Hyperacute Venous Stroke II - Clinical Case Summary
Hyperacute Venous Stroke II - Clinical Case Summary
Hyperacute Venous Stroke II - Clinical Case Summary
SummaryHistory
56 year old male presented with acute onset right facial droop, right arm weakness, and both difficulty speaking and comprehending
Exams performed
Noncontrast head CT; CT perfusion; CTA of the neck including the head with opacification of the dural sinuses; CTA of the head; Post contrast CT of the head for venocapillary pool analysis; MR noncontrast T1-w sequence; MR diffusion (dwi/adc) sequences; MR flair; MR susceptibility (swi) sequence
Prior available imaging reports
Non-Contrast CT Head
1. Focal left retrosylvian vasogenic edema matching the vein of Labbe' venous egress territory. Whether there is cytogenic edema in this area representing venous stroke remains indeterminate. There is acute thrombus in multiple branches of the left vein of Labbe' without apparent concurrent left transverse sinus thrombosis. There is no hemorrhagic conversion.
CT Perfusion
1. There is a focal area of reduced brain perfusion in the left retrosylvian area corresponding to oligemia resulting from thrombosis of the left vein of Labbe' (evident on the noncontrast head CT).There is both collateral zone physiologic hyperemia in the collateral zone surrounding the retrosylvian oligemic area plus evidence of re-routing of venous egress into the left superior sylvian vein complex and left lateral tentorial venous confluence. This accounts for the increased blood volumn (increased CBV) in the cavernous sinus and left transverse sinus.
CTA of the Neck
1. Negative for venous occlusion; negative for otomastoid or paranasal sinus infection/tumor. The CTA of the neck included the head with good opacification of the major dural sinuses, all of which were patent.
CTA of the Head
1. CTA head evidence of re-routed venous egress into the lateral tentorial venous confluence. The cortical veins are not well seen on either sided, because of the timing of a CTA versus a CTV. No arterial stenosis nor occlusion was evident.
Post contrast head CT (venocapillary pool analysis)
1. There is a 2 cm. focal area of virtually absent CT density in the venocapillary pool within the left retrosylvian area plus nonfilling of the vein of Labbe'; findings are consistent with venous stroke. There is no evidence of left transverse sinus thrombosis, nor evidence of arterial occlusion in the same area. The dominant routes for re-routing of the remain retrosylvian veins is into the cavernous sinus via left superior sylvian vein/sphenoparietal sinus route and into the left lateral tentorial venous confluence/left transverse sinus route.There is altered blood brain barrier with leak of contrast into the area of vasogenic edema (vein of Labbe' oligemic zone).
MR pre and post contrast T1-w sequence
1. There are focal changes in the left retrosylvian area consistent with thrombosis of the vein of Labbe' and evidence of focal tissue edema and cortical laminar necrosis (completed venous infarction).
2. The area of ischemic penumbra surrounding the dense ischemic core exhibits features of dysautoregulation, including minimal contrast leak, plus venous congestion in both cortical and deep temporal parenchymal medullary veins.
MR Diffusion
1. Acute, venous related, cortical infarction is evident in the left lateral retrosylvian regions. Most of the area of vasogenic edema (ischemic penumbra) evident on prior imaging is not MR diffusion positive.
MR Flair
1. FLAIR is positive in the site of the left lateral retrosylvian cortical laminar necrosis, which represent s the dense ischemic core of this venous infarction. FLAIR is also positive for vasogenic in the region surrounding the site of dense ischemic core, and regional dural thickening from pial/dural venous collateral egress.
MR susceptibility
1. There is SWI evidence of abnormal subcortical parenchymal density in tissue adjacent to the left retrosylvian cortical necrosis. This change likely represents sequestered blood in the venocapillary pool and is an indication of venous ischemic tissue injury. There is SWI evidence of venous dysautoregulation in the ischemic penumbra surrounding the dense ischemic core with pial vein dilatation plus fuzzy margins, as well as hyperemia in the collateral left superior sylvian vein complex where veins are dilated but margins are sharply delimited. Thus, venous post ischemic dysautoregulation is also similar to the ischemic penumbra dysautoregulation after arterial ischemia.
1. Focal left retrosylvian vasogenic edema matching the vein of Labbe' venous egress territory. Whether there is cytogenic edema in this area representing venous stroke remains indeterminate. There is acute thrombus in multiple branches of the left vein of Labbe' without apparent concurrent left transverse sinus thrombosis. There is no hemorrhagic conversion.
CT Perfusion
1. There is a focal area of reduced brain perfusion in the left retrosylvian area corresponding to oligemia resulting from thrombosis of the left vein of Labbe' (evident on the noncontrast head CT).There is both collateral zone physiologic hyperemia in the collateral zone surrounding the retrosylvian oligemic area plus evidence of re-routing of venous egress into the left superior sylvian vein complex and left lateral tentorial venous confluence. This accounts for the increased blood volumn (increased CBV) in the cavernous sinus and left transverse sinus.
CTA of the Neck
1. Negative for venous occlusion; negative for otomastoid or paranasal sinus infection/tumor. The CTA of the neck included the head with good opacification of the major dural sinuses, all of which were patent.
CTA of the Head
1. CTA head evidence of re-routed venous egress into the lateral tentorial venous confluence. The cortical veins are not well seen on either sided, because of the timing of a CTA versus a CTV. No arterial stenosis nor occlusion was evident.
