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/.
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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.
CA0476-MR Susceptibility SWI
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CA0476-MR Susceptibility SWI
Case ReportExam
Prior Study
1. Markedly reduced CT density in the venocapillary pool within the left pons, and both cerebellar hemispheres, as above. These areas are all included in the dense ischemic core.
2. There is a very recent left deep cerebellar reperfusion hemorrhage, which when combined with the stroke-related brain swelling, has producing mass effect with early upward transtentorial herniation
3. Lack of venous egress in the left cerebellum is indicative of venous collapse, and is likely the basis for the reperfusion hemorrhage.
4. Old infarct in the left P3 PCA perfusion zone.
MR Diffusion
1. Multicentric cerebellar and left pontine infarctions are evident, as listed above. Stroke age is likely 6-8 hours or beyond. There is a chronic completed infarction with encephalomalaica in the left P3-PCA perfusion zone.
2. There is hemorrhagic conversion with hematoma in the left deep central cerebellar watershed zone.
3. There is apparent sequestered infarction in the right deep deep central cerebellar watershed zone.
4. There is early upward transtentorial herniation.
MR FLAIR
1. Multicentric infarctions are listed above; stroke age is likely 6-8 hours or beyond. There is an old left P3 infarction with encephalomalacia in the lateral ventral temporal lobe. There is wide spread age-related ischemic demyelination in the centrum semiovale bilaterally.
2. There is hemorrhagic conversion with hematoma in the left deep central cerebellar watershed zone.
3. There is sequestered infarction in the right deep deep central cerebellar watershed zone; this can be confirmed on MR-swi sequence.
4. There is early upward transtentorial herniation.
Findings
General
There is abnormal blooming SWI artifact producing SWI signal loss within the left intradural vertebral artery and in two sites in the basilar (mid & distal) consistent with presence of recent mural or intraluminal thrombus.
There is abnormal blooming SWI artifact producing SWI signal loss in the left posterior medullary segment of PICA consistent with occlusion of the lateral hemispheric trunk of the distal left PICA. The mesial trunk was remained patent.
There is a wide area of sequestered infarct in the right deep cerebellar watershed zone. It is surrounded by tissue with near-normal SWI signal. Notice how the right cerebellar sequestered infarct matches the underlying anatomic cerebellar parenchymal layered distribution. Sequestered infarcts, if they persist, develop when there is NO restoration of transcapillary blood flow. Hemorrhage is the result of reperfusion into the infarction site, especially when there if venous outlet obstruction as in this case, see below. On later MR imaging they present with ring enhancement and occasionally are resected, as possible tumor. The cytopathology in these cases reveals completely fibrin-filled vessels within venocapillary bed and small arteries and veins, plus extensive parenchymal hemosiderin deposition; they are labelled “chronic completed strokes”. However, these sequestered infarct are also seen in acute stroke imaging, as in this instance. In acute sequestered infarcts the blood products represent stagnated blood products within the venocapillary pool rather than being extraluminal as in hematomas. The technical basis for positive SWI is high levels of deoxyhemoglobin cause phase dispersion and signal loss on all T2-w sequences, especially the SWI sequence.
There is a hematoma (reperfusion hemorrhagic conversion) in the left deep cerebellum. Notice, how hematomas appear as a confluent blood products and act as a solid mass. There are also smaller areas of sequestered infarct in other parts of the left AICA-PICA complex separate from the hematoma. The hematoma is roughly 2.5 cm in diameter and produces mass effects, as described previously.
There is blooming artifact in the outer left cerebellar veins consistent with cortical venous stasis or thrombosis, or both. Venous outlet obstruction is often associated with hemorrhagic conversion, as in this case.
There is chronic hemosiderin along the margins of the old left P3 stroke.
Impression
2. Sequestered infarct is evident in the deep central right cerebellar hemisphere. Hematoma is present in the deep central left cerebellar hemisphere.
3. SWI evidence of blooming artifact in the left cerebellar cortical veins consistent with venous collapse in mainly the AICA-PICA perfusion zone; hence, the hemorrhagic conversion in this territory.
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.
