Abstract Number ‐ 224: Stroke Mimic—Patient with Symptomatic Amyloid‐Related Imaging Abnormalities Presenting with Stroke‐like Symptoms.

Introduction Amyloid‐related imaging abnormalities (ARIA) are rare phenomena in patients taking monoclonal antibodies directed against amyloid beta in Alzheimer’s disease clinical trials. The pathogenesis is unclear, but may be due to an induced inflammatory microangiopathy. While the majority of cases are asymptomatic and resolve without intervention, a small subset can experience symptoms of sudden or uncertain onset. Given the relative rarity of this phenomena and the striking imaging findings, ARIA can be misdiagnosed as ischemic stroke or primary microangiopathy when presenting with acute‐subacute symptoms. Following diagnosis there is no clinical consensus on the optimal management and approaches range from withdrawal of the study drug to pulse‐dose steroids. Methods We present a case study of a patient admitted to our inpatient stroke service after 4 days of rapidly progressive confusion and sudden vision loss with MRI workup reporting subacute stroke. The findings were ultimately determined to be secondary to ARIA. Results A 67‐year‐old man with early onset Alzheimer’s disease enrolled in a clinical trial for donamemab presented with four days of marked cognitive decline including increased forgetfulness, confusion, and episodic hallucinations following an episode of abrupt vision loss. An outpatient MRI brain demonstrated subcortical hyperintensity that was initially reported as a subacute left occipital stroke. Notably, an MRI performed 3 months prior showed no abnormality. Neurological exam was remarkable for right superior quadrantanopia, memory impairment, and mild confabulation. Repeat MRI demonstrated FLAIR white matter hyperintensities and extensive susceptibility artifact in the left parieto‐occipital lobe, consistent with an inflammatory cerebral amyloid angiopathy (or ARIA). Spot EEG demonstrated no associated epileptiform discharges. Patient was treated with 7‐day course of IV Solumedrol and had improvement in visual symptoms. He was discharged on a prednisone taper and a followup MRI brain 4 weeks later showed near‐ complete resolution of the previously noted subcortical white matter changes. Conclusions ARIA can be seen in patients receiving anti‐amyloid monoclonal antibody treatments. Surveillance MRIs have been implemented to screen for such cases as a minority of patients with ARIA present with symptoms. As noted with this case study, a relatively acute presentation and imaging characteristics can lead to an initial misdiagnosis as subacute ischemic stroke. Vascular neurologists should be aware of this clinical entity, noting the natural history and treatment are not well established. This patient was treated aggressively as an inflammatory cerebral amyloid angiopathy with IV steroids and noted positive outcome. More research is required to establish the optimal acute medical management of patients with ARIA.