64 year old male on aspirin and Plavix presenting with acute gait difficulty and left visual field problems.

CT Head; CT Perfusion; CTA Neck; CTA Head; CTA Venocapillary Pool; MR Diffusion; MR Flair; MR Susceptibility

Noncontrast CT head
1. There is focal hyperdensity in the distal basilar apex consistent with acute thrombus.
2. There is no discernable cytogenic edema, and certainly no obvious edema to confirm stroke-age outside the treatment window.
3. There is focal tissue (minimal) volume loss in the caudal surface of the right cerebellum, likely from prior ischemic event or prior trauma.

CT perfusion
1. Short segment acute thrombus is evident on the included head CTA located in the distal basilar apex.
2. Delayed PCA filling (prolonged TTP) is related to retrograde PCA filling from the circle of Willis.
3. Chronic reduced CBV is evident in the caudal Rt. cerebellum, but no discernable hyperacute stroke is evident.
4. Remember: ischemic injury occurs within minutes and it is not uncommon for the offending thrombotic occlusion to have recanalized prior to the CT perfusion, and yet the site be positive on DWI.

CTA of the neck
1. There is a focal roughly 50% stenosis of the left vertebral artery origin.

CTA of the head
1. Acute thrombus in the distal basilar artery apex with limited filling of the SCA perfusion zones to the rostral cerebellum  and superior vermis.
2. There is retrograde filling of the supervermic arteries, but not the superior cerebellar arteries, as yet. This is likely an effect of delay in filling. Correlate with delayed CTA.

Post contrast head CT (venocapillary pool analysis)
1. Acute thrombus in the distal basilar artery (last 3mm’s), and of the basilar apex.
2. The PCA’s and at least part of the P1 segments fill retrograde from the circle of Willis.
3. There was at least some antegrade filling of the SCA’s plus there is likely pial collateral arising from the AICA & PICA sources, which is sufficient to increase the rostral cerebellar & superior vermic CT density in the venocapillary pool to within normal limits.
4. No focal reduced CT density within the venocapillary pool is evident to confirm completed stroke in the rostral cerebellum, rostral brain stem, nor occipital poles.

MR Diffusion
1. Admixture of hyperacute and acute thromboembolic infarctions involving distal PICA branches in both cerebellar hemispheres, the distal basilar perforator to the Rt. cerebral peduncle,  the basilar tip perforators to the mesial thalamus, the right cerebral peduncle,  and the Rt. posterior mesial choroidal perforators to the dorsal Rt. thalamus, and the P4 branches to both occipital polar areas.
2. The most recent infarcts are in the Rt. mesial thalamus, the Rt. cerebral peduncle, and the Rt. occipital polar regions.
 
MR flair
1. Multicentric hyperacute to early acute (6 hours to 1 day) thromboembolic infarctions are evident involving: the distal PICA branches in both cerebellar hemispheres, the distal basilar perforator to the Rt. cerebral peduncle, the basilar tip perforators to the mesial thalamus, the Rt. posterior mesial choroidal perforators to the dorsal Rt. thalamus, a mesial P4 larger infarction right mesial occipital lobe, and finally, multiple small very distal the P4 branches to both occipital poles.

MR  susceptibility (SWI) sequence
1. There is SWI susceptibility blooming artifact in the site of the distal basilar thrombus.
2. There is reduced venous egress from the Rt. mesial occipital infarction site, plus evidence of  intraluminal venous stasis/thrombosis. These are findings of early sequestered stroke.
3. There is no evidence of hemorrhagic conversion.

1. Acute (hyperdense thrombus on CT) intraluminal thrombus in the distal basilar artery segment. CTA reveals intraluminal thrombus covering the origins of the SCA and PCA arteries bilaterally. There is retrograde pial collateral present for all the occluded branches. No clear infarction is evident on CTA. There is focal right cerebellar encephalomalacia from a prior ischemic event. There is a smooth, <40% proximal left vertebral stenosis. 

2. Subsequent MR (performed at 10-12 hours later) demonstrates multicentric distal branch post embolic types of infarctions involving the cerebellar PICA territories bilaterally, The upper and lower right thalamus, the right hippocampus (P2-PCA segment), bilateral P4-PCA distal branches to the occipital pole (more on right than left). The source for the emboli is likely from the heart or aorta.

1. This case illustrates what happens with a recent  (hyperacute) secondary embolic shower; secondary sites are all the stem arteries in neck or head. Primary emboli arise from sites outside the primary afferent input arteries (i.e. brachiocephalic, carotid or vertebral arteries); primary sites are likely aortic or cardiac. The actual sites of hyperacute ischemic injury are positive on diffusion and negative or minimally positive on FLAIR. Smaller emboli end up in the most terminal branches of the pial vessels or within perforators. Larger emboli may stop in the more proximal larger arterial trunks or divisions downstream from the initial thrombus. Emboli develop as clot lysis proceeds. In this case the stroke pattern affects arterial territories that cannot be explained as arising from  a single CNS stem artery. The infarctions are similar in stroke-age, but not necessarily in depth and duration.

2. It is not uncommon to find no clear source for the emboli in the head & neck; implying a primary cardiopulmonary source, or paradoxical embolization from atrial septal defect.

3. This case also illustrates the findings associated with early sequestered infarction, as exhibited in the mesial right occipital infarct. In this site the MR diffusion & FLAIR are positive. Additionally, there is reduction in size of the cortical veins in the right occipital area (compared to the left) indicating reduced transcapillary blood flow. Finally, and most significant, there is early susceptibility artifact on the MR-swi in the venocapillary blood pool within the stroke-zone. This finding means the dense ischemic core has had no transcapillary blood flow and there  is now venous stasis; in other words the transcapillary blood flow is sequestered and accumulating deoxyhemoglobin creates the signal loss on SWI. Sequestered infarcts later become chronic sequestered infarcts which pathologically exhibit fibrin obliteration of the vessel lumina and extensive parenchymal hemosiderin deposition.

4. This case also illustrates how the ventral part of the thalamus is supplied by perforators arising from the basilar apex and P1 segment, while the dorsal aspect is supplied by perforators arising from the posterior mesial & lateral choroidal arteries, which arises as branches off the P1/2 junction. This separate source for the ventral vs dorsal aspect of the thalamus also occurs in the mesencephalon, the medulla, and the centronuclear structures in the cerebrum. 

Watch the included summary video for this instructional case.