Post contrast head CT
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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.
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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.
CA0473-Post contrast head CT
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CA0473-Post contrast head CT
Case ReportExam
Prior Study
1. Hyperacute basilar and left intradural vertebral artery thromboses with multicentric both arterial and watershed strokes involving multiple posterior fossa arteries, as described above.
2. There is early mass effect including compression of the 4thventricle, effacement of prepontine cisterns, and clear evidence of early upward transtentorial herniation.
3. Focal lesion within the deep central left cerebellum is likely a site of hemorrhagic conversion with very acute hematoma.
CT Perfusion
1. The TTP, CBF, & CBV changes consistent with completed infarctions in both SCA’s, the left AICA, the left PICA, the right cerebellar watershed zones, and possibly the left pons.
2. Absent MTT signal (out of scale sign) indicates virtually no transcapillary blood flow to generate MTT data. This is can occur with either sequestered infarction, or hemorrhagic transformation, or both. Differentiation between these two stroke complications is, best exhibited on the MR susceptibility sequence.
3. CTA head (included with our CT perfusion protocol) demonstrates patency of the left intradural vertebral artery and of the caudal basilar artery at this time, despite the CT-hyperdensity seen on the noncontrast CT head .
4. There is an old infarct with an encephalomalacic defect in the left temporal lobe (PCA-P3 segment perfusion zone).
CTA Neck
1. Diffuse atherosclerotic vascular disease is evident in the aorta with ulcerative plaque formation.
2. There is focal left ICA stenosis of 50% and a focal right ICA stenosis of 60%.
3. The proximal left vertebral artery is occluded at its’ origin, but is reconstituted at the C5 level from cervical soft tissue collaterals. The high cervical and intradural vertebral segments are within normal limits.
CTA Head
There is intraluminal basilar artery thrombus in its distal segment. It does allow some antegrade blood flow with contrast partially filling the residual basilar lumen. However, there is very limited filling of the major basilar artery branches.
The circle of Willis collateralizes the basilar tip and the PCA perfusion zones.
The Lt. PICA is patent but only fills the mesial inferior vermic branches. The right PICA is occluded at its’ origin but the right caudal cerebellar hemisphere receives pial collateral from the patent right AICA and from the patent mesial left PICA.
The left intradural vertebral artery segment has an irregular lumen, which is an indication of intercurrent recanalization of a previous thrombosed arterial segment.
Findings
Post contrast head CT
Pial Collateral Gap
The proximal prepontine segments of the superior cerebellar arteries (SCA) are opacified, but none of the rostral cerebellar hemispheric branches on either side. There is cytogenic edema in the SCA perfusion zones bilaterally.
Despite the recanalizaation of the intradural segment of the left vertebral artery and patency of the proximal basilar artery, there is very limited filling of the left AICA-PICA complex vessels except for the inferior vermic branches PICA branches in the mesial cerebellar and inferior vermic areas.
There are retrograde right AICA branches filling the outer surface of the right caudal cerebellum, but not the right cerebellar watershed zone. The left PICA is patent but only fills the mesial cerebellar and inferior vermic pial arteries. On the left the AICA is occluded. Thus, there is no filling of the distal cerebellar hemispheric branches on the left. As expected there is a resultant pial collateral gap in the deep central right cerebellar watershed zone, and a pial collateral gap affecting most of the left cerebellar hemisphere.
Venocapillary Pool CT Density
There is reasonably normal CT density within the venocapillary pool in the peripheral aspects of the right caudal cerebellum and inferior vermis, but virtually absent venocapillary in filling in the deep right cerebellar watershed zone.
There virtually absent CT density in the venocapillary pool within the superor vermis and rostral cerebellar SCA perfusion zones.
The outer and central parts of the right pons have reasonable CT density. On the other hand there is significant reduction in CT density (indicating stroke) in the central and outer aspect of the upper left pons, while the CT density is near normal for both cerebral peduncles. These findings indicate patency of proximal segment of both SCA’s, the right AICA, but nonfilling of the left basilar perforators and nonpatency of the left AICA.
The region of minimally hyperdensity in the central left cerebellar infarction is consistent with a very recent (not yet clear CT hyperdense) hemorrhage.
Venous Egress Status
The outer surface cerebellar hemispheric veins are not opacified on the left, but are, partially present on the right, which indicates significant restricted venous egress from the left cerebellar hemisphere. The veins over the rostral cerebellum and superior vermis also remain unopacified (i.e. evidence of markedly reduced transcapillary blood flow).
There is evidence of upward transtentorial herniation and displacement of the pons against the clivus consistent with mass effect produced by the combined areas of post-ischemic bilateral cerebellar cytogenic edema and the left cerebellar hematoma.
Impression
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.
Recommendations
Consider MR to evaluate for tissue ischemia that is not revealed on the CT perfusion or CT venocapillary pool and to evaluate status of intramedullary veins
