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
CT perfusion
Purpose
Recognize the effects of venous collateral egress hyperemia, especially in dural sinus thrombosis. The effects of patent venous collaterals dominates CT perfusion in CVT. High flow collateral routes are evident on CT perfusion, as sites of rapid (high flow) TTP and MTT; CBV and CBF are usually within normal range. Cortical vein egress abnormalities are often subtle, except for the internal cerebral veins.
Recognize evidence of the actual venous stroke (focal low or absent CBV); the stroke zone, however, is often obscured by the changes related to collateral venous egress or parenchymal vasogenic edema making detection of venous stroke less evident in venous stroke compared to arterial stroke.
Recognize dural CVT by the effect of dural wall collateralization (increase TTP and normal or low CBV) or by the lack of collateralization and lack of flow (absent TTP and absent CBV).
Recognize CT perfusion changes of pial hyperemia associated with CVT. This can occur on either side of a dural sinus or on just one side because of compartmentalized channels within a dural sinus.
The included CTA (included in our CVT protocol) mainly images arterial filling and delayed opacification may simulate CVT.
Be aware that intercurrent seizure activity can produce focal high flow regions. This is especially true if there has been hemorrhagic conversion. In this case, the venous egress is into expected dural sinuses rather than altered pathways.
Purpose
Recognize the effects of venous collateral egress hyperemia, especially in dural sinus thrombosis. The effects of patent venous collaterals dominates CT perfusion in CVT. High flow collateral routes are evident on CT perfusion, as sites of rapid (high flow) TTP and MTT; CBV and CBF are usually within normal range. Cortical vein egress abnormalities are often subtle, except for the internal cerebral veins.
Recognize evidence of the actual venous stroke (focal low or absent CBV); the stroke zone, however, is often obscured by the changes related to collateral venous egress or parenchymal vasogenic edema making detection of venous stroke less evident in venous stroke compared to arterial stroke.
Recognize dural CVT by the effect of dural wall collateralization (increase TTP and normal or low CBV) or by the lack of collateralization and lack of flow (absent TTP and absent CBV).
Recognize CT perfusion changes of pial hyperemia associated with CVT. This can occur on either side of a dural sinus or on just one side because of compartmentalized channels within a dural sinus.
The included CTA (included in our CVT protocol) mainly images arterial filling and delayed opacification may simulate CVT.
Be aware that intercurrent seizure activity can produce focal high flow regions. This is especially true if there has been hemorrhagic conversion. In this case, the venous egress is into expected dural sinuses rather than altered pathways.
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.