Moya moya, f/u pial synangiosis: surveillance. MRI: There are areas of T2 hyperintensity in the subcortical and deep cerebral white matter bilaterally. There is no evidence of intracranial hemorrhage, mass, or acute infarct. The ventricles and basal cisterns are unchanged in size and configuration. There is no midline shift or herniation. The orbits, skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable.MRA: There are postoperative findings related to bilateral pial synangiosis. There is apparent focal loss of flow-related signal in the distal portion of the otherwise patent right superficial temporal artery at the microcraniotomy site, but there is abundant underlying pial vasculature. There is a small caliber left superficial temporal artery diffusely, but there is abundant underlying pial vasculature. There is severe steno-occlusive disease of the supraclinoid right internal carotid artery and proximal right middle and anterior cerebral arteries. There is also severe steno-occlusive disease throughout the length of the left internal carotid artery and proximal right middle and anterior cerebral arteries. There are numerous moyamoya collateral vessels. The posterior cerebral circulation is intact.
1. MRI: Stigmata of moyamoya disease with what may represent chronic ischemic disease, but no acute infarction. The degree of cerebrovascular steno-occlusive disease is similar to the prior exam. 2. MRA: Findings related to bilateral pial synangiosis with apparent focal loss of flow-related signal in the distal portion of the right superficial temporal artery at the microcraniotomy site, which may be due to stenosis or artifact, but there is abundant underlying pial vasculature. The left superficial temporal artery is of diffusely small caliber, but there is abundant underlying pial vasculature. 