Back to Transcapillary Case 06 - Hyperacute Stroke

Case221d

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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.

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Case221d

Findings

Supratentorial Intradural arterial circulation (for details see Arterial Stroke Module)

There is a primary stem intradural/extradural, or proximal intradural ICA high grade stenosis or occlusion.

There is no flow-limiting stenosis or mulicentric stenoses of a secondary stem, division, trunk or pial intracranial artery affecting either the supra or infratentorial arteries.

The circle of Willis is incomplete.

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 evidence of collateral re-routing of the intracranial pial arteries.

There is evidence of widespread pial artery stenoses without secondary cause (SAH, encephalitis, meningitis). In a middle age or younger patient distal small vessel stenoses raise the possibility RCVS (reversible angiitis in younger patients), versus primary CNS angiopathy (PACNS), diabetic vasculopathy or inherited CADASIL syndrome in young and middle aged adults.

There is evidence of widespread proximal and/or distal vasospasm in the context of pregancy, or complications of drug therapy, and associated with thunderclap headaches in younger patient to suggest reversibel vasospastic disorder (RCVS) or migraine vasculopathy.

Infratentorial Intradural arterial circulation (for details see Arterial Stroke Module)

There is high cervical or intradural vertebral artery thrombosis.

There is stenosis or thrombosis of all or part of the basilar artery.

Given there is high-grade stenosis or thrombosis of the basilar artery, there is adequate retrograde collateral filling the distal basilar & its branches.

There is high grade stenosis or thrombosis of all or part of the superior cerebellar artery (SCA)anterior inferior cerebellar artery (AICA), the posterior inferior cerebellar artery (PICA).

Supra & infratentorial venous Circulation (for details see Venous Stroke Module)

There is reduced venous egress, stasis, or thrombosis of the deep venous system (septal veins, thalamostriate veins & ICV's, vein of Galen and deep medullary veins).

There is reduced venous egress, stasis, or thrombosis of the major cerebral (frontal veins, veins of Trolard, veins of Labbe', superior sylvian veins, basal vein of Rosenthal or any of the posterior fossa veins).

There is acute dural sinus stenosis or thrombosis (sagittal, transverse, straight, transverse, torcula, sigmoid, jugular bulb).

There is increased or decreased blood flow through the mesial or lateral tentorial venous confluence, the vertex venous confluence, the sphenoparietal sinus/cavernous sinuses, inferior petrosal sinus.

Other

No other abnormalities are noted.