81 years, Female, lung cancer, persistent headaches for a few months. Dementia stable. There is mild motion degradation on almost all of the sequences which limits detection for small lesions. Within this limitation, no evidence of abnormal parenchymal or meningeal enhancement is seen to suggest metastatic disease. No intracranial mass or mass effect. There is no evidence of recent ischemia or hemorrhage. There are multiple scattered foci of susceptibility particularly in the parieto-occipital lobes which were present on prior study. There is moderate degree of T2/FLAIR hyperintensity in the bilateral periventricular and subcortical white matter which is nonspecific but compatible with chronic small vessel ischemic disease and/or posttreatment changes. There is mild global parenchymal volume loss commensurate with patient's advanced age. No hydrocephalus. No extra-axial collections. Bilateral lens implants are noted. Calvarium and extracranial soft tissues are unremarkable. There is mild prominence of the retroodontoid soft tissues which may related to CPPD for example. There is associated mild narrowing of the spinal canal at the craniocervical junction.
1. Examination is motion degraded which limits sensitivity for small lesions. There is however no appreciable evidence of metastatic disease on the current study. No intracranial mass or mass effect.2. Multiple scattered foci of chronic microhemorrhage, which may represent amyloid angiopathy, and grossly similar to prior. Also no significant change in multiple patchy areas and scattered foci of FLAIR hyperintensity in the white matter which are nonspecific and may be related to chronic small vessel ischemic disease and/or posttreatment changes.3. Mild narrowing of the spinal canal at the craniocervical junction related to retro-odontoid soft tissue, which may be due to CPPD but is incompletely assessed.