72 year old male with transient left sided weakness; history of diffuse vascular disease; evaluate for arterial stenosis.

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

Noncontrast head CT
1. Age related changes and chronic post-ischemic lacunar infarct in the mesial Lt. thalamus.
 2. No hyperacute post ischemic changes are evident.
 
CT perfusion
1. Changes consistent with Lt. ICA afferent obstruction (occlusion or high-grade stenosis) which slows the left hemispheric blood flow but does not had an obvious effect on CBV or CBF.
 2. There is ocal reduced perfusion in the left MCA-PCA watershed zone.
 3. There is delayed, but compensated circulation, in the Lt. PICA perfusion zone.
 
CTA of the neck
1. There are tandem Rt. carotid stenoses, the combination of which, are likely flow-limiting. However, the distal right ICA appears to fill normally.
2. There is diffuse atherosclerotic ulcerative plaque disease in left common carotid; there is no intimal dehiscence, no intraluminal soft clot, nor high grade stenosis.
3. Lt. ICA is occluded in its’ cervical segment just above the carotid sinus; there is limited functional EC-IC collateralization through the ophthalmic collateral with patent but reduced size of the intradural left ICA.
4. The Lt. vertebral artery has an origin stenosis and becomes completely occluded at the dural ring;  The left intradural vertebral segment and the Lt. PICA origin are both occluded, but the distal PICA branches appear to fill in retrograde manner from the Lt. AICA. The Rt. vertebral is occluded in its’ proximal segment but is reconstitued by costocervical collaterals at the C3 level. The Rt. PICA origin is occluded but distal branches fill in retrograde from the Rt. AICA.
 
CTA of the head
1. There is a right proximal vertebral artery occlusion, which is reconstituted at C3 and is patent beyond this point. However, the right PICA is occluded at its origin. Its’ distal branches fill retrograde from the right AICA. The patent right intradural vertebral supplies the left intradural vertebral and left PICA in a retrograde manner (the left vertebral was occluded at the dural ring).
2. There is occlusion of the Lt. cervical ICA just after the carotid sinus. EC-IC collateral reconstitute the Lt. ICA in the cavernous and ophthalmic ICA segments. Distal carotid branch arterial filling on the left is delayed and cannot be fully assessed until the delayed post contrast head CTA.
3. Cerebral arteries on the right appear fully opacified, as are the pial arteries in the posterior fossa on this initial post contrast head CTA. There is a distal basilar non flow-limiting stenosis.
 
Post contrast head CT (venocapillary pool analysis)
1. Despite extensive atherosclerotic vascular disease in the cervical region causing a delay in cerebral and cerebellar filling rates. The delayed post contrast head CT, however, demonstrates functional pial collateral to all areas of the cerebrum and cerebellum. As a result, there is normal CT density in the venocapillary pool in all areas that appeared abnormal on the CT perfusion.
 
MR diffusion and Flair sequences
1. Negative MR diffusion nor cytogenic edema on FLAIR without evidence of an acute ischemic event in any areas of prolonged TTP or reduced CBV..
 
MR Susceptibility
1. Negative SWI sequence
 
Final Summary for Case 8 stroke imaging CT, CTA, CT perfusion & MR.
1. Diffuse atherosclerotic arterial disease with segmental occlusion of the proximal Rt. vertebral, Lt. high cervical vertebral and proximal Lt. IAC.
2. Only minimal EC-IC collateral is present through the Lt. ophthalmic artery.
3. There are tandem extradural ICA stenoses on the Rt.
4. There is ulcerative plaque in the Lt. common carotid.
5. The intradural afferent circulation is delayed, but does completely fill arteries in both the cerebrum and the posterior fossa via complete circle of Willis and functional retrograde pial collateral.
6. Despite extensive extradural vascular disease, there is no sites of oligemia are evident on the delayed post contrast analysis of the venocapillary pool and no evidence of an acute event on MR dwi/FLAIR/swi.

1. There is atherosclerotic mural thickening of the left common carotid with stenosis between 30-40%. However, there is ulcerative plaque in the ICA bifurcation. The proximal left ICA sinus segment is opacified, but the left ICA is not opacified beyond this point. The noncontrast CT demonstrated intraluminal clot, and the CTA confirmed the same. Intracranially, there is collateral to the left ICA from the circle of Willis and the left ophthalmic artery. The proximal segment of the right vertebral artery is occluded from it's origin to C6. where it is reopacified via collaterals. The left vertebral artery is occluded above C1 and includes the intradural segment. The left PICA is collateralized from AICA-PICA connections.

2. The first pass CTA perfusion is grossly abnormal indicating virtually no flow to the left cerebrum. However, on the second pass CTA, the venocapillary pool has virtually normal transcapillary blood pool with no significant focal dropout to suggest acute completed stroke or even reduced blood flow. The MR diffusion and MR flair confirm that there has been no actual acute ischemic event causing cytogenic edema. 

1. This case is an example of a patient with extensive cervical atherosclerotic disease, including multiple sites of occlusion in primary cervical stem arteries, can have symptoms without actually causing a tissue level stroke. In other words, the oligemic event had only enough depth & duration to cause electrical dysfunction, but not enough to initiate the ischemic cascade. Hence, the MR diffusion remained normal despite an abnormal CT perfusion. The symptoms resolved typical of a TIA.

2. This case also illustrates how CT perfusion and the initial pass CTA can over estimate areas of oligemia, because the initial 1st pass data set is acquired in the arterial phase, which doesn’t include enough time for collateralization to occur.  In this example, the delayed CTA (which adds the second contrast bolus to the already circulating 1st bolus) demonstrated no reduction in the CT density within the venocapillary pool implying fully functional pial collateralization including the area of reduced CBV on the CT perfusion.  Remember, however, a normal delayed CTA  doesn’t necessarily preclude tissue level ischemia, as illustrated in Case 7 of this instructional case series. It only takes 3 minutes of severe oligemia to cause tissue injury. If reperfusion occur shortly after the ischemic event and prior to stroke protocol imaging, the CTA can appear normal or near normal. 

Watch the included summary video for this instructional case.