PURPOSE: The aim of this study was to evaluate poststapedectomy-delayed facial palsy etiopathogenesis, risk factors, evolution, and prevention. MATERIALS AND METHODS: Seven hundred six stapedectomies performed in 580 patients were reviewed. In all patients who developed delayed facial palsy, the dates of onset and subside of facial palsy, the anatomic and pathologic predisposing factors, and a possible history for recurrent labial herpetic lesions were considered. The House-Brackmann (H-B) grading system was used to evaluate the facial function. Virus-specific immunoglobulin (Ig) G and IgM antibodies against herpes simplex virus type 1 (HSV-1) were determined by enzyme-linked immunosorbent assay (ELISA) 3 weeks after the onset of the paralysis. The results were compared with a control group without a history of recurrent herpes labialis. RESULTS: Poststapedectomy facial palsy developed in 7 out of 706 procedures. All 7 patients referred a history of recurrent labial herpetic lesions. One patient showed a facial palsy H-B grade II, 2 a grade III, and 3 a grade IV. After acyclovir therapy, 6 subjects recovered completely, whereas 1 maintained an H-B grade II. An increased IgG antibody titer was found in 6 of the patients with delayed facial palsy and in 1 out of 7 controls. Mean IgG titer was 1:14,050 in the subjects with delayed facial palsy and 1:2,300 in controls (P <.001). CONCLUSIONS: Poststapedectomy-delayed facial palsy is likely caused by a reactivation of HSV-1, latent within the geniculate ganglion. The activation of the latent virus is more frequent in patients with a history of herpes labialis and can be prevented by an adequate acyclovir therapy.
PURPOSE: The aim of this study was to evaluate poststapedectomy-delayed facial palsy etiopathogenesis, risk factors, evolution, and prevention. MATERIALS AND METHODS: Seven hundred six stapedectomies performed in 580 patients were reviewed. In all patients who developed delayed facial palsy, the dates of onset and subside of facial palsy, the anatomic and pathologic predisposing factors, and a possible history for recurrent labial herpetic lesions were considered. The House-Brackmann (H-B) grading system was used to evaluate the facial function. Virus-specific immunoglobulin (Ig) G and IgM antibodies against herpes simplex virus type 1 (HSV-1) were determined by enzyme-linked immunosorbent assay (ELISA) 3 weeks after the onset of the paralysis. The results were compared with a control group without a history of recurrent herpes labialis. RESULTS: Poststapedectomy facial palsy developed in 7 out of 706 procedures. All 7 patients referred a history of recurrent labial herpetic lesions. One patient showed a facial palsy H-B grade II, 2 a grade III, and 3 a grade IV. After acyclovir therapy, 6 subjects recovered completely, whereas 1 maintained an H-B grade II. An increased IgG antibody titer was found in 6 of the patients with delayed facial palsy and in 1 out of 7 controls. Mean IgG titer was 1:14,050 in the subjects with delayed facial palsy and 1:2,300 in controls (P <.001). CONCLUSIONS: Poststapedectomy-delayed facial palsy is likely caused by a reactivation of HSV-1, latent within the geniculate ganglion. The activation of the latent virus is more frequent in patients with a history of herpes labialis and can be prevented by an adequate acyclovir therapy.
Authors: Maggie A Kuhn; Shruti Nayak; Vladimir Camarena; Jimmy Gardner; Angus Wilson; Ian Mohr; Moses V Chao; Pamela C Roehm Journal: Otol Neurotol Date: 2012-01 Impact factor: 2.311