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Wk 5, Case 4 - Review

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Patient History

New left-sided weakness.

Findings

CT Head:

Brain: Focal loss of gray-white differentiation in the right paramedian frontal lobe at the vertex involving the superior frontal gyrus and right precentral gyrus to lesser extent.

Ventricles and sulci: Mild prominence of the ventricles.

Veins: Diffusely increased attenuation in the superior sagittal sinus as well as several cortical veins, suspicious for venous thrombosis. Otherwise, brain parenchymal architecture is within normal limits. Remainder of gray-white differentiation is preserved.

Arteries: Intracranial vascular calcifications are faintly present involving the petrocavernous ICAs.

Other: Imaged paranasal sinuses are predominantly clear. No mastoid effusions.

No suspicious osseous abnormalities.

CT Perfusion Head:

Perfusion imaging is markedly suboptimal secondary to extensive motion artifact during the examination. Scanning was not performed to the top of the vertex as well.

Limited perfusion sequences demonstrate increased mean transit time in the right paramedian frontal lobe corresponding to the area of loss of gray-white differentiation with decreased cerebral blood flow.

CTA Head (with adequate venous opacification):

Dural venous sinuses: Marked expansion of the superior sagittal sinus with a large filling defect along the proximal segment. No extension into the transverse sinuses or the inferior aspect of the superior sagittal sinus. Additional foci of thrombosis involving several draining cortical veins bilaterally including the right vein of Trolard with minimal reconstitution. Transverse, sigmoid,and jugular bulbs are patent. Cervical jugular veins are patent. Paired internal cerebral veins are grossly patent as well as the vein of Galen and straight sinus.

Arteries: Petrocavernous and supraclinoid internal carotid artery segments are patent. Anterior, middle and posterior cerebral arteries are patent without stenosis. Anterior communicating artery is present. Bilateral posterior communicating arteries are patent. Intracranial V4 segments and basilar artery are patent.

No evidence of aneurysm or vascular malformation.

MRI Brain:

Area of T2/FLAIR hyperintense signal abnormality involving the cortex and subcortical white matter in the right posterior frontal high convexity region with no restricted diffusion. Associated foci of signal loss on SWI within the depth of the right central sulcus.

Remainder of the brain parenchyma is normal in signal intensity. Mild diffuse prominence of the cerebral sulci with commensurate dilatation of the supratentorial ventricles. Mild dilatation of the fourth ventricle. Sellar region is grossly normal. Craniocervical junction is unremarkable. No other areas of intracranial or extracranial hemorrhage. No territorial restricted diffusion to suggest acute or subacute infarction. Orbits are grossly normal. Trace mucosal thickening of the paranasal sinuses. Mastoid cells are clear.

MR Venogram:

Filling defects within the superficial/cortical veins (right greater than the left) and superior aspect of the superior sagittal sinus, consistent with venous sinus thrombosis. Otherwise, normal contrast enhancement within the major intracranial venous sinuses including the inferior sagittal sinus, internal cerebral veins, straight sinus, transverse sinuses, and sigmoid sinuses.

Conclusion

CT/CTA/CTP:

1. Superior sagittal sinus thrombosis with additional thrombosis of several large draining cortical veins including the right vein of Trolard. Evidence of venous infarct involving the right superior frontal gyrus without evidence of hemorrhagic conversion. Perfusion imaging was not performed at the vertex in the region of the infarct and is significantly degraded by motion, but does demonstrate at risk ischemic tissue in the right paramedian frontal region.

2. Remainder of the major dural venous sinuses are patent without evidence of thrombosis.

3. No significant intracranial arterial stenosis or vascular cut off.

4. No significant stenosis of the cervical carotid or vertebral arteries.

Case Disucssion

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

MRI

CTP

CT

Brain

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