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For Private Practices
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10 topics, 49 min.
10 topics, 47 min.
10 topics, 43 min.
10 topics, 43 min.
10 topics, 43 min.
Interactive Transcript
Report
Patient History
88-year-old female with left-sided weakness.
Findings
CT Head:
Brain Parenchyma: Hypoattenuation in the right cingulate gyrus in the ACA territory, suggestive of a chronic infarct. Corresponding calcification in the location of the A3 segment of the ACA, which could represent embolus. No hemorrhage, cerebral edema, acute cortical infarction, mass, mass effect, or midline shift. Large burden of chronic small vessel ischemic change.
Ventricles and Sulci: Normal for age.
Extra-Axial Spaces: No extra-axial fluid collection.
Paranasal Sinuses: Normal.
Mastoid Sinuses: Normal.
Orbits: Normal.
Cranium and Bones: Normal.
Soft Tissues: Normal.
CTA Head:
Mild arteriosclerotic calcification of the cavernous and supraclinoid segments of the bilateral ICAs, which result in minimal luminal irregularity without flow-limiting stenosis.
Bilateral MCAs are patent in the M1 through M4 segments.
Bilateral A1 through A2 segments are patent. Anterior communicating arteries present.
Focal high-grade stenosis of a right pericallosal branch just proximal to the bifurcation into calcified branches described on the noncontrast CT. The left branch demonstrates more dense calcification with occlusion more distally. The right calcified branch appears to be patent beyond the calcification. Additional narrowing of the left pericallosal branch that begins more proximally with some reconstitution more distally.
Slight left dominance of the vertebral arteries. Bilateral V4 segments are widely patent. Basilar artery is widely patent. Cerebellar arteries are unremarkable.
Bilateral PCAs are widely patent. Diminutive bilateral posterior communicating arteries.
No evidence of intracranial aneurysm.
CTP Head:
Tmax >6.0s: 24 cc
CBF<30%: 0 cc
CBV<42%: 0 cc
Qualitative analysis: Area of elevated Tmax in the right posterior cingulate gyrus, corresponding to hypoattenuation seen on concurrent noncontrast head CT. No corresponding decrease in CBF or CBV.
Area of increased Tmax identified by RAPID software in the left cerebellum is favored to be artifactual.
CTA Neck:
Mild atherosclerotic calcification of the aortic arch with common origin of the brachiocephalic and left common carotid arteries, normal variant.
Bilateral common carotid arteries are tortuous but widely patent.
Right internal and external carotid arteries are widely patent.
Predominantly calcific atherosclerotic plaque at the origin of the left external carotid artery resulting in approximately 70% luminal narrowing of the external carotid artery, though evaluation of the degree of stenosis is limited by blooming artifact from the calcification. External carotid artery remains patent. Left internal carotid artery is widely patent.
Bilateral vertebral arteries are widely patent. Left vertebral artery is slightly larger than the right vertebral artery.
No evidence of dissection, aneurysmal dilatation, or vascular malformation.
Aerodigestive tract: Normal.
Thyroid: Normal.
Parotid and submandibular glands: Normal.
Lymph nodes: No pathologically enlarged or suspicious lymph nodes.
Upper Chest: Imaged portion of the chest appears unremarkable.
Bones: Degenerative changes of the cervical spine.
Conclusion
1. No acute intracranial abnormality. Chronic-appearing right ACA territory infarction centered in the right cingulate gyrus with calcified embolus in the region of the right ACA.
2. Accompanying high-grade focal narrowing/occlusion in the right pericallosal artery proximal to the bifurcation into calcified branches seen on the noncontrast CT. Finding is favored to represent a chronic focal occlusion with consequent chronic calcification of its branches.
3. Elevated Tmax involving the posterior right cingulate gyrus without a corresponding decrease in CBF or CBV, suggesting an area of ischemia. Although a core infarct is not detected by CTP, it is suspected by the noncontrast CT. MRI with diffusion imaging would be more sensitive, if clinically warranted.
Case Discussion
Faculty
Vivek S Yedavalli, MD, MS
Assistant Professor of Neuroradiology and Director of Stroke Imaging
Johns Hopkins University
John Kim, MD, MRMD, (MRSC™)
Associate Professor, Radiology
University of Michigan
Tags
Vascular
Perfusion
Neuroradiology
CTP
CT
Brain
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