New weakness and paresthesia. History of left ventricular thrombus. BRAIN MRI:The wedge-shaped subcortical/cortical biparietal T2-hyperintense lesions that probably represent previous ischemia/infarct remain unchanged. The associated foci of susceptibility effect remain unchanged, reflecting hemosiderin staining or mineral deposition. The scattered T2 hyperintense foci of signal intensity in the cerebral white-matter, predominantly frontoparietal, remain unchanged and are nonspecific. There is no diffusion restriction or new intracranial hemorrhage. There is no mass-effect or midline shift. The ventricles and the other CSF-containing spaces are mildly enlarged, reflecting mild underlying brain volume loss.Minimal mucosal thickening in the paranasal sinuses and right mastoid air cells is nonspecific. There is no gross orbital abnormality.CRANIAL MRA:There is no significant steno-occlusive lesion of the major intracranial arteries or aneurysm. The basilar artery and the V4 segments of the vertebral arteries are slightly smaller than expected which might be developmental (especially given the lack of calcification on the CT scan from February 5, 2016 and the relatively large posterior communicating arteries). This is unchanged since the previous examination.
1.No acute brain infarct or new intracranial hemorrhage. Biparietal small chronic infarcts with hemosiderin staining or mineral deposition remain unchanged. Mild-to-moderate, for age, cerebral nonspecific white-matter lesions are most suggestive of chronic microvascular ischemia.2.Cranial MR angiography shows no significant arterial stenosis.