The focal epilepsy affects more than 30 million patients worldwide and is commonly caused by brain injuries, such as stroke. However, it is not clear why some episodes cause the pathology, while others do not.
A new study by researchers from the Brigham and Women’s Hospital, A founding member of the Mass General Brigham health care system, he found that a common brain circuit can link different locations of disease-causing lesions. In a paper published in JAMA Neurology, researchers used a technique called Mapping the injury network to identify this brain circuit with findings pointing to possible targets for brain stimulation.
“We are learning more and more about Where Cerebral Epilepsy Comes Here and what brain circuits we need to modulate to treat patients with epilepsy. Using a wiring diagram of the human brain, mapping the network of lesions allows us to Look beyond the location of the injury and map their connected brain circuitry,” said senior author Frederic Schaper, an instructor in neurology at the Harvard Medical School and a scientist at the Brigham and Women’s Center for Brain Circuit Therapeutics.
Schaper and the team studied 5 datasets more than 1,500 patients with brain injuries. Participating centers in the U.S. and Europe included Brigham and Women’s Hospital, Massachusetts General Hospital, Boston Children’s Hospital, Northwestern University and Turku University Hospitals in Finland, Maastricht in the Netherlands, and Barcelona in Spain. They analyzed a variety of brain injuries, such as strokes, trauma, and tumors, allowing them to Find common network connections related to epilepsy in different regions and types of brain damage.
One of the datasets included combat veterans from the Vietnam Head Injury Study, which was originally designed in the decade of 1960 because brain damage caused by shrapnel wounds combat resulted in a significant increase in the occurrence of epilepsy.
“In our studies, up to 50% of Vietnam combat veterans suffered at least one seizure after injury, sometimes many years after injury,” explained co-author Jordan Grafman of the Shirley Ryan AbilityLab in Chicago. However, he added, “it’s not clear why these marks in some places cause epilepsy and in others don’t.”
The Brigham researchers compared the locations of brain damage in patients who developed epilepsy with those who did not, and found that the marks associated with epilepsy were distributed throughout the brain.
However, these same injury locations were connected to a common brain network, suggesting that brain connections disrupted by the injuries, rather than the locations of the damage themselves, were key. These findings may have clinical implications for predicting epilepsy risk after brain damage.
“If we can map a lesion to the brain network we identified, we might be able to estimate the likelihood of someone getting epilepsy after a stroke. This is not yet a clinical tool, but we will lay the groundwork for future studies investigating the use of human brain networks to predict epilepsy risk,” Schaper said.
The key brain connections they identified they were not on the surface of the brain, but they were found deep in regions called basal ganglia and in the cerebellum. The authors stated that for decades, these deep structures have been shown to modulate and control epileptic seizures in animal models and are hypothesized to act as a brain ‘lock’. Based on these findings, the researchers analyzed data from 30 patients with resistant epilepsy to medications that underwent deep brain stimulation (DBS) for RTTie up seizures. They found that they fared much better if the DBS site was connected to the same brain network and identified him using brain injuries.
“When programming a DBS electrode to improve seizures, it’s difficult to know which place to stimulate because it can take months before a patient’s seizures improve,” said senior author Michael Fox, associate professor of neurology at the University of the Harvard Medical School and founding director of the Brigham and Women’s Center for Brain Circuit Therapeutics. Identifying this brain circuit for epilepsy can help us target the right place to improve patient outcomes,” Schaper said.
The authors noted that the current study was a retrospective analysis that used existing datasets and a wiring diagram of healthy individuals. When available, future analyses could use something similar in patients and prospectively test the usefulness of this circuit as a clinical tool. “We now know more about which brain circuits may play a role in both causing and controlling epilepsy, opening up promising opportunities to guide our therapies. Future clinical trials are needed to determine whether this circuit can effectively guide brain stimulation treatment for epilepsy and benefit patients,” Schaper concluded.
