Back to Transcapillary Case 06 - Hyperacute Stroke

Case221e

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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"). 

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Case221e

Findings

Pial Collateral Analysis (for details see Arterial Stroke Module)

Does the pial collateral reach the distal end of the arterial thrombus (good if yes). If it does not there is a pial collateral gap.

There is an incomplete circle of Willis contributing to delayed collateral filling (increases probability of stroke w/ intercurrent hypotension).

The post contrast head CT demonstrates reasonable retrograde pial collateral, but, the CT density within venocapillary pool within the stroke-zone appears exaggerated, compared to the contralateral side, reflecting vasodilatation indicating post ischemic dysautoregulation.

The post contrast head CT demonstrates reasonable retrograde pial collateral, and the CT density within the venocapillary pool now appears normal on the delayed CT, as well indicating the pial collateral effectively supplies the underlying brain.

The post contrast head CT demonstrates fair retrograde pial collateral but the CT density within venocapillary pool, although present, appears significantly reduced from expected normal.

There is hyperemia in basal ganglia and thalamic perforating artery territories with increased venocapillary pool CT density consistent with moyamoya disease physiology

There is oligemia in brain with a "usual watershed distribution" with both incomplete retrograde pial collateral and reduced or absent venocapillary pool CT density evident on both the initial & delayed post contrast CT head.

There is oligemia in brain with an end-of the-line watershed distribution with both retrograde pial collateral but reduced or absent venocapillary pool CT density evident in the region of the shifted watershed zone.

Repeat analysis of the venous egress on the delayed post contrast head CTA reveals persistent evidence of reduced opacification or absence of cortical veins, deep central veins, or of the dural sinuses.

Other

No other findings abnormalities are noted.