Female, 25 years old, with posterior headache for two months, history of meningoencephalitis, history of low-grade B-cell lymphoma. Assess for infection, vasculitis, CNS lymphoma. Innumerable punctate foci of susceptibility are seen scattered through the cerebral hemispheres with a fairly symmetric distribution and a frontal lobe predominance. Prior exams did not included susceptibility-weighed images, so assessment for interval changes cannot be made. Also seen is a relatively small number of scattered foci of T2 hyperintensity involving the cerebral white matter. These are predominantly subcortical, though the anterior right corpus callosum is also involved. None of the above lesions is associated with significant edema or mass effect. The T2 hyperintense lesions have significantly improved from the exam of 4/26/15, and appear relatively similar to the exam of 5/10/15. No evidence of any pachymeningeal or leptomeningeal enhancement is seen. No large parenchymal enhancing lesions are seen. There is a punctate focus of enhancement in the right superior frontal gyrus (image 286 series 1201), and another associated with a right frontal white matter T2 lesion (image 234 series 1201). There may also be subtle speckled enhancement associated with the anterior right corpus callosum.No definite restricted diffusion is seen. No acute intracranial hemorrhage or any pathologic extra-axial fluid collection is evident. The ventricular system is normal in size and morphology.Bone marrow signal is within normal limits. Mucosal thickening is evident in the right sphenoid sinus. Multiple enlarged lymph nodes are seen in the visualized neck soft tissues.
Since the prior exam obtained in April, 2015, the size and number of scattered T2 hyperintense white matter lesions in the cerebral hemispheres have significantly diminished. Relatively few lesions persist on the current exam, and these are largely subcortical with the exception of the right corpus callosum, and they exert no mass effect. Susceptibility imaging was not performed on the prior studies, but on today's exam, there are innumerable punctate foci of susceptibility indicating chronic microhemorrhage distributed relatively symmetrically in the cerebral hemispheres, with preference for the frontal lobes. There also appear to be a few small foci of enhancement as described above, some of which are associated with T2 lesions. The appearance and distribution of the findings necessitate a fairly broad differential diagnosis including the sequelae of prior infection (perhaps viral), post-infectious or immune mediated inflammation, and especially a primary or secondary CNS vasculitis. Presence of innumerable microhemorrhages argues against demyelinating disease. The findings are distinctly uncharacteristic for primary CNS lymphoma. The possibility of intravascular (angiocentric) lymphoma would, however, be a reasonable consideration as this condition can mimic vasculitis on imaging.