None traumatic intracranial hemorrhage. Intractable hypertension. Gross patient motion is most pronounced on the susceptibility-weighted sequences and the postcontrast sequences.BRAIN MRI:While there is apparent increase in the size of the intraparenchymal hemorrhage just deep to the right postcentral sulcus since prior CT scan, this is probably related to better conspicuity of the hemorrhage which was partly isoattenuating on the CT scan. The hemorrhage now measures in the axial plane 4.6 cm x 2.0 cm and 3.7 cm in the sagittal plane. It is heterogeneously T1/T2-hyperintense with T1/T2 central hypointensity and has a complete T2 hypointense rim. It is associated with relatively moderate surrounding T2 hyperintensity, reflecting edema and also mass-effect, which are not significantly changed since the prior CT scan. Accounting for diffusion signal alteration within the hematoma, there is no acute infarct.Despite gross patient motion, there is abnormal contrast enhancement external to the hemosiderin rim. This is most pronounced along the anterior aspect of the hemorrhage. However, contrast enhancement at this stage is nonspecific and may reflect a reactive process. There is no separate focus of abnormal brain contrast enhancement.Susceptibility-weighted imaging is markedly limited by patient motion. There are foci of deep T2-hypointensity in the deep aspect of the right cerebellar hemisphere, right thalamus and brainstem, probably representing hemosiderin staining. These show no associated edema.There are chronic lacunar infarcts involving the head of the right caudate nucleus, pons, and right cerebellar hemisphere. There is also patchy and confluent T2-hyperintensity in the cerebral white-matter, which is nonspecific but likely reflect chronic microvascular ischemia. There is focal thinning involving the mid body of the corpus callosum with increased T2 signal.Chronic right orbital medial and inferior wall blowout fractures are present. There is no other gross orbital abnormality. There is no destructive skull lesion.HEAD MRA:Mild irregularity of the cavernous internal carotid arteries, especially on the left, may reflect atherosclerosis. However, there is no significant stenosis, occlusion or gross aneurysm of the major intracranial arteries.NECK MRA:There is irregularity at the carotid bulbs, right more than left, and the proximal vertebral arteries, suggestive of atherosclerosis. However, there is no flow-limiting stenosis in the cervical carotid or vertebral arteries.
1.The anterior right parietal intraparenchymal hemorrhage shows heterogeneous signal but is likely late subacute or even chronic at this stage. It is associated with adjacent parenchymal contrast enhancement, the significance of which is difficult to determine as it might be also reactive to the hemorrhage at this stage. Associated perilesional edema and mass-effect are not significant changed since the CT scan from the day prior. 2.There is suggestion of hemosiderin staining without edema in the right cerebellar hemisphere, right thalamus and brainstem. The distribution of these is suggestive of hypertensive etiology. The susceptibility weighted sequences are nondiagnostic because of gross patient motion and other foci of hemorrhage would be difficult to rule out.3.Chronic infarcts are present in the right cerebellar hemisphere, right caudate nucleus and the pons. In addition, there are changes of chronic microvascular ischemia. 4.Cervical and head MRA show atherosclerosis but no significant, flow-limiting stenosis. There is also no gross intracranial aneurysm. 