| Objective Firstly to establish the model of posttraumatic epilepsy (PTE) induced by fluid percussion injury (FPI) in rats. Then the technique of electric cortical stimulation (ECS) was used in this model to evaluate the effect of ECS on the PTE rats' seizures and EEG, and explore its treatment program, potential mechanism and safety, so provide evidence for treating pharmacological intractable epilepsy patients.Methods⑴Fifty adult male Sprague-Dawley (SD) rats were randomly divided into two groups (40 FPI, 10 shams). To produce severe traumatic brain injury (TBI) in sober rats, we used the fluid percussion device rapidly injecting fluid volumes into the cranial cavity. The changes of rats' behaviors, histological analysis and electroencephalographic (EEG) were observed in the six months following FPI. In this study, animals showing seizures more than two times during the entire period of monitoring were considered epileptic.⑵PTE rats were divided randomly into two groups: stimulation group(n=5), sham stimulation group(n=5).Rats in stimulation group were inserted cortical electrodes in subdural space, then deliver electrical stimulation for two weeks. Sham stimulation groups didn't receive any stimulation and the other treatment was the same as stimulation group. At last, transmission electron microscope (TEM) was used to investigate the ultramicrostructural changes in the stimulated cerebral cortex.Results⑴Animals that died immediately or within the first week after FPI were included in statistical analysis of mortality, but excluded from other analyses. The mortality rate in animals subjected to FPI was 30 %( 12/40). Data from experiment indicated that 42.9 %( 12/28) of injured animals developed epilepsy, with a latency period between 3 weeks and 6 months. Behavioral and electrographic seizures were not observed in control group animals.⑵In this study, ECS significantly reduced the wave amplitude of stimulated cortex with 3 mA current, the suppressing effect lasting for 5～12 seconds. EEG returned to normal after stopping-stimulation. When a seizure occurs, rapidly deliver targeted electrical stimuli on rat cortex. The results show that the seizure activity was not controlled by ECS, but the spike frequency and background activity were reduced. The TEM shows capillary endotheliocyte swelling, neuronal degeneration, cytochondriome cavitations, synaptic vesicle reducing, presynaptic membrane and postsynaptic membrane thickening, but the ECS group rats were less ultrastructural changes than the sham stimulation group.Conclusions⑴These results demonstrate that the FPI in sober rats induces a PTE syndrome with electrographic, behavioral, and pathologic characteristics similar to those of human PTE. The chronic epileptic rat model induced by FPI might be a stable, reliable and maneuverable model of epilepsy. The PTE model can be served as an effective tool for human PTE studies in the near future.⑵These results support the idea that ECS applied in an appropriate manner at seizure onset could abort seizures in rats. TEM observations have indicated that the ECS may be a safe tool. However, it is very difficult to definite the true effects of the ECS owing to the limitation of time and funds in this study. Future investigations are likely to study the delayed effect of ECS by means of a long-term observation and study.
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