Multiple cranial neuropathy associated with herpes zoster in a human immunodeficiency virus-positive patient: a case report

Background: Multiple cranial neuropathy associated with varicella-zoster virus (VZV) reactivation is an uncommon but clinically significant complication in people living with human immunodeficiency virus (HIV). VZV remains latent in sensory ganglia after primary infection and may reactivate under immunosuppressive conditions, leading to Ramsay Hunt syndrome (RHS) with concomitant involvement of the facial and vestibulocochlear nerves. HIV infection itself rarely causes cranial neuropathies, but coinfection with VZV can result in complex polyneuropathic presentations that are insufficiently documented in the literature. Case presentation: We report the case of a 32-year-old HIV-positive male who presented with a 3-month history beginning with sudden right sensorineural hearing loss, followed by acute tinnitus, otalgia, intense vertigo, and post-herpetic right peripheral facial paralysis, in the context of auricular vesicular lesions consistent with RHS and otitis media. He also reported dysphonia characterized by a rough, low-pitched voice, globus sensation, and frequent throat clearing. Otologic examination revealed yellow crusts on the helix and external auditory canal without tympanic membrane abnormalities, while voice assessment showed a grade, roughness, breathiness, asthenia, strain score of 2 (asthenia 1, breathiness 1), a Voice Handicap Index-30 of 11 (mild vocal disability), and a World Health Organization Quality of Life-Brief assessment score of 78. Discussion: This case illustrates how simultaneous auditory, vestibular, facial, and laryngeal involvement may signal multiple cranial neuropathy due to VZV reactivation in an immunocompromised host, underscoring the importance of early recognition and comprehensive neurotologic and laryngologic evaluation to optimize timely diagnosis and management.