The link between human herpesvirus-6 (HHV-6) and other viruses and febrile convulsions (FC) in 65 children (mean age 18 months) with a first episode of simple FC (Group 1) compared to 24 children (mean age 19 months) with a febrile syndrome without FC (Group 2), was examined at the University of Modena, and the Civil Hospital of Sassuolo, Italy. HHV-6 was found in 23/65 of group 1 patients and 12/24 of group 2; adenoviruses in 9/65 of group 1 and in 0/24 of group 2. Of 35% FC cases testing positive for HHV-6,only 17% had the typical exanthema. In the HHV-6 infected group, children who developed FC had lower total immunoglobulins, especially IgM. Children with FC were more likely to have a family history of FC and circulating granulocytes. Of 57 patients followed for 2 years, 9 (15%) had a second FC, and HHV-6 reactivations were three times more frequent in this group. [1]

COMMENT. The authors speculate that several viruses, especially HHV-6, may be implicated in causation of febrile convulsions in two thirds of cases, and may be reactivated to induce recurrences. The heredity factor is also important, involving a reduced immune response to viral infection in susceptible children. Those who develop FC with HHV-6 infection have a marked granulocytosis and reduced immunoglobulins, IgA and IgM. The influence of enhanced cytokine production in FC is unproven.

Febrile seizures caused by fever induced by HHV-6 infection and roseola are not always simple in type. They are frequently prolonged, recurrent, and complex, and sometimes a manifestation of encephalitis or encephalopathy. For additional reports of HHV-6 infection and febrile seizures, see Ped Neur Briefs Sept 1994, and Progress in Pediatric Neurology II, 1994:410-411.

Iron deficiency anemia and febrile convulsions are linked in a study from the University of Naples, Italy [2]. Anemia (Hgb <105 g/l, serum iron <5.4 mcmol/1) occurred in 30% of FC cases compared to 10% in the non-FC control population. Iron deficiency anemia has also been associated with a case of reversible focal neurologic deficits, and with breath-holding spells. (Progress in Pediatric Neurology I, 1991:397-398).