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Viruses in febrile convulsions
  1. HELEN LEWIS, Consultant Paediatrician
  1. Department of Paediatrics & Child Health
  2. Trafford General Hospital, Moorside Road
  3. Davyhulme, Manchester M41 5SL, UK

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    Editor,—A study from Japan has produced evidence of human herpes 6 virus (HHV6) infection in 21 of 105 children with febrile convulsions.1

    Those with HHV6 infection at the time of a first febrile convulsion were younger and more likely to have had a convulsion with complex features (prolonged, clustering, or partial seizure or post-ictal paralysis) than those in whom there was no evidence of HHV6 infection. The authors have suggested that febrile convulsions associated with this virus might be the result of direct invasion of the central nervous system rather than simple fever.

    More than 20 years ago, an investigation in north west London showed that a viral aetiology could be implicated in 86% of 73 children after their first febrile convulsion—by combining the results of techniques available for viral diagnosis (tissue culture, mouse inoculation, electron microscopy, complement fixation tests, and interferon assays).2

    A disseminated viral illness was shown by isolating a virus from the blood, CSF, or urine in 20 (27%) of the children. The viruses isolated included serotypes of adenovirus, echovirus, Coxsackie virus, parainfluenza, measles, and cytomegalovirus. Children with “complex” convulsions had a similar spectrum of viral and bacterial findings as those with simple convulsions. We concluded that many common viruses can invade the blood or CSF, and that systemic invasion produced both fever and convulsion. The viruses identified were common pathogens in infants in our community. The HHV6 virus had not yet been identified, although it was known that roseola infantum was often associated with febrile convulsions in children less than 1 year old, when roseola had its peak incidence.3

    Today, the expansion of techniques of rapid viral diagnosis, including the polymerase chain reaction, might lead to recognition of more “neurotropic” viruses and further support the proposition that a febrile convulsion occurs when a child with a genetic predisposition is exposed to a systemic virus or bacterium at a susceptible stage in brain development.


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