Clinical question: 17 year old male with sickle cell disease, concern for microvascular disease seen on CT. Evaluate for microvascular disease. Acute ischemia.Signs and Symptoms: Microvascular disease seen on CT MRI of the brainNo diffusion weighted abnormalities are appreciated.Punctate lesions which are hyperintense on T2 and FLAIR MRI are present in the left centrum semiovale and to a lesser degree right centrum semiovale.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 minor opacities. The visualized portions of the mastoid air cells are clear. Mastoid air cells appear to be a hypoplastic The visualized portions of the orbits are intact.Incidental note is made of marked bilateral nasopharyngeal adenoidal hypertrophy.There is diffuse marrow replacement present.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. In general the intracranial vasculature is fairly patulous.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 posterior cerebral arteries bilaterally with medium-sized P1 segments. The vertebral arteries are similar in size.
1.There are some punctate periventricular white matter lesions present bilaterally more on the left than the right side which are nonspecific. They could be vascular related. The location is along the watershed distribution. This could be microembolic though they could also be related to hypoperfusion2.There is no evidence for intracranial cerebrovascular occlusive disease.3.Marked bilateral nasopharyngeal adenoidal hypertrophy. There is a nonspecific finding.4.There is no evidence for acute ischemic cerebral infarction.