Case Notes
History
81 year old female presenting with acute onset mental status change, dizziness, nausea, and gait imbalance.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
CT Head1. Hyperdense thrombus is evident in the distal basilar artery extending into the left P1 PCA segment.
2. Multiple recent strokes (readily apparent cytogenic edema sites) involving Lt. PICA and both P4 segments of the PCA were evident on noncontrast CT placing these ischemic events outside the hyperacute treatment timeline on the right and within the timeline on the left. There is an evolving older left PICA stroke. There is parenchymal hypdensity in the deep cerebellar watershed zones, which could be recent ischemia or chronic age-related ischemic demyelination. It is likely there has been recent thrombus in the intradural vertebral artery initially occluding the left PICA, which has then undergone clot lysis with distal secondary embolization to downstream arteries.
CT Perfusion
1. Known acute thrombus in distal basilar artery
2. Focal completed stroke is evident in Lt. PICA perfusion area and early stroke in the Lt. mesial occipital P4-PCA perfusion zone. Reperfusion (increased CBV & CBF) is evident in the Lt. occipital Ischemic zone.
CTA Neck
1. Focal left vertebral artery stenosis without intraluminal soft clot; estimated stenosis is 50% by NASCET & physiologic criteria. This stenosis could be related to an atherosclerotic plaque or from recanalization of a recent thrombus.
2. Occluded distal mesial cerebellar hemispheric branches off the Lt. PICA. The left PICA origin is present but reduced in size consistent with recanalization of a prior thrombus.
CTA Head
Focal intraluminal thrombus is present in the distal basilar artery segment. It produces a partial luminal narrowing of the distal segment basilar and Rt. P1 segment. There is persistent antegrade blood flow in the basilar artery including filling of the basilar tip and its thalamic perforators.
There is proximal stenosis of the Rt. PCA initial segment with limited filling of the distal Lt. PCA branches.
The circle of Willis is complete allowing the P-com’s to collateralize the right PCA’s. The distal P4 trunk arteries are well opacified on the right but are less so on the left (likely in process of clot lysis and recanalization). Arteries are patent bilaterally in the areas of post ischemic cytogenic edema.
Distal Lt. PICA distal branches are partially collateralized from ipsilateral AICA. The mesial left PICA cerebellar hemispheric arteries are not opacified at all.