Presentation
Acute loss of consciousness.
Patient Data
Hypodensity and reduced grey-white matter differentiation anteromedially in both frontal lobes and the right head of caudate nucleus and lentiform nucleus. Bifrontal gyral swelling. Possible hyperdense ACom and right proximal A2. No hemorrhage, surface collection, mass effect or midline shift. Basal ganglia calcifications. The ventricles and basal cisterns are symmetric and normal for age. Normal density of the superior sagittal sinus.
Impression
Suspected bilateral ACA infarcts - CTA and CTP advised.
Aortic arch demonstrates anatomical variation with four vessels with the left vertebral artery originating from the arch.
Contrast filling defect is seen within the distal right common carotid just proximal to the carotid bulb and extending cranially with 50% luminal narrowing extending over a length of 20 mm. The right internal carotid demonstrates no contrast filling from C1-C6.
The left common carotid also demonstrates contrast filling defect from the carotid bulb extending caudally with no contrast seen in the internal left carotid from C1-C6.
The intracranial bilateral ICAs are non opacified with some reconstitution of contrast present within the right cavernous ICA and left supraclinoid ICA from the posterior circulation, hypoplastic left PCOM noted.
Right A1 segment demonstrates contrast filling defect corresponding to the hyperattenuating vessel noncontrast scan. Potential collateral filling of the A2 segment which is of reduced caliber and irregular relative to the left. No filling defects identified within the bilateral M1 and M2 segments.
Small linear filling defect within the origin of the basilar artery could represent small nonocclusive thrombus. Multifocal narrowing and irregularity of the right V1 segment with good opacification distally.
Mild calcified atheroma involving the bilateral carotid bulbs and ICAs.
Large volume of bilateral ACA territory demonstrates elevated MTT and TTP with corresponding reduced CBV and CVF. The majority of the perfusion abnormality indicated core infarct with some penumbra in the left MCA territory.
Case Discussion
On review of external prior imaging (not available for upload) and following discussion with the INR and stroke teams, the timeline is:
Pre existing disease:
moderate right cervical ICA stenosis
left cervical ICA occlusion
left MCA territory had developed pial collaterals
good vertebrobasilar circulation, patient ACom and Pcom arteries.
Current episode:
acute right cervical ICA thrombosis and near occlusion causing right A1 distal embolism
right M1 supplied by good right Pcom artery
right ACA territory infarction as no cross flow from Acom artery
left MCA territory supplied by pial collaterals (confirming compensation of chronic ICA occlusion), ischemic due to no cross flow Acom artery (collaterals were maintaining enough perfusion with help from the Acom artery)
There was no endovascular option for ECR due to the severe bilateral cervical ICA disease and patient co-morbidities. The patient progressed to further infarct both MCA territories in the next 24 hours and was palliated, dying 3 days later.
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