Background: Although a number of susceptibility genes and environmental factors have been identified, precise mechanism that triggers febrile seizures (FS) is still unclear. However, it is known that pH changes have central role in the control of electrical activity in brain, leading to seizures. Brain alkalosis is known to enhance neuronal excitability and promote epileptiform activity.
Objective: The aim of this study was to assess the association between febrile seizure and hypocapnea and the role of hypocapnea in the development of febrile seizures.
Patients and Methods: The present study was an observational, case-control, study that was conducted on 100 patients who were recruited form Aswan University Hospitals. The patients were divided into the following groups: Group I: 50 children with febrile seizure (defined as: seizures in children in association with fever of 38.0 C or more without definitive evidence of neurological disorders, central nervous system infection, or metabolic abnormalities). Group II: 50 age- and gender-matched children with febrile illness, but without convulsions working as a control group.
Results: We found that there was statistically significant difference between patients and control groups in terms of hypocapnea (p < 0.001). Patients were more likely to have hypocapnea at admission. In addition, there were statistically significant differences between patients and control groups in terms of acidosis at admission (p < 0.001) and alkalosis at admission (p < 0.001). Patients were more likely to have acidosis or alkalosis.
Conclusion: Hypocapnea is significantly associated with febrile seizures. In our study, we found that children with febrile convulsion had significantly higher rate of hypocapnea than normal controls. In addition, it is apparent that presence of hypocapnea is associated with the type of seizure, but not with the duration of the attack.