72 years Female (DOB:11/15/1943)Reason: evaluate for stroke History: L-sided weakness, extensive aneurysmal burdenPROVIDER/ATTENDING NAME: JAMES J WALTER RICHARD J KRAIG MRI of the brainThere is a small focus of diffusion restriction present in the right centrum semiovale measuring approximately 10 mm in size which is high signal on FLAIR and T2 imaging.There is a focus of encephalomalacia present in the left inferior parietal lobule and adjacent precuneusThere is a mild degree of periventricular and subcortical confluent hyperintense white matter lesions present identified on the FLAIR and T2 images.Some patchy T2 and FLAIR signal hyperintensities are present in the thalami, brainstem and basal gangliaA subdural effusion the posterior fossa is likely related to atrophy.Punctate foci of signal loss are identified on susceptibility weighted imaging within the cerebellar hemispheres approximately 2 or 3 in each cerebellar hemisphere. These were also present on the prior examNo abnormal mass lesions are appreciated intracranially. No intracranial hemorrhage is identified. No edema is identified within the brain parenchyma.The visualized portions of the paranasal sinuses are clear. 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 a 10 mm x 9 mm aneurysm present along the left internal carotid artery originating from the posterior aspect of the clinoidal segment with any 2.5-mm in neck and suprasellar extension which abuts the optic nerve. There is fusiform ectasia of the left internal carotid artery at the distal cavernous segment where it dilates up to 7 mm in diameter. Immediately distal to this ectasia the internal coronary narrows down to 2.5 mm after which the aneurysm originates. The aneurysm abuts the left optic nerve. The aneurysm appears stable when compared to the prior exam. There is 40% narrowing of the left internal carotid artery at the distal cavernous segment.The right vertebral artery functionally appears to and in the right posterior inferior cerebellar arteryThere is a stenosis present at the distal left vertebral artery at the vertebrobasilar junction where there is approximately 80% stenosis over a 10 mm segment. There is 40% narrowing basilar artery along its midportion.The right P1 segment appears be occluded approximately 4 mm from its origin and the left P1 segment is stenotic approximately 7 mm from its origin where it narrows down to 1 mm diameter.There is a short segment 80% stenosis at the proximal left middle cerebral artery at the M1 segment with associated poststenotic dilation. This was also present on the prior exam. It does not appear to have progressed significantly.There is no evidence for intracranial aneurysm or cerebrovascular occlusion.The anterior communicating artery is identified. The posterior communicating arteries are not readily identified. The vertebral arteries are similar in size.
1.There is an acute lacunar infarct present in the right centrum semiovale.2.A 10 mm left internal carotid artery aneurysm at the clinoid segment is stable compared to the prior exam. This is associated with suprasellar extension. The aneurysm abuts the left optic nerve.3.There is 80% stenosis at the distal left vertebral artery near the V-B junction associated with milder narrowing of the basilar artery. The LVA appears to be effectively the sole supply to the basilar artery. It is associated with tandem foci of narrowing in the basilar artery.4.80% stenosis at the proximal left M1 segment.5.There is occlusion of the right P1 segment.6.There is a high-grade stenosis along the proximal left P1 segment.7.There are multiple old lacunar infarcts present in the brainstem and thalami. These were also present on the prior exam.8.There is a focus of encephalomalacia in the left parietal lobe. This was also present on the prior exam.9.Periventricular and subcortical white matter lesions of a moderate degree are nonspecific. At this age they are most likely vascular related. 10.Cerebellar microhemorrhages are stable.