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Figure 1: (a) MRI. T2 coronal view. Hemosiderine deposition into right hemisphere due to hemorhagic transformation. (b) Diffusion. Damage into territories of both superior cerebellar arteries. Cortical hypersignal because of cytotoxic edema. Subacute ischemia. (c) MRA: Axial reconstruction. Left posterior cerebral artery of fetal origin. Hyperplasic left posterior communicant artery. Severe hypoplasia of left P1 segment. (d) Coronal reconstruction. There is no union between intracranial vertebral arteries (V4 segment). Left vertebral dominance. Right posteroinferior cerebellar artery merges from ipsilateral vertebral ar tery. Antero-inferior cerebellar artery looks thin, with scarce dista l flow. Hypoplasic left P1 segment, with fetal origin. (e) FLAIR. Axial view of subacute ischemia in both cerebellar hemispheres, in the territory of anterior superior cerebellar arteries

Figure 1: (a) MRI. T2 coronal view. Hemosiderine deposition into right hemisphere due to hemorhagic transformation. (b) Diffusion. Damage into territories of both superior cerebellar arteries. Cortical hypersignal because of cytotoxic edema. Subacute ischemia. (c) MRA: Axial reconstruction. Left posterior cerebral artery of fetal origin. Hyperplasic left posterior communicant artery. Severe hypoplasia of left P1 segment. (d) Coronal reconstruction. There is no union between intracranial vertebral arteries (V4 segment). Left vertebral dominance. Right posteroinferior cerebellar artery merges from ipsilateral vertebral ar tery. Antero-inferior cerebellar artery looks thin, with scarce dista l flow. Hypoplasic left P1 segment, with fetal origin. (e) FLAIR. Axial view of subacute ischemia in both cerebellar hemispheres, in the territory of anterior superior cerebellar arteries