The role of interleukins in idiopathic epilepsy

Aim: Epilepsies were classified under three main headings as focal, generalized and unknown according to the latest ILAE 2017. The etiologies are classified as metabolic, immune, structural, genetic, infectious and unknown. Epileptogenesis is still not fully elucidated. It has been stated that the increase in the release of excitatory substances such as voltage-gated ion channels and glutamate responsible for the pathophysiology. Recently, it has been suggested that the disruption of the blood-brain barrier and the increases in glutamate secretion are triggered by both systemic inflammation and neuroinflammation. In this study, we intented to clarify the relationship between epilepsy and inflammation by measuring IL-17A, IL-23, IL-6 and IFN-γ levels. Patients and Methods: Twenty-seven patients between 0-18 years of age who applied to the Pediatrics Neurology outpatient clinic between October 2018 and June 2020, were included in the study. Cases with epileptic encephalopathy, epileptic status, patients with intellectual disability and developmental delay were not included. Twenty-eight children with similar age groups and genders were determined as the control group. IL-17A, IL-23, IL-6 and IFN-γ levels were measured in the plasma serum. National hospital seizure severity scale scores (NHS3) were used for seizure severity. Simultaneous EEG and cranial MRI were performed. Results: In this study, 53 patients were diagnosed as idiopathic epilepsy. Twenty-seven patients of 53 ones met the study criteria. IL-17A and IL-6 levels were measured at the time of diagnosis and at the 6th month of the treatment. When we compare IL-17A and IL-6 levels at the time of diagnosis with 6th months of treatment, we found that 6th mounth levels were were higher (p=0.001 for IL-17A, p=0.020 for IL-6). On the other hand, when the patient group was compared with the control group, IL-17A level was higher in the control group than the patient group at the time of the diagnosis (p=0.043). There was no correlation between NHS3 scores and cytokine levels. The NHS3 scores of our cases were low, with an average of 5.67 point(min 2- max 12 point). Conclusion: There was no difference in inflammatory markers (IL-17A, IL-6) at the beginning compared to the control group on the other hand, IL17-A and IL-6 levels were found to be high despite drug treatment at the end of the six-month follow-up in our uncomplicated childhood epilepy group. This indicates that ongoing epileptogenesis may cause secondary inflammation.