 Diffusion restriction with faint ADC hypointensity and T2 hyperintensity is present involving multiple cortices, most prominently involving parietal lobes, however this finding can be found throughout the supratentorial brain. Additionally, similar-appearing findings are present involving the bilateral putamen and caudate as well as right pulvinar. Note is made of asymmetric predominant biparietal atrophy compared to the only mild prominence of the ventricles and remaining sulci. There are a few scattered small punctate foci of T2 hyperintensity within the primarily subcortical white matter without associated mass effect, restricted diffusion, susceptibility abnormality, or enhancement. The cerebellar tonsils are in normal position. There are no masses, mass effect or midline shift. The pituitary gland is normal in size. There are no extraaxial fluid collections or subdural hematomas. Flow voids are present within the major vessels indicating patency. Mucosal thickening can be found within right ethmoid air cells. The remaining paranasal sinuses and mastoid air cells are clear. There is an 8 mm focus of extra-axial enhancement in the right CP angle which slightly enters the porus acusticus, with a dural tail. This does not abut the adjacent pons or cerebellum. There is no abnormal enhancement elsewhere within the brain.
The constellation of MRI features is most suggestive of Creutzfeldt Jacob disease (CJD). The differential diagnosis would also include hypoglycemic encephalopathy. Given the lack of recent anorexic event history, acute ischemia as an etiology of the findings is unlikely; given the rapid progression of worsening dementia, a mitochondrial disorder etiology is felt to be unlikely; and given the lack of T1 hyperintensity within the globus pallidi and thalami, hepatic encephalopathy is also felt to be unlikely.