Presentation
Acute hemiplegia.
Patient Data
Non-contrast CT
Hyperdense right MCA. No acute intracranial hemorrhage. Normal grey-white differentiation is maintained except where there appears to be a frontal operculum and insular infarct with gliosis and volume loss.
CT perfusion
Perfusion shows increased MTT throughout the right MCA territory with slightly increased CBV and preserved cortical CBF. Reduction of CBF is, however, seen in the right basal ganglia.
Findings are those of a large penumbra and small basal ganglia core.
CT angiogram
Filling defect in the M1 segment of the right MCA, just distal to the origin. There is some arterial flow past this.
No other arterial occlusion, filling defect or significant stenosis identified. Normal opacification of the circle of Willis. Two vessel aortic arch, with a bovine configuration (normal variant). Mild calcification of the arch. The carotid arteries opacify normally. Mild calcification at the carotid bifurcation bilaterally, without significant stenosis. The vertebral arteries opacify normally.
Conclusion
Acute right MCA thromboembolism, with filling defect in the right MCA M1 segment. Associated large penumbra on CT perfusion with small basal ganglia infarct core.
The patient was treated with IV tPA and proceeded to angiography for endovascular clot retrieval.
Cerebral angiography
The right common carotid artery injection showed no evidence of a proximal right MCA occlusion. Distal right M2 clot identified but too distal for clot retrieval.
Established infarct of the lentiform and body of caudate. No cortical infarct. The previously demonstrated right M1 filling defect is no longer present on today's time-of -flight angiogram (not shown).
There is also an old frontal operculum and insular infarct with gliosis and volume loss.
Case Discussion
This case illustrates both the utility of perfusion in identifying core vs penumbra and demonstrates a common pattern whereby an M1 occlusion causes striatocapsular infarction (end-arteries) but not cortical infarction if reperfusion and collateral flow is sufficient.
It also shows how challenging it can be when acute and chronic infarcts co-exist.
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