Hyperacute Arterial Stroke VII - Clinical Case Summary
Hyperacute Arterial Stroke VII - Clinical Case Summary
Hyperacute Arterial Stroke VII - Clinical Case Summary
SummaryHistory
64 year old female presenting with acute onset Rt. hemiparesis, left gaze deviation and aphasia; no depressed level of consciousness; history of hypertension.
Exams performed
CT Head; CT Perfusion; CTA Neck; CTA Head; CTA Venocapillary Pool; MR Diffusion; MR Flair; MR Susceptibility
Prior available imaging reports
Noncontrast head CT
1. Changes consistent with hyperacute stroke in the Lt. lateral lenticulostriate and Lt. superior division MCA region. This makes the likely level of occlusion in the Lt. M1/2 level.
2. No intracranial hemorrhage nor hyperdense (acute) thrombotic arterial segments are evident.
CT perfusion
1. Acute stroke changes with focal prolonged TTP and MTT plus moderate reduction in CBF and CBV centered in the Lt. orbitofrontal artery with some involvement of the Lt. rostral lentriculostriate, and Lt. anterior insular M3 perfusion zones. The tissue at risk is surrounded by areas of physiological hyperemia.
CTA of the neck
1. Proximal right vertebral artery stenosis in the 50-60% range with no other abnormality noted in the remaining cervical arteries or veins. This accounts for the slowed flow on CT perfusion in the Rt. PICA perfusion zone.
CTA of the head
1. There is a short stenosis at the origin of the Lt. superior division MCA; there is minimal post stenotic dilatation placing the stenosis in the 50-60% range; there is, at this time, reasonable antegrade blood flow. Presumably, the original thrombus has recanalized restoring antegrade flow. This segment of the artery now appears as a stenosis rather than an occlusion. The current stroke is the result of the original thrombus rather than the current stenosis.
2. There is subtle leak of contrast around the distal Lt. MCA arteries consistent with the minimal blood brain barrier leak associated with post ischemic arteriopathy.
Post contrast head CT (venocapillary pool analysis)
1. There is a short segment proximal superior division MCA stenosis consistent with a recanalized artery rather than underlying fixed arterial atherosclerotic stenosis. Since the stroke-zone includes the lenticulostriate and lateral orbitofrontal perfusion zone in addition to the superior division MCA, the initial thrombotic occlusion must have involved the M1/2 ICA segments.
2. Persistently reduced CT density in the venocapillary pool within the Lt. lateral orbitofrontal and anterior insular cortex with enough oligemia to fall within the ischemic penumbra. The oligemia in the posterior insula and the Lt. lateral lenticulostriate perforator regions appear less extensive. Correlate with stroke protocol MR.
3. There is no hemorrhagic conversion at this time.
4. There subtle loss of BBB in the distal Lt. MCA (M4) pial branches consistent with post-ischemic arteriopathy.
5. Stroke-age, based on the findings on the noncontrast CT would fit the hypeacute timeframe.
MR diffusion
1. Acute post ischemic injury affecting most of the superior division of the MCA and the left orbitofrontal region, and the left lenticulostriate perforator region consistent with an original afferent block at the left M1/2 junction (secondary stem) site, although no thrombus remains.
2. The ischemic changes are worse (likely dense ischemic core) in the rostral lateral lenticulostriate perfusion zone (especially in the rostral basal ganglia and caudate head), plus the lateral orbitofrontal perfusion zone, plus the anterior insular M3 arterial perfusion zone. Less advanced ischemic changes are evident in the distal M4 MCA superior division perfusion zone. There is less involved interval brain interposed between the rostral larger stroke and the distal cortical ischemic cortex. This pattern is consistent with initial thrombus, subsequent rapid clot lysis, and secondary distal embolization.
3. There is no hemorrhagic conversion.
MR Flair
1.There is well delineated cytogenic edema in the Lt. M3 and M4 MCA cortex, the Lt. lateral lenticulostriate perforator zone, & the Lt. lateral orbitofrontal perfusions zones consistent with stroke age beyond 8-10 hours.
2. The edema is clearly more evident in the anterior insular (rostral M3 arteries) and in the Lt lateral orbitofrontal artery perfusion zones than in the M4 MCA cortical areas indicating a difference in depth and duration of the ischemic event.
3. There is no apparent hemorrhagic conversion including the punctate hyperdensity on the noncontrast head CT (thus, represents incidental asymmetric BG calcification).
4. There is an old MCA stroke is evident in the Rt. posterior insular area.
MR SusceptibiIity
1. Left orbitofrontal artery stroke has evidence of sequestered infarct (dense ischemic core) within the stroke-zone. All other areas of left hemispheric ischemic change do not have sequestered infarction components. In this case the brain served by the left lateral orbitofrontal artery actually has evidence of sequestered infarction (caused by virtually no transcapillary filling), yet the lateral orbitofrontal pial branches are all opacified.
