Bilateral Facial Nerve Palsy associated with COVID-19 and Ep
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A 20-year-old male, with no relevant previous medical history, was admitted due to bilateral facial weakness. Two weeks before, he noticed odynophagia and fever of 39ºC without cough. He associated significant asthenia with headache, myalgia, nausea, and vomiting and he was treated with levofloxacin 500mg qd for 7 days.

One week after, during an initial improvement of the respiratory symptoms, he presented acute right facial weakness. He was diagnosed with right peripheral facial palsy and was treated with prednisone 60 mg/24h with a tapering schedule. The following week he noted left facial weakness and was referred again to the emergency room.

On neurological examination, there was a bilateral facial paresis. The rest of the examination was unremarkable, including other cranial nerves, strength, sensory examination, and deep tendon reflexes. Based on the COVID-19 pandemic at that time, a nasopharyngeal swab RT-PCR was performed for SARS-CoV-2 with positive results. Serum SARS-COV2 antibodies (qualitative IgM-IgG) were detectable at that time. He also had a positive heterophile test indicating a recent Epstein-Barr virus (EBV) infection.

Brain MRI raised the diagnosis of bilateral facial neuritis. The cerebrospinal fluid (CSF) showed protein levels of 80 mg/L and 9 cells/?L. CSF PCR was negative for SARS-CoV-2, Epstein-Barr virus, enterovirus, herpes simplex, and varicella-zoster, cytomegalovirus, and Parechovirus.

Antiganglioside antibodies (IgM and IgG) were negative in serum and CSF. Neurophysiological studies revealed a severe neuropathy of the facial nerve bilaterally, with discrete signs of active denervation. The Blink Reflex showed delayed R1 and R2 responses and the absence of R2c response, with no peripheral nerve abnormalities. A follow-up examination 3 weeks later showed an almost complete facial palsy recovery. Neurophysiological studies showed facial nerve improvement with no peripheral nerve abnormalities.