Epileptic seizures are frequently caused by brain tumors. Traditional anti-epileptic treatments do not acquire satisfactory responses. Preoperative and postoperative seizures seriously influence the quality of life of patients. Thus, tumor-associated
epilepsy (TAE) is an important subject of the current research. The delineation of the
etiology of epileptogenesis in patients with primary brain tumor may help to find the
novel and effective drug targets for treating this disease. In this review, we describe
the current status of treatment of TAE. More importantly, we focus on the factors
that are involved in the functional connectivity between tumors and stromal cells.
We propose that there exist two modes, namely, long-range and short-range modes,
which likely trigger neuronal hyperexcitation and subsequent epileptic seizures. The
long-range mode is referred to as factors released by tumors including glutamate
and GABA, binding to the corresponding receptor on the cellular membrane and
causing neuronal hyperactivity, while the short-range mode is considered to involve
direct intracellular communication between tumor cells and stromas. Gap junctions
and tunneling nanotube network are involved in cellular interconnections. Future
investigations focused on those two modes may find a potential novel therapeutic
target for treating TAE.