Hyperacute Arterial Stroke IV - Clinical Case Summary
Hyperacute Arterial Stroke IV - Clinical Case Summary
Hyperacute Arterial Stroke IV - Clinical Case Summary
SummaryHistory
81 year old female presenting with acute onset mental status change, dizziness, nausea, and gait imbalance.
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. Hyperdense thrombus is evident in the distal basilar artery extending into the left P1 PCA segment.
2. Multiple strokes involving Lt. PICA and both P4 segments of the PCA; cytogenic edema is already evident on noncontrast CT placing these ischemic events outside the hyperacute treatment timeline. Estimated stroke age is at least 10 hours. It is likely there has been 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 Lt. PCA perfusion zone within the mesial Lt occipital lobe. Ischemia is likely present in the occipital deep white matter bilaterally.
CTA of the neck
1. Focal left vertebral artery stenosis without intraluminal soft clot; estimated stenosis is 50% by NASCET & physiologic criteria.
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 of the head
1. Focal intraluminal thrombus is present in the distal basilar artery segment. It produces a partial luminal narrowing of the 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.
2. There is partial narrowing of the basilar lumen and of the Rt. PCA origin. The circle of Willis is complete allowing the P-com’s to collateralize both PCA’s. The distal P4 trunk arteries are patent bilaterally into the area of cytogenic edema.
3. Distal Lt. PICA branches are partially collateralized from ipsilateral AICA. The mesial left PICA cerebellar hemispheric arteries are not opacified.
Post contrast head CT (venocapillary pool analysis)
1 .Known hyperdense acute thrombus in the distal basilar artery. All pial arteries (SCA, basilar tip, and PCA) are opacified without pial collateral gap
2. Partial filling of the left PICA is evident on the head CTA, but there is virtually no CT density in the venocapillary pool in the left tonsillar and mesial left cerebellum PICA perfusion zone. There is partial but reduced CT density in the lateral left cerebellum and the left middle peduncle.
3. Only minimal reduction in the venocapillary pool is in the occipital polar areas indicating ischemic penumbra and the area involved in less than the oligemic tissue based on the CT perfusion. These findings indicated substantial collateralization at this time. Whether the areas in the ischemic penumbra go on to completed infarction is indeterminate by CTA. MR imaging would be of value in determining the extent of the ischemic injury.
CTA final impression
1. Distal segment basilar artery thrombosis with mainly circle of Willis collateral to distal basilar tip and PCA trunks. Thus, there is filling of all pial arteries. However, there is reduced CT density in the venocapillary pool in the subcortical white matter bilaterally (dense ischemic core). Findings are most consistent with initial hypoperfusion from thromboembolism than has now recanalized except in the distal basilar artery. The depth and duration of the initial ischemic insult resulted in deep white matter occipital stroke.
2. Limited filling the left PICA and limited left AICA collateral has resulted in completed stroke in the mesial caudal cerebellum (dense ischemic core) and ischemic changes in the remaining left cerebellum (likely in the ischemic penumbra.
3. Bilateral deep cerebellar white matter post ischemic changes likely in the ischemic penumbra category.
MR diffusion
1. The diffusion maps (both DWI and ADC) are positive for hyperacute stroke in both mesial occipital areas (P4 PCA perfusion zones).
2. There are separated small DWI positive areas in the right occipital lobe, which again are consistent with recent secondary emboli.
3. The diffusion maps (both DWI and ADC) are positive for stroke in the mesial left cerebellum and left peritonsillar region corresponding to the peritonsillar and mesial hemispheric trunks of the Lt. PICA.
MR flair
1. Recent FLAIR positive ischemic events in multiple sites including the mesial occipital lobes (P4 segment PCA perfusion zones) and in the Lt PICA (affecting the mesial cerebellar and peritonsillar trunks only). Stroke-ages are variable, as above.
2. Embolic source is likely (originally) thrombus in the left intradural vertebral artery segment based on FLAIR findings. This original thrombus likely occluded the left PICA resulting in mesial left cerebellar infarction, which is why this stroke is older than the others.
MR GRE (no swi was obtained)
1. GRE demonstrates phase artifact (representing hemosiderin or deoxyHgb) in the post medullary segment of the left PICA and in the distal basilar thrombus.
2. There is no hemorrhagic conversion. There are small sites of prior parenchymal chronic blood products of no acute significance.
1. Hyperdense thrombus is evident in the distal basilar artery extending into the left P1 PCA segment.
2. Multiple strokes involving Lt. PICA and both P4 segments of the PCA; cytogenic edema is already evident on noncontrast CT placing these ischemic events outside the hyperacute treatment timeline. Estimated stroke age is at least 10 hours. It is likely there has been 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 Lt. PCA perfusion zone within the mesial Lt occipital lobe. Ischemia is likely present in the occipital deep white matter bilaterally.
CTA of the neck
1. Focal left vertebral artery stenosis without intraluminal soft clot; estimated stenosis is 50% by NASCET & physiologic criteria.
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 of the head
1. Focal intraluminal thrombus is present in the distal basilar artery segment. It produces a partial luminal narrowing of the 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.
2. There is partial narrowing of the basilar lumen and of the Rt. PCA origin. The circle of Willis is complete allowing the P-com’s to collateralize both PCA’s. The distal P4 trunk arteries are patent bilaterally into the area of cytogenic edema.
