Back to Transcapillary Case 06 - Hyperacute Stroke

Case221i

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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.

MR diffusion
Acute, nonhemorrhagic, right superior division MCA, right frontal ACA, plus both the right A1/2 and  M1/2 perforator zone basal ganglia infarctions, estimated stroke age is consistent with 3-5 days of age.

MR T2-2 turbo spin-echo sequence
Recent, nonhemorrhagic, right, MCA/ACA transcapillary type of stroke with estimated stroke age of 3-5 days.
There is moderate focal cytogenic producing a4-5 mm midline shift and early optic hydrops (raised intracranial pressure)

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Case221i

Findings

MR SWI

There is venous prominence (hyperemia) of the deep medullary veins without blooming artifact, which can reflect physiologically increased venous flow rate, or can be the result of congestion associated with a downstream venous outlet obstruction.

There is SWI venous prominence within the deep medullary veins with blooming artifact, which implies significant venous stasis rather than physiologic hyperemia.

There is reduction in size of the ipsilateral major deep central veins indicating significant reduction in transcapillary blood flow.

There is SWI blooming artifact in proximal arteries indicating recent thrombosis.

There is SWI blooming along major cortical veins indicating recent thrombosis.

​There is SWI susceptibility artifact in the parenchyma included within the stroke-zone indicating sequestered infarction (i.e. cortical laminar necrosis or parenchymal sequestered infarctions).

There is SWI susceptibility artifact within the stroke-zone to indicate hemorrhagic conversion.

There is SWI signal consistent with abnormal or physiologic brain calcification (focal absent nodular signal loss). It should be noted that chronic brain nodular calcification (as in sequelae of neonatal infections) are often not evident as a signal loss on SWI.

Other

No other abnormalities are noted.