UTSA reduces seizures by eliminating neurons in the newborn.

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UTSA reduces seizures by eliminating neurons in the newborn.

Epilepsy seizures occur in one in ten people who have suffered a head injury (head injury). However, new research at the University of Texas at San Antonio (UTSA) has uncovered an innovative approach to slowing the progression of epilepsy. UTSA researchers have successfully eliminated new neurons that developed after brain damage to reduce seizures in mice. They believe that this technique could potentially reduce post-injury epilepsy.

"We already know that new neurons contribute to epilepsy, but we didn't know if we could target them after a trauma, after the onset of seizures," said Jenny Hsieh, president of the Semmes Foundation and professor of cell biology and director of the UTSA Brain Health Consortium.

"Having the ability to do so would be clinically relevant, because the warning signs of epilepsy are the seizures themselves."

People who suffer a head injury as a result of gun violence or a car accident are at greater risk of seizures. During a seizure, there is an abnormal and sudden electrical disturbance in the brain that causes various symptoms: strange movements of the head, body, arms, legs or eyes, such as stiffening or trembling. Lack of reaction, staring, chewing, lip smacking and even strange visual images are also signs of an epileptic seizure.

According to the U.S. Centers for Disease and Control, emergency room visits, hospitalizations and deaths related to CBT have increased by 53%. Those who have a seizure one week after a head injury are 80% more likely to have another post-traumatic seizure.

Seizures usually occur when there is a scar in the brain as a result of the injury. Often, new neurons generated as a result of brain damage do not migrate or develop normally. If left untreated, these cells can contribute to the development of epilepsy.

Hsieh and his colleagues at the University of Texas at San Antonio systematically removed the new neurons that formed within eight weeks of a seizure in mice. The UTSA team then monitored convulsive activity in mice and observed that treated mice had a 65% reduction in convulsions compared to untreated mice. This effect required more than four weeks of continuous treatment.

"Now we know that we can remove new neurons after the initial attacks," says Hsieh. "Although we cannot stop the first crises, we can try to prevent secondary crises. It's very exciting and can lead to new therapeutic strategies."

Although these results support the role of new neurons in the development of epilepsy, they also suggest that other factors are involved.

"We found that once treatment was completed, seizure reduction was not permanent. This could be due to abnormal changes in the epileptic brain, such as chronic inflammation or reactive astrocytes, affecting the development of new neurons. We are currently exploring these possibilities," said Hsieh.