71 years Male (DOB:7/2/1944)Reason: L side weakness History: L side weaknessPROVIDER/ATTENDING NAME: DAVID HOWES DAVID HOWES MRI brain:There is a small focus of diffusion restriction present in the right frontal lobe and insular cortex of the top of the operculum measuring 11 x 9 mm axial dimensions. 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.There is a punctate focus of signal loss and susceptibility imaging in the right pons. Another focus of punctate signal loss is present subcortical white matter of the left cingulate gyrus and another in the left periventricular white matter. Another is present in the medial aspect of the right temporal lobe subcortical white matter. Several foci of punctate signal loss and susceptibility are present in the cerebellar hemispheres. Another is present in the right frontal lobe subcortical white matter. Still another one is present in the periventricular white matter adjacent to the trigone of the right lateral ventricle. Another 0 scattered in the subcortical white matter of the temporal lobes and occipital lobesThere is a mild degree of periventricular and subcortical punctate hyperintense white matter lesions present identified on the FLAIR and T2 images. There are patchy T2 and FLAIR hyperintense lesions present in the brainstem. There are punctate foci of T2 and FLAIR hyperintensity in the thalami and basal ganglia.On susceptibility imaging there is prominent transmitted medullary veins which are lower in signal and appear larger than the left-sided counterparts. Additionally couple cortical veins that are more prominent on the right side versus the left. This corresponds to the precentral and prefrontal territories. This may represent hypoxia.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 relative paucity of vasculature in the right middle cerebral artery territory versus the left. A separate superior division branches not clearly identified. Some the supply to the superior division originates from a small branch of the distal M1 segment which includes a frontal opercular branch, however, prefrontal and precentral arteries are not clearly depicted on this exam distally. There is an occluded the right precentral artery present at the distal M2 segment on the right side. The left posterior communicating artery is medium-sized. The right posterior communicating artery is not readily visualized. Anterior communicating artery is small.There is no evidence for intracranial aneurysm.
1.Occlusion of the right precentral artery at the distal M2 segment and suspected more proximal occlusion of the right prefrontal artery.2.Small focus of infarction is present in the right frontal lobe extending to the insular cortex near the top of the operculum which corresponds to the occluded right precentral artery.3.Findings were discussed with clinical service.4.Periventricular and subcortical white matter lesions as well as some patchy lesions in the brainstem of a mild degree are nonspecific. At this age they are most likely vascular related. 5.Punctate lesions in the thalami and external capsules are suspected to be related to old lacunar infarcts.6.There multiple microhemorrhages present. Anomaly in cerebellum and brainstem but also periventricular white matter and subcortical white matter. The pattern is nonspecific. It could represent a combination of hypertension and amyloid angiopathy.