 There is global volume loss with superimposed progressive diffuse increase of ventricular caliber which is out of proportion to the degree of sulcal prominence. Although the ventricles are stable to minimally larger compared to 4/10/2015, they have been significantly enlarging from 12/6/2014 exams. There is no evidence of transependymal CSF resorption. There are multiple scattered new punctate foci of restricted diffusion within the cerebral hemispheres representing acute/subacute small vessel ischemic strokes. There is unchanged T2 hyperintense signal in the globus pallidus bilaterally which is nonspecific. There are nonspecific periventricular and subcortical white matter T2 hyperintensities likely representing chronic microvascular ischemic changes. There are small scattered microhemorrhages in the cerebellum in the also in the cerebral hemispheres which were felt to be present on the prior degraded exam. There is no extra-axial fluid collection with resolution of remote bilateral hemispheric subdural collections as noted on recent CTs. There is no mass effect or midline shift.
1.Progressive diffuse ventriculomegaly out of proportion to sulcal prominence, consistent with worsening, favored to represent hydrocephalus/NPH in the appropriate clinical setting. Also underlying progressive volume loss which may related to Alzheimer's.2.Scattered bilateral acute punctate nonhemorrhagic infarcts upon background of probable chronic small vessel ischemic changes.3.Stable nonspecific T2 hyperintensity associated with the globus pallidi, which could relate to a metabolic etiology. No other deep grey abnormal signal or diffusion restriction to suggest findings specific to CJD.