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.
CA0467-MR Susceptibility SWI
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CA0467-MR Susceptibility SWI
Case ReportHistory
Exam
Prior Study
1. There is Lt. primary-stem ICA thrombosis affecting both the intracranial/extradural and the entire intracranial portions of the Lt. ICA.
2. Only minimal peripheral pial collateralization is evident; the bulk of the Lt ICA perfusion zone is within the dense ischemic core. The addition of the virtually no venous egress to no afferent arterial input is consistent with sequestrated form of stroke, which if large enough in size typically has a very poor clinical outcome. This patient did not survive this stroke.
3. There is no current hemorrhagic conversion.
4. There is early, but definite, downward incisural herniation.
MR Diffusion
1. There is a variation of diffusion MR imaging characteristic of completed arterial stroke, severely limited transcapillary flow and venous collapse. The DWI sequence is positive only on the periphery of the stroke-zone while the bulk of stroke is NOT hyperintense. Meanwhile the ADC is positive (hypointense) throughout the entire stroke-zone. This is the most advanced state for a dense ischemic core type of stroke. Presumably, the altered diffusion is the result of high tissue levels of deoxyhemoglobin causing phase shift signal loss. This is an ominous finding and will not likely respond favorably to interventional stroke therapy. It may however, cause malignant brain swelling, which may require emergent cranial decompression.
MR Flair
1. Acute thrombus is now evident in the high cervical Lt. ICA, as well as the intradural ICA.
2. Aypical MR diffusion appearance related to suppression of signal most likely caused by the susceptibility artifact associated with high levels of deoxyhemoglobin within areas of venous stasis. This is consistent with a sequestered infarction, which is the worst form of arterial stroke. This involve all but the outer periphery of the left ACA and left MCA perfusion zone. Strokes of this type will not likely respond favorably to interventional stroke therapy.
3. There is evidence of mesial parahippocampal gyrus displacement, which is indicative of the start of downward brain herniation. This patient may, therefore, require cranial decompression if malignant brain swelling occurs.
4. There is a small mesial lenticulostriate perforator stroke without features of sequestered infarct.
Findings
MR SUSCEPTIBILITY SEQUENCE (SWI)
The SWI sequence demonstrates blooming artifact in the left intradural ICA indicating acute arterial thrombus through out the primary and secondary intradural afferent circulation. Thrombus in the extradural arteries is obscured by skull base artifact on SWI, but there was clot in the left extradural ICA on the FLAIR sequence.
There is SWI blooming artifact throughout all the left deep medullary veins and many of the lateral cerebral veins consistent with venous stasis. The SWI signal loss is also related to the susceptibility artifact produced by high concentration of deoxyhemoglobin within the stagnant venocapillary pool in the affected areas.
There is also evidence of venous collapse based on the combination of both blooming artifact in major efferent cortical veins and non-filling of other veins without blooming; this includes the Lt. deep cerebral vein (ICV), which does not fill at all. The caudate veins also demonstrate venous stasis with blooming artifact. In essence, these venous changes confirm the virtual shutdown of transcapillary blood flow with no evidence of any reflow throughout any of the stroke-zone. These are the features of an acutely sequestered infarcts. With no reflow, as evident in this case, the stroke effects are irreversible. Acutely sequestered infarcts can be large in size, as in this case, or very small and scattered as evident in Case 7.
The dural sinuses remain patent because of normal blood flow in the right carotid circuit and in the left PCA and in the posterior fossa.
Impression
2. There is SWI blooming artifact throughout all the deep medullary veins and many of the lateral cerebral veins consistent with advanced venous stasis or venous collapse or a combination.
3. The Lt. deep cerebral vein (ICV) does not fill at-all, and the caudate veins demonstrate venous stasis.
4. The Lt. basal vein of Rosenthal does not fill indicating virtually no transcapillary venous egress from the ventromesial cerebral cortex.
5. The major veins over the vertex of the Lt. hemisphere and the superior sagittal sinus in the same area exhibit susceptibility blooming artifact consistent with venous thrombosis/collapse of veins draining the dorsal cerebral cortex.
Recommendations
A summary 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.
