Case Notes
History
72 year old male with transient left sided weakness; history of diffuse vascular disease; evaluate for arterial stenosis.Exam
2 minute delayed post contrast head CTA with: analysis of pial collateralization, plus a comparative analysis of the CT density within the venocapillary pool (using the initial and delayed post contrast CTA’s), plus an analysis of venous egress. This part of the CTA is referred to as either the delayed post contrast CTA or the 2nd pass CTA, since it is performed after the 2nd contrast bolus. It has the benefit of recirculation effects, and twice the contrast load, as the initial post contrast head CTA. The delayed post contrast CTA is used to detect distal pial collateralization and to assess the CT-density within the parenchymal venocapillary pool, which provides the best CTA evidence of ischemic injury.
Purposes
1. To identify any, and all, sites of intracranial afferent block (either occlusion or combination of tandem stenosis and an incomplete circle of Willis);
2. To determine whether the observed pial collateral gap observed on the CTA head finally reaches the proximal thrombus on the delayed post contrast CTA head (considered fair collateral). However, this tissue may still be at risk for ischemic injury;
3. If the a pial collateral gap remains on the delayed post contrast head CTA, then tissue within the gap will likely be in the dense ischemic core and become a completed stroke (ischemic cascade plus glutamate cascade leading to liquefactive necrosis or sequestered infarct or both).
4. Given there is observably reasonable pial collateral, it does NOT ensure that there is perfusion of the underlying tissue. To assess whether the existing pial collateral actually perfuses the underlying brain parenchyma, a comparative analysis is made between the CT contrast density within the venocapillary pool in the affected region on the initial post contrast CTA with the CT density on the delayed post contrast CTA, and that is compared to unaffected comparable region on the contra lateral side. At-risk tissue (ischemic penumbra) will exhibit a partial rise in CT density between the 1st and the 2nd post contrast CTA, but it will not reach normal range compared to unaffected brain. Tissue that shows little or no rise in CT density in the venocapillary pool will be within the dense ischemic core. The areas of significantly reduced & absent parenchymal contrast CT density are at higher risk of hemorrhagic conversion upon reperfusion (spontaneous or therapeutic). Note: analysis of the CT density in the venocapillary pool and CT perfusion are both approximations of tissue actual perfusion based on changes in concentration of the contrast media in tissue over time. Thus, an initial short-term high depth-duration oligemic event can occur, initiating the ischemic cascade. But the afferent block can quickly clear, which means tissue injury can be initiated, but the antegrade blood flow is restored. In this circumstance, tissue injury will have occurred, but the restroration of pial blood flow will appear as normal or near normal on both the CT perfusion and the CT density within the venocapillary pool. Thus, both the CTA and CT perfusion may underestimate tissue injury, which is why the stroke protocol MR is of value, since actual tissue injury will always show up, in some fashion, on MR diffusion sequences.
5. Given there is an ICA stenosis/occlusion, is there effective EC-IC collateral;
6. In the context of restricted intradural afferent arterial blood flow obstruction (in the absence of a primary stem occlusion), has regional hypoperfusion produced oligemia in the expected anastomotic border zones producing a watershed stroke pattern;
7. In the context of an ICA thrombosis, tandem stenoses, incomplete portions of circle of Willis, or a combination of these, is there a shift in the location of the anastomotic border zones such that oligemia produces an end-of the-line watershed stroke pattern. Low flow ischemia within the end-of the-line portion of a shifted watershed can account strokes that involve tissue not primarily affected by the thrombus.
8. To evaluate the state of venous egress, at least for the major veins (note: SWI is the most effective of assessing flow in the deep parenchymal medullary veins).
Purposes
1. To identify any, and all, sites of intracranial afferent block (either occlusion or combination of tandem stenosis and an incomplete circle of Willis);
2. To determine whether the observed pial collateral gap observed on the CTA head finally reaches the proximal thrombus on the delayed post contrast CTA head (considered fair collateral). However, this tissue may still be at risk for ischemic injury;
3. If the a pial collateral gap remains on the delayed post contrast head CTA, then tissue within the gap will likely be in the dense ischemic core and become a completed stroke (ischemic cascade plus glutamate cascade leading to liquefactive necrosis or sequestered infarct or both).
