Confusion, expressive aphasia. There is relatively symmetric cortically based mild restricted diffusion involving the bilateral parietal and occipital lobes and to a lesser degree frontal, and possibly temporal lobes with corresponding subtle T2/FLAIR signal hyperintensity. There is no evidence of restricted diffusion within the basal ganglia. There is additional patchy and confluent increased T2/FLAIR signal within the periventricular and subcortical white matter which is nonspecific but compatible with mild chronic small vessel ischemic changes. Susceptibility weighted images reveal several punctate foci of susceptibility artifact for example in the left frontal subcortical white matter, right paramedian right frontal lobe, and right parietal subcortical white matter in a nonspecific distribution and compatible with prior microhemorrhages.There is a punctate focus of enhancement involving the left precentral gyrus along the cortex. No additional pathological enhancement is identified. The ventricles and sulci are within normal limits. The basal cisterns remain patent. There is no midline shift or mass effect. No extra-axial fluid collection is identified. Normal flow-voids are demonstrated in the major intracranial vascular structures. The midline structures and craniocervical junction are within normal limits. The orbits, skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable.
1.Areas of bilateral cortical restricted diffusion, primarily in the parietal and occipital lobes. Differential considerations include infectious encephalitis, postictal state, metabolic encephalopathy, prion disease (although the overall distribution is somewhat atypical for CJD), and subacute cortical ischemia.2.Punctate focus of nonspecific enhancement involving the left precentral gyrus. Given cortical restricted diffusion, this may reflect component of subacute injury. Comparison with prior MRI would be helpful if available.3.Mild chronic small vessel ischemic changes.