Case Notes
History
76 year old male presenting with acute slurred speech, left sided weakness, and left facial droop.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. Hyperacute thrombus in M1 and M2 segments of the Rt. MCA
2. The post-ischemic stroke changes affect the Rt. orbitofrontal artery, the rostral lateral lenticulate perforators, and the anterior portion of the intrasylvian MCA superior-division branch perfusion zones; these involved areas are likely beyond the IV treatment window.
3. The posterior M3 sylvian arterial perfusions zone may have some post ischemic changes, but likely are at least partially spared by pial collateral. The same is true for most of the lateral cortex.
CT Perfusion
CT perfusion evidence of prolonged filling rate (prolonged TTP/MTT) affecting mainly the Rt. lateral orbitofrontal perfusion zone with lesser post ischemic changes in the Rt. lateral basal ganglia (lateral lenticulostriate perforator perfusion zone) and the anterior insular M3 perfusion zones. However, the CBV is only minimally reduced in most areas and is only partially reduced in the right orbitofrontal artery perfusion zone indicating at least reasonable retrograde pial collateralization in most of the area included in the prolonged TTP zone.
CTA Neck
1. Abnormal Rt. cervical carotid with 70% stenosis at carotid bifurcation/proximal ICA area with distal luminal partial collapse. The Rt. ICA lumen becomes very small after the calcified nodular plaque at the posterior genu, and finally terminates before the subclinoidal segment. The Rt. ICA lumen is reconstituted just after the dural ring.
2. Other major cervical arteries have age-related changes without flow-limiting stenoses.
CTA Head
1. Tandem Rt. ICA occlusions. The first is at the intrapetrous ICA segment with reconstitution of the ICA at the dural ring. The anterior vertical segment of the ICA is opacified, but the Rt. M1 secondary stem is occluded just after the exit of the anterior temporopolar artery. The thrombus involving the lateral M1 segment primarily occludes the lateral lenticulostriate perforators. The thrombus involving the Rt. M2 segment primarily occludes the Rt. lateral orbitofrontal artery. All of these sites area at risk of stroke depending on the extent of ultimate pial collateralization.
2. There is shifting of the watershed zone because of the M1 occlusion and hypoplastic Rt. P-com. This combination creates and end-of the-line underperfused secondary stroke in the anterior Rt. insular M3 branch perfusion zone.
3. There is reasonable pial collateral supplying cortical M4 perfusion zones vessels on this initial post contrast head CTA.