MR Susceptibility SWI
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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.
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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.
CA0389-MR Susceptibility SWI

CA0389-MR Susceptibility SWI
Case ReportExam
Prior Study
1. Prior occlusion of the posterior M3 trunk off the superior division Lt MCA, which has good pial collateral preventing extension of the stroke to most of the posterior superior division perfusion zone.
2. There is acute thrombus in single artery (artery to the central sulcus). The affected perfusion zone for this artery is much smaller than its’ full (normal) perfusion territory, which indicates there has been substantial retrograde pial collateralization from the A4 (ACA) pial vessels. However, there remains a small pial collateral gap in the mid-insula and the adjacent frontoparietal opercular cortex. In this case, the affected area includes the tongue part of the primary facial motor area, which correlates with the patients presenting symptom of dysarthria.
3. The improved CT density in the venocapillary pool is a good indication that the extent of final stroke-zone will remain quite small.
MR DWI/Flair Sequences
Both the DWI & ADC maps are positive for a small stroke in the mid-insular and intrasylvian frontoparietal cortices.
Very subtle edema is evident with the affect cortex is consistent with a hyperacute stroke timeframe.
Findings
MR susceptibility
SWI is positive for intraluminal thrombus in both the posterior trunk of the M3 arteries and in the acutely thromboses artery to the central sulcus. This indicates the proximal thrombus (which is not hyperdense) likely preceeded the hyperdense single acutely thrombosed, artery to the central sulcus. Thus, it is likely that the early (probably clinically silent) thrombus underwent clot lysis with secondary embolization affecting the origin of the artery to the central sulcus, which in turn produced the current acute symptoms or dysarthria. This accounts for the inconsistency between the punctate hyperdensity on the noncontrast head CT and the wider zone of prolonged TTP on the CT perfusion sequence.
The physiologic hyperemia in the collateral zone with vasodilatation evident on the CTA is confirmed on this SWI exam by evidence of venous prominence of the intrasylvian veins without any blooming artifact. It also matches the increase CBV on the CT perfusion and is outside the diffusion positive stroke-zone.
Impression
2. Physiologic hyperemia is present adjacent to the stroke-zone, as expected.
3. No venous egress abnormality is evident.
Recommendations
A 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.