Diagnosis: Cerebral infarction, unspecifiedClinical question: assess for stroke MRI of the brainNo diffusion weighted abnormalities are appreciated.The CSF spaces are appropriate for the patient's stated age with no midline shift. There are punctate foci of signal hyperintensity present in the pons. Additionally there is a hypointense focus on susceptibility imaging located at the expected location of the right thalamus and adjacent internal capsule and centrum semiovale.The right cerebral peduncle is asymmetrically smaller than the left cerebral peduncle.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 a minor opacity in the right frontal sinus and some mucosal thickening in the left maxillary sinus.. 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 medium size. The posterior communicating arteries are barely visible. The left vertebral artery is larger than the right vertebral artery.MRA neck:The MRA of the neck is degraded by patient motion which occurred during the dynamic phase of the exam and is a result and noncontrast MRA of the neck could no longer be performed. To the extent of visualization possible on the basis of NASCET criteria significant stenosis at the carotid bifurcations is not suspected.The origins of the great vessels from the aortic arch and the origins of the vertebral arteries are not adequately assessed on this exam due to motion artifact.
1.The MR angiogram of the neck is degraded significantly by patient motion as detailed above. Although there is no convincing evidence for stenosis at the carotid bifurcations a subtle abnormality could be overlooked. In addition the origins of the great vessels from the aortic arch and the vertebral arteries are not adequately evaluated.2.There is no evidence for acute cerebral ischemic infarction.3.No evidence for intracranial cerebrovascular occlusive disease.4.Findings suggest a prior hemorrhage involving the right thalamus and adjacent centrum semiovale with associated adjacent encephalomalacia and Wallerian degeneration.5.Periventricular and subcortical white matter changes of a mild degree are nonspecific. At this age they are most likely vascular related. 6.Microhemorrhages in the pons are suggestive of hypertensive etiology based on location7.A small lesion in the left thalamus is suspected to be related to prior lacunar infarct8.Signal changes in the brainstem are likely vascular related.