This review highlights mechanisms and biomarkers linked to seizures in glioma patients, suggesting new treatment strategies.
Epilepsy is a frequently occurring complication in patients with gliomas that substantially impairs their quality of life. The onset of epilepsy in patients with gliomas is driven by multiple mechanisms, including tumour‑induced compression of the peripheral neural network, the release of neurotransmitters and inflammatory factors by tumour cells, alterations in the tumour microenvironment, and changes in gene expression. Collectively, these factors contribute to the abnormal excitability of local neurons, ultimately triggering seizures. Seizures occur in approximately 30 to 90% of patients with glioma, with a higher incidence observed in those with low‑grade gliomas. The type and frequency of seizures are closely associated with tumour characteristics, such as tumour type, location, and growth rate. The current treatment strategies for glioma‑related epilepsy (GRE) primarily involve antiepileptic drugs (AEDs) and tumour‑directed therapies. While AEDs are effective in managing seizures, they show limited efficacy in some patients. Efforts have increasingly focused on identifying biomarkers and elucidating the molecular mechanisms underlying GRE, with the aim of developing more targeted and effective treatment approaches. The present review provides a comprehensive overview of the latest advancements in GRE research.
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Chen et al. (2025) studied this question.
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