Headache. Visual field defect. There is restricted diffusion lesions on bilateral occipital lobes indicating acute ischemic infarct.. There is no evidence of hemorrhagic conversion.There is a linear focal encephalomalacia seen on the right side of upper pons suggesting chronic infarct.Multiple scattered bilateral centrum semiovale and periventricular white matter high signal intensities on FLAIR images indicate nonspecific small vessel disease.The ventricles, sulci and cisterns are symmetric and unremarkable. The midline structures and cranial-cervical junction are normal. Normal flow voids are identified in the major intracranial vessels. The paranasal sinuses and mastoid air cells are clear.3D time of flight MOTSA MRA brain images with maximum intensity projections of the anterior/posterior intracranial circulation demonstrate subtle irregularities of bilateral MCA M1 segments. However, there is no significant (more than 50%) luminal stenosis or intracranial arterial aneurysm. Vertebrobasilar system shows focal signal loss on the right PCA proximal P3 segment. This could represent a embolus but could also be an artifactual finding.3D MRA neck post-gadolinium images with maximum intensity projections of the cervical vasculature demonstrate non visualization of the left vertebral artery proximal segment from its ostium. This can represent segmental occlusion of the left vertebral artery.The right vertebral artery ostium shows signal loss indicate focal luminal stenosis. However, this is more likely due to tortuosity related artifacts. Bilateral common carotid arteries and internal carotid arteries appear to be normal.
1. Acute ischemic infarctions on bilateral occipital lobes (PCA territories) without hemorrhagic transformation.2. Non visualization of the left vertebral artery from its ostium to the level of C4, likely represent occlusion.3. Atherosclerotic changes of intracranial arteries.