# Unmasking the Great Mimic: An Atypical Presentation of Giant Cell Arteritis With Recurrent and Isolated Diplopia

## TL;DR

A rare case of giant cell arteritis (GCA) presented with only recurring diplopia, highlighting the condition's ability to mimic other disorders and the importance of early detection.

## Contribution

This case report highlights the atypical presentation of GCA with isolated diplopia, expanding clinical awareness of its non-classical manifestations.

## Key findings

- GCA was diagnosed in a patient with isolated, recurrent diplopia and no classical symptoms.
- High-dose corticosteroid treatment resolved diplopia and normalized inflammatory markers.
- The case suggests intracranial vasculitis or ophthalmic artery ischemia as possible mechanisms for diplopia in GCA.

## Abstract

Giant cell arteritis (GCA) is a well-recognized vasculitis, typically presenting with headaches, scalp tenderness, jaw claudication, polymyalgia rheumatica, or constitutional symptoms. In stroke and transient ischemic attack (TIA) clinics, GCA is primarily considered in cases of visual loss due to ophthalmic artery involvement. However, diplopia as an isolated manifestation of GCA is exceedingly rare, making early recognition challenging. We present the case of a 75-year-old man who attended our TIA clinic with seven recurrent episodes of transient binocular diplopia. Notably, he lacked the classical features of GCA, including headache, scalp tenderness, jaw claudication, or visual loss. There was no history of fever, night sweats, weight loss, or other systemic symptoms. His neurological examination was unremarkable, and he denied any recent trauma or medication changes. However, routine inflammatory markers revealed a significantly elevated erythrocyte sedimentation rate (ESR) and CRP, raising suspicion for an underlying inflammatory process. An urgent rheumatology assessment and temporal artery ultrasound demonstrated increased intima-media thickness in the superficial temporal, frontal, and axillary arteries, confirming the diagnosis of GCA. He was promptly initiated on high-dose prednisolone (1 mg/kg) with a structured 16.5-month tapering regimen. Following treatment, his diplopia resolved completely, and inflammatory markers normalized. At both three-month and six-month follow-ups, he remained asymptomatic. To our knowledge, this is an extremely rare case of GCA presenting with isolated, recurrent diplopia rather than the typical pattern of visual loss. We propose that the underlying mechanism may involve intracranial vasculitis affecting the posterior circulation, particularly the midbrain and pons, or ischemia of the extraocular muscles due to ophthalmic artery involvement. This case highlights the protean nature of GCA, reinforcing its reputation as the “great mimic.” Clinicians should maintain a high index of suspicion for GCA in older patients presenting with transient diplopia, even in the absence of classical symptoms. Routine ESR and CRP testing in TIA clinics could facilitate early diagnosis, preventing irreversible visual or cerebrovascular complications.