Researchers at the University of Colorado at Boulder may have pinpointed a new explanation for the onset of adult seizures caused by traumatic brain injuries.
According to lead researcher Daniel Barth, a psychology and neuroscience professor at UC Boulder, neurons have been the focus of seizure research for a long time. Now Barth and his team of researchers have found that micro-glial cells cluster in areas of the brain where traumatic injuries have occurred, release cytokines that increase excitability of nearby neurons, by which seizures occur.
“When there has been serious damage to the brain, such as a head injury or infection, the immune system is activated and tries to counteract the damage and repair it,” Barth said. “These glial cells migrate to the damaged area and release chemicals called cytokines that, unfortunately, also profoundly increase the excitability of the neurons that they are near.”
For the study, researchers applied the bacterium lipopolysaccharide to the brain to activate the micro-glial cells. The glial cells then surrounded the area where the bacterium had been applied and began releasing cytokines, exciting the neurons enough to cause seizures. When the team applied drugs that either blocked activation of the glial cells or the impact of the cytokines on the neurons, “all signs of increased brain excitability and seizures were abolished.”
“The thought is that maybe there is a window of opportunity where we could go in after an injury and administer one of these immune response inhibitors and stop a process that we think is going to lead to epilepsy,” Barth said. “So instead of giving anti-seizure drugs, which have no effect in preventing or subsequently treating post-traumatic epilepsy, we could give some anti-immune drugs which may actually stop the process of developing epilepsy in the first place.”
Results of the study were published in the July issue of the journal Brain.