16 year old female presenting with a severe headache, nausea and vomiting. Patient had photophobia but had no focal complaints nor findings on exam. Patient was on birth control.
 

Noncontrast CT head; CTA of the head; Delayed post contrast head CT; Pre and/or post contrast T1-w MR; MR diffusion; MR FLAIR; MR swi Followup exams: head CTV, MR T1-w, MR dwi, MR swi

Noncontrast head CT
1. Acute thrombosis is evident within the posterior (parietal/occipital) segments of the superior sagittal sinus extending into the torcular herophile and the straight sinus.   There is no apparent cortical or deep central vein CVT.
   
CT perfusion: No CT perfusion is available

CTV of the neck: No CTV neck is available
   
CTV of the head
1. Evidence of partial recanalization of dural sinus thromboses, which include the parietal-occipital segments of the SSS, the torcular herophile, the initial segment of the transverse sinuses, and the straight sinus. Multiple effective routes of collateral venous egress are present, as listed above. There is also some antegrade venous blood flow after partial recanalization.
   
Post contrast head CT (venocapillary pool analysis)
1. Dural sinus thrombosis is evident affecting the distal SSS, the straight sinus, the torcula, and both mesial segments transverse sinuses proximal to the lateral tentorial venous confluences. There is moderate venous congestion in the deep central venous system. The venous congestion accounts for the size effacement of the upper third ventricle.
2. There is no evidence of venous stroke nor hemorrhagic conversion.
   
Noncontrast T1-w  MR
1. There is evidence of recent thrombus within the distal SSS, straight sinus, torcula, and initial transverse sinuses. The age of the thrombus is acute, since the clot evolution has not yet change into the met-hemoglobin phase (which would appear hyperintense).
2. There is evidence of deep central venous congestion now affecting the deep medullary veins indicating at least moderate venous congestion. There is no hemorrhagic conversion nor acute hydrocephalus nor clear evidence of optic hydrops.
   
MR diffusion is negative for venous stroke.
   
MR flair
1. There is some FLAIR abnormality in the vein of Galen, the apex of the straight sinus, and within the left channel within the torcula consistent with recent thrombus. However, many areas of known thrombus appear as flow voids and potential dural sinus patentcy. 
2. There is no subependymal edema to confirm early hydrocephus.
3. There is no parenchymal edema in the centronuclear structures. 

MR susceptibility
1. There is moderate-grade venous congestion in the deep central vein system (both subependymal veins, ICV's and vein of Galen) secondary to the venous egress block within the straight sinus and beyond. There is physiologic venous vasodilation of cortical veins in both cerebral hemispheres reflecting re-routing effects; there is no evidence of cortical vein occlusions.

1. Acute thrombosis of the distal superior sagittal sinus, the torcula, and the straight sinus. There is fully functional venous collateralization via collateral pial veins, collaterals in the dural sinus walls and the pial-dural venous confluences.

2. There is no brain edema, venous ischemia, nor hydrocephalus despite the venous egress blocks, because of the venous collateralization.

3. The follow-up CT venogram demonstrated recanalization of all the dural sinuses, but not the torcula. However, the torcula collateralization remains functional.

1. This case illustrates the functional re-routing pathways of cortical venous egress in the context of distal SSS, mesial transverse, and torcular dural sinus CVT. Collateralized, dilated, cortical veins flow retrograde in mutliple directions. They flow into the superior sylvian vein complex and then out through the cavernous sinus; they flow retrograde into the vein of Labbe' and then into the lateral tentorial venous confluence before finally passing into the lateral segments of the patent transverse/sigmoid sinuses

2. This case illustrates how the expansile venous plexus in the wall of the dural sinuses prevents obstruction to venous egress, despite the presence of intraluminal dural sinus clot. In essence, the dural sinus wall venous plexus provides an immediate "jump graft" for the occluded dural segment CVT. The dural wall collateral can then drain into patent sinuses or patent major veins at the pial/dural anastomotic sites. Or they can drain through emissary venous channels to extracranial veins.

3. This case illustrates the two major available supra to infratentorial pial collateral pathways available in the context of vein of Galeln or straight sinus venous occlusion. These pathways include: 1. the superior vermic vein complex pathway, and 2. the lateral anastomotic vein (LAM) to petrosal venous plexus pathway. A third pathway exists through the basal vein of Rosenthal into superficial veins along the ventral side of the mesencephalon, pons and hypothalamus. In this case, these collateral pathways were only partially effective leaving moderate deep central venous congestion.

Watch the included summary video for this instructional clinical case.