Neuro_MR_Brain: 5 M, right-sided weakness.

CLINICAL HISTORY: 5 year-old with left MCA territory infarct.

 

FINDINGS: 

 

BRAIN: 

 

There is evolution of previously seen acute left MCA territory infarct involving the left frontal lobe, insula, and left basal ganglia, with increased edema and associated gyral swelling and sulcal effacement from prior exam. Additional small infarcts in the region of the genu of the left internal capsule/hypothalamus, and punctate infarct in the left temporal lobe are also again seen. No evidence of hemorrhagic conversion. No new infarct identified. No midline shift. 

There is no mass. 

No abnormal extracerebral collections are present. 

 

INTRACRANIAL ANGIOGRAM AND VESSEL WALL IMAGING: 

 

Redemonstration of occlusion of the distal post bifurcation left M1 segment extending into proximal M2 of the anterior division of the MCA. Linear appearing defect in the supraclinoid left internal carotid artery extending into the M1 segment, while this finding raises possibility of dissection, no evidence of dissection flap is seen on other sequences including high-resolution spin echo vessel wall images and is likely artifactual. There is narrowing of the proximal nondominant left A1 segment.

No flow-limiting stenosis right anterior circulation or posterior circulation, or vessel wall enhancement.

No evidence of flow-limiting stenosis or dissection in the cervical vasculature. Left vertebral artery is dominant. 

Dural venous sinuses are patent.

 

IMPRESSION: 

 

1.  Evolution of acute infarcts involving the anterior and deep left MCA territory, as well as punctate infarct in the genu of the left internal capsule/hypothalamus, likely ACA territory. No new infarct. 

 

2.  Unchanged occlusion of distal post bifurcation left M1/proximal M2 of the anterior division of the MCA. Stable narrowing of the proximal nondominant left A1.

 

3.  Vessel enhancement of occluded distal left M1/proximal M2, as well as left A1 segment and prebifurcation M1 segment, suggesting inflammatory etiology of stenoses and occlusion. Basal ganglia and genu of internal capsule infarcts likely due to involvement of nonvisualized small vessels from left M1 and A1. Findings favored to represent cerebral arteriopathy of childhood, less likely early manifestation of unilateral or asymmetric moyamoya disease. Follow-up recommended. 

 

4.  No flow-limiting stenosis or dissection in the cervical vasculature. 

(Cerebral arteriopathy of childhood)