85 years Male (DOB:4/4/1931)Reason: r/o stroke History: right sided weaknessPROVIDER/ATTENDING NAME: DAVID G BEISER DAVID G BEISER MRI of the brainThere is diffusion restriction present along the left parietal lobe involving left postcentral gyrus and some the adjacent left superior parietal lobule extending down to the level of the insula and a small portion of the left temporal lobe.There is a mild to moderate degree of periventricular and subcortical punctate hyperintense white matter lesions present identified on the FLAIR and T2 images.On susceptibility weighted imaging there are are several periventricular punctate foci of signal loss present which are nonspecific and in isolation of unknown clinical significance.. Additionally within the left sylvian fissure at the left M1 M2 junction there is a focus of blooming artifact. This corresponds to blood supply to the patient's area of diffusion restriction. Additionally there is intravascular signal hyperintensity on FLAIR imaging on a branch of the left middle cerebral artery.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 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. The left A1 segment is larger than the right A1 segment. In general the time of flight signal is diminished. There appear to be fewer vessels in the left sylvian fissure compared to the right sylvian fissure and the left M1 segment appears slightly smaller than the right M1 segment. The left angular artery is identified but is diminutive relative to the contralateral side. Additionally the left posterior parietal artery is not readily identified.There is no evidence for intracranial aneurysm or cerebrovascular occlusion.The anterior communicating artery is identified and is medium size. There is fetal origin of the right posterior cerebral artery. The right vertebral artery is larger than the left vertebral artery.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. There is an 70% stenosis at the origin of the left vertebral artery. The left vertebral artery is smaller than the right vertebral artery.
1.Findings are compatible with acute ischemic cerebral infarction involving the left parietal lobe including the left postcentral gyrus, some of the adjacent left superior parietal lobule, some of the left posterior insular cortex and small portion of the left temporal lobe.2.Findings are suspicious for occlusion of at least one branch of the left middle cerebral artery most likely the M2 and M3 junction. If this is isolated to the left posterior parietal artery is suspected within the infarct would appear to be near-complete.3.70% stenosis at the origin of the left vertebral artery.4.Findings were discussed with the neurointensive care unit fellow at the time of the exam. Discussion also centered around intervention. It decided based on the fact of the patient's NIH stroke scale score improved from 19 to 11 and the fact that it appeared that the much of the left middle cerebral artery territory was patent that intervention was not warranted.