MR FLAIR
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.
CA0397-MR FLAIR
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CA0397-MR FLAIR
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 all or at least part of the divisions and major branch arteries distal to the left M1/2(MCA) junction site.
2. The ischemic changes are worse in the lateral orbitofrontal and the anterior insular M3 arterial perfusion zones. Less advanced post ischemic diffusion changes are evident in the distal M4 MCA superior division and the lateral lenticulostriate perfusion zones.
3. There is no hemorrhagic conversion.
Findings
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 now is beyond 8-10 hours. The cytogenic swelling does partially compress the left lateral ventricle, but it does not produce enough mass effect to cause any brain herniation.
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 between these ischemic events. There is also less cytogenic edema (less FLAIR conspicuity) in the mid M4 areas than are evident in the more rostral and caudal M4 areas. This suggests the clot lysis caused secondary distal M4 embolization to the retrosylvian regions.
There is no apparent FLAIR positive signal in the recanalization site in the superior division MCA.
There is no apparent hemorrhagic conversion including the punctate hyperdensity on the noncontrast head CT (which actually represents incidental asymmetric BG calcification).
There is an old MCA stroke is evident in the Rt. posterior insular area.
Impression
2. The ischemic changes are worse (more prominent FLAIR signal and more tissue swelling) in the lateral orbitofrontal and the anterior insular M3 arterial perfusion zones. Less advanced post ischemic diffusion changes are evident in the distal M4 MCA superior division and the lateral lenticulostriate perfusion zones.
3. There is no hemorrhagic conversion nor FLAIR evidence of sequestered infarction.