2. Reduced left side cortical vein filling likely reflects the reduced overall transcapillary filling rate despite normal or even dilated distal pial arteries on the CTA. This again points out the disconnect between conspicuity of the pial arteries and whether they provide adequate transcapillary filling through their penetrating arteries.
1. Changes consistent with hyperacute stroke in the Lt. lateral lenticulostriate and Lt. superior division MCA region. This makes the likely level of occlusion in the Lt. M1/2 level.
2. No intracranial hemorrhage nor hyperdense (acute) thrombotic arterial segments are evident.
CT perfusion
1. Acute stroke changes with focal prolonged TTP and MTT plus moderate reduction in CBF and CBV centered in the Lt. orbitofrontal artery with some involvement of the Lt. rostral lentriculostriate, and Lt. anterior insular M3 perfusion zones. The tissue at risk is surrounded by areas of physiological hyperemia.
CTA of the neck
1. Proximal right vertebral artery stenosis in the 50-60% range with no other abnormality noted in the remaining cervical arteries or veins. This accounts for the slowed flow on CT perfusion in the Rt. PICA perfusion zone.
CTA of the head
1. There is a short stenosis at the origin of the Lt. superior division MCA; there is minimal post stenotic dilatation placing the stenosis in the 50-60% range; there is, at this time, reasonable antegrade blood flow. Presumably, the original thrombus has recanalized restoring antegrade flow. This segment of the artery now appears as a stenosis rather than an occlusion. The current stroke is the result of the original thrombus rather than the current stenosis.
2. There is subtle leak of contrast around the distal Lt. MCA arteries consistent with the minimal blood brain barrier leak associated with post ischemic arteriopathy.
Post contrast head CT (venocapillary pool analysis)
1. There is a short segment proximal superior division MCA stenosis consistent with a recanalized artery rather than underlying fixed arterial atherosclerotic stenosis. Since the stroke-zone includes the lenticulostriate and lateral orbitofrontal perfusion zone in addition to the superior division MCA, the initial thrombotic occlusion must have involved the M1/2 ICA segments.
2. Persistently reduced CT density in the venocapillary pool within the Lt. lateral orbitofrontal and anterior insular cortex with enough oligemia to fall within the ischemic penumbra. The oligemia in the posterior insula and the Lt. lateral lenticulostriate perforator regions appear less extensive. Correlate with stroke protocol MR.
3. There is no hemorrhagic conversion at this time.
4. There subtle loss of BBB in the distal Lt. MCA (M4) pial branches consistent with post-ischemic arteriopathy.
5. Stroke-age, based on the findings on the noncontrast CT would fit the hypeacute timeframe.
MR diffusion
1. Acute post ischemic injury affecting most of the superior division of the MCA and the left orbitofrontal region, and the left lenticulostriate perforator region consistent with an original afferent block at the left M1/2 junction (secondary stem) site, although no thrombus remains.
2. The ischemic changes are worse (likely dense ischemic core) in the rostral lateral lenticulostriate perfusion zone (especially in the rostral basal ganglia and caudate head), plus the lateral orbitofrontal perfusion zone, plus the anterior insular M3 arterial perfusion zone. Less advanced ischemic changes are evident in the distal M4 MCA superior division perfusion zone. There is less involved interval brain interposed between the rostral larger stroke and the distal cortical ischemic cortex. This pattern is consistent with initial thrombus, subsequent rapid clot lysis, and secondary distal embolization.
3. There is no hemorrhagic conversion.
MR Flair
1.There is well delineated cytogenic edema in the Lt. M3 and M4 MCA cortex, the Lt. lateral lenticulostriate perforator zone, & the Lt. lateral orbitofrontal perfusions zones consistent with stroke age beyond 8-10 hours.
2. The edema is clearly more evident in the anterior insular (rostral M3 arteries) and in the Lt lateral orbitofrontal artery perfusion zones than in the M4 MCA cortical areas indicating a difference in depth and duration of the ischemic event.
3. There is no apparent hemorrhagic conversion including the punctate hyperdensity on the noncontrast head CT (thus, represents incidental asymmetric BG calcification).
4. There is an old MCA stroke is evident in the Rt. posterior insular area.
MR SusceptibiIity
1. Left orbitofrontal artery stroke has evidence of sequestered infarct (dense ischemic core) within the stroke-zone. All other areas of left hemispheric ischemic change do not have sequestered infarction components. In this case the brain served by the left lateral orbitofrontal artery actually has evidence of sequestered infarction (caused by virtually no transcapillary filling), yet the lateral orbitofrontal pial branches are all opacified.
