Tumor-associated epilepsy is an important contributor to morbidity in patients with brain tumors. Proposed pathophysiological mechanisms to explain these effects range from neuronal and glial dysfunction to deranged vascular homeostasis, to ionic and pH changes. Perilesional tissue alterations play a vital role in the generation of tumor-associated seizures. Clinical studies have determined that tumor-associated seizures are usually focal with secondary generalization and often resistant to

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... epileptic drugs. Tumor histopathological characteristics and location are independent factors that impact seizure burden. Further understanding of the mechanisms of tumor-associated epilepsy may lead to new types of treatments targeted at perilesional tissue alterations. Key WorDs • brain tumor • epilepsy • seizure • tumor-associated seizure • pathophysiology 1 Abbreviations used in this paper: BBB = blood-brain barrier; DNET = dysembryoplastic neuroepithelial tumor; FCD = focal cortical dysplasia; GABA = γ-aminobutyric acid; LEAT = long-term epilepsy-associated tumor; PBT = primary brain tumor.