Case Notes
History
51 year old female presenting with an acute left facial droop, left side weakness, and mental status change. Patient was able to be seen in the ER within 1 to 1.5 hours after the onset of symptoms.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 HeadRt. parapharyngeal space is abnormal with enlarged high cervical ICA with hyperdensity consistent with an acute high cervical ICA dissection.
Apparent recent, but not hyperacute Rt. parietal subcortical ischemic event.
CT Perfusion
Reduced arterial circulation rate in the Rt. cerebral intradural ICA watershed perfusion zone in the usual centrum semiovale. There is evidence of good pial collateral resulting in normal cortical CBV. Distinct site of actual infarction (low CBV) is not detected. The right ICA dissection was evident on the included post contrast head CTA.
CTA of the Neck
1. Rt. mid and high cervical ICA acute dissection w/ patent limited antegrade blood flow beyond the 70% stenosis.
2. Early features of FMD of the high cervical left ICA.
3. Incomplete circle of Willis (posterior ring) because of very hypoplastic P-com’s.
CTA of the Head
1. Rt. mid and high cervical and intrapetrous ICA acute dissection w/ flow restriction limiting (but not occluding) antegrade blood flow. There are hypoplastic P-coms causing the posterior circle of Willis to be incomplete. Thus, the pial collateral is better in the frontal and temporal regions than in the parietal region, which has shifted the watershed toward the posterior parietal and MCA-PCA watershed areas. There are likely two ischemic events; one is older and the other more recent.
2. Early features of FMD of the high cervical left ICA.