Febrile seizures or convulsions refer to generalized or focal convulsions, seen in children between the ages of 6 months and 5 years, caused by a sudden increase in body temperature. During an attack, which usually lasts for between one and five minutes, the child will typically lose consciousness, roll back his/her eyes, go stiff, and displays jerking movements of the body. Febrile convulsions can be of a simple or complex nature. The simple form involves the entire body, lasts for a lesser time, and does not recur for the next 24 hours, while the complex form focuses on a part of the body, lasts for a longer time, and recurs within a day. Febrile seizures are thought to occur in 2-5% of children between the ages of 6 months and 5 years. Up to 75% of these are cases of simple febrile seizures.
The most important factor while making a diagnosis of febrile convulsions is to rule out underlying meningitis and encephalitis. Simple seizures are easy to treat, and are usually not a cause for concern. In any case, the underlying cause for the high fever needs to be arrived at. Management involves controlling the fever, and preventing dehydration. Recurrence risk is generally low, and gets progressively lower as the child grows older. However, in patients with a family history of the condition, the recurrence risk may be as high as 50%. Prognosis is fairly good. Only about 1% of affected patients go on to develop epilepsy in later life.
As mentioned earlier, a family history of febrile convulsions in first degree relatives increases the recurrence risk of these seizures by about 50%. In addition, if either or both of the parents have a history of childhood febrile convulsions, then there is a 10-20% risk of having an affected child. Researchers are of the opinion that mutations in genes causing neuronal hyperexcitability could lead to febrile convulsions.
An autosomal dominant locus on chromosome 8q was the first genetic locus found to be associated with the condition (FEB1). Since then, several different loci have been discovered. These include the SCN1A (Sodium Channel, Neuronal Type I, Alpha Subunit), GPR98 (G Protein-Coupled Receptor 98), and GABRG2 (Gamma-Aminobutyric Acid Receptor, Gamma-2) genes, and several other loci on chromosomes 19p, 6q, 18p, 21q22, and 3p24.