To describe clinical–radiographic dissociation in cerebral amyloid angiopathy–related inflammation (CAA-ri) and considerations for surveillance imaging to detect subclinical neuroinflammation during immunosuppressant therapy.

CAA-ri is an immune-mediated response to vascular β-amyloid deposition, typically demonstrating concordant clinical and radiographic improvement with corticosteroids. The significance of radiographic progression in the absence of clinical decline remains unclear, particularly during transition to maintenance immunosuppression.

Case report.

A 68-year-old male with HTN, HLD, and T2DM presented with subacute cognitive decline and was diagnosed with CAA-ri based on clinical and MRI findings. He was treated with corticosteroids, followed by transition to mycophenolate mofetil due to a relapsing course. He demonstrated marked clinical improvement with progressive cognitive recovery (MoCA 13→19→27) and return to near-baseline function. Two months after steroid taper and approximately four months into mycophenolate therapy, surveillance MRI demonstrated new right frontal and temporal vasogenic edema. Despite these findings, he remained neurologically asymptomatic with continued cognitive improvement, consistent with clinical–radiographic dissociation. Given concern for ongoing subclinical inflammation and delayed time to efficacy of steroid-sparing therapy, corticosteroids were reinitiated while continuing mycophenolate. The patient remains clinically stable with planned serial imaging and close follow-up.

This case highlights clinical–radiographic dissociation in CAA-ri, suggesting that radiographic progression can occur due to subclinical neuroinflammation. These findings support the role of surveillance MRI in clinically stable patients and emphasize the need to individualize treatment decisions based on both clinical and radiographic disease. Further studies are needed to define biomarkers and optimal monitoring strategies during maintenance immunosuppression.