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.
CA0396-MR Diffusion
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CA0396-MR Diffusion
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 significantly reduced CT density in the venocapillary pool is evident within the Lt. lateral orbitofrontal and anterior insular cortex with enough oligemia. Other affected areas (i.e the posterior insula and the Lt. lateral lenticulostriate perforator zones) improve their CT density toward normal; these could be in the ischemic penumbra.
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.
Findings
MR diffusion
There is positive diffusion (acute post ischemic injury) affecting most of the superior division of the MCA, a part of the inferior MCA division supplying the superior temporal gyrus, and the left orbitofrontal region consistent with the original afferent block at the left M1/2 junction site. The middle temporal gyrus and the anterior temporal polar perfusion zones are spared ischemic injury by PCA (P3 trunk) pial collaterals. This matches the CT perfusion which demonstrated increased CBV in the anterior temporal polar area and the centrum semiovale areas.
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 cortical perfusion zones. There is even less involved brain, interposed between the rostral stroke versus the distal cortical ischemic injury. This non uniform pattern is consistent with an initial thrombus, subsequent rapid clot lysis, and secondary distal embolization with variable distal ischemic consequence.
There is no hemorrhagic conversion.
Impression
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.
