MR Diffusion
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.
CA0459-MR Diffusion
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CA0459-MR Diffusion
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. Likewise, there is very little venous opacification consistent with minimal or no transcapillary blood flow and possible deepm medullary venous collapse.
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.
Findings
MR diffusion
The diffusion maps display a very abnormal, relatively unusual appearance. The DWI sequence within in the central aspects of the stroke zone exhibits almost no hyperintense signal, while the ADC has the usual hypointense signal. The DWI is only hyperintense on the outer margins of the stroke-zone. This reversed appearance of the DWI map is likely related to a virtual total lack of transcapillary blood flow and additionally to venous stasis or even venocapillary thrombosis. This matches the findings on the delayed post contrast CTA, which exhibited no rise in CT-density. Venous stasis results in desaturation of blood and high levels of deoxyhemoglobin. The deoxyhemoglobin causes a susceptibility artifact which dephases the T2-w signal which results in virtually no signal; hence hypointense signal on both the DWI & ADC sequences. The positive DWI along the outer cortex matched areas where some reflow from pial collaterals remained on the CT venocapillary pool analysis.
This combination of marginally positive DWI and globally positive ADC is indicative of both dense ischemic core. But combined with venous stasis and/or total venous collapse, It indicates all of the affected area will undergo completed infarction, but whether it proceeds on to liquefactive necrosis or becomes a sequestered infarction depends on whether spontaneous clot lysis clears the afferent block or not. This scenario has the potential for malignant brain swelling and downward herniation, which is evident in this case. This patient did not survive this ischemic event.
There is an additional punctate area of positive diffusion restriction in a single mesial perforator occlusion on the right. It is located adjacent to the foramen of Monro. This likely is a secondary embolic stroke from proximal clot lysis. The diffusion characteristics of acute stroke have the usual appearance, as opposed to the sided stroke.
Impression
2. Atypical 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. These findings are consistent with an acutely sequestered infarction, which is the worst form of arterial stroke. Strokes of this type typically will not likely respond favorably to interventional stroke therapy.
3. There is a small mesial lenticulostriate perforator stroke without features of sequestered infarct.
