CTA Head
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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.
CA0472-CTA Head
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CA0472-CTA Head
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 4th ventricle, 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.
Findings
CTA of the head
Supratentorial Intradural Arterial Circulation
The supratentorial arteries are all patent. There are scattered sites of intimal irregularity without occlusion or flow limiting stenosis.
The posterior circle of Willis is incomplete, but is sufficient to provide collateral to the P1 segments and the basilar apex (source arteries for the thalamic perforators. The right PCA arises primarily off the right ICA (fetal variant) and supplies the right PCA territory. The left t P-com does fill the left PCA in a retrograde manner. The left P1 part of the circle of Willis is partially involved by the thrombus and is, at least, not fully functional at this time.
In the anterior circle of Willis the right A1 is hypoplastic and both ACA’s fill predominantly from the left.
Infratentorial Intradural Arterial Circulation
The intradural right vertebral artery is developmentally small. Its’ lumen has irregular plaque and the right PICA is not opacified. There is retrograde filling of the distal intradural right vertebral artery and some right hemispheric branches.
The intradural left vertebral artery is patent, but has irregular intimal margins, which is likely from recanalized. The left PICA is patent, but only fills the mesial branches (inferior vermian artery). None of the left hemispheric AICA or PICA branches are opacified.
There is intraluminal soft clot filling most of the distal segment basilar artery. The left AICA is not clearly opacified. The proximal segments of both SCA’s are opacified, but none of their distal cerebellar hemispheric or superior vermic branches are opacified.
The right PICA is occluded, likely on a chronic basis, since minimal plaque is evident at its’ likely takeoff from the right intradural vertebral artery segment. The right AICA is patent providing pial collateral to the caudal right cerebellar hemisphere. Pial collateral to the right inferior vermis and mesial right cerebellum is derived from the patent left mesial PICA inferior vermic branches.
Venous Circulation
It is too early to opacify the venous system.
Other
No other findings are present to suggest a different cause for symptoms than stroke.
Impression
2. The circle of Willis collateralizes the basilar tip and the PCA perfusion zones.
3. 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.
