Clinical question: r/o intracranial pathologySigns and Symptoms: headache MRI of the brainNo diffusion weighted abnormalities are appreciated.There are several periventricular and subcortical punctate hyperintense white matter lesions present identified in each hemisphere on the FLAIR and T2 images.The CSF spaces are appropriate for the patient's stated age with no midline shift. No abnormal enhancing mass lesions are appreciated intracranially. No intracranial hemorrhage is identified. No edema is identified within the brain parenchyma.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 partial opacification of the right sphenoid sinus. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact. The left eye lens is thin.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 right posterior cerebral artery has a fetal origin. The left posterior communicating artery is small and 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 no significant stenosis along the course of the vertebral arteries. MRV brain:The dural venous sinuses are patent. Straight sinus, internal cerebral veins and basal veins are identified and appear patent.
1.No evidence for acute ischemic cerebral infarction.2.No evidence for intracranial cerebrovascular occlusive disease.3.No evidence for extracranial cerebrovascular occlusive disease.4.No evidence for dural sinus thrombosis.5.Periventricular and subcortical white matter signal changes of a mild degree are present which are nonspecific. They are likely of little clinical significance given their size and number at this age.