Spastic left hemiparesis, abulia. History of hypertension, DM, developmental delay, and stroke causing left hemiparesis, and high grade right > left carotid stenosis. MRI: There has been interval evolution of diffuse right cerebral hemisphere white matter infarction, particularly in the corona radiata, with associated encephalomalacia, susceptibility effect, and Wallerian degeneration. There are also diffuse left cerebral hemisphere white matter T2 hyperintensities, mainly in a periventricular distribution, which are not significantly changed. There is diffuse cerebral volume loss, right more than left. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, skull, and scalp soft tissues are grossly unremarkable. There are right maxillary and left sphenoid sinus retention cysts.MRA: There is redemonstration of high-grade steno-occlusive disease involving the bilateral cavernous through supraclinoid internal artery segments with reconstitution of flow at the circle of Willis via the left posterior communicating artery. There is nevertheless paucity of flow-related enhancement to the right middle and anterior cerebral arteries. There is irregularity involving the left P2 segment. The bilateral cervical internal carotid arteries are diffusely diminutive. The posterior intracranial circulation and major cervical arteries are otherwise intact.
1. Diffuse chronic right cerebral hemisphere white matter hemorrhagic infarction, particularly in the corona radiata. There are also diffuse left cerebral hemisphere white matter T2 hyperintensities, mainly in a periventricular distribution, likely related to chronic small vessel ischemia, which are not significantly changed. Otherwise, no evidence of acute infarct. 2. Redemonstration of high-grade steno-occlusive disease involving the bilateral cavernous through supraclinoid internal artery segments with reconstitution of flow at the circle of Willis via the left posterior communicating artery. There is nevertheless paucity of flow-related enhancement to the right middle and anterior cerebral arteries. There is also irregularity involving the left P2 segment. The bilateral cervical internal carotid arteries are diffusely diminutive. The posterior intracranial circulation and major cervical arteries are otherwise intact. 