Crisp D E, Bray P F, Bloomer L C
Pediatrics. 1983 Feb;71(2):163-5.
A 4-year-old boy developed typical acute polyneuritis at 2 years of age and returned to fully normal status in 2 months. When he was 4 years old, an identical neurologic syndrome recurred at the same time that his sister was determined to have classic infectious mononucleosis. Both siblings then had positive Monospot tests. The boy with recurrent symmetrical neuropathy had an initial Epstein-Barr virus-viral capsid antibody (EBV-VCA) serum titer of 1:160 and this dropped to 1:40 after 1 month. A persistent complement fixation titer to cytomegalovirus (CMV) of 1:64 was measured in his serum and his concentrated CSF contained a CMV complement fixation antibody titer of 1:32, a rare finding in an age-matched control group. Cultures of his urine, buffy coat, and saliva for CMV were negative. Electrophoresis of his CSF revealed oligoclonal bands, several of which were also present in his serum. It seems most likely, but not proven, that the clinical paralysis was caused initially by a CMV infection and that the Epstein-Barr virus infection reactivated the latent CMV to produce the recurrent weakness.