree of cortical venous prominence of all the cortical veins is more than expected and appears to be part of the physiologic response to the dural sinus thromboses.
Blooming artifact is evident in the straight sinus and torcula. It is difficult to evaluate other sinuses, because of bone artifact.
Impression
There is physiologic venous vasodilation of cortical veins in both cerebral hemispheres reflecting re-routing effects; there is no evidence of cortical vein occlusions.
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.
