Back to Venous Case 01 - Hyperacute Stroke

Case210f

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Case Notes

History

29 year old female presenting acutely with dysarthria, apahsia, facial droop. Patient was in an automobile accident 3 weeks earlier. Patient is not on birth control meds.

Exam

Prior Study

CT Head
There is widespread acute thrombosis within the superior sagittal sinus, the torcular herophile, the straight sinus, and both transverse sinuses. There may be partial thrombosis within the high cervical jugular veins.
There is acute thrombus in the lateral surface vertex cortical veins adjacent to the superior sagital sinus, and in the right basal vein of Rosenthal, and in the right ICV, and in the vein of Galen. There is focal vasogenic edema in the right dorsal thalamus and caudate with local mass effect consistent with significant right deep central venous egress obstruction (vasogenic edema). Whether cytogenic edema is present from venous infarction is indeterminate. There is early optic hydrops and right temporal ventriculomegaly consistent with early effects of CVT induced raised intracranial pressure.
 
CT Perfusion
CT perfusion features of dural sinus thrombosis with dural wall collateralization affecting  the SSS, the torcula, and the left transverse sinus. The right transverse sinus is apparently thrombosed without dural wall collateralization. There is significant venous congestion within the right subependymal venous plexus, as a result of venous egress block in the right ICV, vein of Galen and straight sinus. There is re-routing of the venous egress through the left superior sylvian vein complex into the cavernous sinus and from supra to infratentorial vein connections through the superior vermian vein and lateral anastomotic mesencephalic vein connections.
 
CTA/CTV/MRV of the neck: No imaging of the neck was obtained.

CTV of the head
There is extensive dural sinus thrombosis, which also involves a short segment of the major cortical veins (the segment adjacent to the dural sinus) bilaterally. Venous egress has been re-routed into the superior sylvian vein complex and the supra to infratentorial connections with the superior vermian vein complex and through the lateral anastomotic vein complex. The former exits through the cavernous sinus into the pharyngeal vein plexus and the lateral through the petrosal veins and perimedullary veins.

CT analysis of the venocapillary pool
No significantly reduced venocapillary CT density was noted to confirm site of venous stroke. However, there is minimally reduced contrast density in the right thalamus consistent with vasogenic edema related to venous congestion. There is thrombosis of the right deep central veins, while the left deep central veins and left septal vein are patent. There is evidence of persistent intraluminal thrombus (empty delta sign) within most of the major dural sinuses.
 

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Section 1

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Case210f

Findings

MR T1-W Sequence without contrast only

​There is luminal abnormal isointensity (lack of flow void) or hyperintensity within one or more dural sinuses (delta sign) indicative of acute thrombus on the noncontrast T1.

​There is evidence of hyperintense or hypointensity  within one or more cortical or central veins on noncontrast T1.

​There is evidence of dilatation of the intraorbital veins, and optic hydrops (dilated CSF space around the optic nerves) on pre or post contrast T1 MR.

​There is evidence of abnormal ventriculomegaly consistent with early hydrocephalus.

​There is evidence of dural sinus filling defect (empty delta sign) indicating thrombosis within one or more dural sinuses on the post contrast T1.

​There is evidence of dural sinus filling defect indicating thrombosis within the cavernous sinus and either its' afferent input or efferent egress veins on the post contrast T1.

​There is evidence of mural enhancement or actual luminal filling defect within a cortical or central vein indicating acute thrombus on post contrast T1.

​There is evidence of mural enhancement or intraluminal filling defect indicating thrombosis in an ophthalmic vein on post contrast T1.

​There is evidence of parenchymal contrast enhancement in the region of the affected venous zone on post contrast T1 indicative of vascular leak.

​There is evidence of pial venous collateral veins (typically appear serpiginous, enlarged size, draining the reversed directiong, with the size changed from being larger next to the dural sinus to being larger at there inception site on the post constrast T1 MR).

​There is prominence of any of the pial/dural anastomotic sites (i.e. vertex venous lacunae, tenorial confluences, or cavernous sinus/retropharyngeal venous plexus) on the post contrast T1-w sequence.

​There is evidence of unexpected regional cortical vein enlargement (arterialization of othersise NL veins), consistent with the combination of a dural AV fistula plus dural sinus stenosis/thrombosis on post contrast T1.

​There is evidence of skull base destruction (infection/tumor) leading to cavernous or dural sinus thrombosis.

There is evidence of hemorrhagic conversion

Other

Other findings are present consistent with a disorder other than CVT.