OBJECTIVE: Delayed facial palsy (DFP) after acoustic neuroma surgery has been reported to occur in up to one third of cases. Reactivation of latent virus has been proposed as an etiology for DFP. However, only retrospective case reports and case series have offered data to support this theory. The objective of this study was to correlate DFP with change in viral titers. PATIENTS AND METHODS: Twenty consecutive patients who underwent acoustic neuroma surgery were prospectively evaluated for viral titers immediately preoperatively and at 3 weeks postoperatively. Viral titers measured included herpes simplex virus 1 (HSV-1), herpes simplex virus 2 (HSV-2), and varicella zoster virus (VZV) and included both IgG and IgM titers. The status of facial nerve function was documented preoperatively and throughout the postoperative period. Patients were categorized according to the presence or absence of DFP. RESULTS: Seven patients developed DFP after acoustic neuroma surgery, while the remaining 13 patients did not. There was no difference in preoperative and 3-week postoperative IgG titers for any of the 3 viruses tested. However, IgM titers were much higher postoperatively in DFP patients for all 3 viruses tested. The average HSV-1 IgM titer rose 92% in DFP patients compared with only 4.5% in the patients who did not develop DFP. Average HSV-2 IgM titers rose 70% compared with a decline of 8.5% in non-DFP patients. Most strikingly, VZV IgM titers rose an average 495% postoperatively among DFP patients compared with a decline of 14% in the non-DFP patients. CONCLUSION: Elevation of the IgM titers of the viruses measured in this study implies that recrudescence of the virus has occurred. The absence of this rise among patients who did not develop DFP implies that viral recrudescence plays a role in the etiology of DFP. These findings support treatment or prophylaxis of DFP with antiviral therapy. Although the finding of normal facial nerve function immediately after acoustic neuroma surgery is an excellent prognostic indicator for the ultimate outcome of facial nerve function, it is not uncommon for the patient to exhibit deterioration of facial nerve function in the first few days to weeks after surgery. When facial palsy is not complete, the prognosis remains excellent. However, when there is total loss of facial nerve function, the final outcome is more variable. Delayed facial palsy (DFP) after acoustic neuroma surgery has been defined as initially normal facial nerve function noted immediately postoperative with subsequent deterioration of facial nerve function. 1 This phenomenon has been noted to occur in up to one third of cases. Numerous causes for this entity have been proposed, including neural devascularization, vasospasm, edema, immune reactions, and viral reactivation. Varicella zoster virus (VZV) and herpes simplex virus (HSV) are ubiquitous, with more than 90% of the adult population demonstrating evidence of prior infection. 2 Reactivation of latent VZV has been implicated as the cause of Ramsay Hunt syndrome. 3 There is mounting evidence that HSV reactivation is the cause of Bell's palsy. 4 In the present study, viral titers for VZV and HSV were assessed before and after acoustic neuroma surgery. DFP and non-DFP patients were compared in an attempt to determine whether there was any correlation between viral recrudescence and DFP.
Intraoperative transcranial facial motor evoked potential monitoring in surgery of cerebellopontine angle tumors predicts early and late postoperative facial nerve function
