BILATERAL FACIAL NERVE PALSY ASSOCIATED WITH MYCOPLASMA PNEUMONIAE INFECTION

Introduction and aims : Bilateral facial nerve palsy is a rare clinical entity, occuring in 0.3% to 2.0% of facial palsy cases. Although its pathogenesis remains unclear, this condition is often associated with systemic diseases and may represent a diagnostic challenge. Mycoplasma pneumoniae is a common cause of respiratory tract illness in children. Neurological complications are the most frequent extrapulmonary manifestation, but, so far, only a few case reports suggested an association between bilateral cranial nerve palsy and M. pneumoniae infection. We describe a patient who developed bilateral facial nerve palsy with a serologically-proved mycoplasma infection. Case report (methods and results): a previously healthy 10-year-old boy was admitted to our department because of sudden onset of peripheral left facial nerve palsy evolved in facial diplegia during the first 24 hours of hospitalization. He had a 15-day history of fever, coughing and vomiting accompanied by asthenia and headache. His physical examination was remarkable for bilateral facial nerve palsy, with no signs of meningism and papilledema, and the remainder of physical examination was normal. He had a positive throat swab culture for S. Pyogenes; chest X-ray, EEG and cerebrospinal fluid examination revealed no pathological findings. PCR for neurotropic virus as well as for Borrelia burgdorferi were negative, but serum M. pneumonie antibodies were positive, indicating an acute infection (IgM and IgG \u2013 titer 1:320). Brain MRI revealed a bilateral and symmetric enhancement of the VII cranial nerves. He was treated with intravenous ceftriaxone for 8 days and oral clarithromycin for 14 days. He rapidly improved, the bilateral nerve palsy resolved completely and spontaneously within 20 days, and no recurrences were noted during his follow-up visits. Conclusions: various infectious agents have been linked to bilateral facial palsy, such as EBV, HIV, Borrelia burgdorferi and Mycoplasma pneumoniae. The spectrum of CNS complications following mycoplasmal infection is wide, but whereas to date the association between encephalitis and mycoplasma infection is accepted, bilateral facial palsy due to M. pneumoniae has been reported in only five cases. Our patient developed a bilateral facial nerve palsy after complained of mild respiratory symptoms; no pulmonary infection was documented but a seroconversion of M. pneumoniae could be detected. The absence of respiratory symptoms in neurologic complications following mycoplasma infection is not a rare event and the number of mycoplasma infections might be higher than recognized so far. Patients presenting with a bilateral facial palsy of unknown origin should be tested for antibodies against M. pneumoniae, regardless of the presence or absence of respiratory symptoms