53 year old female who presented with acute onset diplopia and imaging evidence of dural sinus thrombosis affecting the torcular herophile, the left mesial transverse sinus, and the parietal segment of the SSS. Patient had evidence of meningitis and right sigmoid region epidural abscess. Patient was treated medically and with a right mastoidectomy. This patient is being reimaged at 10 days after the initial imaging.
 

Noncontrast CT head; MRV of the head; Pre and post contrast T1-w MR; MR diffusion; MR FLAIR

Initial admission imaging Initial imaging at the time of presentation demonstrated right coalescent mastoiditis, evidence of meningitis and dural sinus thrombosis affecting the torcula, left transverse sinus and the parietal segment of the SSS. There was a punctate area positive on both FLAIR and MR diffusion in the left superior vermic area (possible ischemic event). The right sigmoid sinus was partially compressed by a small epidural abscess, but was otherwise patent.
   
CT of the head
1. Acute thrombus has progressed and is now evident in most of the superior sagittal sinus (SSS), the straight sinus, the torcular herophile, the right transverse sinus and the initial segment of the left transverse sinus. The hydrocephalus seen on initial imaging has resolved.
   
CT perfusion: No CT perfusion imaging is available
   
CTV of the neck: No neck CTV imaging was available
   
MRV of the head
1. There are progressive dural CVT changes (compared to the initial MRV) with widespread dural sinus thromboses (SSS, torcula, and both transverse sinuses). The lateral aspect of the left transverse sinus wall is opacified but drains not through its' lumen to the sigmoid sinus, but rather into dural emissary channels. There is no apparent cortical vein thrombosis. The major veins are all patent; the vertex veins interconnect across the midline through the vertex venous lacunae. The pial/dural anastomoses combine with expanded dural wall venous plexes, and opened emissary venous channels to provide the dominant means of cerebral venous egress in this case, where there is thrombosis of both sigmoid sinuses.
   
Post contrast head CT (venocapillary pool analysis): No delayed post contrast CT was available
   
Pre and post contrast T1-w MR
1. Multiple dural sinus thromboses, as above, without cortical vein occlusions, and without venous infarction (the MR-diffusion is now negative in the left superior vermis).
2. Reasonably functional collateral venous drainage is present utilizing expansion of the dural wall venous plexes, the left lateral tentorial venous confluence connected to the superior sylvian venous plexus egress route. The major venous egress routes for the deep central and subependymal veins appear through supra to infratentoral connections through the superior vermic vein and LAM collaterals ultimately draining into the petrosal veins. The minimal evidence of persistently raised CSF pressure. There are expected post operative changes in the right mastoid area.
   
MR Diffusion
1. The MR diffusion is now negative with no positive signal in the left superior vermis to confirm a completed stroke in this area.
   
MR Flair
1. Progressive dural sinus thromboses now exhibit positive FLAIR signal in the SSS and the right transverse/sigmoid sinuses and right high cervical IJ vein. There is persistent, unchanged positive FLAIR signal in the right otomastoid region, as expected. There is resolution of the prior evidence of active meningitis. There is resolution of the subependymal edema;  there is no parenchymal vasogenic edema remaining in the left superior vermis. Optic hydrops is the only evidence that the dural sinus thrombosis has raised intracranial CSF pressure.
   
MR Susceptibility: No MR susceptibility imaging was available.

1. S/P right otomastoidectomy and removal of the epidural abscess. Likewise, the features of acute meningitis have improved.

2. The observable thrombus in the dural sinuses has increased to now involve the right transverse sinus and the distal half of the superior sagittal sinus.

3. The venous collaterals remain fully functional with evidence of brain swelling, nor venous infarction, nor hydrocephalus. The rostral cerebellar positive DWI signal, seen previously, has resolved.

1. Hyperintensity on a noncontrast T1-w MR indicates the thrombus now contains met-Hgb, which usually begins after  4-6 days. In this case, there were no noncontrast head CT or T1-w MR on the initial imaging with which to compare the current followup imaging in order to determine progression. Intraluminal thrombus can be detected on post contrast CT or MR exams, but, less well, for a variety of reasons. Hence, the noncontrast exams (especially CT) are helpful in detecting hyperacute thrombus in the first place. The MR flair does demonstrate positve signal in some of the sites of thrombosis, but not all, making it less helpful.

2. The positive MR flair and MR diffusion (indicating an acute ischemic event, as was found in the left superior vermis) on the initial MR -diffusion exam, is now negative on this second followup MR-diffusion exam. This is consistent with a transient ischemic event, which did not progress to completed infarction.  The most likely cause of the positive diffusion was thrombus in the left superior vein complex, which quickly recanalized. 

3. Following medical therapy (for acute meningitis) the positive FLAIR signal along the cortical surfaces has returned to normal; this is confirmation of a definite positive response to therapy.

4. Head MRV and the post contrast T1-w MR exam both exhibit all the expected features of multicentric dural sinus CVT with functional venous collateral egress, in this case, through very complex venous re-routing. There is no venous egress through the sigmoid sinuses to the internal jugular veins. Therefore, venous egress has utilized multiple pial/dural connections and expanded intradural wall venous plexes to reach the left superior sylvian vein-cavernous sinus egress pathway, and to a lesser extent, transcranial emissary venous collateral pathways. These routes of venous egress have been sufficiently effective to prevent parenchymal edema and to keep the ICP at only minimally elevated levels. The deep venous system egress utilized supra to infratentorial pial collaterals for venous egres (superior vermic and LAM-petrosal venous routes); these have been effective, since there is no appreciable centronuclear brain edema.

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