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.
CA0398-MR Susceptibility SWI
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CA0398-MR Susceptibility SWI
Case ReportExam
Prior Study
1. There is a short segment proximal superior division MCA stenosis consistent with a recanalized artery rather than underlying fixed arterial stenosis. Since the stroke-zone includes the lenticulostriate and lateral orbitofrontal perfusion zone in addition to the superior division MCA, the initial thrombotic occlusion must have involved the M1/2 ICA segments.
2. Persistently reduced CT density in the venocapillary pool within the Lt. lateral orbitofrontal and anterior insular cortex with enough oligemia to fall within the ischemic penumbra. The oligemia in the posterior insula and the Lt. lateral lenticulostriate perforator regions appear less extensive. Correlate with stroke protocol MR.
3. There is no hemorrhagic conversion at this time.
4. There subtle loss of BBB in the distal Lt. MCA (M4) pial branches consistent with post-ischemic arteriopathy.
5. Stroke-age, based on the findings on the noncontrast CT would fit the hypeacute timeframe.
MR Diffusion
1. Acute post ischemic injury affecting most of the superior division of the MCA and the left orbitofrontal region, and the left lenticulostriate perforator region consistent with an original afferent block at the left M1/2 junction (secondary stem) site, although no thrombus remains.
2. The ischemic changes are worse (likely dense ischemic core) in the rostral lateral lenticulostriate perfusion zone (especially in the rostral basal ganglia and caudate head), plus the lateral orbitofrontal perfusion zone, plus the anterior insular M3 arterial perfusion zone. Less advanced ischemic changes are evident in the distal M4 MCA superior division perfusion zone. There is less involved interval brain interposed between the rostral larger stroke and the distal cortical ischemic cortex. This pattern is consistent with initial thrombus, subsequent rapid clot lysis, and secondary distal embolization.
3. There is no hemorrhagic conversion.
MR FLAIR
There is well-delineated cytogenic edema in the Lt. M3 and M4 MCA cortex, the Lt. lateral lenticulostriate perforator zone, & the Lt. lateral orbitofrontal perfusions zones consistent with stroke age beyond 8-10 hours.
The edema is clearly more evident in the anterior insular (rostral M3 arteries) and in the Lt lateral orbitofrontal artery perfusion zones than in the M4 MCA cortical areas indicating a difference in depth and duration of the ischemic event.
There is no apparent hemorrhagic conversion including the punctate hyperdensity on the noncontrast head CT (thus, represents incidental asymmetric BG calcification).
There is an old MCA stroke is evident in the Rt. posterior insular area.
Findings
MR susceptibility
There is abnormal SWI susceptibility artifact in the Lt. orbitofrontal region consistent small areas of sequestered infarction (deoxyHgB within in capillary bed from venous stasis within the dense ischemic core). This is not hemorrhagic conversion. All other areas of left hemispheric ischemic change do not have sequestered infarction components.
Clear evidence of the site of the original thrombus is not evident (no blooming artifact along the proximal arterial walls of M1 or M2 on the left). However, the site of the recanalized arterial segment in obscured by skull base artifact.
There is an overall reduction in the size of the left cerebral veins, the ICV, and the thalamostriate veins compared to the contralateral right side. There is no blooming of the deep medullary veins to confirm venous stasis. This reduction in vein size reflects the reduced transcapillary blood flow making malignant unlikely at the current time.
There is no venous hyperemia to confirm that the vasodilatation,evident on the CTA was actually physiologic (veins are dilated in physiologic edema). Rather, the reduced veins size and evidence of BBB leak on the CTA is more consistent with post-ischemic arteriopathy.
The conspicuity of the deep medullary veins , the left cortical and the deep central veins is reduced indicating either there is less transcapillary blood flow or the transcapillary blood flow is delayed by the cytogenic edema in the left hemisphere. There is no evidence that any of the major veins are actually thrombosed.
Impression
2. The reduced left side cortical vein filling reflects the reduced overall transcapillary filling rate despite normal or even dilated distal pial arteries on the CTA. This again points out the disconnect between conspicuity of the pial arteries and whether they provide adequate transcapillary filling through their penetrating arteries.
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.
