Diagnosis: AphasiaClinical question: assess for stenosisSigns and Symptoms: R MCA syndrome MRI of the brainNo diffusion weighted abnormalities are appreciated.There are punctate foci of T2 signal hyperintensity in the thalami bilaterally as well as the posterior limb of the left internal capsule. There are patchy foci of signal hyperintensity present in the midbrain and pons. There is atrophy of the cerebral peduncles. The left cerebral peduncle has signal hyperintensity associated with it as well as greater atrophy than on the right side. There is atrophy of 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 are clear. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact. The right eye lens is thin.There are subdural effusions present in the posterior fossa.A punctate foci of T2 hyperintensity without associated FLAIR hyperintensity along the right cerebellar hemisphere.MRA brain:There is a 70% stenosis present at the left carotid siphon at the distal aspect of the cavernous segment of the left internal carotid artery.The proximal portion of the anterior temporal artery of the left middle cerebral artery is not readily appreciated. This is along the tortuous loops of the left middle cerebral artery.There is 70% stenosis at the distal most aspect of the left vertebral artery at its junction with the vertebrobasilar junction. There is 40% stenosis at the distal aspect of the right vertebral artery just proximal to the vertebrobasilar junction. There is mild narrowing of the basilar artery along its midportion just distal to the origins of the anterior inferior cerebellar arteries.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 left A1 segment is small and tortuous. The right A2 segment is larger than the left A2 segment. The anterior communicating artery is small The posterior communicating arteries are intact. 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 25% stenosis present at the origin of the left internal carotid artery. The left internal carotid artery appears attenuated throughout its course possibly related to a distal stenosis. There is no significant stenosis along the course of the vertebral arteries. The left vertebral artery smaller than the right vertebral artery.
1.There is no evidence for acute ischemic cerebral infarction.2.There is 70% stenosis present at the distal left internal carotid artery. There is associated attenuation of the left internal carotid artery proximal to this suggesting this may be hemodynamically significant.3.Findings raise the question of stenosis at the proximal portion of the inferior division of the left middle cerebral artery. The left anterior temporal artery of the left middle cerebral artery is nondominant. Please note that this may be artifactual due to tortuosity and low flow in this vessel.4.There is 70% stenosis at the distal most aspect of the left vertebral artery at its junction with the vertebrobasilar junction. There is 40% stenosis at the distal aspect of the right vertebral artery just proximal to the vertebrobasilar junction.5.There are multiple punctate lesions present in the brainstem and thalami which are suspected to represent prior lacunar infarct. This affects the left thalamus and brainstem more than the right as some findings that suggest Wallerian degeneration on the left side.6.Periventricular and subcortical white matter lesions of a mild degree are nonspecific. At this age they are most likely vascular related. 7.Old lacunar infarct in the right cerebellar hemisphere.