 BRAIN:There is no diffusion abnormality. There is cystic encephalomalacia in the superior left frontal gyrus that extends posteriorly into the left parietal lobe, as well in the left occipital and posteromedial temporal lobes, corresponding with previously seen infarcts in the left ACA, PCA, and to lesser degree MCA territories. There is associated volume loss and ex vacuo dilatation of the left supratentorial ventricular system.There is expected evolution of intraparenchymal hemorrhage in the left basal ganglia with a rim of susceptibility artifact and encephalomalacia, overall decreased in size compared to prior. There is a punctate focus of susceptibility artifact in the right basal ganglia, unchanged. There is a punctate focus of susceptibility in the genu of the left internal capsule, possibly seen on prior examination and better seen on the current study.There is associated volume loss of the corpus callosum as well as the left cerebral peduncle, consistent with Wallerian degeneration. Normal flow voids are identified in the major intracranial vessels. The paranasal sinuses and mastoid air cells are clear.MRA:Please note that the prior MRA was technically degraded, therefore comparison is not possible. There is signal within the distal bilateral vertebral arteries, within the basilar artery, distal bilateral internal carotid arteries and carotid siphons and bilateral anterior, middle and posterior cerebral arteries. No arterial stenoses, occlusions, arteriovenous malformations, or aneurysms are identified.
1.Evolution of multiple prior infarcts as described above with resultant encephalomalacia and expected evolution of left basal ganglia hemorrhage.2.MRA without significant stenosis in the anterior or posterior circulation. Note that the prior MRA was technically degraded and direct comparison is not possible.