Article published in Texas A&M Today
TBI is among the leading causes of injury-related death and disability in the United States, with an estimated 5 million people living with the challenges of a long-term TBI-related disability. With symptoms ranging from “mild” to “severe,” individuals who suffer from TBIs can develop a wide range of long-term consequences such as poor motor balance, depression, post-traumatic stress disorder (PTSD), dementia, epilepsy and premature death.
Spontaneous recurrent seizures (SRS) may occur in the months or years following the injury, which is commonly referred to as post-traumatic epilepsy (PTE). Currently, there is no effective treatment or cure for PTE; therefore, there is a critical need to develop animal models to help further understand and assess the mechanisms and interventions related to TBI-induced epilepsy.
- Samba Reddy, a professor in the Department of Neuroscience and Experimental Therapeutics at the Texas A&M University College of Medicine, and his team have created a novel experimental model that is able to successfully replicate the same spontaneous recurrent seizures that occur in humans who develop TBI-induced epilepsy. Their findings were recently published in the journal Experimental Neurology. This research, funded by grants from the Department of Defense, can be used to test medical treatments to prevent seizures and other neuropsychiatric conditions in military personnel.
This is a game-changing model on many fronts, Reddy said.
In addition to long-term EEG analysis, Reddy’s team profiled a longitudinal change in the brain in two other major areas: brain tissue histology and behavioral patterns. Behaviorally, the test subjects showed sensory and behavioral functional deficits as well as long-term memory dysfunction — too often overlooked facets of the condition in humans that can negatively affect the quality of life and independent functioning.
In neuropathology analysis, the researchers’ findings showed degeneration of principal neurons and a loss of inhibitory interneurons in the brain. Interneurons normally function as a brake to slow electrical activity, so loss of these special neurons causes excess electrical activity in the brain. There was also an increased incidence of mossy fiber sprouting, which is a hallmark cellular change found in temporal lobe epilepsy.