Prolonged epileptic seizures may cause serious problems that will continue for the rest of a patient’s life. As a result of a seizure, neural connections of the brain may be incorrectly rewired, that may result in seizures that are difficult to control with medication.
In a recent study involving a rat epilepsy model, researchers showed that a change in the function of gamma- aminobutyric acid (GABA), a leading neurotransmitter in the brain, that evokes harmful neural connections to occur.
After a prolonged convulsive seizure, GABA accelerates brain activity, instead of the inhibitory effect of the transmitter. The accelerated effect of GABA was inhibited for three days with a drug called bumetanide, administered soon after a seizure. Two months after the seizure, the amount of harmful connections detected in the brain was significantly lower. Most importantly, the number of convulsive seizures diminished markedly.
In this study, new indications may be found for bumetanide in the treatment of epilepsy. Bumetanide is a diuretic already in clinical use. Extensive clinical studies have already been conducted with bumetanide regarding its ability to reduce the amount of convulsions or prevent them entirely in the acute phase of seizures. This, however, is the first time that bumetanide has been found to have a long-term effect on the neural network structure of the brain.
Further study of the newly identified mechanism may eventually help limit the complication of epilepsy and prevent the onset of permanent epilepsy after an individual serious seizure. It may also be possible that a similar mechanism is responsible for the onset of epilepsy after a traumatic brain injury.
The research team in their next step, intends to study bumetanide both by itself and in combination with other clinically used drugs, to find out the ways in which it may offer additional benefits in the treatment of epilepsy in combination with and even in place of currently used antiepileptic drugs.