Status post acute CVA for 2 month followup. Episode of left sided weakness and dysarthria. MRI HEAD: There is global parenchymal volume loss. There is redemonstration of T2 hyperintense lesions in theright hemispheric watershed territory as well as small foci of hyperintensity in the basal ganglia, cerebellum and brain stem. There are new T2 hyperintense lesions in the right parietal lobe and right posterior temporal lobe adjacent to the craniotomy site. There is no evidence of acute intracranial hemorrhage, mass, or acute infarct. There are scattered foci of susceptibility artifact, consistent with chronic microhemorrhages. The ventricles and basal cisterns are unchanged in size and configuration. There is no midline shift or herniation. The skull and extracranial soft tissues are unremarkable. There is moderate mucosal thickening of the bilateral maxillary sinuses and scattered mucosal thickening of the bilateral ethmoid sinuses. The right ICA flow void is again absent. MRA HEAD: Exam is degraded my motion artifact. There is evidence of right STA-MCA bypass in the interval. There is redemonstration of occlusion of the right internal carotid artery along the cavernous and opthalmic segments but reconstituted along the communicating segment via the PCOM, unchanged from prior exams. Antegrade flow is present in the distal left internal carotid artery, the distal vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries. There is no evidence for intracranial aneurysm. The anterior communicating artery is identified. The left posterior communicating artery not definitively visualized. The vertebral arteries are similar in size.
1. No evidence of acute infarct or intracranial mass effect.2. Unchanged occlusion of the right internal carotid artery at the ophthalmic segment with flow-related enhancement of the right anterior and middle cerebral arteries via collaterals and right STA-MCA bypass.3. Multiple foci of chronic watershed infarcts in right cerebral hemisphere again seen as well as lacunar infarcts in the basal ganglia, cerebellum and brain stem. Compared to 1/11/2015, new areas of T2/FLAIR hyperintensity in the right parietal lobe and right posterior temporal lobe are compatible with evolution of previously seen acute infarcts on MRI 1/11/2015 as well as some adjacent to the interval craniotomy which are compatible with postsurgical change. I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.