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.
CA0474-MR Diffusion
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CA0474-MR Diffusion
Case ReportExam
Prior Study
1. Markedly reduced CT density in the venocapillary pool within the left pons, both rostral cerebellar hemispheres, most of the left caudal cerebellar hemisphere, and the deep portion of the right cerebellar hemisphere. 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 produced 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 left cerebellar hemorrhage.
4. Old infarct in the left P3 PCA perfusion zone.
Findings
MR Diffusion
There is abnormal positive diffusion (hyperintense DWI & hypointense ADC maps) within the perfusion zones of both SCA perfusion zones, the left AICA-PICA perfusion zones, the Rt. deep central cerebellar watershed zone, and the Lt. pontine perforators.
However, the areas of positive diffusion contain central areas of absent signal. The absent signal is related to the susceptibility artifact produced by acute blood products containing high levels of deoxyhemoglobin. In this case, there is a coalescent hematoma in the deep central part of the left cerebellar hemisphere, and intravascular stagnated (sequestered) blood with the venocapillary pool in the deep central part of the right cerebellar hemisphere. These two sites have different morphological features, which are more obvious on the SWI sequence, and will be discussed there.
There is no diffusion abnormality in the distribution of the circummesencephalic artery, nor in the P1/P2/basilar tip perforators.
There is a small acute cortical infarction along the Lt. mesial cortex in the posterior part of the parahippocampal gyrus (distal left P4 mesial artery perfusion zone). It does not affect the left visual cortex.
There is no diffusion positivity, as expected, in the old lateral occipital encephalomalacic site (prior P3 PCA infarction).
Impression
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.
