CHICAGO - Fever-induced childhood seizures, known as febrile seizures, can be terrifying for parents to witness. The full-body convulsions, which mostly affect children six months to five years old, can last from mere seconds up to more than 40 minutes. Currently, children are not treated with daily anticonvulsant medication to prevent these seizures even when they recur repeatedly because toxic side effects of existing treatments outweigh potential benefits.
While scientists know these seizures typically occur when a fever is above 100.4 degrees Fahrenheit (38 degrees Celsius), the exact mechanism at work has been unclear.
Now, in a new study appearing in the June 12, 2013 issue of The Journal of Neuroscience, a team of Northwestern Medicine researchers has identified a new key factor in the generation of febrile seizures, leading to a new therapeutic target for humans. The team further found that nimodipine, a commonly available L-type calcium-channel blocker, dramatically reduced the incidence and duration of febrile seizures in animals.
"Until now, most scientists believed L-type calcium channels, pores in the membrane that allow calcium into cells, were not engaged in the initiation of the brain electrical activity," said the study's lead author Marco Martina, MD, associate professor in physiology at Northwestern University Feinberg School of Medicine. "We show that the activation of these channels, which are temperature sensitive, actually drives the electrical activity, not just follows it. As such, these channels may play a key role in seizure associated with high body temperature. Consequently, we can develop better treatments for toddlers and reduce the risk of negative outcomes."
Febrile seizures affect about five percent of children in the United States and are mostly benign, but do carry a risk of negative long-term consequences on brain development.
In this study, the Northwestern team used
|Contact: Marla Paul|