Seven cases of encephalitis and 5 of aseptic meningitis caused by an outbreak of enterovirus 71 (EV71) during the summer of 1997 are reported from the Otsu Municipal Hospital, Shiga, Japan. Skin and mucosal involvement included hand-foot-and-mouth syndrome in 7 and herpangina in 2. The interval between fever and initial CNS symptoms, including headache, nausea, vomiting, and neck stiffness, was 0 to 5 days. Major neurological manifestations, localized to cerebral hemispheres, brainstem, cerebellum, and diencephalon, included seizures in 5, coma or somnolence in 6, truncal ataxia in 5, and diabetes insipidus in 1. MRIs performed in 7 patients were normal in 6 and showed high-intensity lesions in the pons in 1. EEGs showed diffuse high voltage slow wave activity in 6, focal changes in 2, and normal recordings in 4. Evidence of recent EV71 infection relied on unusually high reciprocal EV71 neutralizing antibody titers in 10 patients and a fourfold change in acute and convalescent-phase serum antibody titer in 2. CSF pleocytosis ranged from 8 to 693 cells/mcL. Attempts to detect the viral genome in CSF, using reverse transcriptase-polymerase chain reaction and Southern blot hybridization procedures, were negative. Clinical recovery was complete in 11, and one, a 2-week-old neonate, developed a motor disorder at several months follow-up. [1]

COMMENT. The nonpolio, RNA enteroviruses include 23 group A coxsackieviruses, 6 group B coxsackieviruses, 31 echoviruses, and 4 enteroviruses (types 68-71). Enteroviruis 71 is associated with hand-foot-and-mouth syndrome, encephalitis, aseptic meningitis, and poliolike paralysis. (AAP 1997 Red Book). The virus is spread from mother to infant at birth, and by fecal-oral and respiratory routes in older children. The incubation period is 3 to 6 days.

EEG in diagnosis and outcome of acute encephalitis was investigated at Helsinki University Hospital, Finland. An analysis of 204 EEG recordings from 98 consecutive acyclovir-treated patients with acute encephalitis found that, in the acute phase, clinical epileptic seizures, and focal abnormalities and periodic complexes in the EEG, but not diffuse background slowing, were predictive of a poor outcome. In follow-up EEG recordings, diffuse slowing was significantly associated with poor outcome. The EEG is valuable in assessment of progression in the level of consciousness and epileptic activity in the unconscious patient with encephalitis. [2]

Of interest, the neonate in the above Japanese study, whose neurologic exam had returned to normal one week after the onset of convulsions and the acute phase of enterovirus 71 meningoencephalitis, had repeated EEGs revealing no abnormalities. The developing motor disorder at several months follow-up could be explained as a lower motor neuron poliolike muscle weakness.