Epilepsy after traumatic brain injury: important new findings

Posted Mar 26 2014 in Uncategorized

Re-cap from earlier
Neurons usually communicate with each other using chemicals known as neurotransmitters, which are either excitatory (meaning the next neuron ‘fires’) or inhibitory (meaning the next neuron stays silent). The main excitatory and inhibitory neurotransmitters in the brain are called glutamate and GABA respectively, and there must be a fine balance between the two for normal function to occur. In epilepsy there is too much glutatmate ‘signalling’ in relation to GABA ‘signalling’, and this can make some neurons hyperexcitable and prone to seizure activity.

 

Background
People who suffer a brain injury – for example through  trauma, stroke or infection – are at an increased risk of developing  epilepsy, and this is often difficult to treat. The precise mechanisms involved are still not fully understood and research is ongoing. In a recent study, scientists in Boston investigated changes in GABA- and glutamate-signalling following traumatic brain injury, to see whether these contribute to the development of epilepsy.

The study
During the study the team used a humane technique to simulate traumatic brain injury in a group of rodents. They then used advanced sensors to measure glutamate signalling and detect epileptic activity in the brain cortex (the folded surface) of each animal. They continued their recordings for between two and four weeks post-injury. In the final stage of the study, the team used immunological methods to measure the number of interneurons (GABA-producing neurons) in the cortex.

A second group of similar but uninjured rodents (known as controls) underwent the same investigations, and the results of the two groups were compared.

Findings
The scientists found that glutamate signalling increased significantly as a result of traumatic injury, and that this was most marked directly next to the site of injury. They also discovered a link between the rise in glutamate and the development and spread of epileptic activity. When they examined the data for the interneurons, the team found that numbers were dramatically decreased in the injured group.

Implications

These findings suggest that when the brain is injured, GABA-producing interneurons in the brain cortex are lost. In some people this causes a toxic build-up of glutamate, which can lead to the production and spread of epileptic activity. If scientists can find a way to protect interneurons immediately following traumatic injury, it may become possible to prevent epilepsy from developing. This may also be applicable to other types of brain injury.

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