59 year old male with COPD who developed tachycardia requiring therapy. Two days later he developed Rt. sided weakness, pupillary dysfunction, and slurred speech. Shortly thereafter, he became somnolent and unresponsive.
 

CT head; CT perfusion; CTA neck; CTA head; Delayed post contrast head CT for analysis of the venocapillary pool; MR diffusion; MR flair; MR susceptibility

CT Head
1. Hyperacute basilar and left intradural vertebral artery thromboses with multicentric both arterial and watershed strokes involving multiple posterior fossa arteries, as described above.
2. There is early mass effect including compression of the 4thventricle, effacement of prepontine cisterns, and clear evidence of early upward transtentorial herniation.
3. Focal lesion within the deep central left cerebellum is likely a site of hemorrhagic conversion with very acute hematoma.

CT Perfusion
1. The TTP, CBF, & CBV changes consistent with completed infarctions in both SCA’s, the left AICA, the left PICA, the right cerebellar watershed zones, and possibly the left pons.
2. Absent MTT signal (out of scale sign) indicates virtually no transcapillary blood flow to generate MTT data. This is can occur with either sequestered infarction, or hemorrhagic transformation, or both. Differentiation between these two stroke complications is, best exhibited on the MR susceptibility sequence.
3. CTA head (included with our CT perfusion protocol) demonstrates patency of the left intradural vertebral artery and of the caudal basilar artery at this time, despite the CT-hyperdensity seen on the noncontrast CT head.
4. There is an old infarct with an encephalomalacic defect in the left temporal lobe (PCA-P3 segment perfusion zone).

CTA of the Neck
1. Diffuse atherosclerotic vascular disease is evident in the aorta with ulcerative plaque formation.
2. There is focal left ICA stenosis of 50% and a focal right ICA stenosis of 60%.
3. The proximal left vertebral artery is occluded at its’ origin, but is reconstituted at the C5 level from cervical soft tissue collaterals. The high cervical and intradural vertebral segments are within normal limits.

CTA of the Head
1. There is intraluminal basilar artery thrombus in its distal segment. It does allow some antegrade blood flow with contrast partially filling the residual basilar lumen. However, there is very limited filling of the major basilar artery branches.
2. The circle of Willis collateralizes the basilar tip and the PCA perfusion zones.
3. The Lt. PICA is patent but only fills the mesial inferior vermic branches. The right PICA is occluded at its’ origin but the right caudal cerebellar hemisphere receives pial collateral from the patent right AICA and from the patent mesial left PICA.
4. The left intradural vertebral artery segment has an irregular lumen, which is an indication of intercurrent recanalization of a previous thrombosed arterial segment.

Post contrast head CT (venocapillary pool analysis)
1. Markedly reduced CT density in the venocapillary pool within the left pons, and both cerebellar hemispheres, as above. These areas are all included in the dense ischemic core.
2. There is a very recent left deep cerebellar reperfusion hemorrhage, which when combined with the stroke-related brain swelling, has producing mass effect with early upward transtentorial herniation.
3. Lack of venous egress in the left cerebellum is indicative of venous collapse, and is likely the basis for the reperfusion hemorrhage.
4. There is an chronic completed infarct in the left P3 PCA perfusion zone.

MR diffusion
1. Multicentric cerebellar and left pontine infarctions are evident, as listed above. Stroke age is likely 6-8 hours or beyond. There is a chronic completed infarction with encephalomalaica in the left P3-PCA perfusion zone.
2. There is hemorrhagic conversion with hematoma in the left deep central cerebellar watershed zone.
3. There is apparent sequestered infarction in the right deep deep central cerebellar watershed zone.
4. There is early upward transtentorial herniation.

MR Flair
1. Multicentric infarctions are listed above; stroke age is likely 6-8 hours or beyond. There is an old left P3 infarction with encephalomalacia in the lateral ventral temporal lobe. There is wide spread age-related ischemic demyelination in the centrum semiovale bilaterally.
2. There is hemorrhagic conversion with hematoma in the left deep central cerebellar watershed zone.
3. There is sequestered infarction in the right deep deep central cerebellar watershed zone; this can be confirmed on MR-swi sequence.
4. There is early upward transtentorial herniation.

MR Susceptibility (SWI)
1. SWI evidence of prior intraluminal thrombus within the left intradural vertebral artery (which in now recanalized). Additionally, there is current hemorrhage in the pontine segment of the basilar artery, and in the posterior medullary segment of left PICA.
2. Sequestered infarct is evident in the deep central right cerebellar hemisphere. Hematoma is present in the deep central left cerebellar hemisphere.
3. SWI evidence of blooming artifact in the left cerebellar cortical veins consistent with venous collapse in mainly the AICA-PICA perfusion zone; hence, the hemorrhagic conversion in this territory.

1. The initial CT and CTA demonstrated a thrombotic occlusion of the proximal, dominant left cervical vertebral artery segment. It recanalizes in the mid cervical region. The left intradural vertebral artery segment appears to be a recanalized vessel with intimal irregularity The right vertebral artery was developmentally hypoplastic leaving the left vertebral artery supplying both caudal cerebellar hemispheres. There is amputation of the distal left PICA branches, non filling of the right PICA, and evidence of intraluminal thrombus in the distal half of the basilar artery with poor filling of the superior cerebellar arteries and the proximal PCA arteries. Distal PCA branches fill from the circle of Willis. The head CT demonstrated cytogenic edema in the caudal aspects of both cerebellar hemispheres. The stroke zone has tumefactive effects from sequestered infarction on  the right and early (isodense) parenchymal hemorrhage on the left. There is evidence of upward transtentorial displacement. There is a completed prior infarction in the caudal left cerebrum. The CTA changes appear to reflect multiple sites of possible acute or subacute intraluminal thrombus that upon recanalization have embolized the both cerebellar hemispheres and likely the rostral brain stem. The delayed CT imaging confirms the severely reduced transcapillary filling in both cerebellar hemispheres consistent with completed infarctions.

2. Follow-up MR diffusion confirms the bilateral cerebellar strokes (positive on both DWI and ADC maps) and the left pontine strokes and the left P4-PCA strokes. MR susceptibility confirms blood products in the right cerebellar hemispheric sequestered infarct and also the deep cerebellar hemisphere on the left. SWI also confirms that there is recanalized clot in the left intradural segment of the vertebral artery. This is the likely source of embolization to sites of posterior fossa structures depending on the original variation in arterial anatomy.

1. This case illustrates what happens with advanced oligemia resulting from a recanalized proximal stem arterial thrombus with widespread secondary distal embolization, in this case mainly into posterior fossa structures.

In this case, there was likely an initial thrombosis of the left intradural vertebral artery. The thrombus then recanalized with downstream secondary embolization into the posterior medullary segment of the left PICA, the left AICA, both SCA’s, terminating in an embolic shower within the distal PCA branches.

A relative large intraluminal embolic thrombus has partially occluded the pontine segment of the basilar artery.

There was also a chronic occlusion of the right PICA and origin occlusion in the left vertebral artery (which was reconstituted by cervical collaterals).

The pial collateralization pattern has been altered by multiple sites of proximal arterial occlusions. As a result, there are end-of the-line hypoperfusion dense infarctions in both cerebellar watershed zones. Additionally, there were primary infarcts in both superior cerebellar artery perfusion zones, and in the left pontine (basilar) perforator zones.

The addition of venous egress obstruction from the lateral superficial veins on the left, likely resulted in venous hypertension sufficient to produce the hemorrhagic conversion in the left cerebellum watershed, as opposed to that in the right cerebellar deep cerebellum.

Watch the included summary video for this instructional case.