Hyperacute Arterial Stroke XI - Clinical Case Summary
Hyperacute Arterial Stroke XI - Clinical Case Summary
Hyperacute Arterial Stroke XI - Clinical Case Summary
SummaryHistory
76 year old male presenting with acute slurred speech, left sided weakness, and left facial droop.
Exams performed
CT head; CT perfusion; CTA neck; CTA head; Delayed post contrast head CT for analysis of the venocapillary pool; MR diffusion; MR flair; MR susceptibility
Prior available imaging reports
CT head
1. 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
1. CT perfusion had 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 of the 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 of the 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 the cortical M4 perfusion zones on the initial post contrast head CTA.
Post contrast head CT (venocapillary pool analysis)
1. Known tandem Rt. carotid circuit occlusions in both the extradural ICA segment and the M1/M2 intradural segments. Pial collateral is good on the delayed post contrast CTA with retrograde filling all distal pial arteries and even outlined the thrombus within the M1/2 ICA segments.
2. CT density within the venocapillary pool is within normal limits in most of the areas of post ischemic cytogenic edema clearly evident on the noncontast head CT. The CT density within the venocapillary pool does not quite reach normal limits in the distribution of the Rt. lateral lenticulostriate perfusion zone. This disparity between the noncontrast CT and the venocapillary pool density implies than there has been intercurrent clot lysis with spontaneous reperfusion occurring since the initial ictus event.
3. There is no venous egress restriction, which is a good indication of reasonable transcapillary blood flow at this time.
4. There is minimal evidence of post ischemic dysautoregulation in the Rt. lateral orbitofrontal artery perfusion zone. This is consistent with vascular changes happening following at least partial reperfusion within the 8 hours post ictus.
MR diffusion
1. Diffusion sequence demonstrates positive restriction consistent with ischemia affecting the Rt. lateral orbitofrontal cortex and the Rt. basal ganglia is consistent with primary thrombosis of their arterial supply and primary type of stroke.
2. Positive diffusion in other areas, as the anterior insula and distal M3 cortex are more consistent with an end-of the-line hypoperfusion type of stroke.
3. Mulitple individual (punctate rather than confluent) strokes in the ACA-MCA watershed zones is evidence that these are terminal arterial type of ischemic injuries.
MR Flair
1. FLAIR imaging demonstrates well-delineated cytogenic edema in the Rt. M1-MCA perfusion indicating the stroke-age is currently well outside the treatment window.
2. Residual marginal acute thrombus in the extradural/intracranial segments of the Rt. ICA consistent with recent thrombosis.
MR Susceptibiliy (SWI)
1. Positive SWI for acute thrombus in the Rt. M2 segment.
2. There is a small area of sequestered infarction (SWI signal loss) in caudate head region, but no hemorrhagic conversion.
1. 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
1. CT perfusion had 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 of the 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 of the 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 the cortical M4 perfusion zones on the initial post contrast head CTA.
Post contrast head CT (venocapillary pool analysis)
1. Known tandem Rt. carotid circuit occlusions in both the extradural ICA segment and the M1/M2 intradural segments. Pial collateral is good on the delayed post contrast CTA with retrograde filling all distal pial arteries and even outlined the thrombus within the M1/2 ICA segments.
2. CT density within the venocapillary pool is within normal limits in most of the areas of post ischemic cytogenic edema clearly evident on the noncontast head CT. The CT density within the venocapillary pool does not quite reach normal limits in the distribution of the Rt. lateral lenticulostriate perfusion zone. This disparity between the noncontrast CT and the venocapillary pool density implies than there has been intercurrent clot lysis with spontaneous reperfusion occurring since the initial ictus event.
3. There is no venous egress restriction, which is a good indication of reasonable transcapillary blood flow at this time.
4. There is minimal evidence of post ischemic dysautoregulation in the Rt. lateral orbitofrontal artery perfusion zone. This is consistent with vascular changes happening following at least partial reperfusion within the 8 hours post ictus.
MR diffusion
1. Diffusion sequence demonstrates positive restriction consistent with ischemia affecting the Rt. lateral orbitofrontal cortex and the Rt. basal ganglia is consistent with primary thrombosis of their arterial supply and primary type of stroke.
2. Positive diffusion in other areas, as the anterior insula and distal M3 cortex are more consistent with an end-of the-line hypoperfusion type of stroke.
3. Mulitple individual (punctate rather than confluent) strokes in the ACA-MCA watershed zones is evidence that these are terminal arterial type of ischemic injuries.
MR Flair
1. FLAIR imaging demonstrates well-delineated cytogenic edema in the Rt. M1-MCA perfusion indicating the stroke-age is currently well outside the treatment window.
2. Residual marginal acute thrombus in the extradural/intracranial segments of the Rt. ICA consistent with recent thrombosis.
MR Susceptibiliy (SWI)
1. Positive SWI for acute thrombus in the Rt. M2 segment.
2. There is a small area of sequestered infarction (SWI signal loss) in caudate head region, but no hemorrhagic conversion.
Overall impression
1. The initial CTA demonstrated tandem calcific atherosclerotic stenoses in the right carotid circuit. There is a 70% luminal narrowing of the proximal cervical ICA. There is substantially reduced right ICA size distal to the stenosis, but there is minimal antegrade flow until the subclinoidal right ICA extradural segment where the lumen is totally occluded. The intradural right ICA branches all have retrograde pial and circle of Willis collaterals except for the proximal right M2-MCA segment. This segment is contains acute thrombus. There is no pial-collateral gap. Delayed post contrast CT imaging does demonstrates reduced capillary perfusion in the right orbitofrontal and anterior insular parenchyma.
