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
CTA of the head
Purpose
Assess for evidence of dural sinus thrombosis and for collateralization of the dural sinus wall including evidence of transcranial emissary veins.
Assess for evidence of cortical vein thrombosis. In many cases of cortical vein thrombosis the diagnosis is made by absence of veins compared to the opposite side. Additionaly, cortical vein & dural sinus occlusion can be inferred by the appearance of the collateral veins and reversed filling pattern. This inability to easily perceive cortical vein thrombotic occlusion as an absence of a vein(s) accounts for its under-reporting.
Assess for re-routing of the venous egress through reversed flow through other pial veins or through the pial/dural interconnections (vertex venous lacunae, mesial and/or lateral tentorial confluences, and the cavernous sinus).
Assess for exaggerated cortical vein prominence that is usually the result of a dural AV fistula in conjunction with dural sinus occlusion. It is often difficult to determine whether the AV fistula is the result of the dural sinus thrombosis collateralization, or whether the AV fistula occurs first, but elevated venous filling pressure causes stasis of flow and secondary dural sinus thrombosis.
Purpose
Assess for evidence of dural sinus thrombosis and for collateralization of the dural sinus wall including evidence of transcranial emissary veins.
Assess for evidence of cortical vein thrombosis. In many cases of cortical vein thrombosis the diagnosis is made by absence of veins compared to the opposite side. Additionaly, cortical vein & dural sinus occlusion can be inferred by the appearance of the collateral veins and reversed filling pattern. This inability to easily perceive cortical vein thrombotic occlusion as an absence of a vein(s) accounts for its under-reporting.
Assess for re-routing of the venous egress through reversed flow through other pial veins or through the pial/dural interconnections (vertex venous lacunae, mesial and/or lateral tentorial confluences, and the cavernous sinus).
Assess for exaggerated cortical vein prominence that is usually the result of a dural AV fistula in conjunction with dural sinus occlusion. It is often difficult to determine whether the AV fistula is the result of the dural sinus thrombosis collateralization, or whether the AV fistula occurs first, but elevated venous filling pressure causes stasis of flow and secondary dural 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.