Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are considered part of a shared disease spectrum. While orbital inflammatory changes have been described in GCA, the presence of increased optic nerve-region metabolic activity in PMR remains unclear. This study aimed to evaluate canalicular optic nerve-region [18F]FDG uptake in patients with clinically isolated PMR. In this retrospective single-center study, PMR patients (without signs and symptoms of GCA), who underwent [18F]FDG PET/CT were included. [18F]FDG uptake in the canalicular optic nerve region was quantified using SUVmax, SUVmean and target-to-background ratios (TBR). Patients with unremarkable [18F]FDG PET/CT served as controls, and patients with GCA were included for comparison. PMR patients (n = 18) showed significantly higher optic nerve-region [18F]FDG uptake compared to controls (median TBR 5.5 [IQR 2.8 - 8.9] vs 2.2 [1.9 - 2.7], p = 0.0006). Patients without immunosuppressive therapy demonstrated higher uptake than treated patients. Notably, untreated PMR patients showed canalicular optic nerve-region uptake values comparable to those observed in active GCA (7.3 [5.9 - 9.8] vs 8.0 [5.2 - 10.0], p = 0.9799). No PMR patient reported visual symptoms. Patients with clinically isolated PMR showed increased [18F]FDG uptake in the canalicular optic nerve region compared with controls, particularly in the absence of immunosuppressive therapy. Uptake values in untreated PMR overlapped with those observed in active GCA. These exploratory findings are compatible with subclinical inflammatory involvement within the GCA-PMR spectrum, but subclinical cranial GCA and non-neural sources of FDG uptake cannot be excluded. Larger prospective studies are required.
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