# A Rare Case of Cerebral Amyloidoma Mimicking Thalamic Glioma in a Rheumatoid Arthritis Patient

## TL;DR

A rare case of cerebral amyloidoma in a rheumatoid arthritis patient was misdiagnosed as a glioma, highlighting the difficulty in diagnosing this condition and the importance of considering amyloidosis in similar cases.

## Contribution

This case report adds to the limited literature on cerebral amyloidoma by emphasizing its diagnostic challenges and the need for improved detection methods in patients with rheumatoid arthritis.

## Key findings

- Cerebral amyloidoma was misdiagnosed as a glioma due to atypical neurological symptoms and imaging findings.
- A brain biopsy confirmed the diagnosis, underscoring the necessity of histopathological evaluation for accurate identification.
- Amyloidosis should be considered in the differential diagnosis of neurological deficits in patients with systemic inflammatory conditions like rheumatoid arthritis.

## Abstract

Amyloidosis, often referred to as “the great imitator”, is a condition characterized by the abnormal deposition of amyloid proteins in various tissues, potentially leading to organ dysfunction. When these deposits localize in the brain, they can disrupt neurological function and present with diverse clinical manifestations, making diagnosis particularly challenging. Cerebral amyloidosis is a rare entity that frequently mimics other neurological disorders, often resulting in significant delays in recognition and management. This case highlights the diagnostic challenge posed by cerebral amyloidosis and underscores its unique presentation. We present the case of a 76-year-old male with a history of rheumatoid arthritis (RA) who developed progressive right-sided weakness over several months. Three years prior, he experienced numbness on the right side of his face and upper limb. Initial imaging identified a small lesion in the left thalamic region, which was originally diagnosed as a glioma. However, due to the worsening of his clinical symptoms, further evaluation was warranted. Subsequent imaging revealed lesion growth, prompting a biopsy that ultimately confirmed the diagnosis of intracerebral amyloidoma. This case underscores the necessity of considering amyloidosis in the differential diagnosis of atypical neurological deficits, particularly in patients with systemic inflammatory conditions such as RA. The initial presentation of hemiparesis resembling a stroke, coupled with non-specific imaging findings and a prior misdiagnosis of glioma, highlights the complexity of cerebral amyloidosis. Only through brain biopsy was the definitive diagnosis established, emphasizing the need for improved diagnostic modalities to facilitate early detection. Further subtyping of amyloidosis, however, requires mass spectrometry-based proteomics or immunohistochemistry to accurately identify the specific amyloid protein involved. Clinicians should maintain a high index of suspicion for cerebral amyloidosis in patients with RA who present with progressive neurological deficits and atypical brain lesions. Early recognition and accurate diagnosis are essential to guiding appropriate management and improving patient outcomes.