 No restricted diffusion to suggest acute infarct. No intracranial mass or mass-effect. The ventricles are within normal limits in size and configuration. There is global parenchymal volume loss with slightly greater involvement of the bilateral parietal lobes similar to prior.There are innumerable foci of susceptibility effect throughout the brain compatible with chronic microhemorrhages, with particular preponderance within the basal ganglia and thalami as well as in the cerebellum. Several of these foci also noted in a peripheral lobar distribution. Allowing for differences in technique, no significant change from prior since 10/14/2014.There is moderate degree of T2/FLAIR hyperintensity in the bilateral subcortical and periventricular white matter as well as the pons and thalami which are nonspecific but compatible with moderate small vessel ischemic disease. Prominent perivascular spaces in the the basal ganglia are also seen.No abnormal parenchymal or meningeal enhancement. Specifically no thickening or abnormal enhancement involving the abducens or other cranial nerves is appreciated. There is symmetric enhancement of the cavernous sinuses. Major flow-voids are preserved. Changes of bilateral intraocular lens replacement. Minimal mucosal thickening in the paranasal sinuses. Paranasal sinuses and mastoid cells are otherwise clear. Bone marrow signal and extracranial soft tissues are within normal limits. MRI ORBITS: Changes of bilateral intraocular lens replacement. No intraorbital mass. No abnormal signal involving the optic nerve or chiasm. No evidence of mass effect. Extraocular muscles appear unremarkable. Minimal enhancement is seen along the optic nerve sheaths which is most likely within normal limits.MRA HEAD
1. No evidence of infarct, intracranial or intraorbital mass, or aneurysm. No lesions along the course of the left abducens nerve are appreciated.2. Moderate chronic small vessel ischemic disease similar to prior. 3. Again seen are numerous foci of chronic microhemorrhages throughout the brain including the basal ganglia, thalami, and cerebellum as well as some in a peripheral lobar distribution. Distribution is consistent with chronic hypertension and/or amyloid angiopathy.4. No significant stenosis in the intracranial or extracranial vasculature in the neck.