The nervous system relies on two opposing forces to function: excitatory signals, which increase the likelihood that nearby neurons will fire, and inhibitory signals, which dampen activity by decreasing that likelihood. Until recently, seizures were thought to begin with an over-activation of excitatory neurons, with inhibitory neurons acting to prevent their spread, but this commonly held belief was never experimentally supported. Led by Dr. Shennan Weiss, a team of researchers at the Jefferson Institute have found evidence to the contrary: increased activation of inhibitory neurons—not excitatory neurons—begin seizures.
In the last twenty years, researchers have found that a spike in inhibition often occurs before seizures in animals. Weiss and his team set out to see if these findings applied to epilepsy in humans. After analyzing thirteen spontaneous seizures in nine epileptic patients, they found that the firing rate of inhibitory neurons peaked well before the firing rate of excitatory neurons. This initial inhibitory activity could be interpreted in one of two ways: it could be a protective mechanism gone awry, or it could be directly responsible for the onset of a seizure.
These findings could have major implications for the study and treatment of epilepsy. According to Dr. Weiss, it may be possible to design treatments like drugs or implantable devices to control the activity of inhibitory neurons. It may also be possible to monitor inhibitory neurons to predict seizures, which would aid in the treatment of epileptic patients.