Mononucleosis is caused by an infection with the Epstein-Barr virus (EBV), a DNA virus in the Herpes virus family. It typically presents with fever, sore throat, malaise, lymphadeno-pathy, and hepatosplenomegaly. It is estimated that 90% of adults have serologic evidence of prior EBV infection. Diagnosis is confirmed by the clinical picture, characteristic hematologic changes, and immunologic findings. Hematologic changes include atypical lymphocytosis of peripheral monocyte cells. Immunologic findings are an elevated heterophil antibody test, the most specific test used for mononucleosis. The heterophile antibody is an IgM antibody produced by infected B lymphocytes. It is not directed against EBV infected cells but rather is a result of the viral transformation of the B cell into a plasmacytoid state induced by the virus. It is present in 90% of cases by the third week of infection. Immunofluorescence techniques are also available to detect antibodies to EBV (50).
Neurologic involvement has been documented in 5.5% of cases with EBV infection (51). Neurologic sequelae are variable and include encephalopathy, meningoencephalitis, seizures, Guillain-Barre syndrome, and cranial neuropathy. Isolated involvement of all 12 cranial nerves has been reported. Facial nerve involvement is a well-recognized sequelae of the infection and was first recognized in 1937 by Gsell (52). The paralysis can be either unilateral (53-55) or bilateral (56), usually presenting as a rapid onset of complete paralysis with typical full recovery of function over the ensuing several weeks (57). Theories of nerve involvement include direct neural cytotoxic injury by the virus, local pressure from viral lymphadenopathy, edema of the facial nerve course, autoimmune response to the antibody-antigen complexes, and vasculitis. Treatment is supportive only and the infection is self-limited with full recovery anticipated. Please refer to Chapter 10 for detailed discussion of EBV.
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