82 years, Female, right hemiparesis, evaluate perfusion/stroke.. There is restricted diffusion involving the left posterior frontal corona radiata consistent with acute infarct. There is an area of FLAIR hyperintensity involving the left parietal lobe with gyriform T1 hyperintensity compatible with laminar necrosis and susceptibility effect within this region likely related to mineralization and/or chronic blood products. There is mild enhancement within this region. There is also a tiny focus of restricted diffusion within this region which may suggest ongoing ischemia. There is also a punctate focus of enhancement slightly superiorly involving the left post central gyrus favored to be related to a subacute infarct.There are multiple foci of susceptibility effect in the brain, predominantly involving the bilateral thalami, basal ganglia, and to a lesser degree cerebellum which are favored to be related to chronic hypertension. Additional peripheral foci involving the right temporal lobe and left parietal lobe may be related to amyloid angiopathy.Several foci of T2/FLAIR hyperintensity are seen in the bilateral subcortical and periventricular white matter, which are nonspecific, but compatible with mild to moderate chronic small vessel ischemic changes. No intracranial mass or mass effect. There is global parenchymal volume loss commensurate with patient's advanced age. No hydrocephalus. No extra-axial collections. Calvarium and extracranial soft tissues are unremarkable.Perfusion images demonstrate relative prolongation of mean transit time at the level of the left inferior frontal lobe and lateral basal ganglia (MTT series 1328 images 13-15) compatible with hypoperfusion in the left MCA territory.
1. Acute infarct involving the left posterior frontal corona radiata.2. Late subacute to chronic left parietal lobe infarct with evidence of laminar necrosis, mild enhancement, and mild volume loss. Within this region however there is a small cortical focus of restricted diffusion which may suggest ongoing/acute ischemia adjacent to an older infarct.3. Multiple foci of chronic microhemorrhage with distribution predominantly favoring a chronic hypertensive etiology. Few additional peripheral foci of chronic microhemorrhage suggest amyloid angiopathy.4. Perfusion images demonstrate relative prolongation of mean transit time at the level of the left inferior frontal lobe and lateral basal ganglia (MTT series 1328 images 13-15) compatible with hypoperfusion in the left MCA territory. Recent CTA demonstrated stenosis in the left supraclinoid internal carotid and M1 segment of the left middle cerebral artery.