Diagnosis: Slurred speechClinical question: vascular stenosisSigns and Symptoms: slurred speech, r side weakness MRI of the brainNo diffusion weighted abnormalities are appreciated.There is a 9 mm hypointense lesion on T2-weighted imaging with surrounding T2 and FLAIR signal hyperintensity and susceptibility effect which is centered in the left cerebellar hemisphere.There are multiple punctate foci of signal loss on susceptibility weighted imaging present in addition to the above described lesion. The lesion present in the hippocampi. There are multiple punctate foci of signal loss on susceptibility imaging located in the thalami bilaterally peduncle and in the basal ganglia bilaterally. There is a slitlike focus of susceptibility effect involving right basal ganglia. There are punctate foci of signal loss and susceptibility weighted imaging in the subcortical white matter as well involving the temporal lobes and left cingulate gyrus.There is a mild degree of periventricular and subcortical punctate hyperintense white matter lesions present identified on the FLAIR and T2 images.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 in the left maxillary sinus associated with a smaller left maxillary sinus compared to the right maxillary sinus. Involution of the maxillary sinus could be related related to silent sinus syndrome. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits demonstrate medial deviation of the left lamina papyracea. This suggests an old medial orbital blowoutMRA 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 not readily. The left A1 segment is larger than the right A1 segment. There is fetal origin of the posterior cerebral arteries bilaterally. The right vertebral artery is small and effectively ends in the right posterior inferior cerebellar artery. There is extracranial origin of the left posterior inferior cerebellar artery. The vertebral arteries are similar in size.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. On the basis of NASCET criteria there is no significant stenosis at the carotid bifurcations. There is no significant stenosis along the course of the vertebral arteries. The left common carotid artery originates from the innominate artery.
1.There is a hemorrhagic lesion present in the left cerebellar hemisphere. Underlying etiology is unclear. If clinically appropriate follow-up exam which may include postcontrast imaging may be of benefit to further evaluate this.2.There are multiple microhemorrhages present as detailed above. The pattern is suggestive - but not confirmatory - of microhemorrhages related to hypertension. 3.Findings suggest an old hemorrhage involving the right basal ganglia which is now in the chronic stage.4.Periventricular and subcortical white matter lesions of a mild degree are nonspecific. At this age they are most likely vascular related. 5.Old left medial blowout fracture and findings suggestive of left silent sinus syndrome.