Purpose:Delayed facial palsy after acoustic neuroma resection may occur in up to 15% of cases. Prognosis is generally good if the palsy does not progress to total paralysis. However, delayed palsy with subsequent total paralysis has a more variable final outcome, which ranges from normal function to permanent total paralysis. This delayed paralysis has been attributed to edema from surgical manipulation of the facial nerve. Steroids and intraoperative decompression of the meatal foramen have been used with some success, but some cases remain refractory to these measures. Herpes simplex virus and varicella-zoster virus are ubiquitous in the population and remain in a latent state in neural ganglia. These viruses are reactivated during times of stress. Trigeminal nerve surgery (partial sensory rhizotomy and microvascular decompression) stimulates reactivation of herpes simplex with manifestations the sensory distribution of the trigeminal nerve in 38-94% procedures. Prevention of this reactivation has been demonstrated in placebo-controlled trials by using prophylactic acyclovir. We present a patient who underwent translabyrinthine resection of an intracanalicular acoustic neuroma and in whom developed otalgia, vesicles on the ear canal and the ipsilateral buccal mucosa, and progressive facial palsy the week after surgery. Serologic evaluation confirmed the diagnosis of herpes zoster oticus. Reactivation of latent virus apparently occurred as a result of surgical manipulation of the facial nerve. This parallels viral reactivation seen in trigeminal nerve surgery. We propose a new theory for an additional cause of delayed facial palsy after acoustic neuroma resection—reactivation of latent herpesvirus resulting from surgical trauma. Acyclovir should be evaluated in clinical trials for a prophylactic role in patients undergoing acoustic neuroma resection or a therapeutic role in patients in whom a delayed postoperative facial palsy develops.