As a subtype of idiopathic generalized epilepsies, absence epilepsy is believed to be
caused by pathological interactions within the corticothalamic (CT) system. Using a
biophysical mean-field model of the CT system, we demonstrate here that the feed-forward
inhibition (FFI) in thalamus, ie, the pathway from the cerebral cortex (Ctx) to the thalamic
reticular nucleus (TRN) and then to the specific relay nuclei (SRN) of thalamus that are also
directly driven by the Ctx, may participate in controlling absence seizures. In particular, we …