The Nerve Less Travelled- Isolated Dysphagia as the Sentinel Symptom of Atypical Ramsay Hunt Syndrome with Cranial Polyneuropathy
摘要
Ramsay Hunt Syndrome (RHS), a neurotropic manifestation of varicella-zoster virus reactivation, is classically characterized by a triad of otalgia, vesicular rash in the external auditory canal, and ipsilateral facial paralysis. While polycranial involvement is a documented but rare phenomenon, cases where lower cranial nerve symptoms precede all classical features are exceedingly uncommon and diagnostically treacherous. A 62-year-old woman presented with sudden-onset severe dysphagia and right otalgia without any cutaneous lesions or facial asymmetry. Otoscopic and fiberoptic laryngoscopic evaluation revealed nonspecific ulceration in the right pyriform fossa with preserved vocal cord mobility prompting an initial differential of malignant or granulomatous etiologies. Hematologic and biochemical workup was non-revealing, while targeted microbiological cultures returned sterile. As her symptoms progressed, a contrast-enhanced MRI of the skull base demonstrated subtle, asymmetric enhancement along the facial and glossopharyngeal nerves on the right. Diagnostic uncertainty persisted until Day 3 of admission, when the patient developed a right-sided Grade III facial nerve palsy and vesicular eruptions over the conchal bowl. A multiplex PCR panel subsequently confirmed varicella zoster virus from saliva, establishing a diagnosis of Ramsay Hunt Syndrome with cranial polyneuropathy involving nerves VII, IX, and X. Prompt initiation of high-dose corticosteroids and oral valacyclovir led to resolution of otalgia and progressive improvement in swallowing function. Facial weakness showed partial recovery at 2-week follow-up. This case underscores the protean manifestations of RHS and the diagnostic complexity it can pose when presenting in an atypical sequence. In elderly patients with unexplained dysphagia and otalgia, clinicians should maintain a high index of suspicion for RHS, even in the absence of its defining features. Advanced imaging and early virologic testing may offer the only clues in such ‘invisible onset’ variants.