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.
CA0475-MR FLAIR
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CA0475-MR FLAIR
Case ReportExam
Prior Study
1. Markedly reduced CT density in the venocapillary pool within the left pons, and both cerebellar hemispheres, as above. 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 producing 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 reperfusion hemorrhage.
4. Old infarct in the left P3 PCA perfusion zone.
MR Diffusion
1. Multicentric cerebellar and left pontine infarctions are evident, as listed above. Stroke age is likely 6-8 hours or beyond. There is a chronic completed infarction with encephalomalaica in the left P3-PCA perfusion zone.
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.
4. There is early upward transtentorial herniation.
Findings
MR FLAIR
FLAIR demonstrates well-formed hyperintense FLAIR signal change consistent with stroke-age beyond 6-8 hours.
FLAIR also exhibits markedly suppressed signal within the left cerebellar hematoma; notice how hematoma effaces the underlying cerebellar parenchymal gray-white matter pattern. There is less signal drop out on the FLAIR in the sequestered infarct in the right cerebellar watershed zone and there is preservation of the layered pattern in the cerebellum. Note also how MR FLAIR tends to have less susceptibility change in a sequestered infarction than it does for hematomas.
There is gliosis around the left occipital encephalomalacia defect, as expected, and age-related ischemic demyelination in the centrum semiovale.
There is enough cerebellar swelling to compress the fourth ventricle and produce early upward transtentorial herniation. Cerebellar tonsils are at the plane of the foramen magnum, but are not below, as yet.
There is abnormal irregular FLAIR signal in the wall of the left intradural vertebral artery consistent with a recanalized prior thrombus. There is positive FLAIR in the residual thrombus in the basilar apex and left P1 segment. Some of the signal in both area may actually be slowed laminar flow effects. This would suggest that the initial thrombotic event was in the left intradural vertebral segment, which then secondarily embolized to the posterior medullary left PICA, as well as sending intraluminal thrombus to the basilar distal segment and emboli to the left P4-PCA perfusion zone. The cerebellar watershed strokes are likely on the basis of an end-of the-line hypoperfusion state (i.e. collateral couldn’t support the right cerebellar watershed zone but was enough to save the caudal cortical areas). The left watershed zone has undergone hemorrhagic transformation.
There is fluid in the right mastoid air cells without aggressive features.
Impression
2. There is hemorrhagic conversion with hematoma in the left deep central cerebellar watershed zone.
3. There is sequestered infarction in the right deep deep central cerebellar watershed zone; this can be confirmed on MR-swi sequence.
4. There is early upward transtentorial herniation.
