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A previously well 33-year-old man was admitted to hospital with a 2-week history of intermittent fever and inguinal lymphadenopathy and a 2-day history of jaundice. Acute hepatitis due to Epstein–Barr virus (EBV) infection was diagnosed based on a positive Paul–Bunnell test result and EBV immunoglobulins G and M and exclusion of other causes (see supplementary data). He was managed conservatively and discharged home after 2 weeks.
Three days after discharge, he developed left-sided facial weakness. He was seen in the medical outpatient clinic and found to have a left-sided facial nerve paresis. He was referred to the hospital 4 days later with worsening facial weakness. On examination, there was bilateral facial nerve paresis, worse on the left than the right (figure 1). The other cranial nerves were normal. Neurological examination of the limbs was normal.
Blood tests showed improving liver function and lymphocytosis (see supplementary data) and a serum angiotensin-converting enzyme (ACE) level of 92 U/l (normal range 25–82 U/l). Cerebrospinal fluid (CSF) examination demonstrated a white blood cell count of 9×106 cells/l, red blood cell count of 2×106 cells/l, protein level of 0.9 g/l and glucose level of 3.1 mmol/l. The findings of the CSF microscopy, culture and Ziehl–Neelsen stain were negative. CSF polymerase chain reactions for EBV, herpes simplex virus, varicella zoster virus, enterovirus, cytomegalovirus and Toxoplasma gondii were negative. The CSF ACE level was 1.67 U/l (normal range <1.2). CSF cytological examination demonstrated occasional red blood cells only. There were matched CSF and serum oligoclonal bands.
MRI brain with intravenous gadolinium showed enhancement within the internal auditory canals bilaterally and extending along the intratemporal left facial nerve (figure 2).
Six weeks later, the patient's facial weakness had improved spontaneously with residual weakness of left eye closure.
Neurological complications, including cranial nerve palsies, meningitis, encephalitis, myelitis and Guillan–Barre syndrome, are associated with 0.5%–7.5% of patients with acute EBV infection.1 The most common cranial nerve involved is the facial nerve, and approximately 35% of reported patients with EBV-associated facial palsy have bilateral facial nerve involvement.2 Although facial nerve palsies associated with acute EBV infection in the paediatric population are reasonably well documented,2–4 there have been few reports of adult cases.5 6
Contrast-enhanced MRI in our patient suggested an inflammatory process affecting both facial nerves. Similar but unilateral changes have been reported in Bell's palsy.7
EBV was the most likely cause of our patient's bilateral facial nerve palsies in view of the recent acute EBV infection. Although CSF EBV polymerase chain reaction was negative, this has been previously described in patients with neurological complications of EBV.5 Neurosarcoidosis was felt to be unlikely despite the slightly raised serum and CSF ACE levels because there were no systemic features of sarcoidosis.
Positive EBV serological test result has previously been reported in patients with Bell's palsy.8 Excluding acute EBV infection might be helpful in the diagnosis of patients with facial palsy, particularly when bilateral, even in cases with no systemic manifestations of EBV infection. Prognosis for EBV-associated neurological complications is good, and treatment is usually not required.1
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
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