Post contrast head CT (venocapillary pool analysis)
1. There is a 2 cm. focal area of virtually absent CT density in the venocapillary pool within the left retrosylvian area plus nonfilling of the vein of Labbe'; findings are consistent with venous stroke. There is no evidence of left transverse sinus thrombosis, nor evidence of arterial occlusion in the same area. The dominant routes for re-routing of the remain retrosylvian veins is into the cavernous sinus via left superior sylvian vein/sphenoparietal sinus route and into the left lateral tentorial venous confluence/left transverse sinus route.There is altered blood brain barrier with leak of contrast into the area of vasogenic edema (vein of Labbe' oligemic zone).
MR pre and post contrast T1-w sequence
1. There are focal changes in the left retrosylvian area consistent with thrombosis of the vein of Labbe' and evidence of focal tissue edema and cortical laminar necrosis (completed venous infarction).
2. The area of ischemic penumbra surrounding the dense ischemic core exhibits features of dysautoregulation, including minimal contrast leak, plus venous congestion in both cortical and deep temporal parenchymal medullary veins.
MR Diffusion
1. Acute, venous related, cortical infarction is evident in the left lateral retrosylvian regions. Most of the area of vasogenic edema (ischemic penumbra) evident on prior imaging is not MR diffusion positive.
MR Flair
1. FLAIR is positive in the site of the left lateral retrosylvian cortical laminar necrosis, which represent s the dense ischemic core of this venous infarction. FLAIR is also positive for vasogenic in the region surrounding the site of dense ischemic core, and regional dural thickening from pial/dural venous collateral egress.
MR susceptibility
1. There is SWI evidence of abnormal subcortical parenchymal density in tissue adjacent to the left retrosylvian cortical necrosis. This change likely represents sequestered blood in the venocapillary pool and is an indication of venous ischemic tissue injury. There is SWI evidence of venous dysautoregulation in the ischemic penumbra surrounding the dense ischemic core with pial vein dilatation plus fuzzy margins, as well as hyperemia in the collateral left superior sylvian vein complex where veins are dilated but margins are sharply delimited. Thus, venous post ischemic dysautoregulation is also similar to the ischemic penumbra dysautoregulation after arterial ischemia.
Overall impression
1. Acute thrombosis of the left vein of Labbe' with venous infarction (with laminar necrosis) in the posterolateral aspect of the left temporal lobe.
2. There is no evidence of left otomastoid infection nor left transverse sinus thrombosis present as a cause for the isolated left vein of Labbe' thrombosis.
2. There is no evidence of left otomastoid infection nor left transverse sinus thrombosis present as a cause for the isolated left vein of Labbe' thrombosis.
Lessons to be learned
1. The retrosylvian (brain) region affected by a vein of Labbe' stroke can simulate an arterial stroke involving the distal MCA, or the MCA-PCA watershed zone. Hence, analysis of any focal retrosylvian edema needs to consider arterial, venous, and watershed types of stroke. Other pathology can also be considered in this area, including complications of otomastoiditis with cerebritis or abscess in the ventral temporal lobe; these abscesses are invariably spread via vein of Labbe' phlebothrombosis.
2. Detection of vein of Labbe' thrombus on noncontrast head CT requires using a wide window viewing, since the hyperdense vein thrombus can be obscurred by adjacent bone density of the skull.
3. The actual venous-stroke zone can have the same appearance on MR T1-w, MR diffusion, and MR swi sequences, as do arterial based strokes; the completed stroke zone evolves in the same manner regardless if the stroke has an arterial or venous cause. In this case the MR swi is positive in both the site of cortical laminar necrosis, and in the adjacent tissue where there a nonspecific (background) positive MR swi signal in tissue; both of these likely represent forms of sequestered infarction (completed parenchymal stroke without reperfusion).
4. Both the post contrast CT and the post contrast T1-w sequences can detect venous dysautoregulation in CVT resulting from significant oligemia. This is based on evidence of parenchymal contrast leak into the the affected ischemic core and/or the ischemic penumbra. Venous dysautoregulation also exhibitis both dilatation (hyperemia) of the cortical or deep central veins or even the deep medullary veins, plus extra-axial contrast leak into the local subarachnoid spaces. There is often some local tissue edema. These findings are similar to the dysautoregulation associated with in arterial ischemia.
5. The re-routing of venous egress, a secondary sign of dural sinus and cortical vein (as in this case) CVT, can even be detect on head CTA. The findings will be more subtle than on CTV or MRV.
2. Detection of vein of Labbe' thrombus on noncontrast head CT requires using a wide window viewing, since the hyperdense vein thrombus can be obscurred by adjacent bone density of the skull.
3. The actual venous-stroke zone can have the same appearance on MR T1-w, MR diffusion, and MR swi sequences, as do arterial based strokes; the completed stroke zone evolves in the same manner regardless if the stroke has an arterial or venous cause. In this case the MR swi is positive in both the site of cortical laminar necrosis, and in the adjacent tissue where there a nonspecific (background) positive MR swi signal in tissue; both of these likely represent forms of sequestered infarction (completed parenchymal stroke without reperfusion).
4. Both the post contrast CT and the post contrast T1-w sequences can detect venous dysautoregulation in CVT resulting from significant oligemia. This is based on evidence of parenchymal contrast leak into the the affected ischemic core and/or the ischemic penumbra. Venous dysautoregulation also exhibitis both dilatation (hyperemia) of the cortical or deep central veins or even the deep medullary veins, plus extra-axial contrast leak into the local subarachnoid spaces. There is often some local tissue edema. These findings are similar to the dysautoregulation associated with in arterial ischemia.
5. The re-routing of venous egress, a secondary sign of dural sinus and cortical vein (as in this case) CVT, can even be detect on head CTA. The findings will be more subtle than on CTV or MRV.
Recommendations
Watch the included summary video for this instructional case.