Varicella-zoster virus-induced glossopharyngeal and vagal nerve palsy presenting with severe dysphagia and delayed acute retinal necrosis: a case report

We present a case of glossopharyngeal and vagal nerve palsy induced by varicella-zoster virus (VZV), which subsequently progressed to acute retinal necrosis (ARN). A man in his 70s presented with severe dysphagia, hoarseness, and a unilateral ulcer on the left soft palate. Serological testing revealed elevated VZV IgM and IgG titers, confirming VZV reactivation, despite the absence of typical vesicular eruptions. The patient received intravenous acyclovir and corticosteroids for lower cranial polyneuropathy; however, dysphagia persisted, necessitating gastrostomy for nutritional support. On day 38 of hospitalization, approximately five weeks following the onset of cranial neuropathy, he developed blurred vision in the left eye, leading to a diagnosis of ARN, confirmed by the detection of VZV DNA in the aqueous humor. Intensified antiviral therapy improved his visual acuity, though the cranial neuropathy required long-term rehabilitation. This case highlights an important diagnostic pitfall: VZV-related lower cranial neuropathy may appear clinically stable yet precede delayed, sight-threatening ocular complications despite standard antiviral therapy. Otolaryngologists should therefore remain vigilant for new visual symptoms during follow-up to prevent irreversible visual loss. • VZV reactivation may involve lower cranial nerves without cutaneous rash. • Delayed acute retinal necrosis (ARN) can develop weeks after initial neuropathy. • Standard antiviral therapy may not prevent delayed ocular complications. • Otorhinolaryngologists should remain vigilant for new visual symptoms.