Clinical question: CVA. Signs and symptoms: New facial droop. Nonenhanced brain MRI:No detectable acute intracranial process and in particular no evidence of acute ischemic stroke as is questioned clinically.Examination demonstrates periventricular and to a lesser degree subcortical foci of flair hyperintensity which are nonspecific however considering patient's stated age of 90 they likely represent microvascular chronic ischemic changes. Signal intensity of brain parenchyma otherwise remains unremarkable. There is moderately enlarged supratentorial ventricular system however with preserved cortical sulci and maintained midline. Prominence of cortical sulci is also noted which is likely within normal for patient of stated age of 90.The signal voids of major intracranial arterial branches are identified.The signal intensity of the intracranial venous sinuses are unremarkable.Calvarium and soft tissues of the scalp are unremarkable.Unremarkable images through the orbits, paranasal sinuses and mastoid air cells.Nonenhanced brain MRA:Bilateral internal carotid are free of are patent across the skull base and in their supraclinoid segments.Bilateral middle cerebral arteries are patent. There is apparent paucity of distal branches of MCA arteries which is believed to be secondary to poor quality imaging. The left anterior cerebral artery is patent. There is partial poor visualization of distal A1 and proximal A2 segments of the posterior cerebral artery which is believed to be secondary to severe tortuosity and suboptimal quality of the study. This finding can be further assessed if clinically deemed necessary with a CTA exam. There is hypoplastic right A1 which is a normal anatomical variation.Prominent bilateral posterior communicating arteries are identified. This anatomical variation (prominent bilateral posterior communicating arteries) resulting in generalized smaller caliber of the vertebral basilar circulation. Right vertebral artery and basilar artery demonstrate uniformly smaller caliber however without evidence of regional vascular lumen compromise or stenosis. A very small hypoplastic left vertebral artery is identified. There is no detectable communication of the left vertebral artery and the basilar artery which may be secondary to its very small hypoplastic size. The left pica branch is also non-detectable on source images or the reformatted images. This could also be secondary to very small size vessel however possibly occlusion cannot be excluded. MRI exam examination however demonstrate no ischemic changes in the distribution of the left vertebral/pica branches.
1.Nonenhanced brain MRI demonstrate no evidence of an acute intracranial process. Foci of flair hyperintensity in the in the subcortical and periventricular white matter of cerebral hemispheres are nonspecific however they are suspected for mild chronic nonhemorrhagic ischemic strokes. Mild to moderately enlarged supratentorial ventricular system without significant change since prior exam or deviation of midline.2.Patent bilateral internal carotid arteries and their distal branches. Uniformly small caliber of vertebrobasilar system secondary to presence of prominent bilateral posterior communicating arteries. The left vertebral artery is extremely small in size and without visualization of its very distal segment or left pica branch. This appearance could be result of very small size of the vessels however less likely possibility of occlusion cannot be entirely ruled out. There is no however no detectable foci of ischemic change in the distribution of the left vertebral/pica branch on MRI exam. If further assessment of intracranial vasculature is clinically deemed necessary follow up with CTA is recommended.