Atypical retrobulbar optic neuropathy after semaglutide escalation

Abstract Semaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1RA), is widely used to manage type 2 diabetes and obesity. Recent pharmacovigilance signals have reported an increased incidence of nonarteritic anterior ischemic optic neuropathy (NAION) among semaglutide users, although the absolute risk remains low. We report a man in his early 30 seconds with class III obesity, obstructive sleep apnea, and prediabetes who developed acute, painless, asymmetric bilateral visual dysfunction four weeks after semaglutide escalation to 1 mg per week. Evaluation revealed retrobulbar optic neuropathy with asymmetric visual field defects, a central scotoma in the left eye, an altitudinal defect in the right eye, preserved optic disc appearance, and markedly delayed visual evoked potentials. Optical coherence tomography and neuroimaging were unremarkable. The presentation was atypical for NAION but did not fully align with classical demyelinating optic neuritis, yielding a mixed clinical picture. Semaglutide was discontinued immediately, and visual function remained stable over serial follow-up with adaptation to a persistent left central scotoma but no further deterioration. This case illustrates an atypical retrobulbar optic neuropathy in close temporal proximity to semaglutide dose escalation and underscores the need for clinical vigilance and strengthened pharmacovigilance as GLP-1RA use expands globally.