Probable Cerebral Amyloid Angiopathy-Related Inflammation Presenting as an Incidental MRI Finding in an Elderly Patient: A Case Report

TL;DR

An elderly woman with no symptoms had MRI findings suggesting CAA-ri, which later led to neurological decline, highlighting the need for early intervention.

Contribution

This case report highlights the risk of progression in asymptomatic CAA-ri and advocates for timely intervention.

Findings

MRI findings consistent with CAA-ri were present in an asymptomatic elderly patient.

Neurological deterioration occurred despite initial lack of symptoms.

Follow-up MRI showed resolution of edema but progression of atrophy.

Abstract

Cerebral amyloid angiopathy-related inflammation (CAA-ri) is a rare but treatable cause of subacute cognitive decline and neurological dysfunction, particularly in the elderly.

We report the case of an 88-year-old woman with mild dementia who was independent in her activities of daily living. She presented after minor head trauma, and brain MRI revealed multiple cerebral microbleeds in the bilateral cortices, cerebellum, and thalamus, along with diffuse fluid-attenuated inversion recovery (FLAIR) hyperintensities, suggestive of probable CAA-ri. Given the absence of symptoms, a strategy of close observation was initially adopted. However, two months later, she developed decreased appetite and gait instability, followed by a transient loss of consciousness at three months, necessitating hospitalization. During admission, she subsequently developed disuse syndrome, resulting in discharge to a nursing facility. Follow-up MRI at six months showed resolution of the prior FLAIR hyperintensities but revealed prominent medial temporal lobe atrophy, supporting the diagnosis of probable CAA-ri.

This case underscores that even in asymptomatic patients with significant MRI findings consistent with CAA-ri, there is a considerable risk of neurological deterioration and functional decline. While some mild cases may experience spontaneous resolution, the presence of widespread edema and multiple microbleeds may necessitate early immunosuppressive intervention, even if the patient is asymptomatic. The clinical silence of asymptomatic CAA-ri should not lead to an underestimation of its potential for progression. A timely assessment of risk and intervention may be crucial to prevent irreversible neurological and functional impairment.

Figures