Semaglutide and Sudden Vision Loss Reveal a Dangerous Eye Syndrome Mimic

This case report matters because it illustrates a potentially life-altering diagnostic pitfall: a pattern of optic nerve findings that closely mimics a brain tumor but actually stems from a vascular eye condition worsened by metabolic disease. As semaglutide use expands dramatically for diabetes and weight loss, clinicians must be alert to ocular risks in this population.

The study presents a single patient — a 38-year-old man with poorly controlled type 2 diabetes mellitus, arterial hypertension, and concurrent semaglutide use — who developed acute, painless vision loss in the left eye. Ophthalmic evaluation found optic disc edema (ODE) in the left eye and optic disc pallor (ODP) in the right, alongside severe nonproliferative diabetic retinopathy and cystoid macular edema bilaterally.

The key finding was that this ODE-plus-ODP pattern, classically associated with Foster Kennedy syndrome caused by intracranial masses compressing the optic nerve, was ultimately a mimic. Comprehensive neuroimaging and systemic workup were unremarkable. Clinicians concluded the right eye pallor represented a prior silent NAION event, and the left eye swelling was an acute new NAION — collectively termed pseudo-Foster Kennedy syndrome.

The implications are significant. NAION is the most common acute optic neuropathy in adults over 50, but its occurrence in a 38-year-old underscores the accelerating vascular damage of poorly managed metabolic disease. Semaglutide has been associated with NAION risk in recent literature, making this case clinically timely.

Caveats are notable: this is a single case report, limiting generalizability. The causal role of semaglutide versus underlying diabetes and hypertension cannot be isolated. Nevertheless, it serves as a critical reminder to perform thorough neuro-ophthalmic evaluation before assuming intracranial pathology.