54 years Female (DOB:5/3/1961)Reason: hx of RA and CNS vasculitis, a/w right sided weakness and pain History: see abovePROVIDER/ATTENDING NAME: LEAH C ANDERSON CELESTE C THOMAS MRI of the brainNo diffusion weighted abnormalities are appreciated.There is a mild degree of periventricular and subcortical punctate hyperintense white matter lesions present identified on the FLAIR and T2 images. This has progressed since 2012 and 2014 and demonstrates minimal progression since 2015.There are multiple punctate T2 and FLAIR hyperintense lesions in the basal ganglia, thalami and brainstem as well as internal capsules. Additional such lesions are present in the cerebellar hemispheres. There are there is a focus of encephalomalacia in the inferior aspect of the right cerebellar hemisphere. There is no other focus of encephalomalacia along the superior aspect of the left cerebellar hemisphere. The pons is small. These lesions have not significantly changed since 2012.There is a punctate focus of signal hypointensity on susceptibility weighted imaging located adjacent to the operculum and the medial aspect of the right inferior frontal gyrus subcortical white matter. Another such lesion is present adjacent along the right superior frontal gyrus subcortical white matter along the deeper portions of the right superior frontal sulcus. In isolation these are of unknown clinical significance.The CSF spaces are appropriate for the patient's stated age with no midline shift. No intracranial mass lesion is appreciated No edema is identified within the brain parenchyma. No abnormal areas of enhancement are identified within the brain parenchyma.Normal vascular flow voids are present in the distal carotid and vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries as well as the internal cerebral veins and superior sagittal sinus.The visualized portions of the paranasal sinuses demonstrate mucosal thickening. The visualized portions of the mastoid air cells are partially opacified. The visualized portions of the orbits are intact.The parotid ducts are dilated. There appears to be accessory parotid gland tissue lateral to the right masticator space.MRA brain:Antegrade flow is present in the distal internal carotid arteries, the distal vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries.There is no evidence for intracranial aneurysm or cerebrovascular occlusion.The anterior communicating artery is identified and is medium size. The posterior communicating arteries are intact. The vertebral arteries are similar in size. The left A1 segment is larger than the right A1 segment. The posterior communicating arteries are medium-sized. MRA neck:There is opacification of the aortic arch, great vessels from the aortic arch and carotid arteries and vertebral arteries. There is no stenosis identified of the great vessels from the aortic arch. The left common carotid artery originates from the innominate artery. On the basis of NASCET criteria there is no significant stenosis at the left carotid bifurcation. There is 55% stenosis at the origin of the RICA. This has progressed since the prior exam from June 2015. There is no significant stenosis along the course of the vertebral arteries.
1.There is a moderate degree of ischemic type lesions in the cerebellar hemispheres, brainstem, basal ganglia and thalami in the chronic stage. These have not substantially changed since October 2012.2.There is no evidence for acute ischemic cerebral infarction.3.There is 55% stenosis at the origin of the right internal carotid artery. This has progressed since previous exams.4.Periventricular and subcortical white matter lesions of a mild degree are nonspecific. They are most likely vascular related. There is mild progression since October 2012.