• Otolaryngol Head Neck Surg · Nov 2002

    Viral titers and delayed facial palsy after acoustic neuroma surgery.

    • Gerard J Gianoli.
    • Ear and Balance Institute, Baton Rouge, LA 70816, USA. gianoli@bellsouth.net
    • Otolaryngol Head Neck Surg. 2002 Nov 1;127(5):427-31.

    ObjectiveDelayed 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 MethodsTwenty 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.ResultsSeven 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.ConclusionElevation 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.

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