3. Distal Lt. PICA branches are partially collateralized from ipsilateral AICA. The mesial left PICA cerebellar hemispheric arteries are not opacified.
Post contrast head CT (venocapillary pool analysis)
1 .Known hyperdense acute thrombus in the distal basilar artery. All pial arteries (SCA, basilar tip, and PCA) are opacified without pial collateral gap
2. Partial filling of the left PICA is evident on the head CTA, but there is virtually no CT density in the venocapillary pool in the left tonsillar and mesial left cerebellum PICA perfusion zone. There is partial but reduced CT density in the lateral left cerebellum and the left middle peduncle.
3. Only minimal reduction in the venocapillary pool is in the occipital polar areas indicating ischemic penumbra and the area involved in less than the oligemic tissue based on the CT perfusion. These findings indicated substantial collateralization at this time. Whether the areas in the ischemic penumbra go on to completed infarction is indeterminate by CTA. MR imaging would be of value in determining the extent of the ischemic injury.
CTA final impression
1. Distal segment basilar artery thrombosis with mainly circle of Willis collateral to distal basilar tip and PCA trunks. Thus, there is filling of all pial arteries. However, there is reduced CT density in the venocapillary pool in the subcortical white matter bilaterally (dense ischemic core). Findings are most consistent with initial hypoperfusion from thromboembolism than has now recanalized except in the distal basilar artery. The depth and duration of the initial ischemic insult resulted in deep white matter occipital stroke.
2. Limited filling the left PICA and limited left AICA collateral has resulted in completed stroke in the mesial caudal cerebellum (dense ischemic core) and ischemic changes in the remaining left cerebellum (likely in the ischemic penumbra.
3. Bilateral deep cerebellar white matter post ischemic changes likely in the ischemic penumbra category.
MR diffusion
1. The diffusion maps (both DWI and ADC) are positive for hyperacute stroke in both mesial occipital areas (P4 PCA perfusion zones).
2. There are separated small DWI positive areas in the right occipital lobe, which again are consistent with recent secondary emboli.
3. The diffusion maps (both DWI and ADC) are positive for stroke in the mesial left cerebellum and left peritonsillar region corresponding to the peritonsillar and mesial hemispheric trunks of the Lt. PICA.
MR flair
1. Recent FLAIR positive ischemic events in multiple sites including the mesial occipital lobes (P4 segment PCA perfusion zones) and in the Lt PICA (affecting the mesial cerebellar and peritonsillar trunks only). Stroke-ages are variable, as above.
2. Embolic source is likely (originally) thrombus in the left intradural vertebral artery segment based on FLAIR findings. This original thrombus likely occluded the left PICA resulting in mesial left cerebellar infarction, which is why this stroke is older than the others.
MR GRE (no swi was obtained)
1. GRE demonstrates phase artifact (representing hemosiderin or deoxyHgb) in the post medullary segment of the left PICA and in the distal basilar thrombus.
2. There is no hemorrhagic conversion. There are small sites of prior parenchymal chronic blood products of no acute significance.
Overall impression
1. There is a dissection of the intradural segment of the left vertebral artery, which appears to have dissected across the origin of the left PICA. Additionally, there is down stream intraluminal thrombus in the distal basilar artery segment mainly on the left portion of the lumen. This causes a stenosis of the left SCA. Both PCA's are opacified, however there is CTA evidence of very low flow state in both P4-PCA perfusion zones and in the left PICA cerebellar perfusion zones. The stroke ages are at least >8-10 hours.
2. MR diffusion confirms the acute (likely > 8 hours) post ischemic changes in the P4-PCA perfusion zones and the mesial aspect of the left PICA perfusion zone. The lateral PICA perfusion is reperfused via AICA-PICA collaterals. None of the sites are hemorrhagic. Thrombus is evident on SWI within the proximal left PICA segment.
2. MR diffusion confirms the acute (likely > 8 hours) post ischemic changes in the P4-PCA perfusion zones and the mesial aspect of the left PICA perfusion zone. The lateral PICA perfusion is reperfused via AICA-PICA collaterals. None of the sites are hemorrhagic. Thrombus is evident on SWI within the proximal left PICA segment.
Lessons to be learned
1. This case illustrates features of secondary embolization. In this case the likely site of initial thrombus was in the left intradural vertebral artery segment, which is revealed on the FLAIR imaging as increased FLAIR signal in the wall. The lumen of the intradural vertebral artery segment has recanalized and currently appears nearly normal. The initial left PICA stroke has features of a subacute stroke event. The GRE points out the site of thrombus in the posterior medullary PICA segment. Clot lysis in the initial intradural vertebral artery has resulted in downstream secondary thrombus being deposited in the distal basilar artery. Additionally, multiple small emboli have caused strokes of differing age within the occipital lobes. This pattern is typical of a secondary embolic pattern, which consists of a proximal major(stem) arterial thrombosis (i.e.the original event) undergoing clot lysis later downstream embolization to branches in the same circuit. It is helpful that FLAIR and SWI can detect residual mural thrombus even after recanalization. If you cannot prove the source for emboli in the head or neck, then the clinical service needs to find a primary embolic source in the heart (i.e. atrial thrombus, patent atrial septal defect, etc.) or in the aorta (i.e. intimal ulcerations, dissection etc.).
Recommendations
Watch the included summary video for this instructional case.