Catatonia, limbic encephalitis. Examination is significantly motion degraded. Within this limitation, there is no restricted diffusion to suggest acute ischemia. No acute intracranial hemorrhage. No intracranial mass or mass-effect. No hydrocephalus. There is generalized global parenchymal volume loss.Multiple foci of T2/FLAIR hyperintensity are seen in the bilateral subcortical and periventricular white matter, which are nonspecific, but compatible with mild chronic small vessel ischemic disease. T2 hyperintensity is noted within the bilateral subinsular white matter which is favored to be related to combination of chronic ischemic change and prominent perivascular spaces. There are few punctate foci of susceptibility effect in the bilateral temporal and occipital lobes compatible with chronic microhemorrhages.No abnormal parenchymal or meningeal enhancement. Major flow-voids are preserved.Sella and orbits are grossly within normal limits. Paranasal sinuses and mastoid cells are clear. Bone marrow signal and extracranial soft tissues are within normal limits.
1. Moderately motion degraded exam demonstrates no evidence of infarct, mass, or mass effect. No clear evidence of encephalitis but consider lumbar puncture for further evaluation as clinically indicated. 2. Multiple areas of T2/FLAIR hyperintensity described above are nonspecific but compatible with mild chronic small vessel ischemic disease. There is generalized global parenchymal volume loss which is mildly prominent for age.3. Few punctate foci of susceptibility effect in the bilateral temporal and occipital lobes compatible with chronic microhemorrhages. Given the peripheral lobar distribution, these may be related to chronic amyloid angiopathy.