4. Given there is observably reasonable pial collateral, it does NOT ensure that there is perfusion of the underlying tissue. To assess whether the existing pial collateral actually perfuses the underlying brain parenchyma, a comparative analysis is made between the CT contrast density within the venocapillary pool in the affected region on the initial post contrast CTA with the CT density on the delayed post contrast CTA, and that is compared to unaffected comparable region on the contra lateral side. At-risk tissue (ischemic penumbra) will exhibit a partial rise in CT density between the 1st and the 2nd post contrast CTA, but it will not reach normal range compared to unaffected brain. Tissue that shows little or no rise in CT density in the venocapillary pool will be within the dense ischemic core. The areas of significantly reduced & absent parenchymal contrast CT density are at higher risk of hemorrhagic conversion upon reperfusion (spontaneous or therapeutic). Note: analysis of the CT density in the venocapillary pool and CT perfusion are both approximations of tissue actual perfusion based on changes in concentration of the contrast media in tissue over time. Thus, an initial short-term high depth-duration oligemic event can occur, initiating the ischemic cascade. But the afferent block can quickly clear, which means tissue injury can be initiated, but the antegrade blood flow is restored. In this circumstance, tissue injury will have occurred, but the restroration of pial blood flow will appear as normal or near normal on both the CT perfusion and the CT density within the venocapillary pool. Thus, both the CTA and CT perfusion may underestimate tissue injury, which is why the stroke protocol MR is of value, since actual tissue injury will always show up, in some fashion, on MR diffusion sequences.
5. Given there is an ICA stenosis/occlusion, is there effective EC-IC collateral;
6. In the context of restricted intradural afferent arterial blood flow obstruction (in the absence of a primary stem occlusion), has regional hypoperfusion produced oligemia in the expected anastomotic border zones producing a watershed stroke pattern;
7. In the context of an ICA thrombosis, tandem stenoses, incomplete portions of circle of Willis, or a combination of these, is there a shift in the location of the anastomotic border zones such that oligemia produces an end-of the-line watershed stroke pattern. Low flow ischemia within the end-of the-line portion of a shifted watershed can account strokes that involve tissue not primarily affected by the thrombus.
8. To evaluate the state of venous egress, at least for the major veins (note: SWI is the most effective of assessing flow in the deep parenchymal medullary veins).
Prior Study
Non-Contrast Head CTThere is a probable left high-cervical ICA acute intraluminal thrombus.
There are expected age related changes and a chronic post-ischemic lacunar infarct in the mesial Lt. thalamus.
No hyperacute post ischemic changes are evident.
CT Perfusion
There are changes consistent with Lt. ICA afferent obstruction (occlusion or high-grade stenosis) which slows the left hemispheric blood flow but has not significantly reduced in the CBV or CBF in either the left ACA or MCA or mesial P4 perfusion zones.
There is reduced perfusion in the left MCA-PCA watershed zone with reduced CBV/CBF/MTT.
There is delayed filling rate in the Lt. PICA perfusion zone, but the increased CBV indicates there is functional pial collateralization.
CTA of the Neck
1. There are tandem Rt. carotid stenoses, the combination of which, are likely flow-limiting. However, the distal right ICA appears to fill normally.
2. There is diffuse atherosclerotic ulcerative plaque disease in left common carotid; there is no intimal dehiscence, no intraluminal soft clot, nor high grade stenosis.
3. Lt. ICA is occluded in its’ cervical segment just above the carotid sinus; there is limited functional EC-IC collateralization through the ophthalmic collateral with patent but reduced size of the intradural left ICA.
4. The Lt. vertebral artery has an origin stenosis and becomes completely occluded at the dural ring; The left intradural vertebral segment and the Lt. PICA origin are both occluded, but the distal PICA branches appear to fill in retrograde manner from the Lt. AICA. The Rt. vertebral is occluded in its’ proximal segment but is reconstitued by costocervical collaterals at the C3 level. The Rt. PICA origin is occluded but distal branches fill in retrograde from the Rt. AICA.
CTA of the Head
1. There is a right proximal vertebral artery occlusion, which is reconstituted at C3 and is patent beyond this point. However, the right PICA is occluded at its origin. Its’ distal branches fill retrograde from the right AICA. The patent right intradural vertebral supplies the left intradural vertebral and left PICA in a retrograde manner (the left vertebral was occluded at the dural ring).
2. There is occlusion of the Lt. cervical ICA just after the carotid sinus. EC-IC collateral reconstitute the Lt. ICA in the cavernous and ophthalmic ICA segments. Distal carotid branch arterial filling on the left is delayed and cannot be fully assessed until the delayed post contrast head CTA.
3. Cerebral arteries on the right appear fully opacified, as are the pial arteries in the posterior fossa on this initial post contrast head CTA. There is a distal basilar non flow-limiting stenosis.