Back to Transcapillary Case 06 - Hyperacute Stroke

Case221c

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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.
 

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Case221c

Findings

Low Neck Evaluation (Aorta, Brachiocephalic, Proximal Common Carotid (CCA) & Proximal Vertebral Arteries)

There is evidence of aortic arch dissection or other abnormality.

There is evidence of occlusion of brachiocephalic arteries.

There is evidence of stenosis of brachiocephalic arteries.

There is evidence of occlusion at the origin of a carotid artery.

There is evidence of stenosis at the origin of a carotid artery.

Given a CCA is occluded, are the vertebral to occipital branch of the external carotid artery (EAC) collateral arcades functional.

There is evidence of occlusion in the proximal segment of a vertebral artery.

There is evidence of stenosis in the proximal segment of either vertebral artery. 

Upper cervical neck & intracranial/extradural evaluation

There is evidence of occlusion at the carotid bifurcation including proximal ICA or ECA or both.

There is evidence of flow-limiting stenoses within either the high cervical carotid or the vertebral arteries, exceeding 60% or less by NASCET standards.

There is dissection, pseudoaneurysm, or intimal web or both in the high cervical ICA's or vertebral arteries.

There is intimal ulceration or intimal dehiscence in the area(s) of carotid plaque.

There is intraluminal soft clot in the area of carotid plaque or pseudoaneurysm.

There is large vessel vasculopathy (FMD) of high cervical or intracranial/extradural ICA or vertebral arteries.

There is focal flow-limiting stenosis/occlusion of the ICA in its' intracranial-extradural segment.

There is focal stenosis or occlusion of the ICA or the vertebral at the dural ring or within the intradural vertebral segment.

There is evidence of reduced size of the either the high cervical carotid or vertebral arteries related to downstream stenosis

There is functional EC-IC collateral with enlargement of the internal maxillary or middle meningeal arteries.

There is increased size of either the ICA or vertebral arteries consistent with exaggerated intracranial flow demand (i.e. collateralization).

There is is evidence of macrovasculopathy of the proximal intradural ICA with stenoses and or abnormal perforators (both lenticulostriate and/or thalamostriate) representing moyamoya collateralization (disease, syndrome or adult moyamoya forms).

There is evidence of meningeal arteries connecting with pial arteries representing moyamoya collateralization.

There is thrombosis of internal jugular or other large neck veins.

There is thrombosis of the sigmoid, transverse, or torcular sinuses.

Other

No other abnormalities are noted.