Patients with gliomas experience worsened quality of life due to epileptic attacks. Over 80% of patients are susceptible to seizures, significantly hindering their treatment and well-being. No cause of epilepsy associated with glioma has been identified; however, some mutations are known to contribute to seizures in various situations. The development of a tumour creates advantageous conditions for abnormal neuronal activity to occur. Identifying a therapeutic target is a significant undertaking that numerous studies are endeavouring to undertake. We investigate the potential correlation of pathophysiological processes in the development of both gliomas and epilepsy, aiming to identify any shared factors. Furthermore, we propose that the mutational profile of different types of gliomas may have an impact on the occurrence or absence of seizures. We conclude that spontaneous neuronal activity arises from both the tumour microenvironment and blood ingress into neuronal networks resulting from the breakdown of the blood–brain barrier.

Approximately 30% of glioma patients are able to survive beyond one year postdiagnosis. And this short time is often overshadowed by glioma-associated epilepsy. This condition severely impairs the patient’s quality of life and causes great suffering. The genetic, molecular and cellular mechanisms underlying tumour development and epileptogenesis remain incompletely understood, leading to numerous unanswered questions. The various types of gliomas, namely glioblastoma, astrocytoma and oligodendroglioma, demonstrate distinct seizure susceptibility and disease progression patterns. Patterns have been identified in the presence of IDH mutations and epilepsy, with tumour location in cortical regions, particularly the frontal lobe, showing a more frequent association with seizures. Altered expression of TP53, MGMT and VIM is frequently detected in tumour cells from individuals with epilepsy associated with glioma. However, understanding the pathogenesis of these modifications poses a challenge. Moreover, hypoxic effects induced by glioma and associated with the HIF-1a factor may have a significant impact on epileptogenesis, potentially resulting in epileptiform activity within neuronal networks. We additionally hypothesise about how the tumour may affect the functioning of neuronal ion channels and contribute to disruptions in the blood–brain barrier resulting in spontaneous depolarisations.