54 year old male with history of epilepsy who presented with a 2 week history of progressive loss of coordination and balance.  On admission the patient was aphasic but without focal findings. Patient is on long term Dilantin.

Noncontrast CT head; CT perfusion; CTA of the neck; CTA of the head; Delayed post contrast head CT; Post contrast T1-w MR; MR diffusion; MR FLAIR; MR susceptibility (swi)

CT head
1. Acute to subacute thrombosis of multiple dural sinuses is evident including the transverse sinuses on both sides, and the straight sinus. Acute venous thrombosis is evident in both of the internal cerebral veins (ICV), the vein of Galen and the right basal vein of Rosenthal. There is edema in the dorsal right thalamus,  but whether this is vasogenic edema or cytogenic edema (venous stroke) is indeterminate. There is also reduced CT density wihtin the superior vermis, but whether this is from prior radiation therapy (with leukomalacia) or whether it is related to retrograde propagation of clot from the vein of Galen into the superior vermian vein complex is indeterminate.

CT Perfusion
1. There is deep central vein thrombosis producing venous congestion in the the subependymal venous system (i.e. caudate, thalamostriate, and deep medullary parenchymal vein), greater on the right than the left.
2. Thrombosis of the straight sinus is evident on the CTA, which is included with the CT perfusion data set, but there is no CT perfusion evidence of collateral flow in the dural sinus wall.

CTV of the neck
1. There is thrombosis (likely chronic) of the right cervical internal jugular vein and the right sigmoid/transverse sinuses.

​CTV of the head
1. There is thrombosis of multiple dural sinuses including the right transverse/sigmoid sinuses and the adjacent right internal jugular vein plus thrombosis of the straight sinus.
2. There is either thrombosis or at least delayed filling of the deep central veins, the vein of Galen, and the right basal vein of Rosenthal on CTA of the head. However, there is thrombus in these veins on the CT head consistent with hyperacute CVT.
3. There is re-routing of venous egress through the left superior sylvian venous complex/sphenoparietal sinus/cavernous sinus and through the left lateral tentorial venous confluence.

Post contrast head CT
1. There is evidence of edema in the dorsal right thalamus which is part of the right ICV venous egress territory.  Whether this edema is vasogenic edema alone related to venous congestion or includes cytogenic edema from venous infarction is indeterminate. However, the partial rise in right thalamic venocapillary pool density makes completed infarction unlikely;  correlate with MR diffusion sequences.
2. Intraluminal clot is evident in the vein of Galen/straight sinus junction (empty delta sign), as well as in the right channel of the torcula and proximal right transverse sinus. There is subependymal venous congestion more prominent on the right than left. There is persistent CVT in the right transverse/sigmoid sinuses and right basal vein of Rosenthal with evidence of thickening (collateralized) dural sinus walls. 

MR T1-w post contrast only
1. Persistent intraluminal thrombosis remains in the vein of Galen/straight sinus junction, straight sinus, right channel of the torcula and all of the transverse sinus. There is partially recanalized clot in the mesial segment of the left transverse sinus. There is expansion and enhancement of the dural sinus walls in the straight sinus and right transverse sinus and in the right lateral tentorial venous confluence, which are then re-routed through the dural wall collateral into the left patent transverse sinus. There is edema in the dorsal thalamus, as seen on prior exams. Whether this represent vasogenic alone or includes post ischemic cytogenic edema is indeterminate. There is evidence of deep medullary and subependymal venous congestion bilaterally.

​MR diffusion
1. Focal, small volume, venous infarction in the right dorsal lateral thalamus. Whether it will proceed to completed infarction or not is indeterminate. The venocapillary pool density in this same area is not absent making it more likely this area will actually undergo tissue infarction.
2. There is lacunar infarction in the right parietal centrum semiovale. Whether this is caused by an arterial or venous thrombosis event is indeterminate. 

MR Flair
1. There is positive FLAIR signal (i.e. post CVT vasogenic edema) in the right thalamus, caudate and basal ganglia. The positve FLAIR signal in the superior vermis may actually be chronic.
2. There is early right lateral ventriculomegaly with increased subependymal edema consistent the hydrocephalus  (internal type).

MR Susceptibility (swi)
1. There is positive SWI blooming artifact (indicating thrombosis) in the right basal vein of Rosenthal and right lateal atrial vein. There is vasodilation of the right mesial occipital cortical veins without blooming artifact to confirm  cortical vein thrombosis. There is moderate grade venous congestion in the deep central venous system bilaterally, but is more prominent on the right than the left. The venous congestion is related to the venous egress block at the vein of Galen/straight sinus junction. Moderate venous congestion is consistent with fair deep venous egress collateral. Deep venous collateral egress routes appear to be mainly through the deep medullary veins and likely some antegrade flow past the apex straight sinus thrombus.

1. There is thrombosis of multiple dural sinuses including the right transverse/sigmoid sinuses and the adjacent right internal jugular vein plus thrombosis of the straight sinus. There is of the deep central veins, the vein of Galen, and the right basal vein of Rosenthal. There is re-routing of venous egress through the left superior sylvian venous complex/sphenoparietal sinus/cavernous sinus and through the left lateral tentorial venous confluence

2. There is venous stasis on SWI in the deep venous system, plus focal, cytogenic edema in the right thalamus consistent with venous ischemia. Whether it will proceed to completed infarction or not is indeterminate, but the venous stasis is usually a precursor of completed venous stroke. 

3. there is evidence of early hydrocephalus, likely on a venous obstruction basis.

1. Acute intraluminal thrombus in dural sinuses, deep central veins, and cortical veins is best seen on the initial screening noncontrast (CT or MR T1-w) studies. Post contrast CT and MR both can obscure the actual intraluminal thrombus, in part because the intrinsic hyperdensity/hyperintensity of the clot can simulate contrast enhancement. Also, contrast in the expanded dural wall can look very similar to a patent vessel lumen.   And finally, there can be capillary ingrowth into a thrombus, which also enhances simulating luminal patency.

2. Evaluation of deep central vein thrombosis is best evaluated on the MR susceptibility (swi) sequence. However, evaluation of superficial cortical vein CVT and dural sinus CVT on SWI is limited by bone (skull) artifact.

3. Grading the severity of the deep central venous system  (into grades 1-4) helps predict patient risk for venous stroke, hemorrhagic transformation, and malignant edema, in cases of ICV, vein of Galen, or straight sinus CVT. The severity of the central venous congestion is a function of the availability of the supra to infratentorial pial collaterals re-routed through the superior sylvian vein pathway and the lateral anastomotic-petrosal vein pathway.

4. Pial, cortical, venous, collateral egress makes use of the local pial veins, the larger regional pial veins, and the pial/dural anastomotic sites (including the vertex venous lacunae, the mesial and lateral tentorial venous confluences, and the sphenoparietal sinus to cavernous sinus connections).

5. Thrombosed dural sinuses employ the venous plexus in the dural sinus walls. The pial/dural connections allow the dural sinuses to empty into major cortical vein pathways, or vice versa. Thus, cerebral cortical veins on one side can pass through the dorsal venous confluence, and exit through opposite side cortical vein pathways. The combination of all these pial/dural and dural wall collateral pathways prevent most cases of extensive CVT to develop venous infarction. As a result, CVT has a more favorable clinical course and clinical outcome than arterial strokes. 

6. In this case, there was chronic venous thrombosis in the right internal jugular vein, which therefore, appeared older than the intercurrent acute dural CVT. Since there is venous CVT of different ages, clinical correlation for underlying hypercoagulable state is recommended.

Watch the included summary video for this instructional clinical case.