Abstract

BackgroundThis study aimed to explore the effects of complex febrile seizures on hippocampal function and the significance of antiepileptic therapy.MethodsA total of 150 children with complex febrile seizures admitted to our hospital from July 2017 to July 2020 were included in the study. The VPA group was given sodium valproate treatment; the LEV group was given levetiracetam treatment; and the observation group was given basic treatment. The efficacy of the patients was evaluated after medication. A complex febrile seizure young mouse model was constructed, and the hippocampal cell morphology and BCL-2 expression of the mice pups were analyzed. A Morris water maze was used to detect the changes in cognitive function of the young mice with complex febrile seizures.ResultsAfter treatment, the recurrence-free rate of the VPA group was significantly higher than that of the observation group (P=0.0045). After 1 month and 6 months, the improvement rate of EEG in VPA group was significantly higher than that in observation group (P<0.05). After treatment, the levels of BCL-2 in the VPA group and the LEV group decreased and were significantly lower than the observation group during the same period (P<0.05), and the M/C of the two groups was significantly higher than the observation group (P<0.05). The neuronal cells in the hippocampus of the young rats in the VPA group and the LEV group were regular, the matrix was more uniform, and nuclear pyknotic cells were occasionally seen. The pathological changes were less obvious than the model group, followed by the degree of pathological changes (0.92±1.31, 0.94±1.24). The incubation period of pups in the model group was significantly higher than that of the normal group, VPA group, and LEV group (P<0.05), and the number of crossing the station area was significantly less than that of the normal group, VPA group, and LEV group (P<0.05).ConclusionsAntiepileptic drugs are effective in preventing the recurrence of complicated febrile seizures (CFS), and the main mechanism may be related to the targeted regulation of BCL-2 on the apoptosis of the hippocampus in the nervous system.

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