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Molecular mechanism may explain how fevers spark seizures

to the cell membrane slowed?

"Trying to get at why the surface receptor levels are reduced requires a whole set of complicated approaches," Macdonald said. "It's like looking out the window and counting the cars on the street: it's easy to count how many are there at any time, but if we want to know where they all came from and where they're all going, that's a whole different problem."

The team's discovery that high temperature reduces cell surface GABA-A receptor levels "raises the idea that one could develop a treatment for vulnerable patients that would prevent them from developing febrile seizures and possibly epilepsy," Macdonald said. Vulnerable patients include children who suffer recurrent febrile seizures, febrile seizures that involve only part of the body (partial instead of generalized), and long-lasting febrile seizures, as well as children with genetic mutations linked to inherited epilepsies. These patients have a higher incidence of developing epilepsy.

"There's a huge incidence of febrile seizures, so even though only a small percentage -- 2 to 4 percent -- progress to epilepsy, it represents a large burden of epilepsy in the world," Macdonald said. "Our findings are attracting attention because they show a novel mechanism for febrile seizures, and now that we know a vulnerable step, we can in principle design therapeutic strategies to overcome it."


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Source:Vanderbilt University Medical Center


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