Back to Transcapillary Case 06 - Hyperacute Stroke

Case221g

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Case Notes

History

54 yo female with an acute left hemiparesis.

Exam

Prior Study

CT Head
Nonhemorrhagic, hyperacute right MCA, superior division, ischemic event.

CT Perfusion
Evidence of a dense ischemic infarction in the right MCA, superior division, perfusion zone and in the right frontopolar ACA perfusion zone and in the right basal ganglia lenticulostriate perfusion zone.
Evidence of a moyamoya (adult) variant affecting the left A1 and M1 segments producing rapid right lenticulostriate perforator blood flow.

Extensive PCA related pial collateralization is evident bilaterally, but it is clearly effective on the left and into the inferior MCA divison on the right. The PCA and thalamoperforator collateral is clearly functional (effective tissue perfusion) in both thalami and in the left cerebrum. It is likely that the combination of choroidal ICA segment stenoses and the left lenticulostriate moyamoya perforator vasculopathy (causing a vascular "steal effect") have combined to result in a transcapillary stroke in the right cerebrum.

CTA of the neck
The cervial arteries are not significantly abnormal to affect intracranial circulation.
There is evidence of a combination of findings indicating the presence of an adult variant of moyamoya syndrome. The lenticulostriate moyamoya vasculopathy is only on the left and this is occuring in an adult patient.

CTA of the head
There is CTA evidence of the adult form of moyamoya syndrome exhibiting bilateral, high grade, choroidal ICA segment stenoses, moyamoya vasculopathy only on the left and evidence of left ethmoid meningeal-pial anastomoses. There are both prominent PCA pial collaterals, and the thalamoperforating collaterals, which appear to preserve parenchymal perfusion in the thalami bilaterally, in all of the left cerebrum and the inferior right MCA territory. The moyamoya vasculopathy maintains flow to the left basal ganglia.
There are tandem stenoses afffecting the right ICA with a flow-limiting extradural, subclinoidal atherosclerotic stenosis and an intradural. flow-limiting, moyamoya clinoidal ICA segment stenosis. These combine along with the hypoplastic A-com and the steal effect of the prominent left lenticulostriate moyamoya vasculopathy to significantly reduce blood flow to the superior division of the right MCA, despite the retrograde PCA pial collateral.

There is CTA evidence of opacification of the  patent proximal secondary stem branches on the right ICA and some distal MCA pial filling. However, this pial circulation is ineffective and there is NO evidence of parenchymal contrast density in affected right superior division MCA perfusion zone, nor in the right basal ganglia. This indicates that the level of arterial obstruction is at the metarteriole/capillary level (i.e "transcapillary type of stroke"). 

Post contrast CT head
There is virtually no rise in the CT density within the venocapillary pool in the distribution of the right MCA superior division consistent with dense ischemic core. There is a partial rise, but not to normal in the right basal ganglia and the right frontopolar region.
The venocapillary pool CT density is near normal in the left cerebrum.

Noncontrast T1-w sequence
Post ischemic cytogenic edema is evident in the right superior division of the MCA and in the rostral aspect of the right ACA, as well  as in the right basal ganglia.
There is slow flow in patent pial branches of the superior division right MCA and slow flow in the proximal right MCA stem segments from circle of Willis collateral that show up on the T1-w sequence that were not as well seen on the head CTA. Thus, pial collateral is reduced, but is at least present on the right. However, it is clear that the extent of pial blood supply does not translate to adequate transcapillary blood flow to avoid initiating the ischemic cascade. 

There is substantial cytogenic edema sufficient to produce a right to left subfalcine shift of roughly 3-4 mms.

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Case221g

Findings

MR Diffusion

There is acute, positive diffusion consistent with acute ischemia in a recognizable arterial perfusion zone in a major stem, trunk, division or pial artery perfusion zone.

There is acute, positive diffusion consistent with acute ischemia in a recognizable perforator, choroidal, or deep subcortical penetrating artery/arteries.

There is acute, positive diffusion consistent with acute ischemia in recognizable centronuclear structures or brainstem perforator zone.

There is acute positive diffusion consistent with acute ischemia in a recognizable watershed zone.

There is acute, positive diffusion consistent with acute ischemia in a recognizable venous egress zone.

There is acute, positive diffusion consistent with acute ischemia within the cortical ribbon consistent with sequestered infarction (laminar necrosis)

There is acute positive diffusion in parenchyma that does not clearly fit into either a recognizable arterial or venous territory, but fits better with terminal artery oligemia and transcapillary ischemic changes.

There is acute, abnormal diffusion within one or both hippocampi indicating a recent seizure event.

There is evidence of intercurrent reperfusion hemorrhage.

Other

No other abnormalities are noted.