New-onset seizure-like activity. History of HTN, HLD, and dementia thought to be Alzheimer's. Some of the images are degraded by patient motion. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There is a defect in the right corona radiata. There is extensive cerebral white matter T2 hyperintensity, which has progressed since 2012. There are scattered punctate foci of susceptibility effect in a predominantly peripheral lobar distribution. There is no abnormal intracranial enhancement. There is diffuse cerebral volume loss, which is more pronounced in the medial temporal lobes. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, skull, and scalp soft tissues are grossly unremarkable. There is mild scattered paranasal sinus mucosal thickening and suggestion of a fluid level in the left maxillary sinus. There is a pannus posterior to the dens, which appears to be somewhat eroded.
1. No evidence of acute intracranial hemorrhage, mass, or acute infarction.2. Extensive chronic probable small vessel ischemic disease or hypertensive encephalopathy, which has progressed since 2012, and chronic lacunar infarct in the right corona radiata.3. Scattered punctate foci of susceptibility effect in a lobar distribution may represent amyloid angiopathy. 4. Diffuse cerebral volume loss, which is more pronounced in the medial temporal lobes, suggests Alzheimer's disease.5. Suggestion of acute sinusitis.6. Pannus posterior to the dens, which appears to be somewhat eroded. This may be a manifestation of rheumatoid arthritis or crystalopathy, for example. 