38 years Male (DOB:11/8/1977)Reason: stroke History: AphasiaPROVIDER/ATTENDING NAME: WILLARD W SHARP TAO W XIE MRI of the brainThere is gyral T2 and FLAIR signal hyperintensity associated with diffusion restriction involving the inferior aspect of the left inferior parietal lobule as well as the left superior temporal gyrus of the left temporal lobe and the lateral aspect of the adjacent left occipital lobe at the level of the cuneus and posterior aspect of the left insular cortex. There are some associated small foci of gyriform susceptibility effect.There are small T2 hyperintense lesions in the pons.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 minor opacities. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact.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 small in diameter. There is fetal origin of the left posterior cerebral artery associated with a hypoplastic left P1 segment. The right posterior communicating arteries is very small. 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 vertebral artery origin is not adequately visualized on this exam.
1.Subacute phase infarction involving the confluence of the left inferior parietal lobule, adjacent left temporal lobe and small portion of the left occipital as well as the posterior aspect of the left insular cortex2.Periventricular and subcortical white matter lesions of a mild degree as well as lesions in the pons are nonspecific. At this age they are most likely vascular related.3. The left vertebral artery origin is not adequately visualized on this exam. The possibility of left vertebral artery origin stenosis cannot be excluded.4.There is no evidence for intracranial cerebrovascular occlusion or stenosis.