50 year old female presenting with acute onset left sided weakness.

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

Noncontrast head CT
1. Dense mural calcification in Rt. ICA which projects over the arterial lumen; this could represent a site of high cervical Rt. ICA flow-limiting stenosis.
2. No clear evidence of a hyperacute stroke is evident.

CT perfusion
1. Reduced perfusion rate in the Rt. cerebral watershed territory, but the area appears physiologically compensated by collateral blood flow.

CTA of the neck
1. Rt. carotid bifurcation has moderate focal stenosis affecting both the EAC & IAC origins in the 50% range.
2. Rt. proximal ICA is occluded just after carotid sinus with apparent intraluminal soft clot consistent with hyperacute thrombus formation.
3. Rt. ICA reopacifies at mid-cavernous segment from ascending pharyngeal artery to infra-lateral trunk EC-IC connection. However, the reopacified ICA has less contrast density and is of smaller size than expected indicating less the fully functional EC-IC collateralization which puts the Rt. hemisphere at risk for hypoperfusion.

CTA of the head
1. Acutely thrombosed Rt. cervical ICA with partial flow restoration at the cavernous level from functional EC-IC connections.
2. Intracranial arteries appear patent. Although the filling rate is delayed, the arterial opacification in the Rt. ICA circuit is less than the left. Additionally, the left A1 segment is hypoplastic. Thus, this combination raises the possibility of a oligemic hypoperfusion in the Rt. carotid watershed areas, which matches the findings on the CT perfusion.

Post contrast head CT (venocapillary pool analysis)
1. There is no pial collateral gap nor evidence of reduced venocapillary CT density to confirm completed infarction in the areas of dysautoregulation.
2. Minimal evidence of post ischemic arteriopathy with subtle intraluminal irregularities, minimal filling delay, and subtle loss of BBB. Findings are consistent with recanalization after recent thromboembolic event.  
3. EC-IC collateral provided by ascending pharyngeal-cavernous sinus EC-IC connection; this delays arterial filling on the right but all distal arteries are patent.
4.  The post ischemic arteriopathy in the second M3 branch could affect the right premotor area, which would account for the symptoms of left sided transient weakness.

MR diffusion
1. There is evidence of hyperacute, multicentric, small-volume embolic-like strokes in the distal M4 branches including those to the arm & trunk area of the primary motor cortex. The sites of ischemia are separate and not confluent. There distribution does correspond to all component sectors of the right cerebral watershed zone. However, watershed ischemia causes a confluent ischemic event. In this case the findings on MR would indicate the basis for the strokes is actually concurrent right MCA secondary embolism from the proximal ICA thrombus.
2. There are older, likely subacute, small embolic strokes present in the Rt. occipital pole.

MR Flair
1. FLAIR positivity is evident in all of the positive diffusion sites. The stroke age is late hyperacute or early acute (3-6 hours)

MR Susceptibility (SWI)
1. There is venous prominence on the right for both the deep and superficial draining veins related to the physiologic hyperemic response to a proximal afferent arterial stenosis. There is no evidence of SWI blooming artifact over any of the veins to suggest abnormal venous stasis.

1. There is hyperacute thrombus in the right cervical ICA beginning just after the carotid sinus. There is non-erosive atherosclerotic changes without high grade stenosis in the Rt. carotid bifurcation. There is a focal nodular calcification in the high cervical Rt. ICA at the skull base, which likely had caused stenosis or occlusion previously. The acute thrombus extends up to the calcification. The Rt. ICA reopacifies in the mid cavernous sinus from EC-IC collaterals. The intracranial vessels opacify normally.

2. Despite good intracranial collateral there is MR diffusion evidence of multicentric, non hemorrhagic, embolic strokes in the distal M4 segment of the Rt. MCA. There are additional sites of positive post embolic ischemic change, as well; however these are in the distribution of terminal P4 PCA branches. Thus, there have been embolic events occurring in different arteries with likely different timeframes.

1. This case illustrates the consequence of having a proximal cervical ICA thrombosis where soft clot remains in the proximal arterial stump and there is functional EC-IC collateral allowing secondary embolization to distal M4 arteries as the process of clot lysis proceeds. Soft clot can also embolize from the distal end of the intraluminal thrombus or in cases of dissection from sites of pseudoaneurysms or sites of intimal dehiscence. Soft clot is distinguished by irregular unsharp margins compared to the sharp margins of an reendothelialized arterial stump.
 
2. Despite the right ICA occlusion, there is evidence of good collateral on CT perfusion and no residual focal reduced venocapillary pool on the head CTA to confirm persistent oligemia in the ischemic zone. This points out how the initial ischemic event(s) can initiate the ischemic cascade, while the rapid collateralization normalizes the CBV and venocapillary pool prior to the stroke imaging. If the ischemic cascade has been initiated, the MR diffusion will be positive.
 
3. This case also points out the disconnect between CT perfusion TTP, which imaged as slow flow in the cerebral watershed zone (mainly the centrum semiovale). However, the actual strokes on DWI were not in the ACA-MCA watershed zone, but rather in the motor cortex plus a few small emboli to MCA penetrating arteries to the frontoparietal and occipital subcortical white matter. Thus, prolonged TTP/MTT are helpful in recognizing slow flow at-risk sites but do not represent  actual oligemic sites. Likewise, reduced CBV & CBF help to recognize sites of potential significant oligemia, but they do not take potential collateralization into account (i.e derived calculations from 1st pass data), and therefore, over estimate the actual stroke-zones.

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