2. The head MR obtained 24 hours after the CTA demonstrates MR diffusion DWI positivity (T2 shine through) in the distribution of the M2 and anterior M3 branches mainly to the right orbitofrontal and anterior insular and Broca's area. Additionally, there are microinfarctions in the terminal M4 branches to the centrum semiovale. There is lesser involvement in the more posterior insular and parietal cortex. There is only one site of positive restriction on MR diffusion and on SWI that is consistent with completed infarction and that site is just lateral to the right caudate.
2. The head MR obtained 24 hours after the CTA demonstrates MR diffusion DWI positivity (T2 shine through) in the distribution of the M2 and anterior M3 branches mainly to the right orbitofrontal and anterior insular and Broca's area. Additionally, there are microinfarctions in the terminal M4 branches to the centrum semiovale. There is lesser involvement in the more posterior insular and parietal cortex. There is only one site of positive restriction on MR diffusion and on SWI that is consistent with completed infarction and that site is just lateral to the right caudate.
Lessons to be learned
1. Several important concept come into play in this case. The first concept is that it is possible for there to be full pial collateralization with no pial collateral gap, plus near normal venocapillary pool CTA and near normal CBV on T perfusion, and yet still have extensive stroke at the tissue level. Stroke occurs when the depth and duration of the ictus oligemia is severe enough to sufficiently reduce ATP to levels sufficient to trip the ischemic cascade alone or the ischemic cascade plus the glutamate cascade. This process is usually initiated by an afferent block lasting for at least 3 minutes without sufficient retrograde collateral. A stroke zone is, therefore, produced by the combination of the afferent block combined with collateral failue, and at times adding venous egress collapse. An afferent block does not cause infarction when collateral is adequate. Once the ischemic cascade begins, there will be some level of ischemic injury. Once the glutamate cascade begins completed stroke is inevitable.
2. The second concept is that the evolution of a stroke depends on reflow (i.e. intercurrent clot lysis plus antegrade or retrograde reperfusion). If reperfusion occurs quickly (as is often seen in emboli), the ictal oligemia can initiate the ischemic cascade with resultant tissue injury (and positive MR diffusion). However, if sufficient reflow occurs before the CTA imaging, the CTA and the CT perfusion can to return to normal or near normal. Reperfusion can help tissue at-risk (ischemic penumbra), which is the basis for stroke therapy. However, if reperfusion occurs after completed stroke, there is a risk of hemorrhagic conversion and reoxydative tissue stress widening the stroke zone.
In this case, the CT perfusion demonstrated only a small zone of reduced CBV. CTA demonstrates good pial collateral. The delayed post contrast CT demonstrates only a small area of significantly reduced CBV (in the right lateral orbitofrontal region. However, the MR diffusion was positive in a much wider territory indicating the CTA underestimated the stroke zone probably on the basis of substantial reflow prior to the CTA exam.
3. The third concept refers to the basis for the partial luminal collapse of a downstream artery (i.e. the right ICA in this case). Reduced luminal downstream right ICA size in the case happened because of high grade stenosis. The second reason, is downstream occlusion in the cavernous segment providing no reason to maintain normal flow rates.
4. The fourth concept is how the imaging differs in recognizing dense ischemic core and sequestered infarctions. The MR-swi is the only sequence to detect the sequerterd infarct in the lateral orbitofrontal parenchyma, which is the site of worst ischemic insult. The CBV and the CTA venocapillary pool did detect this as the area as the site of least perfusion. The MR diffusion and FLAIR sequences were sensitive to the entire stroke zone and were more prominent in the orbitofrontal area but neither could differentiae ischemic penumbra from dense ischemic core.
5. And finally FLAIR is the best study to demonstrate the very sharp transition between affected tissue versus unaffected tissue so characteristic of an arterial type of stroke.
2. The second concept is that the evolution of a stroke depends on reflow (i.e. intercurrent clot lysis plus antegrade or retrograde reperfusion). If reperfusion occurs quickly (as is often seen in emboli), the ictal oligemia can initiate the ischemic cascade with resultant tissue injury (and positive MR diffusion). However, if sufficient reflow occurs before the CTA imaging, the CTA and the CT perfusion can to return to normal or near normal. Reperfusion can help tissue at-risk (ischemic penumbra), which is the basis for stroke therapy. However, if reperfusion occurs after completed stroke, there is a risk of hemorrhagic conversion and reoxydative tissue stress widening the stroke zone.
In this case, the CT perfusion demonstrated only a small zone of reduced CBV. CTA demonstrates good pial collateral. The delayed post contrast CT demonstrates only a small area of significantly reduced CBV (in the right lateral orbitofrontal region. However, the MR diffusion was positive in a much wider territory indicating the CTA underestimated the stroke zone probably on the basis of substantial reflow prior to the CTA exam.
3. The third concept refers to the basis for the partial luminal collapse of a downstream artery (i.e. the right ICA in this case). Reduced luminal downstream right ICA size in the case happened because of high grade stenosis. The second reason, is downstream occlusion in the cavernous segment providing no reason to maintain normal flow rates.
4. The fourth concept is how the imaging differs in recognizing dense ischemic core and sequestered infarctions. The MR-swi is the only sequence to detect the sequerterd infarct in the lateral orbitofrontal parenchyma, which is the site of worst ischemic insult. The CBV and the CTA venocapillary pool did detect this as the area as the site of least perfusion. The MR diffusion and FLAIR sequences were sensitive to the entire stroke zone and were more prominent in the orbitofrontal area but neither could differentiae ischemic penumbra from dense ischemic core.
5. And finally FLAIR is the best study to demonstrate the very sharp transition between affected tissue versus unaffected tissue so characteristic of an arterial type of stroke.
Recommendations
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