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Facial Nerve Paralysis in Acute Otitis Media: Cause and Management Revisited

Abstract Facial nerve paralysis (FNP) complicating acute otitis media (AOM) is thought to be mediated by intrafallopian inflammatory edema and consequent ischemia with neuropraxia. Presumably this occurs either through (1) preexistent bony dehiscences, (2) physiologic canaliculi between the middle ear and fallopian canal, or (3) the vascular connections between the fallopian canal and the mastoid air cells. 1 , 2 , 3 Although there is little scientific evidence, it has been proposed that the bacteria that causes the AOM also produces the facial paralysis. In the postantibiotic era, the incidence of FNP complicating AOM is 0.2%, 4 , 5 and therefore the traditional treatment is geared toward timely eradication of the inciting pathogen with antimicrobial therapy. Wide myringotomy generally is recommended for decompression and culture. We report three cases of facial paresis that began 6 to 8 days after treatment for ipsilateral AOM was initiated. Urgent myringotomy universally revealed minimal or no effusion, and failure to place a tube resulted in early closure. All went on to full facial recovery with antibiotics and steroids. We interpret this and available experimental data as evidence that the pathogenic mechanism of FNP in AOM is related to a slowly evolving neuritis, the cause of which still remains uncertain.