Could Epilepsy Drugs Treat Ischemic Stroke?

Retigabine (Ezogabine)—a drug for the treatment of epilepsy—helped protect the brain against the negative impact of ischemic stroke, according to a new study.

“Cerebral ischemic stroke is a worldwide cause of mortality/morbidity and thus an important focus of research to decrease the severity of brain injury. Therapeutic options for acute stroke are still limited,” said the study’s authors.
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“Although KCNQ channel openers, such as retigabine, have emerged as anti-epilepsy drugs, their effects on ischemic injury remain unknown. Here, we investigated the protective effects of M-channel openers on stroke-induced brain injury in mouse photothrombotic and middle cerebral artery occlusion (MCAo) models,” they said.

For the study, researchers at the School of Medicine at the UT Health Science Center analyzed mice that had undergone ischemic stroke, comparing those treated with the drug to a control group of untreated mice.

Researchers believed that by using the drug to stop the electrical activity of nerve cells in the brain, they could hasten the recovery of those cells after stroke.

During a balance beam exercise, the treated mice showed no difficulty with ambulation, balance, or turning around on the beam, while untreated mice displayed a significant loss of coordination.

Further, the brain tissue of retigabine-treated mice was significantly less damage in comparison to the control group.

The investigators noted that since retigabine is approved by the FDA as an anticonvulsant drug, doctors could use it off label to treat their stroke patients, but clinical trials will need to be conducted before the drug can be approved as stroke therapy.

The complete study is published in the February issue of the Journal of Neuroscience.

-Michelle Canales

Reference:

Bierbower SM, Choveau FS, Lechleiter JD, et al. Augmentation of M-type (KCNQ) potassium channels as a novel strategy to reduce stroke-induced brain injury. J Neurosci. 2015 February [epub ahead of print] doi: 10.1523/JNEUROSCI.3805-14.2015.