 Evaluation of the MRI study is slightly limited by mild motion artifact, especially on the coronal sequences.The ventricles and sulci are prominent consistent with volume loss greater than expected for age. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There is nonspecific FLAIR hyperintensity in the periventricular distribution which is nearly confluent, especially posteriorly along the occipital horns which may be minimally ex vacuo dilated. FLAIR hyperintensity is also noted within the splenium of the corpus callosum. Thin intrinsic gyriform T1 hyperintensity is noted within the bilateral occipital lobes, parietal lobes near the perirolandic areas, posterior temporal lobes, left greater than right side. There is also involvement of the insular cortex. There is no significant associated volume loss, susceptibility, or FLAIR hyperintensity in these locations. There may be some areas of superimposed subtle enhancement in this distribution as well. There is intrinsic T1 signal hyperintensity and minimal T2 signal hyperintensity in the dorsal thalami.There is no diffusion abnormality. There is no midline shift or herniation. No extra-axial fluid collection is identified.There is fluid noted within the mastoid air cells bilaterally, right greater than left. Normal flow-voids are demonstrated in the major intracranial vascular structures. The midline structures and craniocervical junction are within normal limits.
1. There is no evidence of acute intracranial abnormality. FLAIR hyperintensity within the splenium of corpus callosum may relate to recent seizure activity. 2 Thin gyriform intrinsic T1 hyperintensity within predominantly the posterior cerebrum bilaterally may represent laminar necrosis from prior cortical injury of unknown etiology, possibly from a prior vascular insult, prolonged seizures, PRES, or less likely ictal hypoxia.3. T1/T2 hyperintensity in the pulvinar bilaterally, which is nonspecific but can be seen relating to degeneration following prolonged seizure activity, as well as metabolic derangements.4. Confluent FLAIR hyperintensity along the lateral ventricular margins, especially posteriorly with possible mild ex vacuo dilatation of the occipital horns. This is nonspecific but may represent areas of gliosis.