Background: The aim of the present study was to investigate if high amplitude high frequency oscillations(haHFOs) could be a biomarker of posttraumatic epileptogenesis. Methods: After an initial craniotomy of rats and...Background: The aim of the present study was to investigate if high amplitude high frequency oscillations(haHFOs) could be a biomarker of posttraumatic epileptogenesis. Methods: After an initial craniotomy of rats and inducement of traumatic brain injury(TBI) through a fluid percussion, recording microelectrodes were implanted bilaterally in different brain areas.Wideband brain electrical activity was recorded intermittently from Day 1 of TBI and continued till week 21. HaHFO analysis was performed during the first 4 weeks to investigate whether the occurrence of this brain activity predicted development of epilepsy or not. Results: Of the 21 rats which received the TBI, 9 became epileptic(E+) and 12 did not(E-). HaH FOs were observed in the prefrontal and perilesional cortices, hippocampus, and striatum in both E+ and E-group. In comparison to the rats in E-, the E+ group showed a significant increase in the rate of haHFO from weeks 1 to 4 after TBI.Conclusion: The results indicate that an increase in the rate of haHFOs after TBI could be an electroencephalographic biomarker of posttraumatic epileptogenesis.展开更多
基金supported by research grants from the National Institutes of Health,USA。
文摘Background: The aim of the present study was to investigate if high amplitude high frequency oscillations(haHFOs) could be a biomarker of posttraumatic epileptogenesis. Methods: After an initial craniotomy of rats and inducement of traumatic brain injury(TBI) through a fluid percussion, recording microelectrodes were implanted bilaterally in different brain areas.Wideband brain electrical activity was recorded intermittently from Day 1 of TBI and continued till week 21. HaHFO analysis was performed during the first 4 weeks to investigate whether the occurrence of this brain activity predicted development of epilepsy or not. Results: Of the 21 rats which received the TBI, 9 became epileptic(E+) and 12 did not(E-). HaH FOs were observed in the prefrontal and perilesional cortices, hippocampus, and striatum in both E+ and E-group. In comparison to the rats in E-, the E+ group showed a significant increase in the rate of haHFO from weeks 1 to 4 after TBI.Conclusion: The results indicate that an increase in the rate of haHFOs after TBI could be an electroencephalographic biomarker of posttraumatic epileptogenesis.
