Although the relationship is not completely understood, traumatic brain injury (TBI) has been determined as a risk factor for epilepsy. A new study involving mice, published in Cerebral Cortex, identified increased levels of a specific neurotransmitter as a contributing factor linking TBI with post-traumatic epilepsy.
The research team, piloted by David Cantu and Chris Dulla, examined the effect of TBI on levels of the neurotransmitter, gamma-amino butyric acid (GABA), in the cerebral cortex, that portion of the brain associated with higher level functions including information processing.
Under normal functions, GABA inhibits neurotransmission in the brain, while glutamate stimulates neurotransmission. After a brain injury damages the cortex, the cells that create GABA, called interneurons, die. This causes a toxic buildup of glutamate, which over stimulates brain activity. This disrupted balance of GABA and glutamate has been identified as a factor in increased epileptic brain activity.
Interneurons play an integral role in preventing the onset of epileptic seizures, and researchers believe if these cells could be preserved, the negative consequences of TBIs could be decreased. This research provides great insight to the effects of severe single head injuries that often occur in contact sports and military service.
Effects of Epilepsy
According to estimates from the Centers for Disease Control and Prevention, more than 2.3 million Americans are affected by epilepsy. As estimated by the Epilepsy Foundation, 15 to 34 percent of TBI patients suffer from post-traumatic epilepsy, and that rate rises to as much as 52 percent amongst TBI patients with active duty military roles.
Millions of Americans suffer TBIs every year, all too often, with dire consequences. Issues with basic skills such as talking, walking, and independent daily living are all possible results of TBIs. In addition to being linked with military service and contact sports, TBIs can be caused by falls that interfere with the brain development of children, and disrupt the delicate brain systems of the elderly.
This study is a significant step toward identifying the relationship between TBI and post-traumatic epilepsy, and although the specific neurological causes of how TBI kills interneurons are yet unknown, the study potentially outlines what happens after brain injury to trigger epilepsy. Comprehending how TBI disturbs normal brain function will allow researchers to develop new therapies to help post-traumatic epilepsy victims recover.
