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.
 

CT head; CT perfusion; CTV of the head; CT venocapillary pool; MR diffusion; MR flair; MR susceptibility

CT Head
1. 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.
2. 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.
3. 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.
4. There is early optic hydrops and right temporal ventriculomegaly consistent with early effects of CVT induced raised intracranial pressure.

CT Perfusion
1. 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.
2. 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.
3. 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.

CTV of the Head
1. 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.
2. 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.

Post contrast head CT (venocapillary pool analysis)
1. 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

MR Non-Contrast T1-W Exam
1. Hyperacute (isodense) thrombus is evident throughout most of the major dural sinuses (SSS, torcula, transverse sinuses, and the straight sinus). There is evidence of at least moderately advance congestion within the deep medullary vein complex and parenchymal edema in the centronuclear structures on the right.

MR Diffusion 
1. Diffusion is positive on both the DWI and ADC maps confirming evidence of post ischemic injury in right basal ganglia, right caudate and right thalamus (i.e. “venous stroke’).

MR T2/FLAIR
1. There is evidence of significant focal vasogenic edema in the dorsal thalamus and minimal basal ganglia edema, plus evidence of deep medullary vein congestion in the right centrum semiovale, the right basal ganglia, the right caudate nucleus, and more prominently in the right thalamus. These are features of significant venous congestion in the right deep venous system. There is retroglobal edema on the right along with bilateral optic hydrops, as well as, limited right lateral venticulomegaly (early hydrocephalus) indicating there is CVT related elevated CSF pressure.

MR susceptibility (SWI)
1. There are extensive venous abnormalities mainly in the right cerebum. There is blooming artifact of thrombosis in multiple dural sinuses and the right deep central veins, and right the BVR. There is venous hyperemia (pial venous collateralization) exhibited in most of the left cortical pial veins associated with re-routing of venous egress. There is both advanced venous congestion and some actual thrombosie within the right subependymal veins caused by the venous blockade at the right ICV, vein of Galen and straight sinus (the combination of which has significantly reduced the possibility of collateral venous re-routing from the right deep venous system.
2. Venous egress re-routing is mainly through the superior sylvian vein complex bilaterally, and mesial and lateral tentorial venous confluences. There is no hemorrhagic conversion.

1. Widespread dural sinus thrombosis

2. Multicentric cortical vein thromboses

3. Deep venous thrombosis with evidence of Venous infarction in the right basal ganglia and right thalamus.

4. There is functional venous egress collateralization for the dural sinus and cortical vein thromboses utilizing the pial-dural confluences (vertex and mesial/lateral tentorial confluences), and the dural sinus walls.

5. Optic hydrops and early ventricular enlargement indicate that there is raised CSF pressure.

1. Deep central venous outlet obstruction (in this case related to right ICV, vein of Galen and straight sinus thrombosis) can cause significant venous congestion. The degree of venous congestion severity can be stratified into grades 1-4 with 1 being minimal, 2 being moderate, and 3/4 being advanced. In this instance, it is in the moderately-advanced state (grade 3), which in this case was sufficient to produce venous-based venous stroke. It has also produced some centronuclear swelling, but as yet, has not produced malignant swelling.
 
2. This case clearly illustrates imaging features of venous collateral re-routing in the context of both dural sinus and cortical vein thromboses. Actual CVT is confirmed by the presence of SWI blooming artifacts conforming to recognizable venous structures. This case also illustrates the appearance of moderately-advanced deep central venous (grade 3) congestion where even the deep medullary and all subependymal veins are dilated. Most of the cortical veins on the right exhibit features of regional pial venous collateralization with dilatation, serpiginous shape, and reversed filling direction. Finally, most of the veins on the left show the hyperemic effects of venous egress re-routing into the superior sylvian vein complex draining into the left cavernous sinus. Physiologically re-routed collateral veins are enlarged but are not as serpiginous as collateral veins, and they connect with other recognizable patent collateral pathways.
 
3. When dural sinus thrombus on the noncontrast T1-w exam is isodense to brain, as opposed the hyperintense, this indicates a very recent (acute) thrombus age, which has not evolved to the state of high met-Hgb enough. Met-hemoglobin is necessary to produce hyperintense signal on noncontrast T1-w sequences.
 
4. This case illustrates how limited cerebral venous egress can elevate venous pressure, which elevates CSF pressure, which can be manifest as optic hydrops, retroglobal orbital edema, and early hydrocephalus.

Watch the included summary video for this instructional case.