Unprovoked seizure. The images are markedly degraded by patient motion. There is gyriform T1 hyperintensity and encephalomalacia along the margins of the left parieto-occipital sulcus. There are also small areas of surrounding high signal on DWI with what may correspond to mildly low ADC values, although these areas are too small to accurately characterize. The previously demonstrated scattered punctate foci of cortical, subcortical, corpus callosal, bilateral basal ganglia, and left cerebellar restricted diffusion have evolved into chronic infarcts. There is also patchy cerebral white matter T2 hyperintensity in the bilateral cerebral hemispheres and pons. The hippocampi appear to be grossly unremarkable. There is no evidence of intracranial hemorrhage or mass. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. There is a left lamina papyracea defect with herniation of orbital fat. There is a small left maxillary sinus retention cyst.
1. No evidence of acute intracranial hemorrhage or mass, although the images are markedly degraded by patient motion.2. Prior infarction along the margins of the left parieto-occipital sulcus with evidence of cortical laminar necrosis. 3. Small areas of surrounding high signal on DWI may represent superimposed recent infarction. Likewise, the previously demonstrated scattered punctate foci of cortical, subcortical, corpus callosal, bilateral basal ganglia, and left cerebellar restricted diffusion have evolved into chronic infarcts.4. Patchy areas of cerebral white matter T2 hyperintensity in the bilateral cerebral hemispheres and pons are nonspecific, but may represent chronic small vessel ischemic disease. 