Abstract

not confirmed histologically, the patient received two months of oral cyclophosphamide, 100mg daily, with clinical brightening of affect and increased motivation. Cyclophosphamide was discontinued upon development of fever, neutropenia, and rash. At 6 weeks post-treatment, a repeatMRI revealed resolution of thewhitematter signal changes, presumably secondary to treatment of an inflammatory component. She subsequently developed progressive worsening of short term memory, gait, and seizures, treated with rivastigmine, memantine, lorazepam, clonazepam, and lamotrigine. The brainMRI remains stable at 17 months post-treatment.Conclusions: Future therapy of CAA/ABRA-type lesions will likely benefit from targeted treatment of the vascular amyloid as well as inflammation for optimal response.

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