79 year old female with sudden onset symptoms including Rt. facial droop, Rt. side weakness; the patient was nonverbal nor following commands; there is known history of secondary diabetes with hyperlipidemia.
 

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

Final Impression for entire CTA 
1. Proximal left M1/M2 thrombus with reasonable pial collateral (pial collateral reaches the proximal thrombus on the delayed head CT.  
2. There remains evidence of persistent significant oligemia mainly in the lateral lenticulostriate perfusion zone (likely completed stroke, and in the anterior insular cortex (ischemic penumbra. Lesser oligemia (tissue at risk) is evident the remaining MCA and lateral orbitofrontal territories.
3. The persistently oligemic sites in the rostral M3-MCA perfusion zones likely affect the white matter deep to Broca’s area, the uncinate fasiculus, the premotor cortex, and the facial portion of the primary motor cortex.
4. The combination of a focal 50-60% stenosis of the proximal right cervical ICA combined with incomplete circle of Willis shifts the watershed zone to the anterior insular area (end of the line watershed pattern), which likely contributes to the anterior insular ischemia. This end of the line ischemic effect is further supported by evidence of pial collateral reaching the M3 arteries in this area on the initial post contrast head CT.
5. Suspicious nodule in the left thyroid. 

Concurrent MR diffusion sequence
1. There is positive diffusion in the same areas corresponding to sites of reduced CBV and CT perfusion and reduced venocapillary pool on the delayed CTA consistent with post ischemic parenchymal injury in the left lateral basal ganglia/caudate body/centrum semiovle, in the lateral orbitofrontal, and in the anterior insula and much of the superior division of the left MCA to the operculum and lateral cortex. However, the degree of positivity is variable with the least prominent (lesser ischemia) involving in the posterior insula and all of the superior division MCA supplied lateral cortex. The most prominent (worst ischemia) is in the perfusion zone of the M1/2 lateral lenticulostriate perforators and the anterior insula.
2. There is reperfusion  hemorrhage into the lateral lenticulostriate perfusion zone, which was positive on DWI but also had significantly reduced CT density within its’ venocapillary pool on delayed CTA.
3. There is minimal subfalcine brain shift secondary to post ischemic cytogenic swelling plus the hematoma in the lateral lenticulostriate perfusion zone.

FLAIR sequence
1. FLAIR demonstrates post ischemic cytogenic edema consistent with ischemic injury in the left lateral lenticulostriate perfusion zone now with reperfusion hemorrhagic conversion. The hematoma produces local mass effect and early incisular herniation.
2. FLAIR demonstrates post ischemic cytogenic edema in the perfusion zones of the Lt. M3 (MCA) arteries to the anterior insula, Lt. lenticulostriate, and to the Lt. lateral orbitofrontal portions of the Lt. hemisphere. These areas did not develop hemorrhagic conversion.

SWI sequence
1. Reperfusion hemorrhage in the left lateral basal ganglia, in the left body of the caudate, in the left posterior frontal corona radiate/centrum semiovale, all of which involve reperfusion into the lateral lenticulostriate perforator territories.
2. There are scattered small areas of sequestered infarction within the dense ischemic core mainly in the anterior suprasylvian and the lateral orbitofrontal subcortical areas.. They represent areas of ischemia which develop no reperfusion resulting in persistent venous stagnation or intraluminal clot within the venocapillary bed, which also creates a signal drop out on SWI.
3. The cytogenic edema and the hematoma combine to produce early mass effect and reduction in cortical vein size.

1. There is acute thrombus in the proximal M1/M2 segment of the intradural left ICA.

2. The CTA demonstrates good retrograde tissue reperfusion. There is no pial-collateral gap; the retrograde pial collateral reaches the distal end of the thrombus.

3. The post embolectomy MR revealed ischemic changes throughout the left MCA and evidence of a reperfusion hemorrhage and an area of intravascular hemosiderin within venocapillary pool in the frontal suprasyvian area consistent with sequestered infarction

1. This case illustrates the features of a hyperacute thrombotic stroke. The arteries caught within the thrombus will likely be part of the completed stroke (dense ischemic core). When the thrombus is in a proximal stem artery the remaining brain needs to survive via collaterals. Altered circle of Willis (incomplete) possibly with additional contralateral carotid or vertebral stem artery stenosis shift the watershed zone from the usual anastomotic border zone to the anterior insula in this case. Thus, two stroke mechanisms are present. First, stroke related to primary arterial M1/2 thrombus directly occluding its’ lentriculostriate perfusion zone. And second, ischemia related to hypoperfusion at the end-of the-line pial collateral perfusion zone within the shifted watershed zone in the anterior insula and lateral orbitofrontal areas. 

2. The point of all stroke therapy is to restore blood supply to the ischemic penumbra (i.e. the shifted watershed zone in this case). The risk is always hemorrhagic conversion or reoxidative stress (i.e. the lateral lenticulostriate area). These areas vulnerable to post therapy complications will invariably be the sites where the CT density in the venocapillary pool remains less than normal on the delayed CTA exam.

Watch the included summary video for this instructional case.