Establishing a mouse model of post-traumatic epilepsy using video-EEG-ECG Monitoring

Additional Authors

Canah McNeal, Department of Biomedical Sciences, East Tennessee State University, Johnson City, TN.

Abstract

Traumatic brain injury (TBI) is a major cause of death and permanent disability. Patients with TBI are at an increased risk of developing post-traumatic epilepsy (PTE), and it has been estimated that PTE may account for up to 20% of symptomatic epilepsy cases in the general population. The process of epileptogenesis is defined as the mechanism by which a brain insult starts a cascade that culminates in the development of spontaneous seizures. Following TBI, the occurrence of seizures has been categorized as immediate (<24 h), early (days), or latent (weeks). These immediate and early seizures are considered to reflect the severity of the injury itself, whereas the latent seizures are thought to result from maturation of epileptogenic pathology. The specific objective of this pilot study was to establish a protocol for video-EEG-ECG of mice following TBI to determine latent PTE development. Mice underwent surgery and EEG-ECG electrodes were placed immediately prior to TBI via controlled cortical impact. We initially chose 2 depth levels of injury (1mm and 1.5mm). We determined that 1.5 mm led to a high mortality rate, leading us to proceed with 1 mm. Currently, we have detected (and verified) seizures in two of four mice at 4 weeks post injury. An additional 8 mice have been EEG analyzed, with potential seizures detected via EEG in five out of eight (awaiting verification). We found that there was post-ictal Atrial-Ventricular block in one mouse. We also observed large fluctuations in heart rate during seizure free periods. Further analysis of ECG recordings is ongoing. Overall, our goal is to establish a 50-60% PTE development rate in our model for future applications. Our findings on ECG abnormalities mimic those observed in other models of epilepsy, suggesting that neuro-cardiac interactions in TBI warrant deeper investigation.

Start Time

16-4-2025 9:00 AM

End Time

16-4-2025 11:30 AM

Presentation Type

Poster

Presentation Category

Science, Technology and Engineering

Student Type

Undergraduate Student

Faculty Mentor

Chad Frasier

Faculty Department

Biomedical Sciences

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Apr 16th, 9:00 AM Apr 16th, 11:30 AM

Establishing a mouse model of post-traumatic epilepsy using video-EEG-ECG Monitoring

Traumatic brain injury (TBI) is a major cause of death and permanent disability. Patients with TBI are at an increased risk of developing post-traumatic epilepsy (PTE), and it has been estimated that PTE may account for up to 20% of symptomatic epilepsy cases in the general population. The process of epileptogenesis is defined as the mechanism by which a brain insult starts a cascade that culminates in the development of spontaneous seizures. Following TBI, the occurrence of seizures has been categorized as immediate (<24 >h), early (days), or latent (weeks). These immediate and early seizures are considered to reflect the severity of the injury itself, whereas the latent seizures are thought to result from maturation of epileptogenic pathology. The specific objective of this pilot study was to establish a protocol for video-EEG-ECG of mice following TBI to determine latent PTE development. Mice underwent surgery and EEG-ECG electrodes were placed immediately prior to TBI via controlled cortical impact. We initially chose 2 depth levels of injury (1mm and 1.5mm). We determined that 1.5 mm led to a high mortality rate, leading us to proceed with 1 mm. Currently, we have detected (and verified) seizures in two of four mice at 4 weeks post injury. An additional 8 mice have been EEG analyzed, with potential seizures detected via EEG in five out of eight (awaiting verification). We found that there was post-ictal Atrial-Ventricular block in one mouse. We also observed large fluctuations in heart rate during seizure free periods. Further analysis of ECG recordings is ongoing. Overall, our goal is to establish a 50-60% PTE development rate in our model for future applications. Our findings on ECG abnormalities mimic those observed in other models of epilepsy, suggesting that neuro-cardiac interactions in TBI warrant deeper investigation.