【Abstract】 Objective To investigate the clinical efficacy of lacosamide combined with sodium valproate in the treatment of children with epilepsy, and to analyze its effects on neurological injury and electroencephalogram (EEG)-related indexes. Methods A total of 97 children with epilepsy were randomly divided into a single group (n=48) or a combined group (n=49). The single group was treated with sodium valproate, based on which the combined group was treated with lacosamide, and both groups were treated for 2 months. The clinical efficacy; neurological deficit, cognitive function, EEG parameters, serum brain injury indexes, and serum microRNAs (miRNAs) levels before treatment and after 2 months of treatment; and the occurrence of adverse reactions during the treatment were compared between the two groups. Results After 2 months of treatment, the total effective rate of the combined group was higher than that of the single group; the China Stroke Scale score, number of spike waves per minute, and serum levels of insulin-like growth factor-1, neuron-specific enolase, central nervous system specific protein β, and glial fibrillary acidic protein, as well as serum relative expression levels of miRNA-106b and miRNA-146a in the two groups were lower/less than those before treatment, and those in the combined group were lower/less than those in the single group; the scores of the Mini-Mental State Examination in the two groups were higher than those before treatment, and the score in the combined group was higher than that in the single group (all P<0.05); and there was no statistically significant difference in the activity rate of α, θ, or δ wave between the two groups (all P>0.05). No statistically significant difference in the total incidence of adverse reactions was observed between the two groups during treatment (P>0.05). Conclusion In the treatment of children with epilepsy, lacosamide in combination with sodium valproate has a better effect than sodium valproate alone, which can reduce neurological injury, improve cognitive function and epileptic discharge, and the mechanism may be related to the downregulated-expression of miRNA-106b and miRNA-146a.

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