Case Notes
History
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 therapy.Exam
Post contrast T1-w MR
Purpose
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 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
CT headAcute 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. Patient has known von-Hippel Lindau syndrome and has had prior treatment of a hemanioblastoma leaving moderately advanced cerebellar atrophy.
CT perfusion
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. 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.
CTA of the neck
There is thrombosis (likely chronic) of the right cervical internal jugular vein and the right sigmoid/transverse sinuses.
CTA of the head
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 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. 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.
Delayed post contrast CT Venocapillary pool analysis
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. 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.