According to the Epilepsy Foundation, more than 2 million people in the United States and about 65 million worldwide suffer from epilepsy. In the U.S., 150,000 new cases are diagnosed each year. About 300,000 people with epilepsy are under the age of 14, and 500,000 are over the age 65. One in 10 people will have a seizure at some point during their life.

Epilepsy can be classified as either idiopathic or symptomatic. Idiopathic epilepsy has no known cause, and the person has no other signs of neurological disease or mental deficiency. Symptomatic epilepsy results from a known condition, such as stroke, poisoning, Lennox-Gastaut syndrome, cerebral palsy and head injury. Although the relationship is not clearly understood, traumatic brain injury (TBI) is a risk factor for epilepsy.

Head trauma is common in today's world. In addition to trauma from vehicle crashes and sporting accidents, head injury is becoming the signature injury of modern warfare. More than 1 million Americans sustain head trauma each year, but fortunately only a minority of these are severe.

So how often does head trauma lead to epilepsy? Head trauma accounts for 5 percent of all epilepsy cases and 20 percent of cases of symptomatic epilepsy. It generally depends on how severe the head trauma. Mild head trauma — with loss of consciousness for less than 30 minutes — is associated with barely increased risk of developing epilepsy compared to the general population.

David Cantu is a postdoctoral scholar at Tufts University School of Medicine and a member of the NIH-funded Institutional Research Career and Academic Development Awards (IRACDA) Program. He and his associate, Chris Dulla, recently conducted a study in mice to investigate head trauma related to epilepsy by studying the effect of TBI on the levels of the neurotransmitter gamma-aminobutyric acid (GABA) in the cerebral cortex, the portion of the brain associated with higher level functions.

Normally, GABA inhibits neurotransmission in the brain while its precursor, glutamate, stimulates neurotransmission. If the cortex is damaged by brain injury, the cells that create GABA (interneurons) die, which leads to a toxic buildup of glutamate overstimulating the brain.

In their study, the researchers noted that this disruption in the balance of GABA and glutamate was a factor in increased epileptic brain activity. Ultimately, these findings suggest that traumatic brain injuries cause damage to the interneurons responsible for creating GABA. Preserving these important cells may help decrease the negative impacts of TBI, particularly for those severe single injuries that often occur in the military service and contact sports.

This study describes a potential outline of what happens after brain injury to trigger epilepsy, but the neurological causes of exactly how TBI kills interneurons after the initial injury remain unknown. That said, understanding how brain injury disrupts normal brain function will allow scientists as well as physicians to develop new treatments and therapies to help people recover from post-traumatic epilepsy — an important step in preserving brain function.