 No evidence for acute intracranial hemorrhage, mass effect, or edema. Ventricular size is normal. There are no midline shift. Basal cisterns are patent.There is no evidence of restricted diffusion.There are dispersed foci of susceptibility signal throughout the brain. A large focus of susceptibility is seen in the left cingulate gyrus and a smaller one in the right frontal lobe. There are linear dark susceptibility signals along the anterior and the posterior interhemispheric fissures, suggestive of old subarachnoid hemorrhage and residual siderosis. Foci of susceptibility artifacts are also seen in the cerebellum. In comparison to the previous study of 2013, these susceptibility foci were present but increased in number and size. These are due to old blood products from microhemorrhages and residual siderosis.The vascular flow voids are unremarkable.MRA BRAIN:The anterior, middle, and posterior cerebral arteries are within the normal limits. Internal carotid arteries are widely patent. Anterior communicating artery is patent. The bilateral posterior communicating arteries are diminutive. The basilar and vertebral arteries are patent with no evidence of stenosis or aneurysm. There is trifurcation of the anterior cerebral arteries. The left jugular branch of the ascending pharyngeal artery is enlarged as is the left posterior meningeal artery, as compared to the contralateral side. There are some meningeal arteries extending to the torcula and adjacent superior sagittal sinus. There is enlargement of the middle meningeal artery bilaterally.MRA NECK:The common carotid arteries, the cervical internal carotid arteries, and the vertebral arteries are widely patent with no evidence of stenosis or aneurysm.
1.No acute findings. No evidence for acute intracranial hemorrhage, mass effect, or edema. No abnormal enhancement.2.MRA of the brain suggests dural arteriovenous fistula with potential posterior meningeal artery and middle meningeal supply to the torcula and superior sagittal sinus.3.Siderosis predominantly involving posterior aspect of the falx, tentorium and adjacent sulci is stable since prior available exams. This suggests a prior history of subarachnoid hemorrhage and possibly subdural hemorrhage.4.Progression of microhemorrhages within subcortical white matter in the supratentorial and infratentorial brain since 2013. It is certainly possible that this progression is related to her thrombocytopenic state associated with CML.5.Findings were discussed with Lauren Ziskind APN at 10:30 am.