Progression of Epileptogenesis and Comorbid Behavior Patterns after Traumatic Brain Injury in Aged Mice
Abstract number :
2.467
Submission category :
6. Cormorbidity (Somatic and Psychiatric)
Year :
2022
Submission ID :
2232903
Source :
www.aesnet.org
Presentation date :
12/4/2022 12:00:00 PM
Published date :
Nov 22, 2022, 05:28 AM
Authors :
Lauren Skrobarczyk, BS – Texas A&M University School of Medicine; Sreevidhya Ramakrishnan, PhD – Texas A&M University School of Medicine; D. Samba Reddy, Phd, RPH, FAAPS, FAAAS – Texas A&M University School of Medicine
This is a Late Breaking abstract
Rationale: Traumatic brain injury (TBI) is a complex condition with varying degrees of risk of developing post-traumatic epilepsy (PTE) and its associated comorbidities. The risk of PTE is high for up to 10 years following injury, and there is an increased risk of falls in older people, resulting in serious consequences, such as head injury. Therefore, the risk of PTE in people aged 65 or older is high. Age can affect the development and manifestation of epilepsy and associated neuropsychiatric disorders, as aged brains have reduced capacity for rapid repair and neuroplasticity. The development of epilepsy and comorbidities is unknown in geriatric populations. In this study, we characterized the progression of epileptogenesis and its comorbidities in aged populations following TBI.
Methods: A controlled cortical impact model of severe TBI was performed on aged mice (15-17 mon) and video-EEG was recorded 24/7 for 4 months via cortical and hippocampal electrodes. Aged sham (uninjured) and young adult TBI cohorts were generated as control groups. EEGs were analyzed for various abnormalities to study the progression of epileptogenesis. Sensorimotor, behavioral, and cognitive tests were performed each month to evaluate neuropsychiatric comorbidities.
Results: Aged TBI mice displayed elevated post-traumatic behavior deficits, heightened anxiety response, and learning memory deficits. They exhibited robust seizures, discharges, and high frequency oscillations (HFOs) compared to sham; however, they showed a significantly lower seizure burden and incidence rate than young adult cohort.
Conclusions: These results show that TBI causes PTE and associated neuropsychiatric comorbidities in older populations, and the clinical manifestation of TBI differs between aged and young populations.
Funding: This research was funded by DOD grants #W81XWH-16-1-0660 and W81XWH2210275
Cormorbidity (Somatic and Psychiatric)