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.
CA0460-MR FLAIR
View Images
CA0460-MR FLAIR
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.
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.
MR Diffusion
1. There is a variation of diffusion MR imaging characteristic of completed arterial stroke, severely limited transcapillary flow and venous collapse. The DWI sequence is positive only on the periphery of the stroke-zone while the bulk of stroke is NOT hyperintense. Meanwhile the ADC is positive (hypointense) throughout the entire stroke-zone. This is the most advanced state for a dense ischemic core type of stroke. Presumably, the altered diffusion is the result of high tissue levels of deoxyhemoglobin causing phase shift signal loss. This is an ominous finding and will not likely respond favorably to interventional stroke therapy. It may however, cause malignant brain swelling, which may require emergent cranial decompression.
Findings
MR FLAIR
The FLAIR sequence has an atypical stroke appearance in the same way that the MR diffusion was atypical. FLAIR demonstrates little free water within the stroke-zone leaving a reduction in FLAIR signal rather than an increase in signal, as is usually seen in acute strokes. The outer margin of the stroke-zone on the left does demonstrate some increase in FLAIR signal related to some free water remaining in the neuropil along the margin of the stroke-zone, which did have some pial collateralization.
The small anterior thalamic pole Rt. P-com perforator stroke exhibits positive FLAIR signal of a recent stroke.
There is increase FLAIR signal throughout the wall of the extradural left ICA consistent with acute Lt. ICA thrombus.
There is already enough brain swelling at this time to cause early compression of the lateral ventricle and early downward transtentorial herniation with mesial displacement of the uncus effacing the left crural cistern. This represents the initial stage of malignant brain edema resulting from venous egress stasis and/or complete venous collapse.
Impression
Aypical 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. This is consistent with a sequestered infarction, which is the worst form of arterial stroke. This involve all but the outer periphery of the left ACA and left MCA perfusion zone. Strokes of this type will not likely respond favorably to interventional stroke therapy.
There is evidence of mesial parahippocampal gyrus displacement, which is indicative of the start of downward brain herniation. This patient may, therefore, require cranial decompression if malignant brain swelling occurs.
There is a small mesial lenticulostriate perforator stroke without features of sequestered infarct.
