54 years, Male, early onset Alzheimer's dementia. No restricted diffusion to suggest acute ischemia. There are numerous foci of susceptibility artifact of variable sizes throughout both cerebral hemispheres, predominantly at the gray-white matter junctions, which are compatible with chronic microhemorrhages. There is also curvilinear susceptibility signal along the left parieto-occipital sulci, compatible with superficial siderosis. No intracranial mass or mass-effect. The ventricles are within normal limits in size and configuration. There is a small area of encephalomalacia in the mesial right temporal lobe medial to the temporal horn (image 14 on axial series) Several foci of T2/FLAIR hyperintensity are seen in the bilateral subcortical and periventricular white matter, which are nonspecific, but compatible with moderate chronic small vessel ischemic changes. Major intracranial vascular 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. No evidence of acute infarct or other acute intracranial abnormality.2. Numerous chronic lobar microhemorrhages of varying sizes in both cerebral hemispheres and left parieto-occipital siderosis probably indicatinga prior hemorrhagic event. This could be seen with amyloid deposition with resultant angiopathy.3. Nonspecific abnormal T2 signal in the periventricular and subcortical white matter to a degree greater than expected for patient age and could also be related to amyloid angiopathy versus chronic small vessel ischemic changes. Correlation with cerebrovascular risk factors is suggested.4. Small area of encephalomalacia in the mesial right temporal lobe likely related to a small chronic infarct.