Working with data from both rats and humans, NYU Langone researchers have confirmed that certain abnormal discharges are likely behind the lag in the time it takes an epileptic brain to process memory signals traveling from the hippocampus to the cortex.
The delay occurs not during but between seizures, and the new findings may suggest the indication of a not-yet-invented implantable device to interrupt the specific memory signals affected by the disorder, according to a news release from the medical school, issued to publicize the study appearing online April 25 in Nature Medicine.
The study authors documented the damaged neurological process by which epileptic signals emanate from the hippocampus as meaningless commands, only to be mistakenly processed like normal memories.
Laboratory rats evidencing abnormal hippocampal discharges had marked trouble navigating to places in which they’d previously found a water source, and the degree of abnormal hippocampal-cortical signaling tracked closely with the level of memory impairment, according to the release.
Meanwhile the team, led by pediatric neurologist Jennifer Gelinas, MD, PhD, found that human epilepsy patients who had their brain signals monitored as part of surgery preparation evidenced similarly abnormal hippocampal discharges between seizures.
These discharges disrupted normal memory-forming connections between brain regions.
“Our study sheds the first light on the mechanisms by which epilepsy hijacks a normal brain process, disrupting the signals needed to form memories,” says Gelinas, adding that many patients she sees in her practice “feel that cognitive problems have at least as much impact on their lives as seizures, but we have nothing to offer them beyond seizure control treatments. We hope to change that.”
NYU Langone says the new findings may help explain why as many as 40 percent of epilepsy patients experience learning difficulties.
The school says the researchers have begun work designing the aforementioned implantable device, hoping such an intervention might neutralize the effects of the abnormal hippocampal discharges.
The release also references related work published last month in Science. In that study, a team led by NYU Langone neuroscientist Gyorgy Buzsaki, PhD, showed that a few highly active, “rigid” neurons perform the same way before and after experiences, while a second set of rarely contributing “plastic” neurons behave differently before and after opportunities for memory consolidation.
“We seem to have evolved with both a stable template of neurons that process what is the same about the things we encounter and a second group that can learn with new experiences,” says Buzsaki. “This new understanding of memory consolidation made possible our insights into epilepsy.”