2. Reduced left side cortical vein filling likely reflects the reduced overall transcapillary filling rate despite normal or even dilated distal pial arteries on the CTA. This again points out the disconnect between conspicuity of the pial arteries and whether they provide adequate transcapillary filling through their penetrating arteries.
Overall impression
1. Acute left MCA ischemic event involving all portions of the left MCA including the perforators (M1/2 -MCA branches) to the basal ganglia, the artery to the anterior temporal pole (M1-MCA branch), and the orbitofrontal (M2-MCA branch). Much of the posterior MCA perfusion zone demonstrates functional collateral. However, the anterior portion of the MCA and the orbital frontal artery perfusion zones display virtually no reperfusion on delayed CTA imaging; this is consistent with dense ischemic core.
2. Focal high cervical vertebral stenosis (50-60% range)
3. Left MCA ischemic event is evident on MR diffusion. There is sequestered infarction (positive on SWI) in Broca's area of the left cerebrum.
2. Focal high cervical vertebral stenosis (50-60% range)
3. Left MCA ischemic event is evident on MR diffusion. There is sequestered infarction (positive on SWI) in Broca's area of the left cerebrum.
Lessons to be learned
1. This case illustrates what can happen when a proximal thrombosis occurs with a short duration by very dense oligemia. In this scenario the ischemic cascade is initiated, which may or may not include the glutamate cascade, but the afferent block is resolved prior to CTA imaging. If the ischemic cascade is initiated the MR diffusion will become positive.
2. This scenario has been played out in this instructional case. By the time the CTA was performed, the only residua of the thrombus was a moderate stenosis (partial recanalized appearance) of the proximal segment of the superior division of the left MCA. All the proximal stem arteries and all othe pial vessels were opacified even on the 1st pass CTA. The 2nd pass CTA venocapillary density was close to normal throughout most of the MCA, but remained moderately reduced in the lateral orbital frontal artery perfusion zone (similar on the CT perfusion). Despite reasonable perfusion on CTA, the MR revealed post ischemic injury throughout much of the superior division MCA and in the lateral orbitofrontal region (this was the most positive part of the DWI). MR-swi revealed sites of sequestered infarction within in the lateral orbitofrontal parenchyma confirming the worst ischemic injury.
3. This case emphasizes the disconnect between reasonably normal CTA findings including the mostly normal CT density within the venocapillary pool versus the MR sequences. The consequence of an initial oligemic event, can be very severe, but reflow prevents the extent of the infarct to be detected on CTA. This case reinforces the need for performing MR soon after the CTA to fully, understand all that the stroke entails. The exception when the timeframe is documented as being hyperacute and within the treatment window, and there is an accessible thrombus. The MRI can wait until after any stroke intervention.
4. This case illustrates the features of physiologic hyperemia in the collateral zone. On CT perfusion the physiologic hyperemia has prolonged TTP/MTT, and increased CBV/CBF. On CTA there is vasodilation and no leak of contrast. On diffusion there is no diffusion positivity. On MR FLAIR there is no acute cytogenic edema. On MR SWI there in venous hyperemia with no blooming artlifact. These features differ from those of post ischemic arteriopathy as seen in other instructional case examples.
2. This scenario has been played out in this instructional case. By the time the CTA was performed, the only residua of the thrombus was a moderate stenosis (partial recanalized appearance) of the proximal segment of the superior division of the left MCA. All the proximal stem arteries and all othe pial vessels were opacified even on the 1st pass CTA. The 2nd pass CTA venocapillary density was close to normal throughout most of the MCA, but remained moderately reduced in the lateral orbital frontal artery perfusion zone (similar on the CT perfusion). Despite reasonable perfusion on CTA, the MR revealed post ischemic injury throughout much of the superior division MCA and in the lateral orbitofrontal region (this was the most positive part of the DWI). MR-swi revealed sites of sequestered infarction within in the lateral orbitofrontal parenchyma confirming the worst ischemic injury.
3. This case emphasizes the disconnect between reasonably normal CTA findings including the mostly normal CT density within the venocapillary pool versus the MR sequences. The consequence of an initial oligemic event, can be very severe, but reflow prevents the extent of the infarct to be detected on CTA. This case reinforces the need for performing MR soon after the CTA to fully, understand all that the stroke entails. The exception when the timeframe is documented as being hyperacute and within the treatment window, and there is an accessible thrombus. The MRI can wait until after any stroke intervention.
4. This case illustrates the features of physiologic hyperemia in the collateral zone. On CT perfusion the physiologic hyperemia has prolonged TTP/MTT, and increased CBV/CBF. On CTA there is vasodilation and no leak of contrast. On diffusion there is no diffusion positivity. On MR FLAIR there is no acute cytogenic edema. On MR SWI there in venous hyperemia with no blooming artlifact. These features differ from those of post ischemic arteriopathy as seen in other instructional case examples.
Recommendations
Watch the included summary video for this instructional case.