BALTIMORE, Md. -- Using a type of mouse genetically prone to petit mal seizures, researchers at Duke University Medical Center reported Monday finding new clues about the precise location in the brain that causes the common childhood form of epilepsy.
The findings may lead to more specific drugs for the disorder with fewer side effects, said Dr. David Hosford, assistant professor of neurology at Duke and the Durham Veterans Affairs Medical Center.
Petit mal or "absence" seizures affect 100,000 children in the United States and account for one-fifth of all childhood epilepsies. About 20 percent of children with petit mal seizures aren't helped by currently used drugs and another 20 percent experience side effects, such as inability to concentrate.
The findings were prepared for presentation by Sarah Caddick, a post-doctoral fellow in neurology at Duke and the Durham V.A. Medical Center, at the American Epilepsy Society's annual meeting. The work was supported by the National Institute of Neurologic Diseases and Stroke and a V.A. merit award.
Children affected by petit mal seizures have up to hundreds of seconds-long lapses of consciousness, during which they stare blankly and may blink rapidly or sway before recovering.
"Absence seizures usually take hold at a critical period in a child's initial education, and may be interpreted as a learning disability or isolate them from other children," Caddick said in an interview at Duke. "If these studies lead to more effective treatments, they can have a more profound effect on a child's development than merely preventing the seizure."
Previously, the Duke researchers had reported that mice with petit mal seizures have an overabundance of a protein called a GABAb receptor in the brain. These receptor proteins are found in cells throughout the body, and respond to a neurotransmitter signal called gamma aminobutyric acid, or GABA, which is one of a dozen or so known neurotransmitter molecules. GABAb
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Contact: Karyn Hede George
georg016@mc.duke.edu
919-660-1301
Duke University
29-Apr-1996