 MRI brain:Signal abnormality within bilateral parietal regions consistent with a history of previous mycotic aneurysm embolization.There are scattered punctate to small foci of T2 hyperintensity within periventricular and subcortical white matter without mass effect, restricted diffusion, or enhancement. Separately there are also punctate to small foci of susceptibility abnormality in both periventricular and subcortical white matter.The ventricles and sulci are normal in size. The cerebellar tonsils are in normal position. There are no masses, mass effect or midline shift. The pituitary gland is normal in size. There is no evidence for intracranial hemorrhage or acute cerebral, brainstem or cerebellar infarction. There are no extraaxial fluid collections or subdural hematomas. Flow voids are present within the major vessels indicating patency. The paranasal sinuses and mastoid air cells are clear. There is no abnormal enhancement within the brain.  MRI cervical spine: Images are motion greater. Given this caveat:There is abnormal material within the extradural, epidural space extending from C4/5 inferiorly to the mid T1 level. This measures up to 7 mm in maximal depth, has a slight rightward predominant location, contains mixed signal characteristics on both T1 and T2, with minimal peripheral enhancement. The adjacent disc spaces and vertebral bodies are normal in appearance. This process effaces the anterior CSF space, however without cord compression or deformation.Alignment is normal. The marrow signal is benign. The cervical and upper thoracic cord is normal in signal without abnormal enhancement. The cervicomedullary junction is normal. The cerebellar tonsils are in normal position. There is no significant degenerative disease, disc pathology, or stenosis.
1.Signal abnormality within bilateral parietal regions consistent with a history of previous mycotic aneurysm embolization.2.There are scattered punctate to small foci of T2 hyperintensity within periventricular and subcortical white matter without. Separately there are also punctate to small foci of susceptibility abnormality in both periventricular and subcortical white matter. It is uncertain if these two processes are related or due to separate etiologies. The distribution of T2 hyperintensity lesions suggest a vasculitic pathology, yet is nonspecific. Susceptibility images may also be secondary to vasculitic related microhemorrhages or due to microimages from other etiologies such as cerebral cavernous malformations, although given patient age amyloid angiopathy and hemorrhagic metastases are felt to be unlikely.3.There is abnormal material within the extradural, epidural space extending from C4/5 inferiorly to the mid T1 level. This measures up to 7 mm in maximal depth, has a slight rightward predominant location, contains mixed signal characteristics on both T1 and T2, with minimal peripheral enhancement. The adjacent disc spaces and vertebral bodies are normal in appearance. This process effaces the anterior CSF space, however without cord compression or deformation. Although subtle, this is grossly stable when compared to a previous CT angiogram of the neck where these foci demonstrate mixed density. The constellation of these features are most suggestive of anterior epidural hemorrhage.