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Title Bullet News - Can we delay the onset of seizures after brain injury?
 
19 March 2009

In the previous article, we talked about the risk of developing temporal lobe epilepsy (TLE) after the brain has been injured in some way. Damage to the brain can occur not only through trauma, but also after a stroke or an episode of status epilepticus. Research has shown that there is often a delay between the 'event' and the onset of chronic seizures, known as the latent period.

   

The excitability of certain neurones in an important memory section of the brain called the entorhinal cortex (EC) has been found to be significantly higher than normal during the latent period. This is due at least partly to a change in the nature of certain ion channels in the membranes of these cells. These channels, called h-channels, are opened or closed by the size of the difference in electrical charge between the neurone and the surrounding fluid. During the latent period, the number of h-channels decreases significantly, which makes these neurones more excitable and more prone to seizure activity.

   

Lamotrigine is a commonly prescribed anti-epileptic treatment, which has recently been shown to enhance the activity of h-channels in neurons. In 2006 Dr Mala Shah and Professor Matthew Walker, at the Institute of Neurology, London, were awarded a grant by Epilepsy Research UK, to find out if lamotrigine administered during the latent period is able to restore h-channel numbers to normal, and delay the onset of TLE.

The project is now complete and the results show that lamotrigine can indeed increase the number of h-channels during the latent period; but, interestingly, numbers remain lower than normal. In addition, the effects of lamotrigine are only temporary and before long h-channel numbers decrease once again. Whether or not this / or a similar drug could delay the onset of TLE is still being investigated.

These findings will form the basis of exciting investigations in the future. They have shown that h-channel numbers in the EC can be restored after traumatic brain injury, but that more effective drugs need to be developed for the full benefits of this to be explored.

These results will be published in the near future.


 
 
 
 
 
 
 
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