Case Notes
History
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.Exam
MR T1-w sequences pre and post contrast
Purpose
Assess the noncontrast T1-w MR for hyperintense thrombus in one or more dural sinuses (i.e. the delta sign).
Assess the noncontrast T1-w MR for hyperintense thrombus in one or more pial or deep central veins.
Assess the noncontrast T1-w MR for blood products (SAH, hemorrhagic conversion).
Note: acute thrombus may be hyperintense on T1-w MR, just as it is hyperdense on CT, but it depends on the presence of met hemoglobin. Therefore,thrombi become hyperintense later than hyperdensity on CT. Hyperacute intraluminal thrombus on noncontrast T1 is more often isodense relative to brain but the isodense clot removes the expected flow void (actually a technical saturation effect).
Assess noncontrast T1 MR for venous congestion within the expanded medullary veins due to distal venous egress block.
Assess post contrast T1 sequences for intraluminal dural sinus thrombosis. T1-w post contrast exams, especially with multiplanar reconstruction, can discriminate enhancement in the dural sinus wall collateral from intraluminal (non enhancing) thrombus (i.e. the empty delta sign), when viewed in cross-section.
Assess post contrast T1 sequence for evidence of pial venous collaterals (typically appear serpiginous, hyperemic, drain the wrong way, the vein size changes from being larger next to the dural sinus to being larger at their inception site).
Assess the post-contrast T1 sequence for post ischemic contrast leak (i.e. venous post sichemic dysautoregulation).
Assess the post-contrast T1 sequence for unexpected exaggerated filling of atypical venous egress routes (i.e. filling into the orbits or posterior fossa veins or the nasopharyngeal venous plexus (evidence of re-routing of intracranial venous egress).
Assess for evidence of raised intracranial pressure, which includes evidence of brain swelling from venous congestion, optic hydrops/retroglobal edema, early hydrocephalus, effaced sulci, and possibly mass effects with herniation. These findings fall under the umbrella of CVT related pseudotumor.
Assess for nasopharyngeal/retropharyngeal infection/tumor with skull base extension and possible dural or cavernous sinus thrombosis.
Purpose
Assess the noncontrast T1-w MR for hyperintense thrombus in one or more dural sinuses (i.e. the delta sign).
Assess the noncontrast T1-w MR for hyperintense thrombus in one or more pial or deep central veins.
Assess the noncontrast T1-w MR for blood products (SAH, hemorrhagic conversion).
Note: acute thrombus may be hyperintense on T1-w MR, just as it is hyperdense on CT, but it depends on the presence of met hemoglobin. Therefore,thrombi become hyperintense later than hyperdensity on CT. Hyperacute intraluminal thrombus on noncontrast T1 is more often isodense relative to brain but the isodense clot removes the expected flow void (actually a technical saturation effect).
Assess noncontrast T1 MR for venous congestion within the expanded medullary veins due to distal venous egress block.
Assess post contrast T1 sequences for intraluminal dural sinus thrombosis. T1-w post contrast exams, especially with multiplanar reconstruction, can discriminate enhancement in the dural sinus wall collateral from intraluminal (non enhancing) thrombus (i.e. the empty delta sign), when viewed in cross-section.
Assess post contrast T1 sequence for evidence of pial venous collaterals (typically appear serpiginous, hyperemic, drain the wrong way, the vein size changes from being larger next to the dural sinus to being larger at their inception site).
Assess the post-contrast T1 sequence for post ischemic contrast leak (i.e. venous post sichemic dysautoregulation).
Assess the post-contrast T1 sequence for unexpected exaggerated filling of atypical venous egress routes (i.e. filling into the orbits or posterior fossa veins or the nasopharyngeal venous plexus (evidence of re-routing of intracranial venous egress).
Assess for evidence of raised intracranial pressure, which includes evidence of brain swelling from venous congestion, optic hydrops/retroglobal edema, early hydrocephalus, effaced sulci, and possibly mass effects with herniation. These findings fall under the umbrella of CVT related pseudotumor.
Assess for nasopharyngeal/retropharyngeal infection/tumor with skull base extension and possible dural or cavernous sinus thrombosis.
Prior Study
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 head
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 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.